Lupus nephritis — Rapid | Doctor’s Passport

Synopsis

Detect renal involvement early in systemic lupus erythematosus, integrate biopsy class with whole-patient activity, coordinate contemporary induction and maintenance, and protect kidneys through adherence, pregnancy planning and complication surveillance.

Screen every person with SLE using blood pressure, creatinine, urinalysis and quantitative protein when abnormal; absence of oedema or urinary symptoms does not exclude nephritis.
New proteinuria, glomerular blood, casts or unexplained renal decline warrants urgent combined nephrology-rheumatology review and timely kidney biopsy when safe.
Anti-dsDNA rise and C3 or C4 fall can support immunological activity but do not prove a renal flare, determine histological class or exclude infection.
Biopsy reports ISN/RPS class plus activity, chronicity, vascular and tubulointerstitial lesions; the reversible-inflammatory and permanent-scar components guide intensity and prognosis.
When biopsy shows focal or diffuse proliferative nephritis, including a membranous component, begin specialist glucocorticoid-sparing induction without avoidable delay; advanced class VI sclerosis will not recover through escalating immunosuppression.
Current BSR guidance supports hydroxychloroquine plus glucocorticoid and a mycophenolic-acid backbone combined with an appropriate B-cell or calcineurin-directed treatment for many new or relapsing proliferative cases, with cyclophosphamide retained for selected severe or unsuitable cases.
Define response with proteinuria, urine sediment, eGFR, pressure, complement, dsDNA and extra-renal activity over time; protein can fall slowly and must not be interpreted alone.
Before declaring treatment failure, verify adherence and exposure, check infection, thrombosis, TMA, pressure and medicine toxicity, and consider repeat biopsy when activity versus scar remains uncertain.
Maintain kidney protection through pressure and protein control, smoking cessation, cardiovascular prevention, vaccination and avoidance of nephrotoxins alongside immune treatment.
Mycophenolate, cyclophosphamide, ACE inhibitors, ARBs and voclosporin are incompatible or unsuitable in pregnancy; switch before conception while renal disease is stable.

Key red flags

New glomerular haematuria, casts, rising proteinuria or kidney dysfunction in SLE needs urgent combined renal and rheumatology assessment even without oedema.

Haemoptysis with falling haemoglobin and diffuse infiltrates may represent pulmonary-renal disease and requires emergency respiratory and renal support.

Thrombocytopenia, schistocytes, haemolysis and organ injury indicates possible thrombotic microangiopathy, APS or TTP rather than uncomplicated immune-complex nephritis.

Fever, urinary symptoms, hypotension or respiratory infection during induction must be assessed before attributing kidney deterioration to immune flare.

Pregnancy with rising pressure, proteinuria or renal dysfunction requires urgent maternal-medicine assessment because pre-eclampsia and nephritis may overlap.

Pulmonary-renal emergency

Haemoptysis, anaemia, hypoxia and diffuse infiltrates with active urine may represent pulmonary haemorrhage and requires immediate multidisciplinary treatment.

Microangiopathic pattern

Severe pressure, platelet fall, schistocytes, haemolysis and neurological or renal injury suggests TMA, requiring an emergency haematology-renal pathway.

Investigation priorities

Urinalysis, microscopy, ACR and PCRFirst step

Identify glomerular inflammation and quantify albumin and total protein using repeatable measures.

Management branches

First-line renal detectionQuantify, triage and biopsy

SLE review identifies new protein, glomerular blood, hypertension or declining renal function.

Repeat a clean urine sample, quantify ACR or PCR, examine sediment, trend creatinine and pressure and assess fluid, thrombosis, infection and extra-renal activity.
Send complement, anti-dsDNA, blood count, haemolysis and targeted cultures while treating hyperkalaemia, pulmonary oedema, severe hypertension or sepsis immediately.
Refer urgently to a combined service and arrange kidney biopsy when safe; do not select induction from protein quantity or serology alone.

Preferred proliferative inductionCombine early and taper steroids

Biopsy shows active class III or IV nephritis, with or without class V, and meaningful reversibility.

Give protocolised intravenous methylprednisolone when severity warrants, then a reduced-dose oral taper with predefined response and toxicity review.
Continue appropriately dosed hydroxychloroquine and use a mycophenolic-acid analogue with the commissioned B-cell or calcineurin-directed partner selected for histology, kidney function and extra-renal disease.
Use cyclophosphamide or another expert alternative when preferred combinations are unsuitable, with infection prophylaxis, fertility preservation and cumulative-exposure safeguards.

Key medicines

Mycophenolate mofetilSpecialist induction commonly starts at 500 mg orally twice daily and increases as tolerated to 1–1.5 g twice daily; maintenance often uses 500 mg–1 g twice daily according to response, toxicity and the protocol.Exclude pregnancy and provide effective contraception; mycophenolate is teratogenic and must be changed before conception. Monitor FBC, liver and renal function, infection and gastrointestinal toxicity, and adjust or withhold for serious infection under specialist advice.

Reduced-dose glucocorticoid inductionFor active proliferative disease, specialists may give intravenous methylprednisolone 250–1,000 mg daily for one to three doses, then oral prednisolone no more than about 0.5 mg/kg/day with a protocolised taper toward 5 mg/day by six months when response permits.Obtain cultures and address infection before or alongside emergency treatment, monitor glucose, pressure, mood, eyes and bone, provide infection and gastric prophylaxis when indicated, and never stop sustained treatment abruptly.

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