Chronic Kidney Disease

Authored by , Reviewed by Dr Adrian Bonsall | Last edited | Meets Patient’s editorial guidelines

This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Chronic Kidney Disease article more useful, or one of our other health articles.

Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Synonym: chronic renal failure

Chronic kidney disease (CKD) describes abnormal kidney function and/or structure. There is evidence that treatment can prevent or delay the progression of CKD, reduce or prevent the development of complications, and reduce the risk of cardiovascular disease (CVD).[1]

The definition of 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.[2]

When symptoms are severe they can be treated only by dialysis and transplantation (end-stage kidney 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.[2]

Accelerated progression of CKD is defined as a sustained decrease in GFR of 25% or more and a change in GFR category within 12 months, or a sustained decrease in GFR of 15 ml/minute/1.73 m2 per year.[1]

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. This is important because the earlier the intervention, the greater the impact.

  • CKD is common, frequently unrecognised and often exists together with other conditions (such as CVD and diabetes).
  • The risk of developing CKD increases with age.
  • A large primary care study (practice population 162,113) suggests an age standardised prevalence of stage 3-5 CKD of 8.5% (10.6% in females and 5.8% in males).[3]

In developed countries, CKD is often associated with old age, diabetes, hypertension, obesity and CVD.[2]

  • Arteriopathic renal disease.
  • Hypertension.
  • Glomerulonephritis.
  • Diabetes.
  • Infective, obstructive and reflux nephropathies.
  • Family history of stage 5 CKD or hereditary kidney disease - eg, polycystic kidneys.
  • Hypercalcaemia.
  • Multisystem diseases with potential kidney involvement - eg, systemic lupus erythematosus (SLE).
  • Neoplasms.
  • Myeloma.

Risk factors

Risk factors include:[1]

Kidney function should be assessed using a combination of GFR and albumin:creatinine ratio (ACR) categories. Increased ACR and decreased GFR are associated with increased risk of adverse outcomes. Increased ACR and decreased GFR in combination multiply the risk of adverse outcomes.:[1]

  • 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.

CKD is usually asymptomatic and often unrecognised because there are no specific symptoms, and it is often not diagnosed, or diagnosed at an advanced stage.[1]


  • It may be discovered by chance following a routine blood or urine test.
  • Specific symptoms usually develop only in severe CKD, 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 CKD.


  • 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 CKD (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 urine ACR. Offer people testing for CKD if they have any of the following risk factors:[1]

  • AKI.
  • CVD (ischaemic heart disease, chronic heart failure, peripheral arterial disease or cerebral vascular disease).
  • Structural renal tract disease, recurrent renal calculi or prostatic hypertrophy.
  • Multisystem diseases with potential kidney involvement - eg, SLE.
  • Family history of end-stage kidney disease (Stage 5 CKD) or hereditary kidney disease.
  • Opportunistic detection of haematuria.

Acute kidney injury (AKI)

  • Making the distinction between AKI and CKD 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 kidney disease

Acute on chronic kidney disease 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.[2]

  • 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 - see separate Assessing Renal Function article. Most laboratories now provide an eGFR when requesting serum creatinine, which should be used in preference to the 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 CKD.
    • 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 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.[4]
    • 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.[4]
    • 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 CKD.
      • 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.
    • Offer a renal ultrasound scan to all people with CKD who:[1]
      • Have accelerated progression of CKD.
      • Have visible or persistent invisible haematuria.
      • Have symptoms of urinary tract obstruction.
      • Have a family history of polycystic kidney disease and are aged over 20 years.
      • Have a GFR of less than 30 ml/minute/1.73 m2.
      • Are considered by a nephrologist to require a renal biopsy.
    • 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:
    • GFR less than 30 ml/minute/1.73 m2, with or without diabetes.
    • ACR 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated.
    • ACR 30 mg/mmol or more, together with haematuria.
    • Sustained decrease in GFR of 25% or more, and a change in GFR category or sustained decrease in GFR of 15 ml/minute/1.73 m2 or more within 12 months.
    • Hypertension that remains poorly controlled despite the use of at least four antihypertensive drugs at therapeutic doses.
    • Known or suspected 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.

General issues[5]

  • 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.
  • Encourage people with CKD to take exercise, achieve a healthy weight and stop smoking.[1]
  • 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, NSAIDs, aminoglycosides.
  • Immunise against influenza and pneumococcus.

In those 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 PCR or ACR, 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.

CVD prevention[6]

  • See also the separate article on 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.
  • Statins:
    • Statins lower death and major cardiovascular events by 20% in people with CKD not requiring dialysis.[7]
    • Offer atorvastatin 20 mg for the primary or secondary prevention of CVD to people with CKD. Increase the dose if a greater than 40% reduction in non-HDL cholesterol is not achieved and eGFR is 30 ml/minute/1.73 m2 or more. Agree the use of higher doses with a renal specialist if eGFR is less than 30 ml/minute/1.73 m2.[8]
  • Folic acid and B vitamin supplements should be offered to all renal patients considered nutritionally at risk from deficiency of folic acid or vitamin B. 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.
  • Oral antiplatelets and anticoagulants:[1]
    • Offer antiplatelet drugs to people with CKD for the secondary prevention of CVD, but be aware of the increased risk of bleeding.
    • Consider apixaban in preference to warfarin in people with a confirmed eGFR of 30-50 ml/minute/1.73 m2 and non-valvular atrial fibrillation who have one or more of the following risk factors: prior stroke or transient ischaemic attack, age 75 years or older, hypertension, diabetes mellitus, symptomatic heart failure.

Blood pressure control[1]

  • Aim to keep the systolic blood pressure below 140 mm Hg (target range 120-139 mm Hg) and the diastolic blood pressure below 90 mm Hg.
  • In people with CKD and diabetes, and also in people with an ACR of 70 mg/mmol or more, aim to keep the systolic blood pressure below 130 mm Hg (target range 120-129 mm Hg) and the diastolic blood pressure below 80 mm Hg.
  • A low-cost renin angiotensin system antagonist - eg, angiotensin-converting enzyme (ACE) inhibitor or angiotensin-II receptor antagonist (AIIRA) should be used for people with CKD and:
    • Diabetes and an ACR of 3 mg/mmol or more.
    • Hypertension and an ACR of 30 mg/mmol or more.
    • An ACR of 70 mg/mmol or more (irrespective of hypertension or cardiovascular disease).
    • A combination of renin-angiotensin system antagonists should not be offered to people with CKD.
  • The National Institute for Health and Care Excellence (NICE) hypertension recommendations (see the separate article on Management of Hypertension) should be used for people with CKD, hypertension and an ACR of less than 30 mg/mmol if they do not have diabetes.
  • In people with CKD, measure serum potassium concentrations and estimate the GFR before starting renin-angiotensin system antagonists. Repeat these measurements between one and two weeks after starting renin-angiotensin system antagonists and after each dose increase.
  • Do not routinely offer a renin-angiotensin system antagonist to people with CKD if their pre-treatment serum potassium concentration is greater than 5.0 mmol/L. Stop renin-angiotensin system antagonists if the serum potassium concentration increases to 6.0 mmol/L or more and other drugs known to promote hyperkalaemia have been discontinued.
  • 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.[6]

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 CKD but current evidence does not support preventative or therapeutic supplementation. However, supplementation of oral vitamin D (either colecalciferol or ergocalciferol) may be beneficial.
  • Patients should receive advice to perform regular moderate exercise.
  • It is recommended that therapeutic decisions should be based on trends, rather than a single laboratory value.
  • Do not routinely measure calcium, phosphate, parathyroid hormone (PTH) and vitamin D levels in people with a GFR of 30 ml/minute/1.73 m2 or more. 
  • Measure serum calcium, phosphate and PTH concentrations in people with a GFR of less than 30 ml/minute/1.73 m2. Determine the subsequent frequency of testing by the measured values and the clinical circumstances. Where doubt exists, seek specialist opinion.
  • Offer bisphosphonates if indicated for the prevention and treatment of osteoporosis in people with a GFR of 30 ml/minute/1.73 m2 or more.
  • Vitamin D supplements in the management of CKD mineral and bone disorders
    • Do not routinely offer vitamin D supplementation to manage or prevent CKD mineral and bone disorders.
    • Offer colecalciferol or ergocalciferol to treat vitamin D deficiency in people with CKD and vitamin D deficiency.
    • If vitamin D deficiency has been corrected and symptoms of CKD-mineral and bone disorders persist, offer alfacalcidol (1-alpha-hydroxycolecalciferol) or calcitriol (1-25-dihydroxycolecalciferol) to people with a GFR of less than 30 ml/minute/1.73 m2.
  • Monitor serum calcium and phosphate concentrations in people receiving alfacalcidol or calcitriol supplements.
  • 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.


Hyperphosphataemia occurs because of insufficient filtering of phosphate from the blood by poorly functioning kidneys. High serum phosphate levels can directly and indirectly increase PTH secretion, leading to the development of secondary hyperparathyroidism. Left untreated, secondary hyperparathyroidism increases morbidity and mortality and may lead to renal bone disease with bone and muscular pain, increased incidence of fracture, bone and joint abnormalities and vascular and soft tissue calcification.

NICE have provided the following guidance:[11]

Dietary management
A specialist renal dietitian should carry out a dietary assessment and give individualised information and advice on dietary phosphate management. Advice on dietary phosphate management should be tailored to the individual patient. If a nutritional supplement is needed to maintain protein intake in children and young people with hyperphosphataemia, offer a supplement with a lower phosphate content.

Phosphate binders - children and young people

  • Offer a calcium-based phosphate binder as the first-line phosphate binder to control serum phosphate in addition to dietary management.
  • If a series of serum calcium measurements shows a trend towards the age-adjusted upper limit of normal, consider a calcium-based binder in combination with sevelamer hydrochloride.
  • For children and young people who remain hyperphosphataemic despite adherence to a calcium-based phosphate binder, and whose serum calcium goes above the age-adjusted upper limit of normal, consider either combining with, or switching to, sevelamer hydrochloride.

Phosphate binders - adults

  • Offer calcium acetate as the first-line phosphate binder to control serum phosphate in addition to dietary management. Consider calcium carbonate if calcium acetate is not tolerated or patients find it unpalatable.
  • For adults with stage 4 or 5 CKD who are not on dialysis and who are taking a calcium-based binder:
    • Consider switching to a non-calcium-based binder if calcium-based phosphate binders are not tolerated
    • Consider either combining with, or switching to, a non-calcium-based binder if hypercalcaemia develops, or if serum PTH levels are low.
  • For adults with stage 5 CKD who are on dialysis and remain hyperphosphataemic despite adherence to the maximum recommended or tolerated dose of calcium-based phosphate binder, consider either combining with, or switching to, a non-calcium-based binder.
  • For adults with stage 5 CKD who are on dialysis and who are taking a calcium-based binder, if serum phosphate is controlled by the current diet and phosphate binder regimen but serum calcium goes above the upper limit of normal, or serum PTH levels are low, consider either combining with, or switching to sevelamer hydrochloride or lanthanum carbonate.

Phosphate binders - children, young people and adults

  • If a combination of phosphate binders is used, titrate the dosage to achieve control of serum phosphate while taking into account the effect of any calcium-based binders used on serum calcium levels.
  • Advise that it is necessary to take phosphate binders with food to control serum phosphate.
  • At every routine clinical review, assess the patient's serum phosphate control, taking into account: dietary phosphate management, phosphate binder regimen and adherence to diet and medication.

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 kidney disease. 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 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/minute may be due to hyporeninaemic hypoaldosteronism in patients with diabetes, hypoadrenalism or as a result of treatment with ACE inhibitors.

See the separate article on Anaemia in Chronic Kidney Disease. If not already measured, check the haemoglobin level in people with a GFR of less than 45 ml/minute/1.73 m2 to identify anaemia (haemoglobin less than 110 g/L). Determine the subsequent frequency of testing by the measured value and the clinical circumstances.[1]


  • Chronic acidosis aggravates hyperkalaemia, inhibits protein synthesis and accelerates calcium loss from bone.
  • Oral bicarbonate supplements in the management of metabolic acidosis: consider oral sodium bicarbonate supplementation for people with both a GFR less than 30 ml/minute/1.73 m2, and a serum bicarbonate concentration of less than 20 mmol/L.[1]

Mineral and bone disorders
See under 'Management', above.

For malnutrition, see under 'Management', above.

Nerological disorders[2]

  • Signs of peripheral nervous system and CNS disorders include peripheral neuropathy, restless legs 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.[2]

CKD can progress to end-stage kidney disease in a small but significant percentage of people. Moderate-to-severe CKD is also associated with an increased risk of other significant adverse outcomes such as AKI, falls, frailty and mortality. As kidney dysfunction progresses, some co-existing conditions become more common and increase in severity. People with CKD are at increased risk of progression to end-stage kidney disease if they have either of the following:[1]

  • A sustained decrease in GFR of 25% or more over 12 months; or
  • A sustained decrease in GFR of 15 ml/minute/1.73 m2 or more over 12 months.

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

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Further reading and references

  1. Chronic kidney disease: early identification and management of chronic kidney disease in adults in primary and secondary care; NICE Clinical Guidelines (July 2014)

  2. Levey AS, Coresh J; Chronic kidney disease. Lancet. 2012 Jan 14379(9811):165-80. Epub 2011 Aug 15.

  3. Stevens PE, O'Donoghue DJ, de Lusignan S, et al; Chronic kidney disease management in the United Kingdom: NEOERICA project Kidney Int. 2007 Jul72(1):92-9. Epub 2007 Apr 18.

  4. Detection, Monitoring and Care of Patients with Chronic Kidney Disease; Renal Association (2011)

  5. Mitra PK, Tasker PR, Ell MS; Chronic kidney disease. BMJ. 2007 Jun 16334(7606):1273.

  6. Cardiovascular Disease in Chronic Kidney Disease; Renal Association (2010)

  7. Palmer SC, Navaneethan SD, Craig JC, et al; HMG CoA reductase inhibitors (statins) for people with chronic kidney disease not requiring dialysis. Cochrane Database Syst Rev. 2014 May 315:CD007784. doi: 10.1002/14651858.CD007784.pub2.

  8. Lipid modification - cardiovascular risk assessment and the modification of blood lipids for the prevention of primary and secondary cardiovascular disease; NICE Clinical Guideline, July 2014 (updated September 2016)

  9. Nutrition in Chronic Kidney Disease; Renal Association (2010)

  10. Chronic Kidney Disease - Mineral and Bone Disorders; Renal Association (2010)

  11. Hyperphosphataemia in chronic kidney disease; NICE Clinical Guideline (Mar 2013)

To Anyone who can help or offer any advice concerning my 93 (strong constitution doesn't match her chronological age) year young mother who is 50% British and 50% Scottish ethnicity, but was born and...

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