Chronic Kidney Disease

Chronic kidney disease (CKD) is a progressive syndrome in which the kidneys lose their ability to filter blood, concentrate urine, excrete wastes, and maintain electrolyte balance.[1] CKD is an important public health issue that consumes major global health care resources. Its worldwide prevalence is estimated at 11-13%.[2]

CKD is a major independent risk factor for cardiovascular mortality, with more severe forms being equivalent to existing coronary artery disease (CAD) in their ability to predict cardiovascular death. CAD is the most common cause of death in CKD patients; they are more likely to die from cardiovascular disease than they are to progress to end stage renal disease.[3]

The two most common contributors to CKD are diabetes and hypertension, collectively accounting for 7 out of every 10 new cases.[4] Less common causes include glomerulonephritis, renal cystic disease, congenital urologic disorders, urinary obstruction, multiple myeloma, amyloidosis, analgesic abuse, and atheroembolic disease.

CKD may occur quickly or may develop over years with few, if any, symptoms until residual renal function is no longer sufficient to maintain homeostasis. Presenting signs and symptoms can include anorexia, weakness, malaise, fatigue, pruritus, nausea, vomiting, and altered mental status. Other signs of CKD can include fluid retention, hypertension, anemia, and electrolyte disturbances. Severe renal dysfunction can present as uremia, a condition which often affects the central nervous system, causing decreased mental status and, in some patients, seizures. There is no specific level of renal dysfunction at which uremia occurs, but once present, it necessitates dialysis.[5]

Risk Factors

Older age.

Family history.

Urinary tract disorders that may increase the risk of kidney damage: urinary tract infections, urolithiasis, chronic urinary tract obstruction.

Systemic medical disorders that increase the risk of kidney damage: diabetes mellitus, hypertension, obesity, excessive alcohol use, autoimmune disorders (e.g., systemic lupus erythematosus), systemic infections (e.g., HIV, hepatitis C), and atherosclerosis.

Nephrotoxic medications (e.g., nonsteroidal anti-inflammatory drugs, radio-contrast dye, aminoglycoside antibiotics).

Tobacco smoking.


Initial diagnosis of CKD is made when the glomerular filtration rate (GFR) is noted to be lower than normal, often estimated via measurement of serum creatinine and other variables. Testing must be repeated, and renal function must be in a steady state over at least 3 months in order to determine that the renal disease is chronic, rather than just acutely changed.

Testing to determine the underlying etiology typically includes urinalysis with examination of sediment under microscope, renal imaging, and renal biopsy in cases of unclear etiology. Urinary protein excretion should be checked, either with spot urine-creatinine or with 24-hour collection. Excessive protein excretion is a sign of glomerular disease and/or overflow proteinuria.

Because the kidneys regulate electrolyte and acid-base balance, as well as the production of red blood cells via erythropoietin, CKD can lead to hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic acidosis, and anemia. Laboratory studies should include a complete metabolic panel and complete blood count, as well as vitamin D and intact parathyroid hormone levels.


The National Kidney Foundation has developed guidelines for classifying chronic kidney disease based on estimated glomerular filtration rate (eGFR).[6] There are several methods of calculating eGFR. Some are more accurate when predicting a lower GFR while others are better used for estimating GFR in patients without advanced renal disease.[7] The following stages are used to classify abnormal kidney function:

  • Stage 1: Normal eGFR ( > 90 mL/min/1.73 m2 for adults) with persistent albuminuria or structural abnormalities.
  • Stage 2: eGFR between 60-89 mL/min/1.73 m2 with persistent albuminuria or structural abnormalities.
  • Stage 3: eGFR between 30-59 mL/min/1.73 m2. (Sometimes divided into stages 3a & 3b.)
  • Stage 4: eGFR between 15-29 mL/min/1.73 m2.
  • Stage 5 (end-stage renal failure): eGFR < 15 mL/min/1.73 m2.

CKD incidence has been increasing since the 1980s, with the most growth seen in stage 3, according to the most recent United States Renal Data System study.[8] Prevalence increases with age. Studies have shown that more than half of patients over 80 years old have stage 3 CKD or higher.[9]


Treatment for CKD aims to slow disease progression and reduce cardiovascular mortality. It is important to address the underlying etiology and to treat associated conditions, such as anemia, hyperparathyroidism, hyperphosphatemia, hypertension, and acidosis. Decreased proteinuria is associated with reduced cardiovascular mortality.[10] Dialysis may be used to compensate for lost kidney function when appropriate. Patients should be assessed by a nephrologist for the possibility of renal transplant. In patients who continue to progress and a need for hemodialysis is anticipated, an arteriovenous fistula should be placed and given time to mature prior to being necessary. This is typically done while patients are in CKD stage 4.

Common indications for dialysis include development of uremia, fluid overload that is no longer responsive to diuretics, and severe electrolyte abnormalities. Care should be taken with elderly patients who have limited life expectancy, as dialysis can lead to a significant decline in functional status.[11]

Dyslipidemia should be assessed and, if present, treated.

In patients with diabetes mellitus or hypertension, aggressive blood glucose and blood pressure control can slow or even halt the decline in GFR. Angiotensin-converting enzyme (ACE) inhibitors may be especially helpful blood pressure medications for diabetic patients, because they are kidney-protective. In patients with diabetes without significant albuminuria, ACE inhibitors can prevent progression to diabetic kidney disease. The same may be true for angiotensin-receptor blockers (ARBs), although evidence is more limited.[12] ACE inhibitors can cause transient increases in serum potassium concentrations, so routine monitoring is essential and dietary potassium may need to be limited.[13]

Specific treatments for underlying disorders should be applied. In some cases, addressing the underlying etiology will slow or halt the loss of kidney function.

Sodium restriction and/or diuretics may be needed to combat fluid retention.[14]

Anemia is common in CKD patients due to the loss of renal erythropoietin production. It is important to investigate other causes of anemia. Supplemental iron should be used if iron deficiency is also present. Once iron stores are adequate, synthetic erythropoietin (EPO) may be used to reach a target hemoglobin of 10-11 g/dL. Some studies indicate that EPO administration does not improve mortality directly. However, since it does reduce the need for transfusions in CKD stages 3-5, mortality is improved as a result of fewer opportunities for transfusion-related side effects.[15]

Dietary phosphorus restriction should be the initial step to manage elevated phosphorous levels. As the disease progresses, the addition of phosphate binders may become necessary to keep phosphate values within a normal range as the kidney may no longer be excreting sufficient amounts. Phosphate is not removed sufficiently with dialysis.

Corrected calcium levels should be monitored, and if found to be low, may be supplemented as needed. Vitamin D levels should be assessed and are often low in CKD patients since the kidneys play a vital role in vitamin D synthesis. Supplements may be given only after phosphate levels are controlled since vitamin D increases phosphate reabsorption in the GI tract.[16]

Exercise can help patients with CKD. Resistance training reduces the catabolic effects of a low-protein diet (0.6 g/kg/day), whereas aerobic exercise may help control blood pressure and lipid levels.[17],[18]

Ultimately, dialysis or kidney transplantation will be necessary for patients who progress to end-stage kidney failure. Early referral to a nephrologist, no later than onset of CKD stage 4 or when the likelihood of renal replacement therapy within 1 year is 10-20%, has been shown to reduce mortality. Other circumstances that warrant early referral include sudden rapid change in eGFR, increased albuminuria, recurrent renal stones, or persistent electrolyte abnormalities.[1] While trying to preserve residual renal function, it is important to avoid nephrotoxic medications and provide renal dosing of essential medications when possible.

Nutritional Considerations

Diets commonly consumed in Western countries are important contributors to CKD and its progression. The Western eating pattern is high in calories, dietary acid and saturated fat from animal products, sodium, phosphorus, and refined sugars, and low in fruits, vegetables, legumes, and other foods high in fiber and antioxidants. Such Western diets contribute to hypertension, insulin resistance, and dyslipidemia that can lead to CKD. Patients with progressive CKD also commonly present with malnutrition, which calls for a meal plan high enough in calories to prevent excessive weight loss.[19] The right kind of diet, as described below, can help reduce progression of CKD, control blood pressure and cholesterol, and may prevent cardiovascular events. The following dietary factors are clinically significant in patients with CKD.

Loss of excess weight. Obesity is an independent risk factor for the development and progression of CKD. Both dietary and surgical interventions that promote loss of excess weight reduce proteinuria and blood pressure.[20] Other obesity-related diseases, including metabolic syndrome and nonalcoholic fatty liver disease, are also significantly associated with microalbuminuria, proteinuria, and an increased risk for CKD.[21],[22] However, among patients with established CKD, obesity is associated with greater survival (discussed below).[23]

Low intake of animal products. A large cross-sectional study found that individuals who follow a vegan diet are less likely to have CKD and less likely to experience proteinuria when compared with omnivores.[24] High dietary acid load is directly related to CKD progression, bone loss, and sarcopenia and is predictive of end-stage renal disease (ESRD) in patients with CKD.[25],[26] Diets rich in animal protein are acid-producing and have also been found to increase the risk for CKD progression and ESRD when compared with diets lower in acid load.[27] Animal products are a chief source of saturated fat in human diets, and saturated fat intake is linked to hyperalbuminuria, with a 33% greater risk in persons with the highest compared with lowest level of saturated fat intake.[28]

A higher dietary ratio of plant to animal protein has been associated with significantly reduced mortality in those CKD patients with lower eGFR values.[29] Perhaps surprisingly, individuals with CKD who reduce their protein intake may initially experience a decrease in eGFR as the body adapts to a lower protein intake and nitrogen burden; in the long term, though, decline in eGFR actually slows. Conversely, a high-protein intake causes hyperfiltration in the short term, with a concomitantly higher eGFR. In the long-term, high protein intake accelerates eGFR decline.[30] Several meta-analyses have shown the benefit of vegan, low-protein diets for reducing CKD progression and shown their ability to defer the need for dialysis by roughly 1 year. Vegan, low-protein diets have also resulted in reductions in secondary hyperparathyroidism, insulin resistance, hyperlipidemia, blood pressure, aldosterone, and endothelin.[31]

Sodium restriction. Evidence indicates that patients with CKD are more salt-sensitive than the general population, and higher sodium intakes are associated with a decline in eGFR.[32] The efficacy of drugs (e.g., ACE inhibitors) that reduce blood pressure and proteinuria is inhibited by higher sodium intakes.[33] A recent Cochrane Review concluded that reducing salt intake decreases proteinuria and blood pressure.[34]

Phosphorus restriction. Hyperphosphatemia is a well-known contributor to bone disease in patients with CKD and is an independent risk factor for mortality in patients with CKD stages 3 and 4.[35] Phosphate additives are especially concerning. Phosphates added as preservatives to both red and white meats may contribute 300-500 mg of phosphorus per day, 80% of which is absorbed in the GI tract; by comparison, absorption of naturally occurring phosphate from plant foods does not exceed 30-40%.[36] Patients with CKD are advised to limit dietary phosphorus to 800-1,000 mg/day and to avoid phosphorus-containing food additives, but these are found in high quantities when consuming processed foods (including prepared frozen foods, dry food mixes, packaged meats, bread and baked goods, soups, and yogurt), which can contribute an additional 700-800 mg of phosphorus per day.[37] Colas and certain other carbonated beverages are also high in readily absorbable, inorganic phosphate.[38]

Potassium restriction (advanced CKD). For those with advanced kidney dysfunction and high potassium levels, potassium may need to be restricted. Use of potassium-wasting vs. potassium-sparing diuretics should also be considered.[39] As potassium typically occurs in healthful foods such as fruits and vegetables, restriction should only be implemented when necessary and preferably under the supervision of a registered dietitian.

Fluid restriction. Medical status, blood pressure, edema, and issues with urine output may necessitate fluid restriction.[39]

Micronutrient status. Patients with CKD are at risk for deficiency of both vitamins and minerals, including B vitamins, vitamin K, magnesium, and selenium. This is due in part to decreased appetite and a decreased sense of smell and taste, leading to decreased food intake.[40] A substantial proportion of patients with CKD stages 4 and 5 have thiamine-insufficient or deficient status, and a low-protein diet increases the number of patients with biochemical indicators of riboflavin deficiency. Biochemical indications of pyridoxine (vitamin B6) deficiency have also been found, and a high percentage of CKD patients have been found to have vitamin K deficiency.[41]

Low intake of magnesium also poses problems for patients with CKD. Several studies have established hypomagnesemia as an independent predictor of kidney function decline, and as an independent predictor of future negative cardiovascular outcomes and mortality in CKD patients.[42] Low magnesium levels in CKD patients are closely linked with vascular changes, including increased intima-media thickness, arterial stiffness, and vascular calcification through increases in inflammation, oxidative stress, vasoconstriction, and hypertension.[43] Selenium is required for synthesis of plasma glutathione peroxidases (GSH-Px) that are synthesized in the kidney. Levels of both are significantly decreased in CKD patients, and supplemental selenium is required to increase GSH-Px in these patients.[44]

According to the Nutrition Care Manual from the Academy of Nutrition and Dietetics, dietary reference intakes should be supplied for B-complex vitamins and vitamin C in patients with CKD. These nutrients are typically found in renal multivitamin formulations. Calcium intakes should be monitored, especially in those with CKD stages 3 and 4, and should not exceed 2,000 mg per day. Iron status should also be monitored using serum ferritin and transferrin saturation, and iron should be supplemented if needed.[39],[45]

Vitamin D supplementation. According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, vitamin D supplementation is indicated when patients with CKD have levels less than 30 ng/mL. Vitamin D deficiency in CKD patients must be avoided in order to reduce a significantly greater risk for doubling of serum creatinine, ESRD, anemia, vascular calcification, cardiovascular events, cardiovascular mortality, and all-cause mortality.[46]

A diet high in fiber and low in saturated fat and cholesterol. Most individuals with chronic kidney disease die from cardiovascular causes before developing ESRD.[47] The dyslipidemia of CKD is characterized by elevated plasma triglycerides and VLDL cholesterol (VLDL-C) and reduced HDL cholesterol (HDL-C) concentrations, which, along with proteinuria, are improved by a vegetarian diet.[48],[49],[50] Another benefit of a vegetarian diet is a high intake of fruits and vegetables. These can lower net acid excretion by approximately a third, which is comparable to administration of 0.5 mEq/kg/day of sodium bicarbonate, an amount clinically used to buffer metabolic acidosis.[26] High fruit and vegetable intakes are also associated with a significant reduction in mortality in CKD patients when compared with low intakes.[51] Dietary and supplemental sources of fiber can also be helpful, and a recent systematic review and meta-analysis concluded that dietary fiber supplementation significantly reduces serum urea and creatinine.[52] High dietary fiber intake is associated with reduced mortality in patients with CKD.[53]

A high-calorie diet. Protein-energy wasting (PEW) is associated with poor clinical outcome and mortality in CKD and is multifactorial. Although reduced food intake due to anorexia and dietary restrictions are obvious contributors, other contributors also include uremia-induced alterations such as increased energy expenditure, persistent inflammation, and acidosis. Endocrine changes such as lower levels of testosterone and thyroid hormone; resistance to insulin, growth hormone (GH), and IGF-1; and elevated levels of glucocorticoids are also significant contributors.[54] Although correct implementation of protein-restricted diets does not induce protein-energy wasting, a relaxation in dietary restriction is warranted for patients with a significant degree of PEW.[26]

Avoiding star fruit. Several reports have noted the toxic effects of Averrhoa carambola in patients with both CKD and end-stage renal failure on dialysis. The primary symptoms are neurological and include hiccoughing, vomiting, asthenia, paresis, muscle twitching, insomnia, mental confusion, convulsion, and coma.[55] The outcome is fatal in some cases despite hemodialysis.[56] The cause is thought to be tubular obstruction by calcium oxalate crystals as well as apoptosis of renal tubular epithelial cells.[57]


Consultation with a nephrologist.

Low-protein diet (0.6-0.8 g/kg and dependent on residual kidney function); protein needs may be slightly higher if diabetic nephropathy is present.[39]

Low-sodium, high-fiber, low-saturated-fat, and low-cholesterol diet.

Possible restriction of potassium and phosphorus, dependent on patient’s CKD stage and laboratory values.

Medical nutrition therapy referral to a registered dietitian to determine appropriate energy, protein, and micronutrient requirements.

Exercise prescription.

Smoking cessation.

What to Tell the Family

CKD increases the risk for heart problems and further loss of kidney function. The family can help the patient make the dietary changes that will help preserve health. These include limiting sodium, restricting total and animal protein intake and following a high-fiber diet. If the patient smokes cigarettes, the family can help with the quitting process. Family members can also encourage regular exercise. All of these lifestyle changes are good for everyone involved.

When necessary, family members can also monitor medication use, to be sure that conditions such as high blood pressure and diabetes are well controlled.


  1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International website. Accessed January 18, 2023.
  2. Hill NR, Fatoba ST, Oke JL, et al. Global Prevalence of Chronic Kidney Disease - A Systematic Review and Meta-Analysis. PLoS ONE. 2016;11(7):e0158765.  [PMID:27383068]
  3. Briasoulis A, Bakris GL. Chronic kidney disease as a coronary artery disease risk equivalent. Curr Cardiol Rep. 2013;15(3):340.  [PMID:23338722]
  4. United States Renal Data System. 2016 USRDS annual data report: Epidemiology of kidney disease in the United States. Accessed January 18, 2023.
  5. Eriksen BO, Ingebretsen OC. The progression of chronic kidney disease: a 10-year population-based study of the effects of gender and age. Kidney Int. 2006;69(2):375-82.  [PMID:16408129]
  6. National Kidney Foundation. Frequently asked questions about GFR estimates. Accessed January 18, 2023.
  7. Matsushita K, Mahmoodi BK, Woodward M, et al. Comparison of risk prediction using the CKD-EPI equation and the MDRD study equation for estimated glomerular filtration rate. JAMA. 2012;307(18):1941-51.  [PMID:22570462]
  8. United States Renal Data System. 2014 USRDS Annual Data Report. Vol. 1 CKD. Chapter 1: CKD in the general population. Accessed January 18, 2023.
  9. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in the United States. JAMA. 2007;298(17):2038-47.  [PMID:17986697]
  10. Currie G, Delles C. Proteinuria and its relation to cardiovascular disease. Int J Nephrol Renovasc Dis. 2013;7:13-24.  [PMID:24379690]
  11. Kurella Tamura M, Covinsky KE, Chertow GM, et al. Functional status of elderly adults before and after initiation of dialysis. N Engl J Med. 2009;361(16):1539-47.  [PMID:19828531]
  12. Lv J, Perkovic V, Foote CV, et al. Antihypertensive agents for preventing diabetic kidney disease. Cochrane Database Syst Rev. 2012;12:CD004136.  [PMID:23235603]
  13. Hsu CY, Chertow GM. Elevations of serum phosphorus and potassium in mild to moderate chronic renal insufficiency. Nephrol Dial Transplant. 2002;17(8):1419-25.  [PMID:12147789]
  14. Krikken JA, Laverman GD, Navis G. Benefits of dietary sodium restriction in the management of chronic kidney disease. Curr Opin Nephrol Hypertens. 2009;18(6):531-8.  [PMID:19713840]
  15. Palmer SC, Saglimbene V, Craig JC, et al. Darbepoetin for the anaemia of chronic kidney disease. Cochrane Database Syst Rev. 2014;3:CD009297.  [PMID:24683046]
  16. Wetmore JB, Quarles LD. Calcimimetics or vitamin D analogs for suppressing parathyroid hormone in end-stage renal disease: time for a paradigm shift? Nat Clin Pract Nephrol. 2009;5(1):24-33.  [PMID:18957950]
  17. Castaneda C, Gordon PL, Uhlin KL, et al. Resistance training to counteract the catabolism of a low-protein diet in patients with chronic renal insufficiency. A randomized, controlled trial. Ann Intern Med. 2001;135(11):965-76.  [PMID:11730397]
  18. Johansen KL. Exercise and chronic kidney disease: current recommendations. Sports Med. 2005;35(6):485-99.  [PMID:15974634]
  19. Shoji T, Nishizawa Y. Chronic kidney disease as a metabolic syndrome with malnutrition--need for strict control of risk factors. Intern Med. 2005;44(3):179-87.  [PMID:15805704]
  20. Navaneethan SD, Yehnert H, Moustarah F, et al. Weight loss interventions in chronic kidney disease: a systematic review and meta-analysis. Clin J Am Soc Nephrol. 2009;4(10):1565-74.  [PMID:19808241]
  21. Musso G, Gambino R, Tabibian JH, et al. Association of non-alcoholic fatty liver disease with chronic kidney disease: a systematic review and meta-analysis. PLoS Med. 2014;11(7):e1001680.  [PMID:25050550]
  22. Thomas G, Sehgal AR, Kashyap SR, et al. Metabolic syndrome and kidney disease: a systematic review and meta-analysis. Clin J Am Soc Nephrol. 2011;6(10):2364-73.  [PMID:21852664]
  23. Kovesdy CP, Kopple JD, Kalantar-Zadeh K. Management of protein-energy wasting in non-dialysis-dependent chronic kidney disease: reconciling low protein intake with nutritional therapy. Am J Clin Nutr. 2013;97(6):1163-77.  [PMID:23636234]
  24. Liu HW, Tsai WH, Liu JS, et al. Association of Vegetarian Diet with Chronic Kidney Disease. Nutrients. 2019;11(2).  [PMID:30691237]
  25. Scialla JJ, Anderson CA. Dietary acid load: a novel nutritional target in chronic kidney disease? Adv Chronic Kidney Dis. 2013;20(2):141-9.  [PMID:23439373]
  26. Scialla JJ. The balance of the evidence on acid-base homeostasis and progression of chronic kidney disease. Kidney Int. 2015;88(1):9-11.  [PMID:26126088]
  27. Banerjee T, Liu Y, Crews DC. Dietary Patterns and CKD Progression. Blood Purif. 2016;41(1-3):117-22.  [PMID:26765365]
  28. Lin J, Judd S, Le A, et al. Associations of dietary fat with albuminuria and kidney dysfunction. Am J Clin Nutr. 2010;92(4):897-904.  [PMID:20702608]
  29. Chen X, Wei G, Jalili T, et al. The Associations of Plant Protein Intake With All-Cause Mortality in CKD. Am J Kidney Dis. 2016;67(3):423-30.  [PMID:26687923]
  30. Bankir L, Roussel R, Bouby N. Protein- and diabetes-induced glomerular hyperfiltration: role of glucagon, vasopressin, and urea. Am J Physiol Renal Physiol. 2015;309(1):F2-23.  [PMID:25925260]
  31. Thilly N. Low-protein diet in chronic kidney disease: from questions of effectiveness to those of feasibility. Nephrol Dial Transplant. 2013;28(9):2203-5.  [PMID:23787548]
  32. Lin J, Hu FB, Curhan GC. Associations of diet with albuminuria and kidney function decline. Clin J Am Soc Nephrol. 2010;5(5):836-43.  [PMID:20299364]
  33. McMahon EJ, Campbell KL, Mudge DW, et al. Achieving salt restriction in chronic kidney disease. Int J Nephrol. 2012;2012:720429.  [PMID:23320173]
  34. McMahon EJ, Campbell KL, Bauer JD, et al. Altered dietary salt intake for people with chronic kidney disease. Cochrane Database Syst Rev. 2015;2:CD010070.  [PMID:25691262]
  35. Martin KJ, González EA. Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat? Clin J Am Soc Nephrol. 2011;6(2):440-6.  [PMID:21292848]
  36. Chauveau P, Combe C, Fouque D, et al. Vegetarianism: advantages and drawbacks in patients with chronic kidney diseases. J Ren Nutr. 2013;23(6):399-405.  [PMID:24070587]
  37. León JB, Sullivan CM, Sehgal AR. The prevalence of phosphorus-containing food additives in top-selling foods in grocery stores. J Ren Nutr. 2013;23(4):265-270.e2.  [PMID:23402914]
  38. Wickham E. Phosphorus content in commonly consumed beverages. J Renal Nutr. 2014;24:e1-e4.
  39. Academy of Nutrition and Dietetics. Nutrition Care Manual. Chronic kidney disease (CKD) stage 1-5 non-dialysis: nutrition intervention. Accessed February 4, 2020.
  40. Clase CM, Ki V, Holden RM. Water-soluble vitamins in people with low glomerular filtration rate or on dialysis: a review. Semin Dial. 2013;26(5):546-67.  [PMID:23859229]
  41. Steiber AL, Kopple JD. Vitamin status and needs for people with stages 3-5 chronic kidney disease. J Ren Nutr. 2011;21(5):355-68.  [PMID:21439853]
  42. Floege J. Magnesium in CKD: more than a calcification inhibitor? J Nephrol. 2015;28(3):269-77.  [PMID:25227765]
  43. Galassi A, Cozzolino M. Magnesium: a renewed player of vascular ageing in diabetic CKD patients? Clin Kidney J. 2014;7(2):93-6.  [PMID:25852855]
  44. Zachara BA. Selenium and selenium-dependent antioxidants in chronic kidney disease. Adv Clin Chem. 2015;68:131-51.  [PMID:25858871]
  45. Swafford C. A current look at renal multivitamins. J Renal Nutr. 2001;21: e33-e42.
  46. Obi Y, Hamano T, Isaka Y. Prevalence and prognostic implications of vitamin D deficiency in chronic kidney disease. Dis Markers. 2015;2015:868961.  [PMID:25883412]
  47. Chan CM. Hyperlipidaemia in chronic kidney disease. Ann Acad Med Singap. 2005;34(1):31-5.  [PMID:15726217]
  48. Rahman M, Yang W, Akkina S, et al. Relation of serum lipids and lipoproteins with progression of CKD: The CRIC study. Clin J Am Soc Nephrol. 2014;9(7):1190-8.  [PMID:24832097]
  49. Azadbakht L, Shakerhosseini R, Atabak S, et al. Beneficiary effect of dietary soy protein on lowering plasma levels of lipid and improving kidney function in type II diabetes with nephropathy. Eur J Clin Nutr. 2003;57(10):1292-4.  [PMID:14506491]
  50. Jibani MM, Bloodworth LL, Foden E, et al. Predominantly vegetarian diet in patients with incipient and early clinical diabetic nephropathy: effects on albumin excretion rate and nutritional status. Diabet Med. 1991;8(10):949-53.  [PMID:1838047]
  51. Gutiérrez OM, Muntner P, Rizk DV, et al. Dietary patterns and risk of death and progression to ESRD in individuals with CKD: a cohort study. Am J Kidney Dis. 2014;64(2):204-13.  [PMID:24679894]
  52. Chiavaroli L, Mirrahimi A, Sievenpiper JL, et al. Dietary fiber effects in chronic kidney disease: a systematic review and meta-analysis of controlled feeding trials. Eur J Clin Nutr. 2015;69(7):761-8.  [PMID:25387901]
  53. Krishnamurthy VM, Wei G, Baird BC, et al. High dietary fiber intake is associated with decreased inflammation and all-cause mortality in patients with chronic kidney disease. Kidney Int. 2012;81(3):300-6.  [PMID:22012132]
  54. Carrero JJ, Stenvinkel P, Cuppari L, et al. Etiology of the protein-energy wasting syndrome in chronic kidney disease: a consensus statement from the International Society of Renal Nutrition and Metabolism (ISRNM). J Ren Nutr. 2013;23(2):77-90.  [PMID:23428357]
  55. Chen LL, Fang JT, Lin JL. Chronic renal disease patients with severe star fruit poisoning: hemoperfusion may be an effective alternative therapy. Clin Toxicol (Phila). 2005;43(3):197-9.  [PMID:15902795]
  56. Tse KC, Yip PS, Lam MF, et al. Star fruit intoxication in uraemic patients: case series and review of the literature. Int Med J. 2003;33:314-316.
  57. Abeysekera RA, Wijetunge S, Nanayakkara N, et al. Star fruit toxicity: a cause of both acute kidney injury and chronic kidney disease: a report of two cases. BMC Res Notes. 2015;8:796.  [PMID:26680759]
Last updated: February 3, 2023