AKT · Renal & urology/Glomerular disease

Glomerulonephritis

Immune-mediated glomerular inflammation — nephritic (inflammatory) vs nephrotic (heavy proteinuria) spectrum

Overview

A group of immune-mediated diseases of the glomerulus presenting along a spectrum from nephritic (haematuria, hypertension, oliguria, mild proteinuria — active inflammation) to nephrotic (heavy proteinuria, hypoalbuminaemia, oedema). The crucial recognitions are rapidly progressive (crescentic) GN — a renal emergency — and matching the syndrome to its commonest cause. Diagnosis usually needs a renal biopsy.

Recognise

NEPHRITIC: haematuria (red-cell casts, 'cola' urine), hypertension, oliguria, mild–moderate proteinuria, AKI — e.g. IgA nephropathy, post-streptococcal, anti-GBM, ANCA-associated, lupus nephritis
NEPHROTIC: proteinuria >3.5 g/day, hypoalbuminaemia, oedema, hyperlipidaemia — e.g. minimal change, membranous, FSGS, diabetic, amyloid
RAPIDLY PROGRESSIVE (crescentic) GN: AKI over days–weeks ± pulmonary haemorrhage (anti-GBM/Goodpasture's, ANCA vasculitis, immune-complex) — a renal EMERGENCY

Red flags

Rapidly progressive GN — rising creatinine + active sediment ± haemoptysis (pulmonary-renal syndrome) → urgent immunology, biopsy and immunosuppression ± plasma exchange
Anti-GBM (Goodpasture's): haemoptysis + AKI + anti-GBM antibodies → plasma exchange + immunosuppression

Differentials & how to tell them apart

IgA nephropathyhaematuria 1–2 days after a URTI ('synpharyngitic'), commonest GN — see its own card

Post-streptococcal GNnephritic 1–2 WEEKS after throat/skin strep, low complement, ASO titre; usually self-limiting in children

Lupus nephritis / ANCA vasculitis / anti-GBMsystemic features + the specific autoantibody — RPGN risk

Thin basement membrane / Alporthereditary haematuria; Alport adds sensorineural deafness + ocular signs

Investigations

Urinalysis + microscopy (red-cell casts = nephritic; quantify protein with ACR/PCR), U&Es/eGFR, albumin/lipids; immunology — ANA/anti-dsDNA/complement (lupus), ANCA (vasculitis), anti-GBM (Goodpasture's), ASO/anti-DNase B (post-strep), hepatitis serology; RENAL BIOPSY is usually definitive.

Management

Biopsy-guided: treat the cause; RPGN → urgent immunosuppression ± plasma exchange; ACEi/ARB + BP control

1Place the patient on the nephritic↔nephrotic spectrum from the urinalysis and protein quantification; send the immunology screen (ANCA, anti-GBM, ANA/dsDNA, complement, ASO) and arrange a renal biopsy.Gate: Rapidly progressive GN (rising creatinine + active sediment ± haemoptysis) is a renal EMERGENCY → urgent immunosuppression ± plasma exchange (anti-GBM/ANCA) — don't wait.
2Treat the specific cause (immunosuppression for lupus/vasculitis/anti-GBM; supportive for post-strep); give RAS blockade for proteinuria/BP and manage the nephrotic/CKD complications.

Treat the specific cause — e.g. immunosuppression for lupus/ANCA/anti-GBM; supportive for post-strep (usually self-limiting)

RPGN: high-dose corticosteroids + cyclophosphamide/rituximab ± plasma exchange — urgent — for crescentic/anti-GBM/ANCA disease

Supportive: BP control with ACE inhibitor/ARB, treat oedema, manage CKD — RAS blockade reduces proteinuria and slows progression

Statin / VTE prophylaxis for nephrotic features — address hyperlipidaemia and thrombotic risk where nephrotic

Key points

Place GN on the spectrum: NEPHRITIC (haematuria + red-cell casts + hypertension + AKI) vs NEPHROTIC (heavy proteinuria + hypoalbuminaemia + oedema). Don't miss rapidly progressive (crescentic) GN — anti-GBM/ANCA/immune-complex → urgent immunosuppression ± plasma exchange. Post-strep = 1–2 weeks after, low complement; IgA = 1–2 days after a URTI.

Monitor & prognosis

Renal function, proteinuria, immunology titres/complement, immunosuppression safety; biopsy response.

Depends on type and speed; RPGN/anti-GBM can destroy kidneys in days untreated; post-strep usually recovers.

Source: KDIGO GN; cross-ref MSK (vasculitis), rheumatology (lupus)