Synopsis
Detect renal involvement in systemic lupus erythematosus, use timely biopsy and activity–chronicity assessment to select treatment, and coordinate modern combination therapy, monitoring and pregnancy planning.
- Lupus nephritis may be clinically silent, so every SLE review includes blood pressure, urinalysis, serum creatinine and quantitative proteinuria rather than waiting for oedema.
- New proteinuria, glomerular haematuria, casts or unexplained kidney dysfunction should trigger urgent combined renal and rheumatology review and timely kidney biopsy.
- Anti-dsDNA rise and C3 or C4 fall support immunological activity but neither proves a renal flare, excludes infection nor replaces urine and biopsy assessment.
- The ISN/RPS classes describe mesangial, proliferative, membranous and sclerosing patterns; class, activity, chronicity and coexisting vascular or interstitial lesions all alter treatment.
- Class III or IV proliferative nephritis, with or without class V, needs prompt induction; class VI reflects advanced sclerosis where immunosuppression cannot restore scarred glomeruli.
- Current 2026 BSR guidance favours glucocorticoid and hydroxychloroquine with a mycophenolic-acid analogue plus obinutuzumab, a calcineurin inhibitor or belimumab for new or relapsing proliferative disease.
- Reduced glucocorticoid exposure and a planned taper are preferred when response and histological risk permit because cumulative steroid toxicity drives long-term damage.
- Hydroxychloroquine is background therapy for most people unless contraindicated, with dose adjustment and retinal screening informed by body weight and kidney function.
- Proteinuria may improve slowly and calcineurin inhibitors can lower it through podocyte effects; assess eGFR, sediment, serology and adherence before calling early non-response.
- Mycophenolate, cyclophosphamide, ACE inhibitors, ARBs and several newer agents are unsuitable in pregnancy; pre-conception switching must be planned while disease is quiet.
- Antiphospholipid-associated thrombosis, thrombotic microangiopathy, infection and medicine toxicity can worsen kidneys alongside immune-complex nephritis and require distinct treatment.
- Long-term kidney protection includes blood-pressure and proteinuria control, vaccination, cardiovascular-risk care, avoidance of nephrotoxins and sustained specialist follow-up after remission.
Key red flags
Hypertension, glomerular blood, casts, rising creatinine and falling complement suggest active class III or IV disease and require urgent biopsy-led care.
Abrupt renal decline, severe hypertension, thrombocytopenia, haemolysis or thrombosis raises antiphospholipid nephropathy or thrombotic microangiopathy and needs urgent multidisciplinary assessment.
Investigation priorities
Detect glomerular inflammation and quantify albumin and total protein loss.
Management branches
A person with SLE develops proteinuria, glomerular haematuria, casts, hypertension or unexplained renal dysfunction.
- Quantify proteinuria, inspect sediment, trend creatinine and pressure, and assess fluid state, extra-renal activity, infection, medicines and thrombosis.
- Send complement, dsDNA, blood count, CRP and cause-directed infection and antiphospholipid tests, treating sepsis and acute renal complications immediately.
- Refer urgently to the combined renal–rheumatology service and arrange timely biopsy when safe; do not infer histological class from protein amount alone.