Miscellaneous renal disorders

Polycystic kidney disease

Generally patients present with symptoms of pyelonephritis or clot colic. Diagnosis is by abdominal palpation, and confirmed on ultrasound. Manage confirmed or suspected UTI with antibiotics as for complicated UTI. Monitor renal function and control the blood pressure.

Interstitial nephritis

The key point is recognition of the condition so that the underlying cause, which is usually a drug, can be stopped. Consider it in any patient with deteriorating renal function, often in the setting of proteinuria, but often with rather unimpressive urine microscopy. Common causative drugs to consider are the non-steroidal anti-inflammatory agents, rifampicin and beta-lactam antibiotics. If the patient has this condition and is on any drug at all, it should be considered a potential cause.

Although the evidence in terms of adequately blinded randomised controlled trials is lacking, many nephrologists argue in favour of using corticosteroids to manage this condition. (1 mg/kg/d for 4-6 weeks). It is probably reasonable to consider this in any patient who is not settling within a day or two of withdrawing the potential offending agent.

Renal tubular acidosis

RTA-1 (distal RTA) has a myriad causes, including dysglobulinaemic autoimmune processes such as Sjogren’s, medullary damage from pyelonephritis, obstructive uropathy, and amphotericin use. It may also be ‘primary’ (i.e. no obvious precipitant). It presents with severe acidosis, often precipitated by an infection, and the associated hypokalaemia may cause muscle weakness. AXR shows nephrocalcinosis in many patients. U&E shows hypokalaemia and raised chloride, there is a normal urea and a normal anion gap metabolic acidosis with a urinary pH above 5.5. Manage it by fixing the potassium FIRST and then giving sodium bicarbonate 2 mmol/kg/d orally in divided doses, usually with potassium supplements as well. Some authorities consider potassium citrate a more logical alternative.

RTA-4 – also a normal anion gap metabolic acidosis, but hyperkalaemia instead of hypokalaemia. Due to aldosterone deficiency, or block in its action. It occurs naturally in diabetes and Addison’s and can also be due to drugs such as NSAIDS, ACE inhibitors, and spironolactone. Treatment is with fludrocortisone 1 mg per day if the cause can’t be removed.

RTA – 2 behaves like RTA-1 except that the requirement for bicarbonate is higher and nephrocalcinosis is unlikely.