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Acute Renal Failure Case Study

Our kidneys are incredible organs that get rid of toxins, retain substances needed by our bodies, and maintain the right balance of electrolytes, minerals, and water. Find out what happens to this 27-year-old when toxins accumulate in her kidneys leading to acute renal failure.

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Clinical pearls, case study: man with type 2 diabetes and stage 1 kidney disease on atkins-like diet.

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Deborah Thomas-Dobersen , Lynn Casey; Case Study: Man With Type 2 Diabetes and Stage 1 Kidney Disease on Atkins-Like Diet. Clin Diabetes 1 January 2005; 23 (1): 46–48. https://doi.org/10.2337/diaclin.23.1.46

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C.S. is a 45-year-old Hispanic man with a 10-year history of type 2 diabetes. He has a glycated hemoglobin of 7.0% and a blood pressure of 130/80 mmHg, treated with an angiotensin-converting enzyme inhibitor for the past 2 years. He has stable background retinopathy and is a nonsmoker. His BMI has been 30 (height 5′10″, weight 210 lb) for the past year. However,lately, he has put himself on the latest high-protein diet (i.e., the Atkins diet).

His weight has dropped by 10 lb, his fasting serum triglyceride level has fallen from 185 to 130 mg/dl, and his blood pressure has decreased to 120/78 mmHg. His LDL cholesterol has remained stable at 102 mg/dl on a statin. His serum creatinine is 0.9 mg/dl, and his 24-hour urine shows a significant increase in microalbumuria from 100 mg/24 hours last year to the current 200 mg/24 hours. He has stage 1 chronic kidney disease indicating kidney damage,with a normal glomerular filtration rate (GFR) of 98 ml/min/1.73 m 2 .

Would the weight reduction, blood pressure, and lipid-lowering accomplished by this high-protein, low-carbohydrate diet be an acceptable choice for a patient who is at significant risk of cardiovascular disease?

What are the recommendations of the American Heart Association (AHA), the National Kidney Foundation (NKF), the National Academy of Sciences, and the American Diabetes Association (ADA) regarding this type of diet for diabetes and/or weight loss?

What has research revealed about appropriate levels of macronutrients for patients such as C.S.?

It is likely that microalbuminuria is the start of a continuum progressing to macroalbuminuria and proteinuria. Microalbuminuria predicts renal disease in diabetes (both type 1 and type 2) and relates to premature mortality. Microalbuminuria is also a marker for pronounced diabetic vascular disease(endothelial dysfunction and chronic low-grade inflammation). Abnormal albuminuria is a major risk factor for cardiovascular complications,predicting increased cardiovascular morbidity and mortality. 1  

Twenty to thirty percent of patients with type 2 diabetes develop evidence of nephropathy. Some patients already have microalbuminuria or overt nephropathy upon diagnosis. Without intervention, 20-40% of those with microalbuminuria progress to overt nephropathy. For those on the continuum from overt nephropathy to end-stage renal disease (ESRD), the greater risk of death from coronary artery disease (CAD) may intervene. 2  

The average adult protein intake in the United States is 15-20% of total calories and has remained consistent from 1909 to the present. 3   Most Americans eat 50% more protein than they need. The Recommended Dietary Allowance (RDA) is 0.8 g of good quality protein per kilogram body weight per day for men and women. The high-protein Atkins and Zone diets recommend 125 g/day (36% kcal from protein) and 127 gm/day (34% kcal from protein),respectively. 4   The initial phases of the South Beach diet are similar, but no specific nutrient intake can be found in the diet's literature. In C.S., the Atkins diet would contribute 1.3 g protein/kg body weight and 36% of total daily calories from protein. Thus, high-protein diets promote a significantly abnormally high protein intake.

There is some evidence that a sustained high-protein diet can adversely affect renal function, especially in people with diabetes with or without mild renal insufficiency. In patients without renal insufficiency, a high-protein diet may act by acutely increasing the GFR and causing intraglomerular hypertension, which may cause progressive loss of renal function. In the Nurses Health Study, 1,624 female nurses between 30 and 55 years of age were followed for a period of > 11 years. The highest quartile of total protein intake, an average of 93 g/day, was significantly associated with a decline in GFR in women with mild renal insufficiency, thus worsening renal disease. 5   Previous studies had shown mixed results of high-protein diets on renal function but had limitations such as small patient numbers, limited follow-up, and a narrow range of protein intake.

Looking at this relationship from another angle, a meta-analysis recently showed that protein restriction retards the rate of decline in GFR, thus lessening kidney damage. The resulting decrease in kidney damage was small and not impressive. However, when studies looking at people with diabetes were combined, a total of 102 patients given a mean protein restriction of 0.7 g/kg/day versus a control group given 1 g/kg/day (a narrow range), showed a more impressive improvement in renal function independent of the original renal function over 22 months. 6   A crosssectional study of > 2,600 people with type 1 diabetes found that a protein intake > 20% of calories was associated with an increased urinary albumin excretion rate. Researchers concluded that people with diabetes should not exceed a protein intake of 20% of calories. 7   Any study in type 1 diabetes is applicable to type 2 diabetes as it relates to nephropathy. Therefore, there is evidence to recommend avoidance of high protein intakes in patients at risk for renal disease, i.e. all patients with type 1 or type 2 diabetes.

Nutrient analysis of high-protein diets is a concern. With some high-protein diets, such as Atkins, come carbohydrate restrictions. Yet high-carbohydrate foods, such as fruits, vegetables, and low-fat dairy products, provide potassium, magnesium, and calcium, which modestly reduce blood pressure. 8   Normal blood pressure is critically important in preventing CAD and microalbuminuria. With high-protein diets and carbohydrate restrictions come decreased-fiber diets. High-fiber diets have many beneficial effects,including weight loss and lower cardiovascular and cancer risks. With high-protein diets come higher intakes of saturated fats, which are potentially atherogenic. 9   In addition, experimental evidence indicates that a high-protein diet and the resultant increase in saturated fat intake may accelerate the progression of renal disease. Increased LDL cholesterol can stimulate mesangial hypertrophy and stimulate cytokine formation, which may ultimately cause tissue injury. In both type 1 and type 2 diabetes, hypercholesterolemia is a predictor of deteriorating kidney function. 10  

The RDA for carbohydrate is set at 130 g carbohydrate/day for adults and children based on the average minimum amount of glucose utilized by the brain to ensure optimal brain function. 11   That pretty much omits Atkins (28-33 g/day) and the early phases of the South Beach diet. Recent AHA guidelines discourage high-protein diets for weight loss,citing potential increased risk for coronary heart disease and renal disease. 12   The most recent ADA technical review on nutrition states that high-protein diets are not recommended until further research establishes their safety. 3   Concerns include renal function and cardiovascular disease. The NKF states in its Kidney Disease Outcomes Quality Initiative guidelines for chronic kidney disease that there is no benefit from a protein intake higher than the RDA of 0.8 g/kg body weight and that this is a reasonable level to recommend for patients with chronic kidney disease in stages 1-3. 13   Thus, many respected nonprofit health care organizations discourage the use of high-protein, low-carbohydrate diets.

Literature reviews of research on the effect of high-protein,low-carbohydrate diets on obesity and lipid levels are not convincing. A review of the literature describing adult outpatient recipients of low-carbohydrate, high-protein diets compared a wide variety of study designs,carbohydrate levels, durations, and calorie levels. Only five studies evaluated low-carbohydrate, high-protein diets for > 90 days, and these were nonrandomized, uncontrolled studies. The three variables that most predicted weight loss were calorie level, duration of calorie restriction, and number of very obese participants in the study. Reduced carbohydrate content was not significantly associated with weight loss. 14  

Another review concluded that populations at risk for renal disease, such as patients with diabetes, should avoid high-protein diets. The authors also caution that evidence suggested that protein intakes in excess of two to three times the RDA may have harmful effects on calcium homeostasis and possibly bone mass, 15   a problem for a population already predisposed to osteoporosis. In addition, a comparison of high-protein, low-carbohydrate diets versus a low-fat diet for weight loss shows them equally effective after 1 year in duration. 16   A recent small, randomized, clinical trial comparing a low-carbohydrate (< 30 g) to a conventional low-fat diet in severely obese patients, including individuals with diabetes, showed no significant difference in weight loss after 1 year, although weight loss was minimal (11 vs. 7 lb). Of interest was that the weight loss on the low-carbohydrate diet did not appear to be sustainable and that blood urea nitrogen levels increased more in the low-carbohydrate group. 17  

Reduced energy intake is an important therapeutic objective for the patient in the case described above. Reduced energy intake would reduce his blood pressure and serum lipids as well as improve his glycemic control. Weight loss was effective in lowering his blood pressure and serum triglycerides, as one would expect. However, the macronutrient content of his diet may have exacerbated the microalbuminuria. Therefore, a patient such as C.S. would be illadvised to stay on the high-protein diet because of the potential risk to his kidney function as shown by his elevated microalbuminuria.

With guidance from a registered dietitian, C.S. started a 1,500-kcal,low-fat diet with a walking program of 2 miles/day, 6 days/week. He was very tired of the restrictive nature of the high-protein diet and welcomed a change. His urine microalbumin level fell to < 50 mg/24 hours.

Two important studies show strategies that work to yield long-term weight loss. In order to determine what strategies work for long-term weight loss,the National Weight Control Registry elicited and studied information from> 800 people who have been successful in this endeavor. Only half had lost weight through weight loss programs. The remainder had lost weight without medical intervention. Keys to success were an average calorie intake of ∼1,400 kcal/day, a low-fat diet (24% of kcal), and a high energy expenditure through exercise (2,800 kcal/week). 18   The Diabetes Prevention Program also documented that a low-fat diet, increased physical activity, and educational sessions with frequent follow-up allowed participants to lose 7% of their body weight and maintain a 5% weight loss for 3 years. 19  

High protein intakes cause higher workloads for kidneys, whose function is to handle amino acid fragments during protein degradation and excrete nitrogen as urea.

There is no research documenting that a high-protein diet maintains weight reduction any better than a low-fat diet, which is safer and offers long-term results.

Safety and efficacy of high-protein, low-carbohydrate diets are a concern for patients with diabetes, regardless of documented kidney disease.

Additional Information

Concerns about the low-carbohydrate diet craze of 11 leading nonprofit consumer, nutrition, and public health organizations are discussed in a format appropriate for both health professionals and patients at the Partnership for Essential Nutrition website: www.essentialnutrition.org .

Deborah Thomas-Dobersen, RD, MS, CDE, is a diabetes educator at the Center for Diabetes and Endocrinology in Arvada, Colo. Lynn Casey, RD, CSR, is a renal dietitian at Renal Care Group, Inc., in Denver, Colo.

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• Case report
• Open access
• Published: 04 August 2009

A 60-year-old man with chronic renal failure and a costal mass: a case report and review of the literature

• Germán Campuzano-Zuluaga 1 ,
• William Velasco-Pérez 1 &
• Juan Ignacio Marín-Zuluaga 1  

Journal of Medical Case Reports volume  3 , Article number:  7285 ( 2009 ) Cite this article

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Introduction

Brown tumors are a rare focal manifestation of osteitis fibrosa cystica, which results from hyperparathyroidism. Chronic kidney failure may lead to secondary or tertiary hyperparathyroidism and thus to osteitis fibrosa cystica and brown tumors.

Case presentation

A 60-year-old man with a history of diabetes mellitus and chronic kidney failure presented with a 15-day history of dyspnea, cough, malaise and fever. Initially, there was little correlation between his history and his physical examination. Various pulmonary, cardiac and infectious etiologies were ruled out. A chest X-ray showed a costal mass that was further verified by tomography and gammagraphy. The mass was suspected of being neoplastic. After a failed biopsy, the mass was removed surgically and on histopathology was compatible with a giant-cell tumor versus a brown tumor caused by hyperparathyroidism. Laboratory tests showed elevated calcium, phosphate and parathyroid hormone concentrations. The patient was diagnosed with a brown tumor secondary to refractory hyperparathyroidism.

Tending towards a diagnosis because it is more frequent or it implies more risk for the patient may delay the consideration of other diagnostic options that, although rare, fit well into the clinical context. The patient presented here was suspected to have an osseous neoplasia that would have had major implications for the patient. However, reassessment of the case led to the diagnosis of a brown tumor. Brown tumors should be an important diagnostic consideration in patients with chronic kidney failure who have secondary or tertiary hyperparathyroidism and an osseous mass.

The first case in the literature reporting a brown tumor was published in 1953 and described a fronto-ethmoidal brown tumor [ 1 ]. However, previous reports of patients with localized forms of osteitis fibrosa cystica (OFC) suggest that the clinical entity was described earlier, at a time when there were few treatment options for chronic kidney failure (CKF) and consequently chronic hyperparathyroidism was more prevalent. Brown tumors are rare osseous lesions that represent a focal manifestation of OFC resulting from hyperparathyroid states. Patients suffering from CKF may develop secondary or tertiary hyperparathyroidism due to altered phosphorus and calcium metabolism. Persistent hyperparathyroidism leads to altered osseous metabolism with bone resorption and tissue changes collectively known as OFC. Our case report describes a patient with poorly controlled CKF who presented with a non-specific clinical picture and no clear diagnosis. Incidentally a costal mass was found and the diagnostic workup that followed led to an unexpected diagnosis.

A 60-year-old man was transferred from the hemodialysis unit to the emergency room because of a 15-day history of malaise, subjective fever, shortness of breath, dry cough, abdominal pain and diarrhea. He also complained of mild anterior thoracic pain not associated with other symptoms and which was not irradiated. He had a 20-year history of type 2 diabetes mellitus (DM) that required insulin, with micro- and macro-vascular complications such as diabetic retinopathy and CKF. He was on hemodialysis and had a history of multiple failed dialysis accesses. He also suffered from arterial hypertension, upper and lower extremity peripheral arterial disease, carotid artery disease, a first degree atrioventricular heart block and had smoked one packet of cigarettes per day for the last 20 years. He was being treated with sevelamer, erythropoietin, folic acid, lovastatin, gemfibrozil, NPH insulin, amlodipine and acetylsalicylic acid, but was not receiving calcium or a vitamin D supplement.

A physical examination revealed the patient to be in a fair condition, with no apparent distress, hydrated, alert and well oriented. He had a heart rate of 92 beats per minute, respiratory rate of 14 breaths per minute, blood oxygen saturation of 97%, arterial blood pressure of 130/70 mmHg and no fever. He had bilateral blindness and mild epistaxis through the left nostril. The thorax was tender to palpation in some costochondral unions, but pain was poorly localized. The vesicular murmur had reduced intensity and no pathologic sounds were auscultated. Peripheral pulses were weak in both the upper and the lower limbs. He had a translumbar hemodialysis catheter. The remaining physical examination was unremarkable.

The patient had stable vital signs and had no signs of systemic inflammatory response. However, because of the patient's previous history of DM, CKF and the presence of leukocytosis, neutrophilia and elevated C-reactive protein upon admission (Table 1 ), we initially ruled out a gastrointestinal or lung infection, or any cardiac cause for the patient's symptoms. The electrocardiogram showed no signs of ischemia, and the chest X-ray showed cardiomegaly, a small left pleural effusion, a circular opacity in the right inferior thoracic region and no signs of consolidation. These findings were initially interpreted as a pulmonary infection, probably a lung abscess, an abscedated nodule or pulmonary tuberculosis. A contrast tomography scan of the chest was ordered for further characterization. Though it showed no parenchymal compromise, a 4 × 1.3 cm lesion was observed on the right dorsal region of the eighth rib. The lesion showed thinning of cortical bone in some areas, preserved cortex and lacked periosteal reaction (Figure 1 ). The radiology staff considered a bone metastasis as a first diagnostic option, and a thoraco-abdomino-pelvic tomography scan was done in search for more lesions and a probable primary tumor. Additional hypodense lesions were observed, including one on the left lamina of L4, acetabulum, and head and neck of the right femur. There was no lymph-node or internal organ compromise. A Tc 99 m Medronate osseous gammagraphy reported a hypermetabolic focus compatible with a neoplastic lesion, concordant in size and location with the costal mass reported in the previous imaging studies. It also revealed generalized osseous compromise compatible with renal osteodystrophy and did not confirm the other lesions described on tomography. A tomography-guided biopsy specimen (Figure 1 ) was obtained, but histopathological analysis reported normal tissue components.

Tomographic image during guided biopsy procedure . Note the heterogeneous 4 × 1.3 cm mass (arrow), with preserved cortical bone and no periosteal reaction or other inflammatory signs. No cysts were identified.

Not being able to reach a clear diagnosis, a careful reassessment of the patient's clinical record led to considering the alternative diagnosis of renal osteodystrophy. This was supported by a history of poorly controlled CKF, elevated calcium (11.2 mg/dl) and phosphorus (5.3 mg/dl) concentrations, a phosphocalcic product of 59.36 mg 2 /dl 2 , and a bone gammagraphy that showed changes compatible with OFC. However, the possibility of neoplasia was still being considered so the mass was removed surgically. Histopathological studies reported an osseous tissue with spindles of fusiform cells in a storiform disposition with abundant multinucleated giant cells, some macrophages and some mononuclear cells. Scarce mitotic activity was observed, and there were no signs of malignancy (Figure 2 ). The pathologist concluded that the findings were compatible with a giant-cell tumor or a brown tumor, both histologically very similar [ 2 ]. Parathyroid hormone (PTH) concentration was 1377 pg/ml. These findings were compatible with refractory hyperparathyroidism, and a diagnosis of a brown tumor of hyperparathyroidism associated with CKF was reached.

Microscopic pathology of surgical specimen . Presence of various multinucleated giant cells (arrows) and spindle arranged cells. Hemosiderin deposits were not observed in the sample. Hematoxylin-eosin stain at 40 × magnification.

The patient continued ambulatory medical treatment with vitamin D, calcium and sevelamer. Two months after discharge, the parathyroid level was 1900 pg/ml and a Tc 99 m Sestamibi scan revealed hyperfunctioning glands despite aggressive pharmacological treatment. Serum calcium and phosphorus levels were within normal limits, 9.4 mg/dl and 3.4 mg/dl, respectively. At the time of writing, the patient was awaiting parathyroidectomy as definite treatment for tertiary hyperparathyroidism associated with severe renal osteodystrophy.

Brown tumors are unusual bone lesions that represent a localized manifestation of OFC induced by hyperparathyroidism, independent of its cause. Increased PTH levels and locally produced tumour necrosis factor α and interleukin 1 (IL-1) by marrow monocytes induce the proliferation and differentiation of pluripotent bone-marrow cells into osteoblasts. These cells produce granulocyte macrophage colony stimulating factor, IL-6, IL-11 and stem-cell factor that induce the migration and differentiation of monocytes into osteoclasts, increasing the number of the latter in the bone tissue. Enhanced activity of osteoclasts and osteoblasts leads to bone resorption and a reduction of bone mineral concentration with an increased proliferation of fibrous tissue and extracellular matrix [ 3 ]. Brown tumors develop in 3% to 4% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of patients with secondary causes of hyperparathyroidism [ 4 ]. However, around half of patients with CKF may develop OFC due to secondary hyperparathyroidism making brown tumors more frequent in these patients. Brown tumors have been reported in patients with primary hyperparathyroidism due to adenomas [ 5 ] and carcinomas [ 6 ] of the parathyroid gland; vitamin D deficiency due to lack of sunlight exposure [ 7 ] or due to intestinal malabsorption syndromes [ 8 ]; and secondary [ 9 ] or tertiary hyperthyroidism [ 10 ] in patients suffering CKF. Hyperphosphatemia with hypocalcemia caused by tubular damage and impaired vitamin D metabolism explains hyperparathyroidism in these patients.

Brown tumors are either mono- or polyostotic benign masses, painless and usually found incidentally. However, they may cause tissue damage to adjacent structures and compressive manifestations such as pain, neuropathies [ 11 ] and myelopathy [ 12 ]. The majority of cases report the maxilla and mandible as the main sites of occurrence [ 9 ]. Other common sites are the clavicles, scapula, pelvis and ribs; however, these lesions may appear in any osseous structure [ 7 ], including chondral tissue [ 13 ]. They are associated with an increased risk of fractures if localized in weight-bearing areas [ 14 ].

Brown tumors arise from foci of OFC and represent a reparative bone process rather than true neoplastic lesions, as there is no hyperplasia or clonal cell proliferation. Typical histopathology describes spindle cells or fibroblasts in areas of osseous lysis, multinucleated giant cells (probably osteoclasts), increased vascularization and accumulation of hemosiderin-laden macrophages, with micro-hemorrhages which confer a brownish appearance to the affected tissue. Cysts and areas of necrosis may be found [ 2 , 5 ]. Brown tumors are histologically similar to giant-cell tumors, giant-cell regenerative granulomas, cherubism and aneurismatic osseous cysts [ 2 , 4 ].

On X-ray imaging, brown tumors appear as lytic lesions with thinned cortical bone that may be fractured. Concurrent changes that suggest OFC such as osteopenia, a "salt-and-pepper" bone appearance, subperiosteal bone resorption and disappearance of the lamina dura around the roots of the teeth, may help differentiate it from other entities [ 4 ]. Tomographic imaging shows an osseous mass, with no cortical disruption, no periosteal reaction or inflammatory signs, a heterogeneous center and areas that suggest cysts [ 14 ]. Magnetic resonance imaging (MRI) shows variable intensities on T2-weighted images and intense enhancement on T1-weighted contrast MRI. MRI may be better for determining the presence of cysts or fluid filled levels; a finding that is very suggestive of a brown tumor [ 14 ]. Osseous gammagraphy is not indicated for the diagnosis of brown tumors; however, isolated hypermetabolic lesions or simultaneous hypercaptation of bone lesions and parathyroid adenomas, when done with Tc 99 m Sestamibi, have been described [ 15 ].

Although differential diagnoses for an isolated bone lesion are extensive, when confronted with a patient with CKF, an osseous mass and laboratory data that show increased levels of calcium, phosphate, phosphocalcic product as well as alkaline phosphatase, it is imperative to determine PTH levels to rule out hyperparathyroidism. Histopathological analysis of the osseous lesion is needed to confirm the diagnosis of a brown tumor. In the case presented here, parathyroid levels were not assessed earlier because another diagnosis, osseous neoplasia, was suspected which posed major prognostic value and risk for the patient. A parathyroid hormone measurement six months earlier reported 570 pg/ml; thus, it is probable that the pathological process evolved during this brief time.

Treatment of brown tumors relies on a definitive control of the underlying hyperparathyroid state. In a patient with CKF, this is achieved through the administration of phosphorus chelators, and calcium and vitamin D supplementation. In patients presenting with tertiary hyperparathyroidism, parathyroidectomy may be required. Osseous lesions usually cease to grow, then shrink and eventually ossify without further consequences for the patient. Surgery is required under certain circumstances, such as: 1) compressive neurologic symptoms over peripheral nerves, cauda equina or spinal medulla; 2) a significant anatomical deformity; 3) risk of a pathologic fracture; 4) when the symptoms or pain do not resolve despite adequate medical treatment and control of the hyperparathyroid state; and 5) when the biopsy does not yield a clear diagnosis, as with the present case [ 9 , 11 , 12 ].

The case presented here illustrates how brown tumors, though rare, should be considered in patients with CKF and an osseous mass. The initial clinical presentation of this patient, a history of DM with a non-compensated CKF and the laboratory studies suggested an infectious process. Retrospectively, these initial complaints and findings could be explained by the patient's renal condition with volume overload, severe anemia, hydro-electrolyte disturbances, as well as altered calcium and phosphate metabolism. Early diagnosis and proper management of CKF enable an optimal control of bone-mineral metabolism, thus decreasing the incidence of OFC and making brown tumors rare lesions. Nevertheless, when confronted with a patient with CKF and an osseous mass, a brown tumor caused by hyperparathyroidism should always be considered in the differential diagnosis.

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Abbreviations

chronic kidney failure

diabetes mellitus

interleukin 1

interleukin 6

interleukin 11

magnetic resonance imaging

osteitis fibrosa cystica

parathyroid hormone.

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Acknowledgements

We thank the following persons: the patient and his family for the information provided and their approval for the publication of this case; the medical staff at the Hospital Pablo Tobón Uribe, especially the Internal Medicine, Radiology, Surgery and Pathology Departments, and the Nephrology and Dialysis Unit; Dr. Victoria Eugenia Murillo for histopathological analysis, case discussion and photomicrography; Dr. John M. Lopera, Dr. Jorge H. Donado and Ana Isabel Toro for manuscript revision and editing.

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Department of Internal Medicine, Hospital Pablo Tobón Uribe, Calle 78B No. 69-240, Medellín, Colombia

Germán Campuzano-Zuluaga, William Velasco-Pérez & Juan Ignacio Marín-Zuluaga

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Correspondence to Germán Campuzano-Zuluaga .

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GCZ summarized and interpreted the patient's medical record and was part of the medical staff, did the literature review and wrote the manuscript. WV and JIMZ helped to interpret the patient's medical record, were part of the medical staff and helped to write and review the manuscript. JIMZ was the principal attending physician and responsible for most medical decisions and interpretations expressed in the article. All authors read and approved the final manuscript.

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Campuzano-Zuluaga, G., Velasco-Pérez, W. & Marín-Zuluaga, J.I. A 60-year-old man with chronic renal failure and a costal mass: a case report and review of the literature. J Med Case Reports 3 , 7285 (2009). https://doi.org/10.4076/1752-1947-3-7285

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Received : 23 December 2008

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DOI : https://doi.org/10.4076/1752-1947-3-7285

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• Hyperparathyroidism
• Parathyroid Adenoma
• Renal Osteodystrophy
• Brown Tumor

Journal of Medical Case Reports

ISSN: 1752-1947

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Decision coaching for people with kidney failure: A case study

Affiliations.

• 1 Department of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark.
• 2 Research Centre for Patient Involvement (ResCenPI), Aarhus University, Aarhus, Denmark.
• 3 Department of Public Health, Aarhus University, Aarhus, Denmark.
• 4 Leeds Unit of Complex Intervention Development (LUCID), Leeds Institute of Health Science, University of Leeds, Leeds, UK.
• 5 Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
• 6 Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark.
• 7 Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
• 8 Centre for Practice Changing Research, Ottawa Hospital Research Institute, Ottawa, Canada.
• 9 School of Nursing, University of Ottawa, Ottawa, Canada.
• PMID: 36734306
• DOI: 10.1111/jorc.12459

Background: Little is known about the usefulness of decision coaching for people with kidney failure facing decisions about end-of-life care.

Objectives: To investigate experiences of people with kidney failure who received decision coaching for end-of-life care decisions.

Design: We conducted a prospective case study bound by time (September to December 2021), location (one nephrology department), and guided by the Ottawa Decision Support Framework.

Participants: Adults with kidney failure facing end-of-life care decisions.

Measurements: A nurse trained in decision coaching screened for unmet decisional needs with the SURE test and provided decision coaching using the Ottawa Personal Decision Guide. Postcoaching, the participants were rescreened using the SURE test and interviewed to explore their experience with decision coaching. Change in SURE test findings was analysed descriptively and systematic text condensation was used for the analysis of interviews. Recorded decision coaching sessions underwent content analysis using the Decision Support Analysis Tool.

Results: Decision coaching was provided to four adults with kidney failure. Median pre-SURE test score was 2.5 (range 2-4) and posttest score was 3 (range 3-4), indicating a decrease in decisional needs. Participants described that decision coaching provided an overview of features of options to consider, identified remaining decisional needs for further discussion with relatives and health professionals and clarified next steps. Median Decision Support Analysis Tool score was 9 (range 8-9).

Conclusions: After decision coaching, results suggest that the participants experienced fewer decisional needs and seemed clearer about the next steps in the decision making process.

Keywords: chronic kidney disease; decision coaching; end-of-life care; health professionals; skills.

© 2023 The Authors. Journal of Renal Care published by John Wiley & Sons Ltd on behalf of European Dialysis & Transplant Nurses Association/European Renal Care Association.

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Chronic Kidney Disease (CKD) Case Study (45 min)

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Mr. Stinson is a 52-year-old male with a history of HTN, DM Type II, CKD, and CHF. He presented to the Emergency Department (ED) complaining of severe itching, nausea, and vomiting.  He appeared pale and is lethargic. He reported shortness of breath and the nurse notes crackles in his lungs. He has now been admitted to your unit.

What additional nursing assessments should be performed?

• Full set of vital signs
• Auscultate heart and lung sounds, as well as peripheral pulses
• Assess skin turgor and edema
• Assess the patient’s dialysis access site for functionality or bleeding

What diagnostic or lab tests would you expect the provider to order?

• Complete metabolic panel (electrolytes, renal function, etc.
• Complete blood count
• Possibly an ABG to assess for acidosis
• Possibly a BNP to assess volume overload and its effect on the heart

Upon further questioning, the patient reports he normally gets dialysis Monday, Wednesday, Friday, but that he skipped dialysis yesterday because he was “not feeling well”. He has +2 pitting edema in his legs. Vital signs are as follows:

HR 102 RR 24

BP 153/97 SpO 2 90%

The patient’s labs result and show the following:

BUN 62 mg/dL Na 134 mg/dL

Cr 3.9 mg/dL Ca 7.8 mg/dL

GFR 13 mL/min/m 2 Phos 5.0 mg/dL

K 6.3 mEq/L Mg 1.6 mg/dL

Gluc 224 mg/dL H/H 8.2 / 30%

pH 7.32 pCO 2 32 HCO 3 – 16

BNP 247 pg/mL

Interpret these lab results and explain their meaning.

• The BUN/Cr and GFR indicate the patient is definitely in kidney failure as his glomerulus is not filtering the blood like it should and the waste products are building up
• His electrolyte abnormalities (hyperkalemia, hyponatremia, hypocalcemia, hyperphosphatemia, and hypomagnesemia) are all indicative of kidney disease and acidosis. The kidneys would normally retain sodium and excrete potassium. In kidney failure, they do the opposite and potassium levels can get very high.
• He is in metabolic acidosis, likely because his kidneys are not able to retain the bicarb buffer like they normally would – this also contributes to the hyperkalemia. As the body tries to balance the H+ ions, it kicks K+ out into the bloodstream.
• His BNP is also elevated, indicating volume overload – this is probably caused both by the kidney failure and not getting dialysis and by the heart failure
• He is anemic – chronic anemia is common in chronic kidney disease patients due to the lack of erythropoietin.

What is going on with Mr. Stinson physiologically?

• Because of his CKD, Mr. Stinson requires dialysis to perform the normal functions of the kidneys, since his aren’t working. He likely felt sick because his potassium was elevated and because of the azotemia (toxins building up in his blood).
• He missed dialysis and therefore he is now even more volume overloaded and azotemic
• This will cause a risk to his heart and lungs because of the overload and the hyperkalemia

The nephrologist is consulted and determines that the patient needs hemodialysis. As soon as possible.  The charge nurse of the dialysis unit is working to create a bed for him and will call back as soon as one is available, hopefully within the hour.

What do you, the nurse, need to consider and assess for Mr. Stinson PRIOR to sending him to dialysis?

• ALWAYS hold antihypertensives before HD (obtain provider order)
• Hold any medications that may be dialyzed off as they will not have their therapeutic benefit (confirm with pharmacist and obtain provider order)
• May require potassium-lowering medications before dialysis if the wait is going to be too long – hyperkalemia can be deadly
• Determine if any medications should be held prior to HD
• Assess full set of vital signs
• Obtain a weight, preferably on a standing scale
• Assess heart and lung sounds, as well as skin/edema

Mr. Stinson goes to hemodialysis, where they are able to pull of 3 L of fluid. He tolerates the procedure well and returns to his room.  

What would you need to assess for Mr. Stinson AFTER he returns from Dialysis?

• Obtain a weight, preferable on a standing scale, to compare to the pre-HD weight. This helps determine how much fluid was pulled off (1 kg = 1 L)
• Obtain a full set of vital sign
• Re-draw a renal function panel as ordered to ensure electrolytes are not in a dangerous range (requires provider order)

What are some important patient education topics for Mr. Stinson before discharge?

• Importance of hemodialysis – he likely didn’t feel well because he NEEDED dialysis.
• Reasons to “skip” dialysis typically involve severe infections and fevers, in which case he should go the following day whenever possible or notify his nephrology team
• Should also reinforce teaching regarding nutrition – foods to avoid (high in potassium) and when to take medications with or without food (especially Phos-Lo and Calcium supplements)

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Nursing Case Studies

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Introduction

Case report, statement of ethics, disclosure statement, funding sources, author contributions, a case of acute kidney injury in a patient with renal hypouricemia without intense exercise.

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Daiki Aomura , Kosuke Sonoda , Makoto Harada , Koji Hashimoto , Yuji Kamijo; A Case of Acute Kidney Injury in a Patient with Renal Hypouricemia without Intense Exercise. Case Rep Nephrol Dial 12 May 2020; 10 (1): 26–34. https://doi.org/10.1159/000506673

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Exercise-induced acute kidney injury (EIAKI) frequently develops in patients with renal hypouricemia (RHUC). However, several cases of RHUC with acute kidney injury (AKI) but without intense exercise have been reported. We encountered a 15-year-old male with RHUC who experienced AKI. He reported no episodes of intense exercise and displayed no other representative risk factors of EIAKI, although a vasopressor had been administered for orthostatic dysregulation before AKI onset. His kidney dysfunction improved with discontinuation of the vasopressor and conservative treatment. Thus, AKI can develop in patients with RHUC in the absence of intense exercise, for which vasopressors may be a risk factor.

Exercise-induced acute kidney injury (EIAKI) is a major complication in patients with renal hypouricemia (RHUC). EIAKI usually develops after intense exercise, such as anaerobic exertion, and is not accompanied by rhabdomyolysis [ 1 ]. However, there are several case reports of patients experiencing EIAKI without intense exercise [ 2-4 ]. Although the pathomechanism and risk factors of EIAKI remain unclear, many reports suggest that an oxidation-reduction imbalance is associated with EIAKI onset [ 5 ]. We herein report a case of acute kidney injury (AKI) in a patient with RHUC in the absence of intense exercise, which may have been caused by an oral vasopressor.

A 15-year-old male complained of strong fatigue after intense exercise since childhood. He had no remarkable medical history apart from allergic rhinitis. After entering high school, he often felt unwell, especially in the morning, and frequently missed classes. He was diagnosed as having orthostatic dysregulation and prescribed amezinium metilsulfate 10 mg/day, but his symptoms persisted. Eight days after the start of treatment he was switched to etilefrine 5 mg/day. However, his fatigue progressively worsened. He was found vomiting and unresponsive after collapsing in the bathroom on the eighth night following the prescription change and taken to the hospital by his family. In the emergency room he exhibited mild consciousness disturbance (Glasgow Coma Scale: E4V4M6) and complained of right lower abdominal pain. Laboratory tests (blood and urine), whole-body computed tomography, and head magnetic resonance imaging did not indicate any abnormalities (serum creatinine level 1.0 mg/dL, uric acid level 7.2 mg/dL). His conscious state and abdominal pain were improved on the next day, but his blood pressure gradually increased from 100/60 to 180/80 mm Hg and his serum creatinine level rose from 1.0 to 5.5 mg/dL during 5 days of admission. He was then transferred to our institution for the treatment of AKI and severe hypertension.

At the time of admission to our hospital the patient was fully conscious and alert. His body temperature was 37.2°C, blood pressure was 161/98 mm Hg, heart rate was 83 beats/min, and respiratory rate was 17 breaths/min. His height was 174 cm and his body weight was 54 kg. Physical examination detected no signs of dehydration, rash, or other abnormalities of the neck, chest, abdomen, or extremities. He had been taking loratadine 10 mg/day for his allergic rhinitis for several months. Both loratadine and etilefrine had been discontinued upon admission to the previous hospital. There was no family history of kidney dysfunction, and he reported no episodes of intense exercise other than daily commuting by bicycle to school. No alcohol consumption, smoking, or illegal drug use were reported. His laboratory data at the time of transfer to our hospital are summarized in Table 1 . Urinalysis showed mild proteinuria (0.66 g/gCr) and elevation of the tubulointerstitial injury marker β2 microglobulin (1,498 μg/L). Hematuria was not observed. His serum level of uric acid was low at 3.2 mg/dL and his fractional excretion of uric acid was high at 49.7%. Laboratory markers of rhabdomyolysis, diabetes mellitus, infection, and collagen diseases such as creatine phosphokinase, hemoglobin A1c, C-reactive protein, and autoimmune antibodies were all within normal range. An electrocardiogram disclosed left anterior hemiblock and nonspecific intraventricular conduction delay that had been detected when he was an elementary school student. A chest X-ray revealed no abnormalities. Ultrasound echography showed bilateral mild kidney swelling with increased renal cortical echogenicity (Fig.  1 ). No stenotic lesions were detected in the aorta or renal arteries, although the resistance index of the intrarenal arteries was slightly high (left 0.69, right 0.69), indicating a circulatory disturbance in the renal microvessels. Hydronephrosis and renal calcification were absent. An ultrasound-guided kidney biopsy performed 3 days after arrival at our hospital showed mild interstitial edema, vascular endothelial cell swelling in the renal interlobular arterioles, and no obvious signs of acute tubular necrosis (ATN) (Fig.  2 ). Treatment with continuous intravenous infusion of extracellular fluids and nicardipine gradually improved his kidney function and hypertension. His serum uric acid level decreased to 1.0 mg/dL (Fig.  3 ), and his fractional excretion of uric acid was at 55.9% at 10 days after admission. He was ultimately diagnosed as having AKI with RHUC and discharged 12 days after transfer to our hospital. Hypouricemia was found in his parents and a sister, indicating a hereditary condition. However, genetic screening did not detect any known causative RHUC mutations on URAT1/SLC22A12 or GLUT9/SLC2A9 .

Main laboratory data on admission to our hospital

Renal ultrasound showed mild kidney swelling with increased renal cortical echogenicity. Hydronephrosis and renal calcification were not observed. Renal imaging findings were similar bilaterally (left 105 × 62 mm, right 115 × 63 mm).

Kidney biopsy specimen findings. Mild interstitial edema and vascular lumen narrowing by endothelial cell swelling (arrow) were detected (periodic acid-methenamine silver stain). No other abnormalities were found, including signs of acute tubular necrosis.

Clinical course of the present case. Vasopressors that had been administered for 15 days were discontinued on admission. After transfer to our hospital, his renal function improved gradually with continuous intravenous infusion of extracellular fluids and nicardipine. The serum uric acid level decreased steadily to 1.0 mg/dL during hospitalization.

Ishikawa et al. [ 6 ] first described EIAKI as AKI with accompanying abdominal or lower back pain after intense exercise, such as a 100-meter dash. EIAKI is differentiated from AKI with rhabdomyolysis by normal or slightly elevated serum myoglobin and creatine phosphokinase levels. EIAKI typically occurs in young males, with more than half having RHUC. Enhanced computed tomography often displays a wedge-shaped contrast defect in the kidneys. As for the clinical course of EIAKI, kidney dysfunction improves naturally without any special treatment [ 1, 7 ]. Although the reported patient had no intense episodes of exercise, EIAKI was diagnosed because he had RHUC, his kidney function recovered naturally, and he was young and male.

Blood pressure and serum creatinine level in our patient increased gradually following admission to the former hospital. As high blood pressure alone might cause AKI, we could not exclude the possible involvement of hypertension in AKI development. However, his serum creatinine level ultimately improved to 0.7 mg/dL after the final discharge despite having been 1.0 mg/dL on first admission, indicating that it had already been elevated by 0.3 mg/dL at the former hospital. Considering the fact that his blood pressure was normal on admission, AKI was thought to have developed before blood pressure elevation. Furthermore, his serum uric acid level was much higher on first admission (7.2 mg/dL) than at discharge (1.0 mg/dL), suggesting AKI onset prior to the former hospital visit. We suspected that AKI caused hypertension, which in turn worsened AKI. The elevation of blood pressure was assumed to be an exacerbation factor of EIAKI rather than its main cause.

The reported patient had no intense episodes of exercise. Lee et al. [ 3 ] described 17 AKI patients with abdominal or lower back pain who exhibited the characteristic patchy kidney sign on enhanced computed tomography. Among them, 5 patients reported no episodes of intense exercise. To the best of our knowledge, there have been 8 patients with EIAKI who did not have any episodes of intense exertion [ 2-4 ], with 5 experiencing infection or analgesic usage before EIAKI onset (Table 2 ), thought to be risk factors of EIAKI in addition to RHUC [ 3, 8, 9 ]. These reports support the notion that EIAKI can develop without intense exercise and the existence of risk factors other than strong exertion. However, to date no reports have focused on the relationship between lack of intense exercise and the etiology and development mechanism of EIAKI.

Clinical findings of current and previous reported cases of EIAKI without strenuous exercise

The pathomechanism of EIAKI is unclear, but renal circulatory disturbance by reactive oxygen species (ROS) is thought to be a main cause [ 5 ]. Intense exercise, such as anaerobic exertion, produces large amounts of ROS, which are rapidly removed by uric acid and other scavengers in the healthy population [ 8 ]. Patients with RHUC have insufficient scavengers, resulting in inadequate ROS removal and the subsequent activation of vasoconstrictive factors, vasoconstriction, and renal ischemia [ 2 ]. Since renal vasoconstriction is known to trigger further vasoconstriction and oxidative stress via activation of the renin-angiotensin system and blood pressure elevation [ 10 ], EIAKI patients are thought to show a vicious cycle between oxidative stress and vasoconstriction – oxidative stress causes stronger vasoconstriction and vasoconstriction causes more oxidative stress – culminating in acute and severe renal injury. In the present case, the patient had been taking vasopressors for orthostatic dysregulation for 15 days prior to the onset of AKI. Amezinium metilsulfate inhibits monoamine oxidase activity and suppresses the uptake of noradrenaline, while etilefrine activates type α1 and β1 adrenaline receptors. Thus, both vasopressors increased cardiac output and the constriction of peripheral vessels [ 11, 12 ]. Bellomo et al. [ 13 ] reported that activation of type α1 adrenaline receptors could cause excessive renal vasoconstriction and decreased renal blood flow in models of healthy renal hemodynamics. Radaković et al. [ 14 ] described that adrenaline induction increased ROS and caused a disruption in oxidant/antioxidant balance. Considering these results and the developmental mechanism of EIAKI (i.e., ROS and renal ischemia), we suspect that the vasopressors may have affected the onset or worsening of EIAKI by increasing ROS, exacerbating vasoconstriction, and forming a vicious cycle of diminished renal hemodynamics. Karasawa et al. [ 15 ] reported a case of EIAKI who was given midodrine, another vasopressor, before the onset of EIAKI, and Saito et al. [ 16 ] described that vasoexpansion by low-dose dopamine improved the resistance index of renal arterioles in 2 cases of EIAKI, implying the relation between vasopressors and EIAKI in clinical settings. Although no studies have directly addressed the relationship between vasopressors and EIAKI, past reports and our own results indicate an importance of catecholamine level homeostasis in the pathogenesis of EIAKI. We suspect that vasopressors may be associated with AKI onset in RHUC patients and may be a risk factor of EIAKI.

Renal biopsy showed no significant abnormalities in the present case. Although patients with EIAKI generally exhibit ATN, Ohta et al. [ 2 ] reported no abnormalities in 6 of 28 renal biopsies from EIAKI patients, which implied that EIAKI could develop without ATN. AKI with renal ischemia often causes ATN. However, tubular necrosis is sometimes absent without a sufficient degree or duration of ischemia, and early treatment for renal ischemia leads to a rapid improvement in renal function in such cases [ 17 ]. In the present patient, vasopressors, which might be a risk factor for EIAKI, were discontinued and intravenous antihypertensive medication was induced just after the first admission. The serum uric acid level was temporarily elevated on admission by AKI, and the patient’s scavenging ability with serum uric acid was thought to be temporarily improved. These factors could have mitigated the vicious cycle between renal vasoconstriction and oxidative stress, reduced the severity of renal ischemia, and prevented ATN development. However, as no studies have addressed the cause or meaning of a lack of ATN in some EIAKI patients, a greater number of studies are needed.

In conclusion, AKI can develop in patients with RHUC without intense exercise, possibly through the use of vasopressors. Further related case reports are needed to clarify the association between vasopressor use and AKI in patients with RHUC.

The present case report adhered to the Declaration of Helsinki. Informed consent for publication was obtained from the patient.

The authors declare no conflicts of interest.

The authors received no specific funding for this work.

D. Aomura drafted the article. K. Sonoda, M. Harada, and K. Hashimoto revised the article critically for important intellectual content. Y. Kamijo revised the article critically for important intellectual content and gave final approval of the version to be submitted.

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Case Report

Treatment of end-stage renal disease with continuous ambulatory peritoneal dialysis in rural guatemala, jillian moore.

1 Harvard Medical School, Boston, Massachusetts, USA

2 Wuqu' Kawoq, Santiago Sacatepéquez, Guatemala

Pablo Garcia

3 Department of Medicine, Saint Peter’s University Hospital, New Brunswick, New Jersey, USA

Peter Rohloff

4 Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA

David Flood

5 Departments of Medicine and Pediatrics, University of Minnesota, Minneapolis, Minnesota, USA

A 42-year-old indigenous Maya man presented to a non-profit clinic in rural Guatemala with signs, symptoms and laboratory values consistent with uncontrolled diabetes. Despite appropriate treatment, approximately 18 months after presentation, he was found to have irreversible end-stage renal disease (ESRD) of uncertain aetiology. He was referred to the national public nephrology clinic and subsequently initiated home-based continuous ambulatory peritoneal dialysis. With primary care provided by the non-profit clinic, his clinical status improved on dialysis, but socioeconomic and psychological challenges persisted for the patient and his family. This case shows how care for people with ESRD in low- and middle-income countries requires scaling up renal replacement therapy and ensuring access to primary care, mental healthcare and social work services.

Case presentation

A 42-year-old indigenous Maya man with a 6-year history of type 2 diabetes presented to a non-profit clinic in a rural agricultural town in Guatemala with weight loss, fatigue and weakness. Six years prior to presentation, he had been diagnosed with diabetes and later admitted to a regional hospital in a coma due to a hyperglycaemic crisis. After discharge from the hospital, the patient lost his job as a construction worker. As he could not afford antidiabetic medications or private physician fees, he abandoned outpatient treatment until being referred to the non-profit clinic.

On presentation, his examination was notable for cachexia, inability to ambulate and severe peripheral neuropathy. His weight was 32.7 kg with a body mass index of 14.5 kg/m 2 , and his blood pressure was 90/60 mm Hg. Random fingerstick blood glucose was over 600 mg/mL (normal <200 mg/mL), serum creatinine was 1.1 mg/dL (normal range 0.7–1.2 mg/dL) and urine albumin to creatinine ratio (ACR) was 40 mg/g (normal <30 mg/g). Haemoglobin A1c testing was not available. He had undergone bilateral cataract surgery approximately 2 years prior to presentation, and ophthalmologic evaluation at that time did not reveal retinopathy. The patient was started on insulin NPH. Following his initial presentation, the non-profit clinic procured point-of-care haemoglobin A1c testing, which resulted at 7.0% (normal range 3.9%–6.5%) 12 months after presentation. Repeat screening creatinine at this time was again normal.

Approximately 18 months after his initial presentation, the patient reported persistent difficulty gaining weight, as well as interval development of severe nausea and anorexia. An evaluation for failure to thrive was initiated at a higher-level laboratory in the regional capital. Results were notable for a serum creatinine of 7.57 mg/dL (glomerular filtration rate 8.5 mL/min/1.732) and blood urea nitrogen of 68.0 mg/dL (normal range 6.0–21 mg/dL), which were confirmed on repeat. Serum potassium, liver function tests, C reactive protein, thyrotropin, HIV, viral hepatitis antibodies, antinuclear antibodies, serum protein electrophoresis and urinalysis (with the exception of the presence of glycosuria) were normal. Haemoglobin was 7.3 mg/dL (normal range 12–16 mg/dL) with normal mean corpuscular volume. A renal ultrasound showed bilateral atrophic kidneys with increased echogenicity, two small non-obstructive echogenic foci suggestive of kidney stones and no significant hydronephrosis. Additional information obtained at this time confirmed that the patient had no known history of hypertension, urinary tract infections (UTIs), nephrolithiasis or exposure to nephrotoxic agents.

The patient was referred to the National Centre for Chronic Renal Disease (UNAERC), an institution in Guatemala City serving as the public nephrology centre. At UNAERC, the aetiology of his end-stage renal disease (ESRD) was not definitively elucidated, and a kidney biopsy was not pursued given the chronic and irreversible nature of his renal disease. Renal replacement therapy was recommended, and the patient was presented two options: twice-weekly haemodialysis at UNAERC, or continuous ambulatory peritoneal dialysis (CAPD) multiple times daily in his home. He chose CAPD, as limited mobility and finances precluded him from travelling to Guatemala City, a 3-hour bus trip each way. The patient initiated home CAPD after an abdominal catheter was placed and a sterile dialysis room was constructed in his home.

As of the writing of this case report, the patient has performed CAPD four times per day for 3 years. Clinically, he has improved considerably. He has more energy, can ambulate and has gained 10 kg. He has experienced no episodes of peritonitis. However, due to severe peripheral neuropathy and weakness, he must always be accompanied outside the home, sleeps with difficulty and requires assistance with most self-care activities in addition to his dialysis exchanges. He has not returned to work.

Socioeconomically and psychologically, the patient and his family have struggled. His wife cannot hold a regular job given her role as primary caregiver, and Guatemala does not have a national disability programme to support individuals who cannot work due to illness or injury. While UNAERC provides free clinical consultations and dialysis supplies, it does not cover other aspects of care including transportation, medications, nutritional supplements, primary care or emergency care. The patient and his family have subsided on donations from the non-profit clinic and their local church, as well as the meagre wages his wife earns weaving belts (US$33 monthly). The patient has four young children, and he worries constantly about the future. His chronic diseases have caused him to feel distress, helplessness and shame, yet he has not been formally evaluated for a mood or anxiety disorder given the lack of mental health practitioners in his rural town.

Global health problem list

• Many people in rural areas of low- and middle-income countries (LMICs) do not receive adequate primary healthcare due to poverty, geographic barriers and health system limitations. Underfunded rural public health systems struggle to prevent, detect and manage chronic diseases, including chronic kidney disease (CKD).
• Given obstacles to renal transplantation, dialysis is often the only feasible option for patients with ESRD in LMICs. Access to dialysis is limited in rural areas, and there is great need for community-based dialysis programmes.
• Debilitating illnesses like ESRD cause economic, social and psychological burdens for patients and their families in LMICs. Access to primary care, mental healthcare and social work services is important for these patients and their families.

Global health problem analysis

This case describes a patient who developed ESRD of uncertain aetiology and who now requires dialysis. This story is increasingly common in LMICs like Guatemala, as a rising prevalence of nephropathies of various causes confers an increasing burden of ESRD and an urgent need to expand access to renal replacement therapy. However, many public health systems do not have the resources or capacity to provide comprehensive care to patients with ESRD. Given the rising rates of renal disease in LMICs, it is essential to reflect on why patients develop CKD, what can be done to prevent this condition, and how to best care for patients when disease progresses to its end stage.

CKD in Guatemala

Guatemala is an LMIC in Central America with a population of 16 million people. While the epidemiology and risk factors for renal disease are not well understood in Guatemala, available evidence including from the Global Burden of Disease Study suggests that, as in other LMICs, the burden of CKD is significant and rising. 1 2 WHO estimates that renal failure mortality in Guatemala in 2007 was 24.7 per 100 000 people, one of the highest rates in the Americas. 3 In the Latin American region, diabetes has been identified as the leading cause of CKD requiring dialysis, and, as of 2013 in Guatemala, 30% of new patients requiring renal replacement therapy had diabetes. 4 Our organisation previously reported high rates of CKD in a rural diabetes cohort, 5 6 data which were consistent with evidence from Mexico showing a strong link between diabetes and renal cause of death. 7

For the patient in this case, the aetiology of CKD remains unknown, and a wide differential includes diabetic nephropathy, nephrotoxic exposure, chronic nephrolithiasis, chronic UTIs and other causes. The patient has a 6-year history of uncontrolled diabetes and has experienced diabetes complications such as hyperglycaemic crisis and severe peripheral neuropathy. However, he does not meet criteria for diabetic kidney disease given that he had no history of diabetic retinopathy, did not have severely increased albuminuria (previously known as macroalbuminuria, ACR >300 mg/g) and had a more rapid progression of renal disease than would typically be expected from diabetes alone. 8 He also did not have a history or laboratory evidence suggestive of other common causes of ESRD—including hypertension, UTIs or nephrotoxic ingestion. Although echogenic foci were found on renal ultrasound, the pattern was not consistent with nephrocalcinosis, and the presence of non-obstructing kidney stones without hydronephrosis in a patient denying a history of symptoms of renal colic makes chronic nephrolithiasis seem less likely as the primary aetiology for his CKD.

In recent decades, there has been an increasing incidence of renal disease of uncertain aetiology in Central America observed in male agricultural workers in coastal areas. This entity has been termed ‘CKD of non-traditional aetiology’ (CKDnT) and is a source of active research throughout the region. The Pan American Health Association (PAHO) recently released a report on CKDnT epidemiology, consensus case definitions and methods for surveillance. 9 In Guatemala, dialysis enrolment rates may be higher along the southwestern coast. 10 11 However, epidemiological studies using dialysis registries are susceptible to confounding as indigenous Maya people, like this patient, tend to live in highland rather than coastal towns and also face barriers to accessing dialysis. 12 The patient described in this case does not meet PAHO technical criteria for a ‘confirmed clinical case of CKDnT’ given the presence of diabetes with diabetic neuropathy. 9

Renal replacement therapy in rural Guatemala

Once a person develops ESRD, the only means of survival are through renal replacement therapy, which includes dialysis—haemodialysis or peritoneal dialysis—or renal transplantation. Like other nephrology-related medicines and technologies, renal replacement therapy is unequally distributed around the world. Millions of people die prematurely each year because they cannot access dialysis or transplantation, particularly in LMICs. 13 14 Even among those who can access renal replacement therapy, there are significant outcome disparities by socioeconomic status and geography. 13 15 16

Kidney transplantation confers survival and quality of life advantages over dialysis. 17 The first renal transplantation programme in Guatemala was launched in the 1980s in the Social Security health system. 18 In 2015, according to data from the National Nephrology Association, there were 117 total kidney transplantations: 68% were performed in the public sector, 15% of transplant recipients were children and 17% involved deceased-donor kidneys. 19 The overall renal transplantation rate in Guatemala in 2013 was 5.6%, which is lower than the overall rate in Latin America of 19.8%. 4 Barriers to expanding access to renal transplantation include limitations in public sector funding, lack of structured waiting lists, incomplete coverage of post-transplant immunosuppression therapy, opt-in organ donation laws and minimal health protection for living donors. 20

In Latin America, rates of dialysis are rising sharply, and haemodialysis is the modality of choice in 90% of cases. 4 Guatemala is unique in that more than half of dialysis patients undertake peritoneal dialysis, giving the country one of the highest per capita rates of peritoneal dialysis in the world. 21 The public nephrology centre, UNAERC, manages a dialysis caseload of approximately 4500 people, of which two-thirds use CAPD. 22 Advantages of CAPD over haemodialysis include allowing rural patients to undertake therapy in their homes, requiring less infrastructure or specialised staff and not depending on the availability of rationed machines. 23 Rural CAPD programmes have been reported in multiple LMICs. 24–26

Patients at UNAERC receive, free of charge, all supplies directly necessary for CAPD: expert nephrology consultation, catheter insertion and maintenance, dialysis solution and laboratory monitoring of dialysis function. Basic survival is the chief concern. Unfortunately, UNAERC is unable to fund treatment for many sequelae of ESRD such as anaemia, mineral bone disease, hypertension, metabolic acidosis or dyslipidaemia. Additionally, the rural public healthcare system is not adequately equipped to meet the considerable primary healthcare concerns of patients with ESRD, which may include insomnia, pruritus, diabetes, hypertension, neuropathy, diarrhoea, sexual dysfunction and depression.

Systemic barriers to primary care in rural Guatemala

The Guatemalan healthcare system is marked by extreme fragmentation, privatisation and inequity. 12 The rural public healthcare system was established following the 1996 Peace Accords, which formally ended a 36-year civil war. The system was designed primarily to deliver basic preventative services to mothers and children. 27 While the disease landscape has shifted considerably since 1996, with chronic conditions comprising an increasingly significant burden, the health system has not been reoriented to this new epidemiology. Overall, the public health system in Guatemala is persistently underfunded; as a per cent of GDP, the country has the lowest government spending on health in Central America. 28

Like the patient in this case report, over half of Guatemalans are indigenous Maya, a group that faces formidable socioeconomic, linguistic and geographic barriers to healthcare. 12 Indigenous populations have high rates of poverty, limited access to education and poor health as measured by a range of indicators including infant mortality, child malnutrition and access to prenatal care. 29 The most reliable data on health disparities between indigenous and non-indigenous people derive from reproductive health surveys, which generally suggest that such poorer health indicators in indigenous groups are not solely explained by poverty and rural residence. 29 There are limited studies on the prevalence and outcomes of diseases like diabetes, cancer or CKD in indigenous areas. Available data show that ethnic disparities exist in both paediatric and adult populations. 30–32

In theory, all Guatemalans can access primary healthcare either within the network of free clinics and hospitals operated by the Ministry of Health (MOH), through a system of employment-based insurance at designated facilities, or at military hospitals. However, in reality, only a small proportion of the population has public or private insurance, particularly in rural areas, and MOH healthcare is limited by resource constraints. For example, patients at MOH health centres may be sent to purchase basic medications or laboratory tests, and certain resources like insulin are typically only available at regional referral hospitals. With these shortcomings in the public health system, many Guatemalans seek care in the private sector. While private sector care is considered more responsive than care delivered at public health centres, private care is expensive and fragmented. In general, the poorest and most marginalised patients are unable to access regular primary care for chronic diseases like diabetes or CKD.

This case illustrates many of the major challenges in accessing chronic disease care for both diabetes and CKD in rural Guatemala. Prior to seeking care at the non-profit clinic, the patient had entered a sickness-poverty cycle due to uncontrolled diabetes: he became too sick to work, then too poor pay for quality healthcare and medications and consequently he became even sicker. On developing CKD, there was no coordination between the public nephrology clinic and his local health centre and no primary care infrastructure to manage his associated symptoms and conditions. His indigenous ethnicity may have also contributed to his poor diabetes control and difficulty accessing high-quality primary care services.

While strengthening the rural public health system would be the most powerful approach to improve primary care in rural Guatemala—and to thereby both prevent and manage chronic disease—in the current political and economic environment, it is difficult to imagine the government dramatically increasing public outlays for chronic disease care. Care coordination and intensive social work interventions are potential strategies to assist patients with ESRD and other complex care needs, and there are examples of such programmes in Guatemala. 30 31 33 34 However, scaling up such interventions would require massive philanthropic or public sector investments.

The patient in this case is fortunate to live in a country providing public dialysis services to impoverished patients with ESRD from rural areas. Nevertheless, although dialysis has prolonged his life, this therapy has not necessarily nurtured his quality of life. With a national kidney transplantation rate of less than 6%, 4 most Guatemalans with ESRD, like the patient in this case, have no reasonable hope for life beyond dialysis. We therefore should consider what makes life worth living for those able to successfully access dialysis in places like rural Guatemala.

Lived experiences of ESRD

The typical trajectory of ESRD resembles those of other organ failures: chronic, progressive debility interposed by episodes of acute decompensation, with death often sudden and unexpected. Like the patient in this report, people on dialysis can survive for years during which they may endure fatigue, weakness, pruritus, insomnia, pain, depression and functional impairment—in addition to the symptom burdens of comorbid conditions. These patients must adhere to a demanding dialysis regimen in order to live, yet they cannot be certain what their lives will entail or how long they will survive.

The patient in this case is a poor, indigenous man whose chronic illnesses have limited him from employment as a construction worker. He lives in Guatemala, a nation infused with legacies of colonialism, racism and oppression. Historically, indigenous people have been viewed by the state primarily as a resource from which to extract unpaid physical labour for the production of commodities and public works. 35 Today, while indigenous people in Guatemala have more rights than in previous generations, the indigenous poor still often sell their labour in the informal economy. Rural men, like this patient, learn to maintain strong bodies to augment their labour potential and their ability to provide for their families. Hence, conditions of poverty and marginalisation lead to chronic illness and impairment, and also cause chronic illness and impairment to be felt more severely. 36

Chronic diseases like ESRD often preclude patients from fulfilling expected roles and may result in altered social identities and self-concepts. 37 The patient in this report tearfully described feeling like ‘a little baby’ unable to provide for his family or carry out basic activities of daily living without assistance from his wife and children. Indeed, those facing illness and impairment may perceive a loss of status within their families and communities, especially when moral worth is tied to a masculinity grounded in strength, endurance and the ability support others—as is common for men in rural Guatemala. Patients on dialysis may also endure tedium—an emptiness of time—as their treatment regimen ‘threatens to overcome, and for some patients, to become the life it extends.’ 38 The patient in this report has found meaning and joy being with his children, singing and praying, but others may not be similarly incorporated into family and community life.

As described in this report, patients on dialysis face significant social and occupational limitations from their time-consuming yet life-supporting treatment. Given the rising number of patients on dialysis in Guatemala and elsewhere who will never receive a kidney transplant, ‘health-related quality of life’—how patients perceive illness and treatment to affect their physical, mental, spiritual, emotional, social and functional well-being—has become an important dialysis outcome measure. 39  Standardised instruments have not been validated in most LMICs, where the focus is more often on basic treatment provision and survival. 40 Nonetheless, for patients on dialysis, poor health-related quality of life, 41 discrepancies between expected and received social support 42 and depressive symptoms 43 have each been found to be associated with increased mortality.

As with other chronic conditions, the impacts of ESRD are not limited to a single patient but rather permeate households and communities. Patients who once earned wages to support their families can no longer work, requiring household roles to shift to replace lost incomes. Furthermore, chronic illnesses like ESRD entail direct costs for medical treatment and indirect costs such as the uncompensated labour of family members who provide caregiving. In countries like Guatemala without universal disability or health insurance programmes, those in poverty are exquisitely sensitive to out-of-pocket catastrophic health expenditures. 44 The patient in this case has successfully performed dialysis for multiple years, in part due to material support received from a local church, extended family and a non-governmental organisation. Other ESRD patients in poverty who lack such support are unlikely to successfully access and sustain dialysis in Guatemala.

In addition to providing resources and basic income, the families and communities of patients with ESRD must often provide intimate care, including feeding, bathing, grooming, dressing and toileting. Although gender roles are shifting, 45 46 in rural Guatemala, as in many cultures, there is a gendered division of labour in which women perform reproductive labour in the private sphere—including tending to the young, elderly and sick—and men perform productive labour in the public sphere. 47 For the man in this case, his wife provides him constant and intimate care, and also works to generate income to provide for their four children.

In summary, the rising rate of patients with ESRD in LMICs will require rapidly scaling up nephrology care and interventions like dialysis and renal transplant. As this case illustrates, comprehensive ESRD care also must include access to primary care, mental healthcare and social work services.

Patient’s perspective

• ‘My dream would be that my kidneys would work again, and that I could stop dialysis…One of the hardest things for us are trips to nephrology appointments in Guatemala City—getting up at 2:00 a.m., bringing my wheelchair, and the long bus rides…You have to have faith in God and a lot of patience with this disease. When I heard the news that my kidneys were failing, I felt that my life was over. It’s an incurable disease, and there isn’t any way for my kidneys to recover. The only option is dialysis, which I will have to do for the rest of my life. Sometimes, I feel like I just don’t want to do dialysis anymore. But when the time comes to do my exchanges, I confront those feelings and just keep going. Like I said, you have to have patience with this disease.’

Learning points

• Health systems in resource-limited countries may struggle to prevent, detect and manage chronic diseases like diabetes and chronic kidney disease.
• Worldwide, rising numbers of patients with end-stage renal disease (ESRD) require expansion of dialysis and renal transplantation, especially in rural areas.
• ESRD has significant impacts on the quality of life of patients and their families.
• Care for patients with ESRD requires meeting the comprehensive needs of these patients, including access to primary care, mental healthcare and social work services.

Contributors: JM and DF conceptualised the manuscript and wrote the first draft. DF and PR led clinical care of the patient. PR and PG critically revised the manuscript.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

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• Open access
• Published: 10 January 2022

Chronic kidney disease and its health-related factors: a case-control study

• Mousa Ghelichi-Ghojogh 1 ,
• Mohammad Fararouei 2 ,
• Mozhgan Seif 3 &
• Maryam Pakfetrat 4  

BMC Nephrology volume  23 , Article number:  24 ( 2022 ) Cite this article

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Chronic kidney disease (CKD) is a non-communicable disease that includes a range of different physiological disorders that are associated with abnormal renal function and progressive decline in glomerular filtration rate (GFR). This study aimed to investigate the associations of several behavioral and health-related factors with CKD in Iranian patients.

A hospital-based case-control study was conducted on 700 participants (350 cases and 350 controls). Logistic regression was applied to measure the association between the selected factors and CKD.

The mean age of cases and controls were 59.6 ± 12.4 and 58.9 ± 12.2 respectively ( p  = 0.827). The results of multiple logistic regression suggested that many factors including low birth weight (OR yes/no  = 4.07, 95%CI: 1.76–9.37, P  = 0.001), history of diabetes (OR yes/no  = 3.57, 95%CI: 2.36–5.40, P  = 0.001), history of kidney diseases (OR yes/no  = 3.35, 95%CI: 2.21–5.00, P  = 0.001) and history of chemotherapy (OR yes/no  = 2.18, 95%CI: 1.12–4.23, P  = 0.02) are associated with the risk of CKD.

Conclusions

The present study covered a large number of potential risk/ preventive factors altogether. The results highlighted the importance of collaborative monitoring of kidney function among patients with the above conditions.

Peer Review reports

Chronic kidney disease (CKD) is a non-communicable disease that includes a range of different physiological disorders that are associated with an abnormal renal function and progressive decline in glomerular filtration rate (GFR) [ 1 , 2 , 3 ]. Chronic kidney disease includes five stages of kidney damage, from mild kidney dysfunction to complete failure [ 4 ]. Generally, a person with stage 3 or 4 of CKD is considered as having moderate to severe kidney damage. Stage 3 is broken up into two levels of kidney damage: 3A) a level of GFR between 45 to 59 ml/min/1.73 m 2 , and 3B) a level of GFR between 30 and 44 ml/min/1.73 m 2 . In addition, GFR for stage 4 is 15–29 ml/min/1.73 m 2 [ 4 , 5 ]. It is reported that both the prevalence and burden of CKD are increasing worldwide, especially in developing countries [ 6 ]. The worldwide prevalence of CKD (all stages) is estimated to be between 8 to 16%, a figure that may indicate millions of deaths annually [ 7 ]. According to a meta-analysis, the prevalence of stage 3 to 5 CKD in South Africa, Senegal, and Congo is about 7.6%. In China, Taiwan, and Mongolia the rate of CKD is about 10.06% and in Japan, South Korea, and Oceania the rate is about 11.73%. In Europe the prevalence of CKD is about 11.86% [ 8 ], and finally, about 14.44% in the United States and Canada. The prevalence of CKD is estimated to be about 11.68% among the Iranian adult population and about 2.9% of Iranian women and 1.3% of Iranian men are expected to develop CKD annually [ 9 ]. Patients with stages 3 or 4 CKD are at much higher risk of progressing to either end-stage renal disease (ESRD) or death even prior to the development of ESRD [ 10 , 11 ].

In general, a large number of risk factors including age, sex, family history of kidney disease, primary kidney disease, urinary tract infections, cardiovascular disease, diabetes mellitus, and nephrotoxins (non-steroidal anti-inflammatory drugs, antibiotics) are known as predisposing and initiating factors of CKD [ 12 , 13 , 14 ]. However, the existing studies are suffering from a small sample size of individuals with kidney disease, particularly those with ESRD [ 15 ].

Despite the fact that the prevalence of CKD in the world, including Iran, is increasing, the factors associated with CKD are explored very little. The present case-control study aimed to investigate the association of several behavioral and health-related factors with CKD in the Iranian population.

Materials and methods

In this study, participants were selected among individuals who were registered or were visiting Faghihi and Motahari hospitals (two largest referral centers in the South of Iran located in Shiraz (the capital of Fars province). Cases and controls were frequency-matched by sex and age. The GFR values were calculated using the CKD-EPI formula [ 16 , 17 ].

Data collection

An interview-administered questionnaire and the participant’s medical records were used to obtain the required data. The questionnaire and interview procedure were designed, evaluated, and revised by three experts via conducting a pilot study including 50 cases and 50 controls. The reliability of the questionnaire was measured using the test-retest method (Cronbach’s alpha was 0.75). The interview was conducted by a trained public health‌ nurse at the time of visiting the clinics.

Avoiding concurrent conditions that their association may interpreted as reverse causation; the questionnaire was designed to define factors preceding at least a year before experiencing CKD first symptoms. Accordingly participants reported their social and demographic characteristics (age, sex, marital status, educational level, place of residency), history of chronic diseases (diabetes, cardiovascular diseases, hypertension, kidney diseases, family history of kidney diseases, autoimmune diseases and thyroid diseases [ 18 ]). Also history of other conditions namely (smoking, urinary tract infection (UTI), surgery due to illness or accident, low birth weight, burns, kidney pain (flank pain), chemotherapy, taking drugs for weight loss or obesity, taking non-steroidal anti-inflammatory drugs, and taking antibiotic) before their current condition was started. Many researchers reported recalling birth weight to be reliable for research purposes [ 19 ]. Moreover, we asked the participants to report their birth weight as a categorical variable (< 2500 g or low, 2500- < 3500 g or normal, and > 3500 g or overweight). Medical records of the participants were used to confirm/complete the reported data. In the case of contradiction between the self-reported and recorded data, we used the recorded information for our study.

Verbal informed consent was obtained from patients because the majority of the participants were illiterate. The study protocol was reviewed and approved by the ethical committee of Shiraz University of Medical Sciences (approval number: 1399.865).

Sample size

The sample size was calculated to detect an association‌ between the history of using antibiotics (one of our main study variables) and CKD as small as OR = 1.5 [ 20 ]. With an alpha value of 0.05 (2-sided) and a power of 80%, the required sample size was estimated as large as n  = 312 participants for each group.

Selection of cases

The selected clinics deliver medical care to patients from the southern part of the country. In this study, patients with CKD who were registered with the above centers from June to December 2020 were studied. A case was a patient with a GFR < 60 (ml/min/1.73 m 2 ) at least twice in 3 months. According to the latest version of the International Classification of Diseases (2010), Codes N18.3 and N18.4 are assigned to patients who have (GFR = 30–59 (ml/min/1.73 m 2 ) and GFR = 15–29 (ml/min/1.73 m 2 ) respectively [ 21 ]. In total, 350 patients who were diagnosed with CKD by a nephrologist during the study period.

Selection of the controls

We used hospital controls to avoid recall-bias. The control participants were selected from patients who were admitted to the general surgery (due to hernia, appendicitis, intestinal obstruction, hemorrhoids, and varicose veins), and orthopedic wards‌ from June to December 2020. Using the level of creatinine in the participants’ serum samples, GFR was calculated and the individuals with normal GFR (ml/min/1.73 m 2 ) GFR > 60) and those who reported no history of CKD were included ( n  = 350).

Inclusion criteria

Patients were included if they were ≥ 20 years old and had a definitive diagnosis of CKD by a nephrologist.

Exclusion criteria

Participants were excluded if they were critically ill, had acute kidney injury, those undergone renal transplantation, and those with cognitive impairment.

Statistical analysis

The Chi-square test was used to measure the unadjusted associations between categorical variables and CKD. Multiple logistic regression was applied to measure the adjusted associations for the study variables and CKD. The backward variable selection strategy was used to include variables in the regression model. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. All p -values were two-sided and the results were considered statistically significant at p  < 0.05. All analyses were conducted using Stata version 14.0 (Stata Corporation, College Station, TX, USA).

In total, 350 cases and 350 age and sex-matched controls were included in the analysis. The mean age of cases and controls were 59.6 ± 12.4 and 58.9 ± 12.2 respectively ( p  = 0.83). Overall, 208 patients (59.4%) and 200 controls (57.1%) were male ( p  = 0.54). Also, 149 patients (42.6%) and 133 controls (38.0%) were illiterate or had elementary education ( p  = 0.001). Most cases (96.9%) and controls (95.7%) were married ( p  = 0.42). The mean GFR for CKD and control groups were 38.6 ± 11.4 and 78.3 ± 10.2 (ml/min/1.73 m2) respectively.

Result of univariate analysis

Table  1 illustrates the unadjusted associations of demographic and health-related variables with CKD. Accordingly, significant (unadjusted) associations were found between the risk of CKD and several study variables including education, history of chronic diseases (diabetes, cardiovascular, hypertension, kidney diseases, autoimmune diseases, and hypothyroidism), family history of kidney diseases, smoking, UTI, surgery due to illness or accident, low birth weight, burns, kidney pain, chemotherapy, taking non-steroidal anti-inflammatory drugs, and taking antibiotics) ( P  < 0.05 for all).

Results of multivariable analysis

Table  2 illustrates the adjusted associations between the study variables and the risk of CKD. Most noticeably, low birth weight (OR yes/no  = 4.07, 95%CI: 1.76–9.37, P  = 0.001), history of surgery (OR yes/no  = 1.74, 95%CI: 1.18–2.54, P  = 0.004), family history of kidney diseases (OR yes/no  = 1.97, 95%CI: 1.20–3.23, P  = 0.007), and history of chemotherapy (OR yes/no  = 2.18, 95%CI: 1.12–4.23, P  = 0.02) were significantly associated with a higher risk of CKD. On the other hand, education (OR college/illiterate or primary  = 0.54, 95%CI: 0.31–0.92, P  = 0.025) was found to be inversely associated with CKD.

The results of the present study suggested that several variables including, education, history of diabetes, history of hypertension, history of kidney diseases or a family history of kidney diseases, history of surgery due to illness or accident, low birth weight, history of chemotherapy, history of taking non-steroidal anti-inflammatory drugs, and history of taking antibiotics may affect the risk of CKD.

In our study, the level of education was inversely associated with the risk of CKD. This finding is in accordance with the results of a study conducted by K Lambert et.al, who suggested that illiteracy or elementary education may raise the risk of CKD [ 22 ]. The fact that education level is associated with health literacy, may partly explain our results that lower education and inadequate health literacy in individuals with CKD is associated with worse health outcomes including poorer control of biochemical parameters, higher risk of cardiovascular diseases (CVDs); a higher rate of hospitalization, and a higher rate of infections [ 23 ].

In the current study, the history of diabetes was associated with a higher risk of CKD. This finding is consistent with the results of other studies on the same subject [ 20 , 21 , 24 , 25 , 26 , 27 ]. It is not surprising that people with diabetes have an increased risk of CKD as diabetes is an important detrimental factor for kidney functioning as approximately, 40% of patients with diabetes develop CKD [ 27 ].

The other variable that was associated with an increased risk of CKD was a history of hypertension. Our result is consistent with the results of several other studies [ 20 , 24 , 25 , 28 ]. It is reported that hypertension is both a cause and effect of CKD and accelerates the progression of the CKD to ESRD [ 29 ].

After controlling for other variables, a significant association was observed between family history of kidney diseases and risk of CKD. Published studies suggested the same pattern [ 24 ]. Inherited kidney diseases (IKDs) are considered as the foremost reasons for the initiation of CKD and are accounted for about 10–15% of kidney replacement therapies (KRT) in adults [ 30 ].

The importance of the history of surgery due to illness or accident in this study is rarely investigated by other researchers who reported the effect of surgery in patients with acute kidney injury (AKI), and major abdominal and cardiac surgeries [ 31 , 32 ] on the risk of CKD. Also, AKI is associated with an increased risk of CKD with progression in various clinical settings [ 33 , 34 , 35 ]. In a study by Mizota et.al, although most AKI cases recovered completely within 7 days after major abdominal surgery, they were at higher risk of 1-year mortality and chronic kidney disease compared to those without AKI [ 31 ].

The present study also showed that low birth weight is a significant risk factor for CKD. This finding is consistent with the results of some other studies. However, the results of very few studies on the association between birth weight and risk of CKD are controversial as some suggested a significant association [ 19 , 36 , 37 ] whereas others suggested otherwise [ 36 ]. This may be explained by the relatively smaller size and volume of kidneys in LBW infants compared to infants that are normally grown [ 38 ]. This can lead to long-term complications in adolescence and adulthood including hypertension, decreased glomerular filtration, albuminuria, and cardiovascular diseases. Eventually, these long-term complications can also cause CKD [ 39 ].

Another important result of the current study is the association between chemotherapy for treating cancers and the risk of CKD. According to a study on chemotherapy for testicular cancer by Inai et al., 1 year after chemotherapy 23% of the patients showed CKD [ 40 ]. Another study suggested that the prevalence of stage 3 CKD among patients with cancer was 12, and < 1% of patients had stage 4 CKD [ 41 , 42 ]. Other studies have shown an even higher prevalence of CKD among cancer patients. For instance, only 38.6% of patients with breast cancer, 38.9% of patients with lung cancer, 38.3% of patients with prostate cancer, 27.5% of patients with gynecologic cancer, and 27.2% of patients with colorectal cancer had a GFR ≥90 (ml/min/1.73 m 2 ) at the time of therapy initiation [ 43 , 44 ]. The overall prevalence of CKD ranges from 12 to 25% across many cancer patients [ 45 , 46 , 47 ]. These results clearly demonstrate that, when patients with cancer develop acute or chronic kidney disease, outcomes are inferior, and the promise of curative therapeutic regimens is lessened.

In our study, the history of taking nephrotoxic agents (antibiotics or NSAIDs drugs) was associated with a higher risk of CKD. Our result is following the results reported by other studies [ 48 , 49 ]. Common agents that are associated with AKI include NSAIDs are different drugs including antibiotics, iodinated contrast media, and chemotherapeutic drugs [ 50 ].

Strengths and limitations of our study

Our study used a reasonably large sample size. In addition, a considerably large number of study variables was included in the study. With a very high participation rate, trained nurses conducted the interviews with the case and control participants in the same setting. However, histories of exposures are prone to recall error (bias), a common issue in the case-control studies. It is to be mentioned that the method of selecting controls (hospital controls) should have reduced the risk of recall bias when reporting the required information. In addition, we used the participants’ medical records to complete/ confirm the reported data. Although the design of the present study was not able to confirm a causal association between the associated variables and CKD, the potential importance and modifiable nature of the associated factors makes the results potentially valuable and easily applicable in the prevention of CKD.

Given that, chemotherapy is an important risk factor for CKD, we suggest the imperative for collaborative care between oncologists and nephrologists in the early diagnosis and treatment of kidney diseases in patients with cancer. Training clinicians and patients are important to reduce the risk of nephrotoxicity. Electronic medical records can simultaneously be used to monitor prescription practices, responsiveness to alerts and prompts, the incidence of CKD, and detecting barriers to the effective implementation of preventive measures [ 51 ]. Routine follow-up and management of diabetic patients is also important for the prevention of CKD. We suggest a tight collaboration between endocrinologists and nephrologists to take care of diabetic patients with kidney problems. In addition, surgeons in major operations should refer patients, especially patients with AKI, to a nephrologist for proper care related to their kidney function. Treatment of hypertension is among the most important interventions to slow down the progression of CKD [ 12 ]. Moreover, all patients with newly diagnosed hypertension should be screened for CKD. We suggest all patients with diabetes have their GFR and urine albumin-to-creatinine ratio (UACR) checked annually. Finally, the aging population and obesity cause the absolute numbers of people with diabetes and kidney diseases to raise significantly. This will require a more integrated approach between dialectologists/nephrologists and the primary care teams (55).

Availability of data and materials

The datasets generated and/or analyzed during the current study are not publicly available due to their being the intellectual property of Shiraz University of Medical Sciences but are available from the corresponding author on reasonable request.

Abbreviations

• Chronic kidney disease

End-stage renal disease

Glomerular filtration rate

Renal replacement treatment

Urinary tract infection

Odds ratios

Confidence intervals

Hypertension

Acute kidney injury

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Acknowledgments

This paper is part of a thesis conducted by Mousa Ghelichi-Ghojogh, Ph.D. student of epidemiology, and a research project conducted at the Shiraz University of Medical sciences (99-01-04-22719). We would like to thank Dr. Bahram Shahryari and all nephrologists of Shiraz‌ University of medical sciences, interviewers, and CKD patients in Shiraz for their voluntary participation in the study and for providing data for the study.

Shiraz University of Medical Sciences financially supported this study. (Grant number: 99–01–04-22719).

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Candidate in Epidemiology, Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran

Mousa Ghelichi-Ghojogh

HIV/AIDS research center, School of Health, Shiraz University of Medical Sciences, P.O.Box: 71645-111, Shiraz, Iran

Mohammad Fararouei

Department of Epidemiology, School of Health, Shiraz University of Medical Sciences, Shiraz, Iran

Mozhgan Seif

Nephrologist, Shiraz Nephro-Urology Research Center, Department of Internal Medicine, Emergency Medicine Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

Maryam Pakfetrat

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Contributions

MGG: Conceptualization, Methodology, Statistical analysis, Investigation, and writing the draft of the manuscript. MP: were involved in methodology, writing the draft of the manuscript, and clinical consultation. MS: was involved in the methodology and statistical analysis. MF: was involved in conceptualization, methodology, supervision, writing, and reviewing the manuscript. The authors read and approved the final manuscript.

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Correspondence to Mohammad Fararouei .

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The study protocol was reviewed and approved by the ethical committee of Shiraz University of Medical Sciences (approval number: 1399.865). All methods were performed in accordance with the relevant guidelines and regulations of the Declaration of Helsinki. The participants were assured that their information is used for research purposes only. Because of the illiteracy of a considerable number of the patients, verbal informed consent was obtained from the participants. Using verbal informed consent was also granted by the ethical committee of Shiraz University of Medical Sciences.

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Ghelichi-Ghojogh, M., Fararouei, M., Seif, M. et al. Chronic kidney disease and its health-related factors: a case-control study. BMC Nephrol 23 , 24 (2022). https://doi.org/10.1186/s12882-021-02655-w

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Received : 14 August 2021

Accepted : 24 December 2021

Published : 10 January 2022

DOI : https://doi.org/10.1186/s12882-021-02655-w

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