NephrologyTier 2Topic

Renal biopsy

What it is

The only way to determine the lesion, the activity, and the chronicity - and the last two decide whether treatment is worth its toxicity
Percutaneous, ultrasound-guided, spring-loaded 16-18G needle; lower pole of the left kidney
Three preparations from the same core:
- Light microscopy (H&E, PAS, silver, trichrome, Congo red)
- Immunofluorescence (IgG, IgA, IgM, C3, C1q, kappa, lambda, C4d in transplants)
- Electron microscopy - deposits and foot process effacement
*Adequacy: >=10 glomeruli for light microscopy (>=25 for a confident focal lesion), >=2 for immunofluorescence and EM*

Major bleeding requiring transfusion or intervention: ~1-2%
Macroscopic haematuria ~3-5%; perinephric haematoma on imaging ~10-90% (mostly clinically silent)
Nephrectomy or death: <0.1%
Non-diagnostic (inadequate sample) in ~2-5%

What the biopsy actually tells you

The lesion - which glomerular, tubulointerstitial or vascular disease
Activity - reversible: crescents, endocapillary proliferation, necrosis, interstitial infiltrate. Treat these
Chronicity - irreversible: glomerulosclerosis, interstitial fibrosis and tubular atrophy, arteriolar hyalinosis. Do not immunosuppress these
Prognosis - interstitial fibrosis and tubular atrophy is the strongest histological predictor of ESKD in almost every glomerular disease
A biopsy that is entirely chronic changes management by stopping you from treating

Nephrotic syndrome in any adult (not children, where MCD is assumed)
Acute nephritic syndrome / suspected RPGN - urgent
AKI of unclear cause not explained by pre-renal, obstruction or a clear ATN history
Unexplained CKD with normal-sized kidneys
Significant proteinuria (>1 g/day) with or without haematuria
Isolated glomerular haematuria - only if there is proteinuria, hypertension or falling eGFR; not for haematuria alone
Systemic disease with renal involvement - SLE, ANCA vasculitis, myeloma, amyloid, sarcoid
Transplant - graft dysfunction, protocol biopsy, DSA, distinguishing rejection from BK nephropathy and CNI toxicity

Small echogenic kidneys (<9 cm) - the answer will be irreversible fibrosis, and the bleeding risk is higher
Classical long-standing diabetes with retinopathy and a bland sediment
Anti-PLA2R-positive membranous with no secondary cause - serology suffices
A child with textbook minimal change disease

Absolute: uncorrectable coagulopathy or thrombocytopenia, uncontrolled severe hypertension, active pyelonephritis or perinephric abscess, a solitary native kidney (relative in expert hands, and not applicable to transplants), an uncooperative patient
Relative: small kidneys, multiple cysts, hydronephrosis, morbid obesity, anatomical abnormality, anaemia

BP <140-160 systolic before the procedure
Platelets >50-100 x10^9/L, INR <1.5, normal APTT
Withhold: aspirin ~5-7 days, clopidogrel 7 days, warfarin (INR <1.5), DOACs 48-72 h (longer in CKD), therapeutic heparin 4-6 h
Uraemic platelet dysfunction: DDAVP 0.3 microgram/kg before biopsy if urea is markedly elevated
Group and hold; consent; ultrasound to confirm two kidneys and exclude hydronephrosis

After

Bed rest 6-8 h, observations, post-procedure Hb
Most bleeding declares within 4-8 h; ~90% within 24 h
Watch for flank pain, hypotension, macroscopic haematuria, falling Hb, clot retention
Complications: AV fistula (~15% on Doppler, usually resolves), perinephric haematoma, page kidney (subcapsular haematoma -> renin-driven hypertension), bowel or liver injury, infection
Bleeding -> resuscitate, CT angiography, embolisation; nephrectomy is a last resort

Lupus nephritis - the clearest example

Class	Histology	Action
I minimal mesangial	Deposits on IF/EM only	Conservative - treat extrarenal SLE
II mesangial proliferative	Mesangial hypercellularity	Conservative
III focal proliferative	<50% glomeruli	*Aggressive immunosuppression*
IV diffuse proliferative	>=50% glomeruli	*Aggressive immunosuppression*
V membranous	Subepithelial deposits	Immunosuppress if significant proteinuria; antiproteinuric therapy if sub-nephrotic
VI advanced sclerosing	>90% globally sclerosed	Conservative / prepare for RRT

*Class III and IV proliferative disease is the finding that most clearly warrants aggressive immunosuppression* - high risk of progressive irreversible damage
Report activity and chronicity indices separately - they answer different questions

Crescents in >25-50% of glomeruli -> RPGN protocol, same admission
Linear IgG -> anti-GBM; plasma exchange + steroid + cyclophosphamide
Pauci-immune with necrosis -> ANCA vasculitis; steroid + rituximab or cyclophosphamide
Congo red positive with apple-green birefringence -> amyloid; type it (mass spectrometry) and treat the clone, not the kidney
Light chain casts with a fractured appearance -> myeloma cast nephropathy; urgent haematology
SV40-positive tubular inclusions -> BK nephropathy; reduce immunosuppression
Tubulitis with interstitial infiltrate in a graft -> TCMR; pulse steroid
Thrombotic microangiopathy -> stop the culprit drug, consider complement inhibition
Predominantly fibrosis and glomerulosclerosis -> *supportive care only; immunosuppression will harm*

For coagulopathy, obesity, a solitary kidney, or the need for simultaneous liver biopsy - bleeding is into the venous system
Smaller cores, lower glomerular yield

Systemic disease requiring tissue confirmation - SLE, ANCA vasculitis, anti-GBM, amyloid, myeloma, sarcoid, IgG4-related disease
Anticoagulation and antiplatelet therapy - the main modifiable bleeding risk
Uraemic platelet dysfunction - corrected with DDAVP, dialysis, or cryoprecipitate
Hypertension - the strongest predictor of post-biopsy bleeding
Solitary kidney, polycystic kidneys, obesity - technical limitations
Transplant recipients - lower bleeding risk (superficial, iliac fossa position) and much more frequently biopsied

A biopsy is a snapshot - repeat biopsy is legitimate when the clinical course diverges from the histology (lupus flare, IgAN progression, graft dysfunction)
Sampling error is real - FSGS is the classic miss (deep juxtamedullary glomeruli affected first); a small core reads as minimal change disease
*The single most useful prognostic number on any renal biopsy is the extent of interstitial fibrosis and tubular atrophy*
Bleeding risk factors: hypertension, high creatinine, low platelets, anaemia, older age, small kidneys, operator inexperience
90% of significant bleeds declare within 24 h - which is why same-day discharge is only appropriate with a defined low-risk protocol and 6-8 h of observation
The commonest error is biopsying too late in RPGN, and biopsying at all when the kidneys are small and the answer is already fibrosis

12 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.