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Instant wisdom – renal medicine

Five quick tips

1. Interpret eGFR and creatinine carefully

Mild to moderate elevation of creatinine (and so reduction in eGFR) may be due to increased release from muscles (large muscle bulk, vigorous exercise or even a large meat meal). If the result is unexpected, repeat the measurement (urgently if the dysfunction is marked) before considering a renal referral. Also, remember to multiply the eGFR by a correction factor of 1.21 for patients of black ethnic origin, and that the eGFR calculation is not applicable to patients with significant oedema, obesity or limb amputations.

2. Unprovoked hypokalaemia is an indicator of possible secondary hypertension

A low, or low normal potassium result should raise the possibility of an underlying cause for hypertension, particularly if the patient is under 30 years old. Both renal artery stenosis (listen for renal or abdominal bruits) and Conn’s syndrome may be the explanation. Other rare causes of hypertension with hypokalaemia include Cushing’s syndrome (look for other features), adrenal tumours and, in the young patient, tubular disorders such as Liddle’s syndrome. These will require specialist assessment.

3. Advise your patients to withhold ACE inhibitors and ARBs during acute GI illness

ACE inhibitors and ARBs have specific effects on the kidney, preventing the angiotensin-II induced increase in efferent glomerular arteriolar resistance and lowering glomerular filtration pressure. This forms the basis of their reno-protective properties, but interferes with the mechanism for maintaining glomerular filtration in the event of a loss of circulating volume, where acute renal failure can occur. Patients on high-dose ACE inhibitors and ARBs, particularly those with vascular disease or established kidney disease, should omit these drugs if they develop a severe gastrointestinal illness lasting more than 24 hours, and should seek medical help.

4. Always check for a palpable bladder in patients with renal impairment

Bladder outflow obstruction is a common cause of renal dysfunction, particularly in men. So, on discovering impaired renal function, check for urinary outflow symptoms, although these may not always be present, or volunteered. Also, before requesting further investigations, examine these patients carefully for an enlarged bladder as evidence of incomplete emptying – relief of the obstruction via a urinary catheter is often all that is required to improve renal function, sometimes back to normal. Such patients should be referred to urological services; they will only require a nephrology assessment if they are left with significant CKD despite relief of the obstruction.

5. Anaemia and CKD does not mean ‘renal anaemia’

Although CKD causes a reduction in erythropoietin production and anaemia, this is not usually clinically significant until patients reach CKD stage 4 (patients with diabetes can sometimes develop anaemia in stage 3B). Patients with evidence of anaemia in earlier stages should have a full assessment, including measurement of ferritin, vitamin B12

and folate. Patients with CKD have a functional resistance to iron, so aim for ferritin levels of above 100µg/l with oral iron supplementation. The target haemoglobin level in CKD is 100-110g/l and therapy with erythropoiesis- stimulating agents is not indicated at levels above this.

Obscure and overlooked diagnoses

Exercise-induced haematuria

Vigorous exercise is a recognised cause of non-visible and occasionally visible haematuria. Patients should have a full assessment to rule out systemic disease, including urinalysis to exclude proteinuria. The haematuria should resolve within one week if the patient refrains from exercise. If the haematuria is persistent or recurrent and particularly if the patient is aged over 50 years, consider cystoscopy to exclude bladder pathology. One specific form of exercise-induced ‘haematuria’ is ‘march haemoglobinuria’. This is thought to result from the traumatic haemolysis of red cells in the feet of long-distance runners.

Orthostatic proteinuria

Orthostatic or postural proteinuria is the development of elevated urinary protein excretion in the upright position. It is a common cause of proteinuria in children and adolescents, but is rare after age 30. The diagnosis is confirmed by comparing a urinary ACR taken first thing in the morning with one taken later in the day. Orthostatic proteinuria is benign.

Autosomal dominant polycystic kidney disease (ADPKD)

This affects between one in 400 and one in 1,000 births, although only about half will have the diagnosis made during their lifetime. Cysts develop in late teens and early 20s, so ultrasound screening of family members should not be conducted until the patient is over 18. Patients may complain of flank pain from infected cysts, sometimes with visible haematuria.

Most patients also have hypertension. All ADPKD patients should be referred for monitoring, as tolvaptan has been shown to reduce progression before the eGFR falls below 60ml/min.

Easily confused 

Heart failure and nephrotic syndrome

Heart failure Nephrotic syndrome

History of heart disease

Usually no history of heart disease

Gradual onset over months

Subacute or acute onset over days to weeks

Swelling confined to feet/lower legs

Swelling may affect hands and face, particularly

first thing in the morning

May be precipitated by an acute cardiac event

May be precipitated by acute viral illness

Dyspnoea common

Dyspnoea rare

JVP raised

JVP not raised

Urine dip normal

Heavy proteinuria

Renal function usually normal

Renal function may be impaired

Serum albumin normal

Serum albumin reduced

 Viral illness and vasculitis

Viral illness Vasculitis

Acute onset

Insidious onset over weeks or months

History of contact with other affected individuals

No history of contact

Upper respiratory symptoms predominate, some myalgia and rarely arthralgia

Predominant symptoms are arthralgia and myalgia, anorexia and weight loss

Fever common

Usually apyrexial

Rash unusual, may be transient and exanthematous

Rash common, typically non-blanching macular, papular or purpuric and often on the lower limbs

Urine dip: trace or 1+ proteinuria

Urine dip: haematuria and proteinuria

CRP mildly elevated

CRP significantly elevated

Renal function normal

Renal function abnormal

Renal calculi and primary loin pain haematuria syndrome

Renal calculi Primary loin pain haematuria syndrome


Rare (<0.1% of population)

Male > female

Female > male

Typically middle aged

Typically young adult

Unilateral loin pain

Begins unilaterally, typically bilateral

Visible haematuria may be present during pain

Visible haematuria typical during pain

Urine dip normal when asymptomatic

Non-visible haematuria usually persistent

Renal imaging with CT/ultrasound usually demonstrates calcification

Imaging normal

Treatment with increased fluids, salt restriction and urological assessment

Treatment with increased fluids, ACE inhibition/ARB therapy and analgesia

Prescribing points

Analgesia in CKD

  • NSAIDs are relatively contraindicated in patients with an eGFR <30ml/min (their use in patients on renin-angiotensin blocking agents is particularly risky).
  • Most opiate metabolites undergo renal excretion. They should be used in low doses with increased dosing intervals and close monitoring. Oxycodone and fentanyl are safer alternatives.

ACE inhibitors/ARBs and proteinuria

ACE inhibitors/ARBs are key treatments in patients with chronic kidney disease but increase the risk of worsening renal function (NICE guidance states an increase of up to 30% in creatinine is acceptable, but continued deterioration should be excluded by a repeat test after a further one to two weeks). Exercise caution before introducing such drugs in patients with stable renal disease and controlled hypertension, particularly in the absence of proteinuria, for fear of doing more harm than good.

Treatment of gout in CKD

Gout is common in patients with CKD.

Acute attacks:

  • NSAIDs are relatively contraindicated.
  • Colchicine doses should not exceed 500µg bd and the duration should be limited.
  • Glucocorticoids, either orally or in the form of a low-dose depot injection, are effective.


  • Prolonged administration of colchicine at doses not exceeding 500µg daily (alternate days if eGFR <30) may help.
  • The starting dose of allopurinol should be 100mg daily and increments made in 50mg steps. Doses of more than 300mg should be avoided. The minimum dose that renders the patient free of attacks should be the aim rather than a specific urate level, as this is often unachievable.

Dr Aroon Lal is a consultant nephrologist at Basildon and Thurrock University Hospital, and an honorary senior clinical lecturer at UCL Medical School

This is an abridged version of a chapter in Instant Wisdom, a guide for GPs distilling years of knowledge, experience and key evidence into 25 easy-to-read chapters, each one covering a different specialty. Pulse is offering an exclusive 15% discount to GPs on the recommended retail price. To take advantage of this offer, visit and enter PUL15 at the checkout.

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