Guidance

1 Recommendations

1 Recommendations

The following guidance is based on the best available evidence. The full guideline gives details of the methods and the evidence used to develop the guidance.

The wording used in the recommendations in this guideline (for example, words such as 'offer' and 'consider') denotes the certainty with which the recommendation is made (the strength of the recommendation). See about this guideline for details.

Terms used in this guideline

Chronic kidney disease (CKD)

Defined as abnormalities of kidney function or structure present for more than 3 months, with implications for health. This includes all people with markers of kidney damage and those with a glomerular filtration rate (GFR) of less than 60 ml/min/1.73 m2 on at least 2 occasions separated by a period of at least 90 days (with or without markers of kidney damage).

Classification of CKD

CKD is classified according to estimated GFR (eGFR) and albumin:creatinine ratio (ACR) (see table 1), using 'G' to denote the GFR category (G1–G5, which have the same GFR thresholds as the CKD stages 1–5 recommended previously) and 'A' for the ACR category (A1–A3), for example:

  • A person with an eGFR of 25 ml/min/1.73 m2 and an ACR of 15 mg/mmol has CKD G4A2.

  • A person with an eGFR of 50 ml/min/1.73 m2 and an ACR of 35 mg/mmol has CKD G3aA3.

  • An eGFR of less than 15 ml/min/1.73 m2 (GFR category G5) is referred to as kidney failure.

Glomerular filtration rate (GFR)

This is abbreviated in the following way in this guideline:

  • GFR: either a measured or an estimated GFR

  • eGFR: estimated GFR (without indicating the method of estimation)

  • eGFRcreatinine: an estimation of GFR using serum creatinine

  • eGFRcystatinC: an estimation of GFR using cystatin C.

Markers of kidney disease

These include albuminuria (ACR more than 3 mg/mmol), urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology, structural abnormalities detected by imaging, and a history of kidney transplantation.

Renin–angiotensin–aldosterone system antagonist

A drug that blocks or inhibits the renin–angiotensin–aldosterone system including angiotensin-converting enzyme (ACE) inhibitors, angiotensin‑receptor blockers (ARBs), direct renin inhibitors and aldosterone antagonists.

Renin–angiotensin system antagonist

A drug that blocks or inhibits the renin–angiotensin system including ACE inhibitors, ARBs and direct renin inhibitors. This group of drugs does not include aldosterone antagonists.

1.1 Investigations for chronic kidney disease

Measuring kidney function

Creatinine-based estimate of GFR

1.1.1 Whenever a request for serum creatinine measurement is made, clinical laboratories should report an estimate of glomerular filtration rate (eGFRcreatinine) using a prediction equation (see recommendation 1.1.2) in addition to reporting the serum creatinine result[2]. [2014]

1.1.2 Clinical laboratories should:

  • use the Chronic Kidney Disease Epidemiology Collaboration (CKD‑EPI) creatinine equation to estimate GFRcreatinine, using creatinine assays with calibration traceable to standardised reference material

  • use creatinine assays that are specific (for example, enzymatic assays) and zero-biased compared with isotope dilution mass spectrometry (IDMS)

  • participate in a UK national external quality assessment scheme for creatinine. [new 2014]

    For more information about implementing this recommendation, see implementation: getting started.

1.1.3 Apply a correction factor to GFR values estimated using the CKD‑EPI creatinine equation for people of African-Caribbean or African family origin (multiply eGFR by 1.159). [new 2014]

1.1.4 In people with extremes of muscle mass – for example, in bodybuilders, people who have had an amputation or people with muscle wasting disorders – interpret eGFRcreatinine with caution. (Reduced muscle mass will lead to overestimation and increased muscle mass to underestimation of the GFR.) [2008]

1.1.5 Advise people not to eat any meat in the 12 hours before having a blood test for eGFRcreatinine. Avoid delaying the despatch of blood samples to ensure that they are received and processed by the laboratory within 12 hours of venepuncture. [2008]

Cystatin C-based estimate of GFR

1.1.6 Whenever a request for serum cystatin C measurement is made, clinical laboratories should report an estimate of glomerular filtration rate (eGFRcystatinC) using a prediction equation (see recommendation 1.1.7) in addition to reporting the serum cystatin C result. [new 2014]

1.1.7 When an improved assessment of risk is needed (see recommendation 1.1.14), clinical laboratories should use the CKD‑EPI cystatin C equation to estimate GFRcystatinC. [new 2014]

1.1.8 Clinical laboratories should use cystatin C assays calibrated to the international standard to measure serum cystatin C for cystatin C-based estimates of GFR. [new 2014]

1.1.9 Interpret eGFRcystatinC with caution in people with uncontrolled thyroid disease because eGFRcystatinC values may be falsely elevated in people with hypothyroidism and reduced in people with hyperthyroidism. [new 2014]

Reporting and interpreting GFR values

1.1.10 Clinical laboratories should report GFR either as a whole number if it is 90 ml/min/1.73 m2 or less, or as 'greater than 90 ml/min/1.73 m2'. [new 2014]

1.1.11 If GFR is greater than 90 ml/min/1.73 m2, use an increase in serum creatinine concentration of more than 20% to infer significant reduction in kidney function. [new 2014]

1.1.12 Interpret eGFR values of 60 ml/min/1.73 m2 or more with caution, bearing in mind that estimates of GFR become less accurate as the true GFR increases. [2014]

1.1.13 Confirm an eGFR result of less than 60 ml/min/1.73 m2 in a person not previously tested by repeating the test within 2 weeks. Allow for biological and analytical variability of serum creatinine (±5%) when interpreting changes in eGFR. [2008]

When to use a cystatin C-based estimate of GFR for diagnosis of CKD

1.1.14 Consider using eGFRcystatinC at initial diagnosis to confirm or rule out CKD in people with:

  • an eGFRcreatinine of 45–59 ml/min/1.73 m2, sustained for at least 90 days and

  • no proteinuria (albumin:creatinine ratio [ACR] less than 3 mg/mmol) or other marker of kidney disease. [new 2014]

    For information about implementing this recommendation, see implementation: getting started.

1.1.15 Do not diagnose CKD in people with:

  • an eGFRcreatinine of 45–59 ml/min/1.73 m2 and

  • an eGFRcystatinC of more than 60 ml/min/1.73 m2 and

  • no other marker of kidney disease. [new 2014]

When highly accurate measures of GFR are required

1.1.16 Where a highly accurate measure of GFR is required – for example, during monitoring of chemotherapy and in the evaluation of renal function in potential living donors – consider a reference standard measure (inulin, 51Cr‑EDTA, 125I‑iothalamate or iohexol). [2008]

Proteinuria

1.1.17 Do not use reagent strips to identify proteinuria unless they are capable of specifically measuring albumin at low concentrations and expressing the result as an ACR. [2008]

1.1.18 To detect and identify proteinuria, use urine ACR in preference to protein:creatinine ratio (PCR), because it has greater sensitivity than PCR for low levels of proteinuria. For quantification and monitoring of levels of proteinuria of ACR 70 mg/mmol or more, PCR can be used as an alternative. ACR is the recommended method for people with diabetes. [2008, amended 2014]

1.1.19 For the initial detection of proteinuria, if the ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested. [2008, amended 2014]

1.1.20 Regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria. [2008, amended 2014]

1.1.21 Quantify urinary albumin or urinary protein loss as in recommendation 1.1.18 for:

  • people with diabetes

  • people without diabetes with a GFR of less than 60 ml/min/1.73 m2. [2008, amended 2014]

1.1.22 Quantify by laboratory testing the urinary albumin or urinary protein loss of people with a GFR of 60 ml/min/1.73 m2 or more if there is a strong suspicion of CKD (see also recommendation 1.1.28). [2008]

Haematuria

1.1.23 When testing for the presence of haematuria, use reagent strips rather than urine microscopy.

  • Evaluate further if there is a result of 1+ or more.

  • Do not use urine microscopy to confirm a positive result. [2008]

Managing isolated invisible haematuria

1.1.24 When there is the need to differentiate persistent invisible haematuria in the absence of proteinuria from transient haematuria, regard 2 out of 3 positive reagent strip tests as confirmation of persistent invisible haematuria. [2008]

1.1.25 Persistent invisible haematuria, with or without proteinuria, should prompt investigation for urinary tract malignancy in appropriate age groups. [2008]

1.1.26 Persistent invisible haematuria in the absence of proteinuria should be followed up annually with repeat testing for haematuria (see recommendations 1.1.24 and 1.1.25), proteinuria or albuminuria, GFR and blood pressure monitoring as long as the haematuria persists. [2008]

Who should be tested for CKD

1.1.27 Monitor GFR at least annually in people prescribed drugs known to be nephrotoxic, such as calcineurin inhibitors (for example, cyclosporin or tacrolimus), lithium and non-steroidal anti-inflammatory drugs (NSAIDs). [2008, amended 2014]

1.1.28 Offer testing for CKD using eGFRcreatinine and ACR to people with any of the following risk factors:

  • diabetes

  • hypertension

  • acute kidney injury (see recommendation 1.3.9)

  • cardiovascular disease (ischaemic heart disease, chronic heart failure, peripheral vascular disease or cerebral vascular disease)

  • structural renal tract disease, recurrent renal calculi or prostatic hypertrophy

  • multisystem diseases with potential kidney involvement – for example, systemic lupus erythematosus

  • family history of end-stage kidney disease (GFR category G5) or hereditary kidney disease

  • opportunistic detection of haematuria. [new 2014]

1.1.29 Do not use age, gender or ethnicity as risk markers to test people for CKD. In the absence of metabolic syndrome, diabetes or hypertension, do not use obesity alone as a risk marker to test people for CKD. [2008, amended 2014]

1.2 Classification of chronic kidney disease

1.2.1 Classify CKD using a combination of GFR and ACR categories (as described in table 1). Be aware that:

  • increased ACR is associated with increased risk of adverse outcomes

  • decreased GFR is associated with increased risk of adverse outcomes

  • increased ACR and decreased GFR in combination multiply the risk of adverse outcomes. [new 2014]

    For information about implementing this recommendation, see implementation: getting started.

Table 1 Classification of chronic kidney disease using GFR and ACR categories

Table 1 Classification of chronic kidney disease using GFR and ACR categories

1.2.2 Do not determine management of CKD solely by age. [new 2014]

Investigating the cause of CKD and determining the risk of adverse outcomes

1.2.3 Agree a plan to establish the cause of CKD during an informed discussion with the person with CKD, particularly if the cause may be treatable (for example, urinary tract obstruction, nephrotoxic drugs or glomerular disease). [new 2014]

1.2.4 Use the person's GFR and ACR categories (see table 1) to indicate their risk of adverse outcomes (for example, CKD progression, acute kidney injury, all-cause mortality and cardiovascular events) and discuss this with them. [new 2014]

Indications for renal ultrasound

1.2.5 Offer a renal ultrasound scan to all people with CKD who:

  • have accelerated progression of CKD (see recommendation 1.3.3)

  • 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/min/1.73 m2 (GFR category G4 or G5)

  • are considered by a nephrologist to require a renal biopsy. [2008, amended 2014]

1.2.6 Advise people with a family history of inherited kidney disease about the implications of an abnormal result before a renal ultrasound scan is arranged for them. [2008]

1.3 Frequency of monitoring

1.3.1 Agree the frequency of monitoring (eGFRcreatinine and ACR) with the person with, or at risk of, CKD; bear in mind that CKD is not progressive in many people. [new 2014]

1.3.2 Use table 2 to guide the frequency of GFR monitoring for people with, or at risk of, CKD, but tailor it to the person according to:

  • the underlying cause of CKD

  • past patterns of eGFR and ACR (but be aware that CKD progression is often non-linear)

  • comorbidities, especially heart failure

  • changes to their treatment (such as renin–angiotensin–aldosterone system [RAAS] antagonists, NSAIDs and diuretics)

  • intercurrent illness

  • whether they have chosen conservative management of CKD. [new 2014]

Table 2 Frequency of monitoring of GFR (number of times per year, by GFR and ACR category) for people with, or at risk of, CKD

Table 2 Frequency of monitoring of GFR (number of times per year, by GFR and ACR category) for people with, or at risk of, CKD

Defining progression

1.3.3 Define accelerated progression of CKD 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/min/1.73 m2 per year. [new 2014]

1.3.4 Take the following steps to identify the rate of progression of CKD:

  • Obtain a minimum of 3 GFR estimations over a period of not less than 90 days.

  • In people with a new finding of reduced GFR, repeat the GFR within 2 weeks to exclude causes of acute deterioration of GFR – for example, acute kidney injury or starting renin–angiotensin system antagonist therapy. [2008, amended 2014]

1.3.5 Be aware that people with CKD are at increased risk of progression to end-stage kidney disease if they have either of the following:

  • a sustained decrease in GFR of 25% or more over 12 months or

  • a sustained decrease in GFR of 15 ml/min/1.73 m2 or more over 12 months. [2008, amended 2014]

1.3.6 When assessing CKD progression, extrapolate the current rate of decline of GFR and take this into account when planning intervention strategies, particularly if it suggests that the person might need renal replacement therapy in their lifetime. [2008, amended 2014]

Risk factors associated with CKD progression

1.3.7 Work with people who have any of the following risk factors for CKD progression to optimise their health:

  • cardiovascular disease

  • proteinuria

  • acute kidney injury

  • hypertension

  • diabetes

  • smoking

  • African, African-Caribbean or Asian family origin

  • chronic use of NSAIDs

  • untreated urinary outflow tract obstruction. [new 2014]

1.3.8 In people with CKD the chronic use of NSAIDs may be associated with progression and acute use is associated with a reversible decrease in GFR. Exercise caution when treating people with CKD with NSAIDs over prolonged periods of time. Monitor the effects on GFR, particularly in people with a low baseline GFR and/or in the presence of other risks for progression. [2008]

Acute kidney injury and CKD

1.3.9 Monitor people for the development or progression of CKD for at least 2–3 years after acute kidney injury, even if serum creatinine has returned to baseline. [new 2014]

1.3.10 Advise people who have had acute kidney injury that they are at increased risk of CKD developing or progressing. [new 2014]

1.4 Information and education

1.4.1 Offer people with CKD education and information tailored to the severity and cause of CKD, the associated complications and the risk of progression. [2008]

1.4.2 When developing information or education programmes, involve people with CKD in their development from the outset. The following topics are suggested.

  • What is CKD and how does it affect people?

  • What questions should people ask about their kidneys?

  • What treatments are available for CKD, what are their advantages and disadvantages and what complications or side effects may occur as a result of treatment/medication?

  • What can people do to manage and influence their own condition?

  • In what ways could CKD and its treatment affect people's daily life, social activities, work opportunities and financial situation, including benefits and allowances available?

  • How can people cope with and adjust to CKD and what sources of psychological support are available?

  • When appropriate, offer information about renal replacement therapy (such as the frequency and length of time of dialysis treatment sessions or exchanges and pre-emptive transplantation) and the preparation required (such as having a fistula or peritoneal catheter).

  • Conservative management and when it may be considered. [2008]

1.4.3 Offer people with CKD high-quality information or education programmes as appropriate to the severity of their condition to allow time for them to fully understand and make informed choices about their treatment. [2008]

1.4.4 Healthcare professionals providing information and education programmes should ensure they have specialist knowledge about CKD and the necessary skills to facilitate learning. [2008]

1.4.5 Healthcare professionals working with people with CKD should take account of the psychological aspects of coping with the condition and offer access to appropriate support – for example, support groups, counselling or a specialist nurse. [2008]

Lifestyle advice

1.4.6 Encourage people with CKD to take exercise, achieve a healthy weight and stop smoking. [2008]

Dietary interventions

1.4.7 Offer dietary advice about potassium, phosphate, calorie and salt intake appropriate to the severity of CKD. [2008, amended 2014]

1.4.8 Where dietary intervention is agreed this should occur within the context of education, detailed dietary assessment and supervision to ensure malnutrition is prevented. [2008]

Low-protein diets

1.4.9 Do not offer low-protein diets (dietary protein intake less than 0.6–0.8 g/kg/day) to people with CKD. [new 2014]

Self-management

1.4.10 Ensure that systems are in place to:

  • inform people with CKD of their diagnosis

  • enable people with CKD to share in decision-making about their care

  • support self-management (this includes providing information about blood pressure, smoking cessation, exercise, diet and medicines) and enable people to make informed choices. [new 2014]

1.4.11 Give people access to their medical data (including diagnosis, comorbidities, test results, treatments and correspondence) through information systems, such as Renal PatientView, to encourage and help them to self-manage their CKD. [new 2014]

1.5 Referral criteria

1.5.1 Take into account the individual's wishes and comorbidities when considering referral. [2008]

1.5.2 People with CKD in the following groups should normally be referred for specialist assessment:

  • GFR less than 30 ml/min/1.73 m2 (GFR category G4 or G5), 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 (ACR category A3), 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/min/1.73 m2 or more within 12 months

  • hypertension that remains poorly controlled despite the use of at least 4 antihypertensive drugs at therapeutic doses (see also Hypertension [NICE guideline CG127])

  • known or suspected rare or genetic causes of CKD

  • suspected renal artery stenosis. [2008, amended 2014]

1.5.3 Consider discussing management issues with a specialist by letter, email or telephone in cases where it may not be necessary for the person with CKD to be seen by the specialist. [2008]

1.5.4 Once a referral has been made and a plan jointly agreed (between the person with CKD or their carer and the healthcare professional), it may be possible for routine follow-up to take place at the patient's GP surgery rather than in a specialist clinic. If this is the case, criteria for future referral or re-referral should be specified. [2008]

1.5.5 People with CKD and renal outflow obstruction should normally be referred to urological services, unless urgent medical intervention is required – for example, for the treatment of hyperkalaemia, severe uraemia, acidosis or fluid overload. [2008]

1.6 Pharmacotherapy

Blood pressure control

1.6.1 In people with CKD aim to keep the systolic blood pressure below 140 mmHg (target range 120–139 mmHg) and the diastolic blood pressure below 90 mmHg[3]. [2008]

1.6.2 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 mmHg (target range 120–129 mmHg) and the diastolic blood pressure below 80 mmHg[3]. [2008]

Choice of antihypertensive agent

1.6.3 Offer a low‑cost renin–angiotensin system antagonist to people with CKD and:

  • diabetes and an ACR of 3 mg/mmol or more (ACR category A2 or A3)

  • hypertension and an ACR of 30 mg/mmol or more (ACR category A3)

  • an ACR of 70 mg/mmol or more (irrespective of hypertension or cardiovascular disease)[4]. [new 2014]

1.6.4 Do not offer a combination of renin–angiotensin system antagonists to people with CKD. [new 2014]

1.6.5 Follow the treatment recommendations in Hypertension (NICE guideline CG127) for people with CKD, hypertension and an ACR of less than 30 mg/mmol (ACR categories A1 and A2), if they do not have diabetes. [new 2014]

1.6.6 To improve concordance, inform people who are prescribed renin–angiotensin system antagonists about the importance of:

  • achieving the optimal tolerated dose of renin–angiotensin system antagonists and

  • monitoring eGFR and serum potassium in achieving this safely. [2008]

1.6.7 In people with CKD, measure serum potassium concentrations and estimate the GFR before starting renin–angiotensin system antagonists. Repeat these measurements between 1 and 2 weeks after starting renin–angiotensin system antagonists and after each dose increase. [2008]

1.6.8 Do not routinely offer a renin–angiotensin system antagonist to people with CKD if their pretreatment serum potassium concentration is greater than 5.0 mmol/litre. [2008, amended 2014]

1.6.9 When hyperkalaemia precludes use of renin–angiotensin system antagonists, assessment, investigation and treatment of other factors known to promote hyperkalaemia should be undertaken and the serum potassium concentration rechecked. [2008]

1.6.10 Concurrent prescription of drugs known to promote hyperkalaemia is not a contraindication to the use of renin–angiotensin system antagonists, but be aware that more frequent monitoring of serum potassium concentration may be required. [2008]

1.6.11 Stop renin–angiotensin system antagonists if the serum potassium concentration increases to 6.0 mmol/litre or more and other drugs known to promote hyperkalaemia have been discontinued. [2008]

1.6.12 Following the introduction or dose increase of renin–angiotensin system antagonists, do not modify the dose if either the GFR decrease from pretreatment baseline is less than 25% or the serum creatinine increase from baseline is less than 30%. [2008]

1.6.13 If there is a decrease in eGFR or increase in serum creatinine after starting or increasing the dose of renin–angiotensin system antagonists, but it is less than 25% (eGFR) or 30% (serum creatinine) of baseline, repeat the test in 1–2 weeks. Do not modify the renin–angiotensin system antagonist dose if the change in eGFR is less than 25% or the change in serum creatinine is less than 30%. [2008]

1.6.14 If the eGFR change is 25% or more, or the change in serum creatinine is 30% or more:

  • investigate other causes of a deterioration in renal function, such as volume depletion or concurrent medication (for example, NSAIDs)

  • if no other cause for the deterioration in renal function is found, stop the renin–angiotensin system antagonist or reduce the dose to a previously tolerated lower dose, and add an alternative antihypertensive medication if required. [2008]

Statins

1.6.15 Follow the recommendations in Lipid modification (NICE guideline CG181) for the use of statins in CKD. [new 2014]

Oral antiplatelets and anticoagulants

1.6.16 Offer antiplatelet drugs to people with CKD for the secondary prevention of cardiovascular disease, but be aware of the increased risk of bleeding. [new 2014]

1.6.17 Consider apixaban in preference to warfarin in people with a confirmed eGFR of 30–50 ml/min/1.73 m2 and non-valvular atrial fibrillation who have 1 or more of the following risk factors:

  • prior stroke or transient ischaemic attack

  • age 75 years or older

  • hypertension

  • diabetes mellitus

  • symptomatic heart failure. [new 2014]

1.7 Other complications

Bone metabolism and osteoporosis

1.7.1 Do not routinely measure calcium, phosphate, parathyroid hormone (PTH) and vitamin D levels in people with a GFR of 30 ml/min/1.73 m2 or more (GFR category G1, G2 or G3). [2008]

1.7.2 Measure serum calcium, phosphate and PTH concentrations in people with a GFR of less than 30 ml/min/1.73 m2 (GFR category G4 or G5). Determine the subsequent frequency of testing by the measured values and the clinical circumstances. Where doubt exists, seek specialist opinion. [2008]

1.7.3 Offer bisphosphonates if indicated for the prevention and treatment of osteoporosis in people with a GFR of 30 ml/min/1.73 m2 or more (GFR category G1, G2 or G3). [2008]

Vitamin D supplements in the management of CKD–mineral and bone disorders

Detailed advice on the management of CKD–mineral and bone disorders is beyond the scope of this guideline. If uncertain, seek advice from your local renal service.

1.7.4 Do not routinely offer vitamin D supplementation to manage or prevent CKD–mineral and bone disorders. [new 2014]

1.7.5 Offer colecalciferol or ergocalciferol to treat vitamin D deficiency in people with CKD and vitamin D deficiency. [new 2014]

1.7.6 If vitamin D deficiency has been corrected and symptoms of CKD–mineral and bone disorders persist, offer alfacalcidol (1‑alpha‑hydroxycholecalciferol) or calcitriol (1‑25‑dihydroxycholecalciferol) to people with a GFR of less than 30 ml/min/1.73 m2 (GFR category G4 or G5). [new 2014]

1.7.7 Monitor serum calcium and phosphate concentrations in people receiving alfacalcidol or calcitriol supplements. [2014]

Anaemia

1.7.8 If not already measured, check the haemoglobin level in people with a GFR of less than 45 ml/min/1.73 m2 (GFR category G3b, G4 or G5) to identify anaemia (haemoglobin less than 110 g/litre [11.0 g/dl], see Anaemia management in people with chronic kidney disease [NICE guideline CG114]). Determine the subsequent frequency of testing by the measured value and the clinical circumstances. [2008]

Oral bicarbonate supplements in the management of metabolic acidosis

Detailed advice on the management of metabolic acidosis is beyond the scope of this guideline. If uncertain, seek advice from your local renal service.

1.7.9 Consider oral sodium bicarbonate supplementation for people with both:

  • a GFR less than 30 ml/min/1.73 m2 (GFR category G4 or G5) and

  • a serum bicarbonate concentration of less than 20 mmol/litre. [new 2014]


[2] eGFRcreatinine may be less reliable in certain situations (for example, acute kidney injury, pregnancy, oedematous states, muscle wasting disorders, and in people who are malnourished or have had an amputation) and has not been well validated in certain ethnic groups (for example, in people of Asian family origin).

[3] The GDG searched for and appraised evidence on blood pressure control, and did not set out to establish definitive safe ranges of blood pressure in CKD. The evidence presented in the full guideline does not therefore include safety of low blood pressure, but some such evidence does exist. The GDG set out a range of blood pressure targets, given in these recommendations, which in their clinical experience will inform good practice in CKD.

[4] The evidence to support these criteria is limited in people aged over 70 years.

  • National Institute for Health and Care Excellence (NICE)