Chronic Kidney Disease (Chronic Renal Failure)

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

The definition of chronic kidney disease (CKD) is based on the presence of kidney damage (ie albuminuria) or decreased kidney function (ie glomerular filtration rate (GFR) <60 ml/minute per 1·73 m²) for three months or more, irrespective of clinical diagnosis.[1] 

When symptoms are severe they can be treated only by dialysis and transplantation (end-stage renal disease). Kidney failure is defined as a GFR of less than 15 ml/minute per 1·73 m², or the need for treatment with dialysis or transplantation.[1]

Progression of CKD is defined as a decline in estimated glomerular filtration rate (eGFR) of > 5 ml/minute/1.73 m² within one year, or >10 ml/minute/1.73 m² within five years.[2] 

Until recently, the emphasis has been on patients needing dialysis or transplantation. It is now realised that less severe CKD is quite common, and monitoring in primary care will enable the minority of patients who go on to develop a more severe form to be detected at any earlier stage.[3] This is important because the earlier the intervention, the greater the impact.

  • A large primary care study (practice population 162,113) suggests an age standardised prevalence of stage 3-5 chronic kidney disease (CKD) of 8.5% (10.6% in females and 5.8% in males).[4]

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In developed countries, CKD is often associated with old age, diabetes, hypertension, obesity and cardiovascular disease (CVD).[1] 

Risk factors

Factors other than the underlying disease process that may cause progressive renal injury include the following:

  • Acute insults from nephrotoxins or decreased perfusion.
  • Proteinuria.
  • Increased renal ammonia formation with interstitial injury.
  • Hyperlipidaemia.
  • Hyperphosphataemia with calcium phosphate deposition.

Kidney function should be assessed by eGFR and CKD is classified on this basis:[2]

  • Stage 1: normal; eGFR >90 ml/minute/1.73 m2 with other evidence of chronic kidney damage (see below).
  • Stage 2: mild impairment; eGFR 60-89 ml/minute/1.73 m2 with other evidence of chronic kidney damage.
  • Stage 3a: moderate impairment; eGFR 45-59 ml/minute/1.73 m2.
  • Stage 3b: moderate impairment; eGFR 30-44 ml/minute/1.73 m2.
  • Stage 4: severe impairment; eGFR 15-29 ml/minute/1.73 m2.
  • Stage 5: established renal failure (ERF); eGFR less than 15 ml/minute/1.73 m2 or on dialysis.

Use the suffix (p) to denote the presence of proteinuria when staging CKD.

NB: patients with a GFR of >60 ml/minute/1.73 m2 without evidence of chronic kidney damage should NOT be considered to have CKD and do not necessarily need further investigation.

The other evidence of chronic kidney damage may be one of the following:

  • Persistent microalbuminuria.
  • Persistent proteinuria.
  • Persistent haematuria (after exclusion of other causes - eg, urological disease).
  • Structural abnormalities of the kidneys, demonstrated on ultrasound scanning or other radiological tests - eg, polycystic kidney disease, reflux nephropathy.
  • Biopsy-proven chronic glomerulonephritis.


  • it usually presents with nonspecific symptoms caused by renal failure, complications - eg, anaemia in chronic renal failure (CRF), and the underlying disease.
  • It may be discovered by chance following a routine blood or urine test.
  • Specific symptoms usually develop only in severe renal failure, and include anorexia, nausea, vomiting, fatigue, weakness, pruritus, lethargy, peripheral oedema, dyspnoea, insomnia, muscle cramps, pulmonary oedema, nocturia, polyuria and headache.
  • Sexual dysfunction is common.
  • Hiccups, pericarditis, coma and seizures are only seen in very severe renal failure.


  • The physical examination is often not very helpful but may reveal findings characteristic of the underlying cause (eg SLE, severe arteriosclerosis, hypertension) or complications of CRF (eg, anaemia, bleeding diathesis, pericarditis).
  • Signs of CKD include increased skin pigmentation or excoriation, pallor, hypertension, postural hypotension, peripheral oedema, left ventricular hypertrophy, peripheral vascular disease, pleural effusions, peripheral neuropathy and restless legs syndrome.

Patients who are at increased risk of developing CKD should be offered screening tests to detect CKD, which should include assessment of the eGFR as well as urinalysis. Offer people testing for CKD if they have any of the following risk factors:[2] 

  • Acute kidney injury (acute renal failure):
    • Making the distinction between AKI and CRF can be very difficult. A history of chronic symptoms of fatigue, weight loss, anorexia, nocturia, and pruritus all suggest CKD.
    • The history and examination will provide clues, but renal ultrasound will provide the most important information. Renal abnormalities on ultrasound, such as small kidneys in chronic glomerulonephritis or large cystic kidneys in adult polycystic kidney disease, will almost always be present in patients with CKD.
  • Acute on chronic renal failure: may have features indicating CKD but also features suggesting a cause of an acute deterioration of renal function - eg, infection.

Investigations are focused on assessment of renal function and therefore stage of CKD, identification of the underlying cause and assessment of complications of CKD.[1] 

  • Assessment of renal function:
    • Serum urea is a poor marker of renal function, because it varies significantly with hydration and diet, is not produced constantly and is reabsorbed by the kidney.
    • Serum creatinine also has significant limitations. The level can remain within the normal range despite the loss of over 50% of renal function.
    • A gold-standard measurement is an isotopic GFR, but this is expensive and not widely available.
    • For most purposes in primary care, the best assessment or screening tool is the eGFR.[5] - see separate article Assessing Renal Function and the Estimated Glomerular Filtration Rate Calculator. Most laboratories now provide an eGFR when requesting serum creatinine, which should be used in preference to calculator above.
  • Biochemistry:
    • Plasma glucose: to detect undiagnosed diabetes or assess control of diabetes.
    • Serum sodium: usually normal, but may be low.
    • Serum potassium: raised.
    • Serum bicarbonate: low.
    • Serum albumin: hypoalbuminaemia in patients who are nephrotic and/or malnourished (low levels at the start of dialysis are associated with a poor prognosis).
    • Serum calcium: may be normal, low or high.
    • Serum phosphate: usually high.
    • Serum alkaline phosphatase: raised when bone disease develops.
    • Serum parathyroid hormone: rises progressively with declining renal function.
    • Serum cholesterol and triglycerides: dyslipidaemia is common.
  • Haematology:
    • Normochromic normocytic anaemia; haemoglobin falls with progressive renal failure.
    • White cells and platelets are usually normal.
  • Serology:
    • Autoantibodies, particularly antinuclear antibodies, classical antineutrophil cytoplasmic antibodies (c-ANCA), protoplasmic-staining antineutrophil cytoplasmic antibodies (p-ANCA), antiglomerular basement membrane (anti-GBM) antibodies (very suggestive of underlying Goodpasture's syndrome) and serum complement.
    • Hepatitis serology: ensure not infected and vaccinate against hepatitis B.
    • HIV serology: performed before dialysis or transplantation.
  • Urine:
    • Urinalysis: dipstick proteinuria may suggest glomerular or tubulointerstitial disease. Urine sediment with red blood cells and red blood cell casts suggests proliferative glomerulonephritis.
    • Pyuria and/or white cell casts suggest interstitial nephritis (especially if eosinophils are present in the urine) or urinary tract infection (UTI).
    • Spot urine collection for total protein:creatinine ratio allows reliable estimation of total 24-hour urinary protein excretion. The degree of proteinuria correlates with the rate of progression of the underlying kidney disease and is the most reliable prognostic factor in CKD.
    • 24-hour urine collection for total protein and creatinine clearance. To detect and identify proteinuria, use urine albumin:creatinine ratio (ACR) in preference, as it has greater sensitivity than protein:creatinine ratio (PCR) for low levels of proteinuria. For quantification and monitoring of proteinuria, PCR can be used as an alternative. ACR is the recommended method for people with diabetes.
    • Patients in whom initial urinalysis reveals microscopic haematuria should have a urine culture performed to exclude a UTI. If a UTI is excluded, two further tests should be performed to confirm the presence of persistent microscopic haematuria.[6] 
    • Patients over 40 years of age with persistent non-visible/microscopic haematuria in the absence of significant proteinuria or a reduced GFR should be referred to a urology department for further investigation.[6] 
    • Serum and urine protein electrophoresis: to screen for a monoclonal protein possibly representing multiple myeloma.
  • ECG and echocardiography: to detect left ventricular hypertrophy and ischaemia, and to assess cardiac function.
  • Imaging of the renal tract:
    • Plain abdominal X-ray: may show radio-opaque stones or nephrocalcinosis.
    • Intravenous (IV) pyelogram: not often used because of potential for contrast nephropathy.
    • Renal ultrasound:
      • Small echogenic kidneys are seen in advanced renal failure.
      • Kidneys are usually initially large and then become normal in size in advanced diabetic nephropathy.
      • Structural abnormalities may be seen - eg, polycystic kidneys.
      • It is also used to screen for hydronephrosis caused by urinary tract obstruction, or involvement of the retroperitoneum with fibrosis, tumour or diffuse adenopathy.
    • Retrograde pyelogram: may be indicated if there is clinical suspicion of obstruction despite a negative ultrasound study finding.
    • Renal radionuclide scan:
      • Useful to screen for renal artery stenosis when performed with captopril administration but is unreliable for GFR of less than 30 ml/minute.
      • Also quantifies differential renal contribution to total GFR.
    • CT scan: to define renal masses and cysts, seen on ultrasound, better; this is the most sensitive test for identifying renal stones.
    • MRI:
      • For patients who require a CT scan but who cannot receive IV contrast.
      • Like CT scan and renal venography, it is reliable in the diagnosis of renal vein thrombosis.
      • Magnetic resonance angiography is also useful for diagnosis of renal artery stenosis, although renal arteriography remains the investigation of choice.
    • Micturating cystourethrogram: for diagnosis of vesicoureteric reflux.
  • Renal biopsy.

Take into account the individual's wishes and comorbidities when considering referral.

  • People with CKD in the following groups should normally be referred for specialist assessment:
    • Stage 4 and 5 CKD (with or without diabetes).
    • Higher levels of proteinuria (ACR ≥70 mg/mmol) unless known to be due to diabetes and already appropriately treated.
    • Proteinuria (ACR ≥30 mg/mmol) together with haematuria.
    • Rapidly declining eGFR (>5 ml/minute/1.73 m2 in one year, or >10 ml/minute/1.73 m2 within five years).
    • Hypertension that remains poorly controlled despite the use of at least four antihypertensive drugs at therapeutic doses.
    • People with, or suspected of having, rare or genetic causes of CKD.
    • Suspected renal artery stenosis.
  • People with CKD and renal outflow obstruction should normally be referred to urological services, unless urgent medical intervention is required.
  • Consider discussing management issues with a specialist in cases where it may not be necessary for the person with CKD to be seen by the specialist.
  • Once a referral has been made and a plan jointly agreed, consider routine follow-up at the person's GP surgery rather than in a specialist clinic and specify criteria for future referral or re-referral.
  • Doctors and patients can use Decision Aids together to help choose the best course of action to take.
  • Compare the options »

General issues[7]

  • Many patients equate kidney disease with renal dialysis. It is important to explain that CKD is a spectrum of disease. Mild CKD is common and rarely progresses to a more severe form later.
  • Explain eGFR and that this will need to be monitored on a regular basis to ensure that the condition is not deteriorating.
  • If relevant, discuss the link between hypertension and CKD and that maintaining tight blood pressure control can limit the damage to the kidneys.
  • Discuss the link between CKD and an increased risk of developing CVD.
  • Patients with diabetes mellitus and CKD should achieve good glycaemic control.
  • Review all prescribed medication regularly to ensure appropriate doses.
  • Avoidance of nephrotoxins - eg, IV radiocontrast agents, non-steroidal anti-inflammatory drugs (NSAIDs), aminoglycosides.
  • Immunise against influenza and pneumococcus.

In newly diagnosed with eGFR less than 60 ml/minute/1.73 m2

  • Review all previous measurements of serum creatinine to estimate GFR and assess the rate of deterioration.
  • Review all medication including over-the-counter drugs; particularly consider recent additions (eg, diuretics, NSAIDs, or any drug capable of causing interstitial nephritis, such as penicillins, cephalosporins, mesalazine).
  • Urinalysis: haematuria and proteinuria suggest glomerulonephritis, which may progress rapidly.
  • Clinical assessment: eg, look for sepsis, heart failure, hypovolaemia, palpable bladder.
  • Repeat serum creatinine measurement within five days to exclude rapid progression.
  • Check criteria for referral (above). If referral is not indicated, ensure entry into a chronic disease management register and programme.


  • The eGFR should be monitored regularly. The frequency will depend on the severity of kidney impairment.
  • Patients with CKD should have the level of proteinuria assessed at least annually.
  • Proteinuria should be assessed by measurement either of the protein:creatinine or albumin:creatinine ratio, ideally on an early-morning urine specimen.
  • Detection of an initial abnormal eGFR result should prompt clinical assessment and a repeat test within two weeks to assess the rate of change in GFR. If the GFR is stable, a further test should be performed after 90 days to confirm the diagnosis of CKD.
  • If the diagnosis of CKD is confirmed, at least three assessments of eGFR should be made over not less than 90 days, to evaluate the rate of change in GFR.
  • Detection of an initial level of proteinuria equivalent to <0.5 g/day of total protein (including levels compatible with microalbuminuria) should be confirmed with a repeat test performed on an early-morning urine specimen. For the diagnosis of microalbuminuria, two abnormal results from three specimens are required.

Cardiovascular disease prevention[8] 

  • See also separate article Prevention of Cardiovascular Disease.
  • Patients with CKD should have an annual formal assessment of their cardiovascular risk factors including lipid profile, BMI, exercise, alcohol and smoking habits, as well as a review of interventions to reduce cardiovascular risk.
  • Patients with CKD and dyslipidaemia should be treated in accordance with current guidance for the general population. Smoking status and action taken should be documented. Patients with CKD and a BMI of >30 kg/m2 should receive dietary advice to assist them in losing weight.
  • Statins should be considered for primary prevention in all CKD stages 1-4 and transplant patients with a 10-year risk of cardiovascular disease calculated as >20%. A total cholesterol of <4 mmol/L or a 25% reduction from baseline, or a fasting low-density lipoprotein (LDL)-cholesterol of <2 mmol/L or a 30% reduction from baseline, should be achieved, whichever is the greatest reduction in all patients.
  • Folic acid and B vitamin supplements should be offered to all renal patients considered nutritionally at risk from deficiency of folic acid or B vitamin deficiency. B12 levels and, serum and red cell folate should be above the lower limit of the reference range in all CKD patients. Red cell folate levels should be checked if MCV remains high despite normal or high serum folate. Serum folate levels and B12 should be checked six-monthly in CKD4/5 and three-monthly in dialysis patients, or more frequently if patients remain anaemic or deficient.
  • CKD patients with established CVD should be prescribed aspirin, an ACE inhibitor, a beta-blocker, and a statin unless contra-indicated. Aspirin is indicated for secondary prevention but not primary prevention of vascular disease in renal failure.
  • Patients on lipid-lowering drug treatment should have total cholesterol reduced by 25% or to below 4 mmol/L, or LDL-cholesterol to below 2 mmol/L, or reduced by 30%, whichever reductions are the greatest.

Blood pressure and hypertension[6] 

  • In patients with CKD, systolic blood pressure should be lowered to <140 mm Hg (target range 120-139 mmHg) and the diastolic blood pressure to <90 mm Hg for the majority.
  • For those with diabetes mellitus or proteinuria of 1 g/24 hours or greater, the systolic blood pressure should be lowered to <130 mm Hg (target range 120-129 mm Hg) and the diastolic blood pressure to <80 mm Hg unless the risks are considered to outweigh the potential benefits.
  • Antihypertensive therapy should be individualised and lowering the systolic blood pressure to <120 mm Hg should be avoided.
  • Angiotensin-converting ennzyme (ACE) inhibitor or angiotensin-II receptor antagonist (AIIRA) treatment should form part of the antihypertensive therapy of patients with CKD and urinary protein excretion of >0.5 g/day unless there is a specific contra-indication.
  • Patients with CKD and proteinuria >0.5 g/day should have their ACE inhibitor or AIIRA and other antihypertensive treatment escalated to achieve the lowest possible level of proteinuria.
  • Hypertension in dialysis patients: dialysis patients should be on a restricted sodium (<5 g/day) diet. Hypertension on dialysis should initially be managed by ultrafiltration.[8] 

Nutrition and physical exercise[9] 

  • All patients with stage 4-5 CKD should have the following parameters measured as a minimum in order to identify undernutrition:
    • Actual body weight (ABW) <85% of ideal body weight (IBW).
    • Reduction in oedema-free body weight (of 5% or more in three months or 10% or more in six months).
    • BMI <20 kg/m2.
  • Recommended daily energy intake: a prescribed energy intake of 30-35 kcal/kg IBW/day is recommended for all patients, depending upon age and physical activity.
  • Oral nutritional supplements should be used if oral intake is below the levels indicated above and food intake cannot be improved.
  • Enteral feeding via nasogastric (NG) tube or percutaneous endoscopic gastrostomy (PEG) may be required if nutrient intake is suboptimal despite oral supplements. Intradialytic parenteral nutrition (IDPN) or intraperitoneal amino acids may be considered for selected cases if tube feeding is declined or clinically inappropriate.
  • Anabolic agents such as androgens, growth hormone or IGF-1 are not indicated in the treatment of undernutrition in adults. Androgens and growth hormone have shown improvement in serum albumin levels and lean body mass but not mortality, and they have significant side-effects.
  • Minimum daily dietary protein intake: a prescribed protein intake of 0.75 g/kg IBW/day for patients with stage 4-5 CKD not on dialysis; 1.2 g/kg IBW/day for patients treated with dialysis.
  • Patients should receive dietary advice to restrict their sodium intake to <2.4 g/day (100 mmol/day or <6 g/day of salt).
  • Patients who develop hyperkalaemia or hyperphosphataemia should receive dietary advice to assist dietary restriction of potassium and phosphate.
  • Deficiencies of fat-soluble vitamins, trace elements and carnitine are prevalent in patients with chronic kidney disease but current evidence does not support preventative or therapeutic supplementation. However, supplementation of oral vitamin D (either cholecalciferol or ergocalciferol) may be beneficial.
  • Patients should receive advice to perform regular moderate exercise.

Mineral and bone disorders[10] 

  • Serum levels of calcium, phosphate, alkaline phosphatase, PTH and calcidiol (25(OH)D) should be monitored in patients with CKD stage 3-5, and patients on dialysis, with a frequency based on stage, rate of progression and whether specific therapies have been initiated.
  • It is recommended that therapeutic decisions should be based on trends, rather than a single laboratory value.
  • Serum calcium, adjusted for albumin concentration, in patients with CKD stage 3-5 not on dialysis should be kept within the normal reference range.
  • Dialysis patients: serum calcium, adjusted for albumin concentration, should be maintained within the normal reference range, measured before a 'short-gap' dialysis session in haemodialysis patients. Ideally, adjusted serum calcium should be maintained between 2.2 and 2.5 mmol/L, with avoidance of hypercalcaemic episodes.
  • Serum phosphate in patients with CKD stage 3-5 (not on dialysis): serum phosphate in patients with CKD stage 3b-5 should be maintained between 0.9 and 1.5 mmol/L.
  • Serum phosphate in dialysis patients (stage 5D): serum phosphate in dialysis patients, measured before a 'short-gap' dialysis session in haemodialysis patients, should be maintained between 1.1 and 1.7 mmol/L.
  • Serum PTH in patients with CKD 3b-5 (not on dialysis): treatment should be considered in patients with CKD stages 3b-5 not on dialysis therapy in whom serum PTH levels are progressively increasing and remain persistently higher than the upper reference limit for the assay, despite correction of modifiable factors.
  • Target range of serum PTH in patients on dialysis should be between 2 and 9 times the upper limit of normal for the assay used. Marked changes in PTH levels in either direction within this range should prompt an initiation or change in therapy to avoid progression to levels outside this range.

Renal replacement therapy

Renal replacement therapy includes haemodialysis, peritoneal dialysis, chronic ambulatory peritoneal dialysis and renal transplantation. See separate article Renal Replacement Therapy and Transplantation.

  • Anaemia: left ventricular hypertrophy, fatigue, impaired cognitive functioning.
  • Coagulopathy.
  • Hypertension: left ventricular hypertrophy, heart failure, stroke, CVD.
  • Calcium phosphate loading: cardiovascular and cerebrovascular disease, arthropathy, soft tissue calcification.
  • Renal osteodystrophy: disorders of calcium, phosphorus and bone, most commonly osteitis fibrosa cystica.
  • Bone changes of secondary hyperparathyroidism: bone pain and fractures.
  • Neurological: uraemic encephalopathy, neuropathy including peripheral neuropathy.
  • Dialysis amyloid: bone pain, arthropathy, carpal tunnel syndrome.
  • Fluid overload: pulmonary oedema, hypertension
  • Malnutrition: increased morbidity and mortality, infections, poor wound healing.
  • Glucose intolerance due to peripheral insulin resistance.
  • Water and electrolyte balance:
    • Patients with CKD pass normal volumes of urine. Precise restriction of fluid intake is only required for patients with oliguric end-stage renal failure. The usual recommendation is for a daily intake of daily urinary output plus 500 ml (for insensible losses).
    • Patients should avoid binge drinking and be vigilant in replacing extra fluid losses in hot weather and during episodes of diarrhoea or vomiting.
    • Severe acute volume overload may require high-dose loop diuretics or dialysis.
    • Dietary restriction to 60 mmol/day each of sodium and potassium is appropriate but compliance is greatly improved with sensible and flexible dietary advice.
    • Loop diuretics (with the addition of a thiazide diuretic if resistant) improve sodium balance and blood pressure.
    • Hyperkalaemia is treated with dialysis if the potassium level rises above 7 mmol/L. Otherwise, treatment is directed towards the cause - eg, excess fruit, chocolate or coffee, gastrointestinal haemorrhage, acidosis or tissue necrosis. Hyperkalaemia with the GFR still above 10 ml/min may be due to hyporeninaemic hypoaldosteronism in patients with diabetes, hypoadrenalism or as a result of treatment with ACE inhibitors.
  • Anaemia: See separate article Anaemia in Chronic Kidney Disease.
  • Acidosis:
    • Chronic acidosis aggravates hyperkalaemia, inhibits protein synthesis and accelerates calcium loss from bone.
    • Correction of metabolic acidosis: venous bicarbonate concentrations should be maintained above 22 mmol/L.[9] 
    • Treated with sodium bicarbonate as long as the patient can tolerate the increased sodium load, as additional sodium may cause fluid overload and worsen hypertension.
  • Mineral and bone disorders: see under Management Section above.
  • Malnutrition: see under Management Section above.
  • Nerological:[1] 
    • Signs of peripheral nervous system and CNS disorders include peripheral neuropathy, restless leg syndrome, sleep disorders, and cognitive impairment.
    • Retained toxins are thought to have a role in these disorders, and intensive dialysis is sometimes associated with amelioration.
    • No specific therapies have yet been developed for these neurological manifestations.

Early diagnosis, regular monitoring and early treatment can prevent development and slow disease progression, reduce complications and the risk of cardiovascular disease, and improve survival and quality of life.[1] 

  • Much of the damage caused by CKD occurs early, when interventions may be much more effective.
  • Rapidly progressive diseases can lead to kidney failure within months. However,  most diseases evolve over decades and some patients do not progress during many years of follow-up.[1] 
  • Patients on chronic dialysis have a high incidence of morbidity and mortality. Patients with end-stage renal disease (ESRD) who undergo renal transplantation survive longer than those on chronic dialysis.
  • CVD is the most common cause of death in patients with CKD. Cardiovascular mortality is doubled in patients with a GFR below 70 ml/minute.

Early diagnosis and good control of potential causes - eg, diabetes, hypertension and urinary tract obstruction.

Further reading & references

  1. Levey AS, Coresh J; Chronic kidney disease. Lancet. 2012 Jan 14;379(9811):165-80. Epub 2011 Aug 15.
  2. Chronic kidney disease; NICE Clinical Guideline (September 2008)
  3. Introducing eGFR - Promoting good CKD Management, Royal College of General Practitioners
  4. Stevens PE, O'Donoghue DJ, de Lusignan S, et al; Chronic kidney disease management in the United Kingdom: NEOERICA project Kidney Int. 2007 Jul;72(1):92-9. Epub 2007 Apr 18.
  5. About eGFR; UK CKD Guide, Renal Association, 2007
  6. Detection, Monitoring and Care of Patients with Chronic Kidney Disease; Renal Association (2011)
  7. Mitra PK, Tasker PR, Ell MS; Chronic kidney disease. BMJ. 2007 Jun 16;334(7606):1273.
  8. Cardiovascular Disease in Chronic Kidney Disease, Renal Association (2010)
  9. Nutrition in Chronic Kidney Disease, Renal Association (2010)
  10. Chronic Kidney Disease - Mineral and Bone Disorders, Renal Association (2010)

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Last Checked:
Document ID:
2422 (v25)