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Glomerulonephritis

  • Background

    Definition and classification

    • Inflammation of the glomeruli.
    • This page discusses primary glomerulonephritides, but glomerular disease can also be secondary to diabetes and multi-system autoimmune or infiltrative diseases.
    • Can be classified by whether they typically present with nephrotic syndrome – minimal change disease, membranous GN, membranoproliferative GN, FSGS – or haematuria/nephritic syndrome – IgA nephropathy, post-streptococcal GN, rapidly progressive GN. However, presentation is often non-specific and asymptomatic.

    Presentation

    • Can be an incidental finding in an asymptomatic individual e.g. with hypertension, proteinuria or haematuria on dipstick, abnormal renal function test, anaemia.
    • Symptomatic presentations include oedema (nephrotic syndrome), frank haematuria, or generally unwell (uraemia, anaemia).

    Management

    • See chronic kidney disease (CKD) and/or acute kidney injury (AKI) for general management of renal impairment. BP control (SBP <130) and ACEi/ARB therapy (esp. if proteinuric) is particularly important.
    • The sections below outline which types of GN may benefit from immunosuppression.

  • Minimal change disease

    Pathophysiology and epidemiology

    • Pathology: podocyte effacement seen on electron microscopy.
    • Commonest cause (90%) of nephrotic syndrome in children.
    • Causes: idiopathic, Hodgkin's lymphoma, NSAIDs, lithium.

    Management and prognosis

    • Usually responds to corticosteroids, especially in kids (90%). 2nd line cyclophosphamide or calcineurin inhibitors (tacrolimus, ciclosporin).
    • Although relapses are common, long-term prognosis is good.

  • Membranous glomerulonephritis

    Pathophysiology and epidemiology

    Diffuse thickening of glomerular basement membrane, due to:

    • Autoimmune reaction to phospholipase A2 receptor (PLA2R) or other podocyte autoantigens.
    • Cancer: lung, prostate, Hodgkin's.
    • Infection: HBV, HCV, TB, malaria.
    • Drugs: NSAIDs, anti-malarials, gold, penicillamine.
    • SLE

    Commoner in adults.

    Management and prognosis

    • Untreated, 50% self-resolve and 50% progress to end-stage kidney disease.
    • Given potential for resolution, only treat in severe nephrotic syndrome, with corticosteroids plus cyclophosphamide.

  • Membranoproliferative glomerulonephritis

    Aka mesangiocapillary glomerulonephritis.

    Pathophysiology and epidemiology

    • Mesangial proliferation (capillary smooth muscle cell proliferation) and thickened glomerular basement membrane.
    • Causes: idiopathic, SLE, HBV/HCV, monoclonal gammopathy, lymphoma.
    • Relatively uncommon. Usually occurs in children or young adults.

    Presentation and prognosis

    • Presents with nephrotic (50%) or nephritic (30%) syndrome, or sometimes just isolated protein- and haematuria.
    • 50% develop end-stage kidney disease in 10 years.

  • Focal and segmental glomerulosclerosis (FSGS)

    Pathophysiology

    • Accumulation of type 4 collagen (sclerosis) in parts (segmental) of some (focal) glomeruli.
    • Typically leads to nephrotic syndrome.
    • Causes: idiopathic, cancer, HIV, obesity.

    Management and prognosis

    • 50% respond to corticosteroids.
    • Further immunosuppression (ciclosporin, cyclophosphamide, MMF, or rituximab) may be beneficial in steroid-resistant FSGS, but many progress to end-stage kidney disease.

  • IgA nephropathy

    Aka Berger's disease.

    Pathophysiology and epidemiology

    • A type of mesangial proliferative nephritis, involving glomerular IgA deposition.
    • Commonest type of glomerulonephritis worldwide.
    • Henoch-Schonlein purpura is sometimes considered a systemic form, as it causes renal IgA deposition.

    Presentation

    • Around 50% present with visible haematuria in the days following an URTI, which is thought to trigger the disease. Flank pain may be present.
    • Remainder mostly present with incidental microscopic haematuria ± proteinuria.
    • Rarely, presents with nephrotic syndrome or rapidly progressive glomerulonephritis (RPGN).

    Management

    Corticosteroids for those with rapidly progressive disease, otherwise benefit is unclear.

  • Post-streptococcal glomerulonephritis

    • Typically 1-2 weeks after pharyngitis or (less commonly) impetigo.
    • Usually presents with haematuria or nephritic syndrome, but can also lead to rapidly progressive glomerulonephritis.
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