ACUTE KIDNEY FAILURE

Specific causes of acute kidney failure

▪   Prerenal failure and acute tubular necrosis
▪   Vascular causes of acute kidney failure
▪   Nephrotoxic causes of acute kidney failure
▪   Glomerulonephritic and vasculitic causes of
    acute kidney failure
▪   Interstitial nephritis as a cause of acute
    kidney failure
▪   'Haematological' causes of acute kidney failure
▪   Hepatokidney Syndrome
▪   Tropical

Glomerulonephritic and vasculitic causes of acute kidney failure

A large number of glomerulonephritic and vasculitic diseases can cause acute kidney failure, sometimes in association with pulmonary haemorrhage. Together they form only 5 to 10 per cent of cases of acute kidney failure, but making the correct diagnosis is of extreme importance because of the management implications. Regrettably, most nephrologists have seen cases where the diagnosis has been much delayed because kidney impairment has incorrectly been attributed to acute tubular necrosis, and infiltrates on the chest radiograph to oedema or infection. This error, which can be catastrophic, should be avoided in patients in whom the cause of acute kidney failure is not obvious, by: 

1. Microscopy of the urine to look for the presence of red cells and red cell casts.
2. The following blood tests:

• measurement of antiglomerular basement membrane (anti-GBM) antibodies—positive in Goodpasture's disease.

• measurement of antineutrophil cytoplasmic antigen antibodies (ANCA)(screening by indirect immunofluorescence test, specific tests for antiproteinase-3 and antimyeloperoxidase antibodies)—positive in microscopic polyangiitis and Wegener's granulomatosis

• estimation of serum complement levels (C3 is depressed in postinfectious glomerulonephritis, mesangiocapillary glomerulonephritis , systemic lupus erythematosus)

• measurement of anti-streptolysin O titre (ASOT—elevated in poststreptococcal glomerulonephritis)

• serological tests for systemic lupus erythematosus

• cryoglobulins  (tests of serum immunoglobulins and for urinary light chains should also be performed).

3. Considering the possibility that pulmonary infiltrates in a patient with acute kidney failure might be due to haemorrhage. The chances of this are increased if there is a history of haemoptysis (associated with several forms of rapidly progressive glomerulonephritis), nasal discharge, or bleeding (associated with Wegener's granulomatosis), or if anaemia is unusually profound and otherwise unexplained. Lung function tests demonstrating an increase in carbon monoxide transfer factor can establish the diagnosis.
4. Performing an urgent kidney biopsy. In any patient with acute kidney failure and an active urinary sediment, kidney biopsy should be performed unless the diagnosis is clear (for example, a classical history of poststreptococcal nephritis, obvious infective endocarditis/shunt nephritis) or there is a strong contraindication, for example a single kidney or serious bleeding disorder.

The possibility of the presence of a rapidly progressive glomerulonephritis/vasculitis constitutes a medical emergency. Anti-GBM disease responds well to immunosuppression with plasma exchange, steroids and cyclophosphamide, but only if treatment is begun before dialysis is required. Immunosuppressive treatment should be given as early as possible in the course of acute kidney failure complicating microscopic polyangiitis/idiopathic rapidly progressive (crescentic) glomerulonephritis, Wegener's granulomatosis, and systemic lupus erythematosus. The urgency is such that it may well be appropriate to start these treatments while the results of blood tests and kidney biopsy are awaited, and to stop them if the findings do not corroborate the initial clinical diagnosis. The management of these patients is complex and patients benefit from the judgement and expertise of specialists.