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Chapter 6: Disorders of the kidney 245

Sex Management
M > F Antibiotics are usually given, although there is no evi-
dencethattheyhaveaneffectontheglomerulonephri-
tis. There is no role for steroids or other specific treat-
Aetiology
ments.
The most common infectious agent is β-haemolytic
General measures are as for acute renal failure and
Streptococcus, Lancefield Group A although other bac-
nephritic syndrome. Dialysis may be required.
teria, viruses and malaria may be causative. A similar
picture is seen in systemic lupus erythematosus.
Prognosis
Pathophysiology Most patients, especially children, have complete clinical
There are subendothelial immune deposits of immune resolution over 3–6 weeks, even in those with crescents
complexes, which may be derived from the circulation on biopsy.
or formed de novo in the kidney. These result in comple- Up to 30% develop progressive renal disease, some-
ment activation and an inflammatory response, causing times becoming manifest many years later with hy-
endothelial cell proliferation. Subepithelial deposits can pertension, recurrent or persistent proteinuria and
lead to a variable degree of proteinuria. chronic renal impairment. Late biopsy may show
glomerulosclerosis, which is thought to be due to
Clinical features the loss of some glomeruli, leading to hyperfiltra-
The disease presents as acute nephritic syndrome tion through the remaining glomeruli, causing grad-
(haematuria, oliguria and variable renal failure), with ual changes to the glomeruli and ultimately renal fail-
malaise and nausea 1–2 weeks after a illness such as a ure. In other cases of persistent disease, the original
sore throat. Mild facial oedema and hypertension are glomerular disease may have been membranoprolif-
variably present. erative glomerulonephritis.
Adults are more likely to develop rapidly progressive

glomerulonephritis (>80% glomeruli affected) and
Macroscopy/microscopy
have incomplete resolution afterwards.
All the glomeruli demonstrate endothelial, epithelial

and mesangial cell proliferation, together with neu-
trophils. Crescents may be formed in severe cases.
Focal segmental proliferative

Immunofluorescence reveals granular deposits of C 3 glomerulonephritis
and IgG.
Electron microscopy shows subepithelial deposits Definition

(called humps or lumpy deposits). Focalsegmentalproliferativeglomerulonephritisischar-
acterised by cellular proliferation affecting only one
Complications segment of the glomerulus and occurring in only a pro-
Severe acute renal failure, rapidly progressive glomeru- portion of all glomeruli.
lonephritis, hypertensive encephalopathy and pul-
monary oedema.
Aetiology
This histological pattern is caused by:
Investigations Primary glomerular diseases such as IgA nephropathy
Renal biopsy is required to make a definitive diagnosis (also called mesangial IgA disease or Berger’s disease)
but may not always be necessary. and Goodpasture’s disease (anti-GBM disease).
Throat swabs, swabs of skin lesions, anti-streptolysin Systemic diseases such as systemic lupus erythe-

Otitre, anti-DNAse B antibodies and other tests may matosus (SLE), microscopic polyarteritis, Wegener’s
identify recent infection. granulomatosis, infective endocarditis and Henoch–
Low plasma complement especially C 3 . Sch¨ onlein purpura.