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Proliferative glomerulonephritis 

Proliferative glomerulonephritis

Chapter:
Proliferative glomerulonephritis
Author(s):

Peter W. Mathieson

DOI:
10.1093/med/9780199204854.003.210805_update_001

Update: The entity of C3 glomerulonephritis has been more accurately defined, and linked in some cases to genetic abnormalities in the complement system (familial complement factor H-related protein 5 (CFHR5) nephropathy in patients of Cypriot origin).

Updated on 25 May 2011. The previous version of this content can be found here.
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date: 30 March 2017

Proliferative glomerulonephritis—which occurs in many conditions—describes the finding of increased cellularity of the glomerulus, which may be due to proliferation of intrinsic glomerular cells, infiltration of leucocytes, or both. Patients will typically have haematuria, and this may be associated with proteinuria and/or impairment of excretory renal function and/or hypertension. Different subtypes of proliferative glomerulonephritis are recognized: 1 Proliferation of mesangial cells—most commonly seen in immunoglobulin A (IgA) nephropathy (see Chapter 21.8.1), but rare variants without IgA deposition may feature IgM or complement 3 (C3) deposition or no immune reactants. The behaviour of these variants is uncertain, but responsiveness to corticosteroid treatment is often seen. 2 Endocapillary proliferation—glomerular hypercellularity is confined within the glomerular capillary tuft; best described in the form of poststreptococcal glomerulonephritis, but can be provoked by other infections; treatment is directed at eradicating underlying infection; most cases recover, but haematuria and proteinuria can persist, and some cases (particularly nonstreptococcal) develop chronic renal failure. 3 Diffuse proliferative glomerulonephritis—some ‘idiopathic’ cases have no preceding history of infection, no evidence of other disease, and no atypical histological features; prognosis and treatment are uncertain. 4 Extracapillary proliferation—produces crescentic glomerulonephritis (discussed in Chapters 21.8.1, 21.8.4, and 21.8.7).

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