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Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.

Nephritic syndrome and rapidly progressive glomerulonephritis

Renal · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Escalate

Oliguria, rapidly rising creatinine, hyperkalaemia, pulmonary oedema, severe hypertension, pulmonary haemorrhage or systemic vasculitis with active urine sediment is a renal emergency. Contact nephrology immediately, obtain time-critical serology and biopsy, and do not delay treatment of a convincing pulmonary-renal syndrome for every result.

Synopsis

Recognise active glomerular inflammation, distinguish its immune patterns rapidly, and secure biopsy and organ-saving treatment before irreversible crescentic injury develops.

  • Nephritic syndrome combines glomerular haematuria, variable proteinuria, reduced GFR, sodium retention, oedema and hypertension; not every component is present.
  • Dysmorphic red cells and red-cell casts strongly support glomerular bleeding, while dipstick blood without red cells suggests haemoglobin or myoglobin instead.
  • Rapidly progressive glomerulonephritis is a clinical trajectory of kidney function loss over days to weeks, usually with crescentic injury on biopsy.
  • The three immune patterns are anti-GBM linear antibody disease, pauci-immune ANCA-associated disease and immune-complex disease such as lupus, IgA or infection-related GN.
  • Normal complement supports but does not prove ANCA or anti-GBM disease; low C3 and/or C4 directs attention toward immune-complex and complement-mediated causes.
  • Pulmonary haemorrhage can present with breathlessness, falling haemoglobin and diffuse opacities without visible haemoptysis, especially after alveolar blood is swallowed.
  • Send ANCA with PR3 and MPO, anti-GBM, ANA, dsDNA, complement, immunoglobulins and infection studies urgently while arranging renal biopsy.
  • Blood cultures and echocardiographic assessment matter when endocarditis is possible because infection-related GN can be worsened catastrophically by blind immunosuppression.
  • Biopsy determines crescents, necrosis, immune deposition and chronic scarring, which changes whether intensive immunosuppression can still recover function.
  • Supportive treatment of hyperkalaemia, pulmonary oedema and severe pressure runs alongside cause-specific therapy; dialysis does not replace immune treatment when recovery is plausible.
  • Cyclophosphamide, rituximab, plasma exchange and high-dose glucocorticoid are specialist treatments with major infection, fertility and cytopenia safeguards, not empirical ward prescriptions.

Key red flags

Rapid kidney trajectory

Creatinine rising across days or weeks, oliguria, new acidosis or potassium elevation indicates RPGN and warrants same-day nephrology even if the absolute creatinine remains modest.

Pulmonary haemorrhage

New hypoxia, diffuse bilateral opacities and falling haemoglobin with active urine sediment may be alveolar bleeding; haemoptysis can be absent and anticoagulation can amplify danger.

Hypertensive fluid emergency

Headache, visual disturbance, encephalopathy, pulmonary oedema or severe pressure with AKI requires controlled emergency blood-pressure and volume treatment while the renal cause is investigated.

Investigation priorities

01
Urinalysis, microscopy and ACR or PCRFirst step

Confirm active glomerular sediment and quantify protein loss.

Management branches

First hoursStabilise and phenotype RPGN

Active urine sediment accompanies a rapid creatinine rise.

  1. Call nephrology, perform ABCDE and assess urine output, potassium, acidosis, severe pressure, pulmonary oedema, anaemia, rash, neurological and respiratory involvement.
  2. Send urgent urine microscopy, protein quantification, ANCA-PR3/MPO, anti-GBM, ANA-dsDNA, complement, immunoglobulins, cultures and infection serology before immune treatment when feasible.
  3. Arrange ultrasound to exclude obstruction and urgent biopsy, while treating hyperkalaemia, fluid overload, sepsis and dialysis indications without waiting for a final immune label.

Key medicines

Intravenous methylprednisolone and oral glucocorticoid inductionUse the biopsy- and diagnosis-specific renal or rheumatology protocol, often beginning with one to three supervised intravenous pulses followed by a reduced-exposure oral taper rather than an unreviewed fixed course.Exclude and treat infection, monitor glucose, mental state, blood pressure, fluid, GI and bone risk, and provide prophylaxis. Steroid alone is inadequate for anti-GBM or organ-threatening ANCA disease.
Cyclophosphamide or rituximab inductionUse only the current specialist weight-, age- and kidney-adjusted intravenous or oral cyclophosphamide schedule, or the licensed vasculitis rituximab infusion regimen, with pharmacy verification and cumulative-dose tracking.Assess infection, hepatitis, immunoglobulins, cytopenia, bladder toxicity, malignancy, fertility and pregnancy. Provide Pneumocystis prophylaxis and vaccination planning; rituximab infusion reactions and late hypogammaglobulinaemia need monitoring.
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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • UKKA glomerular disease guideline commentaryCurrent UK commentary on biopsy, induction and disease-specific glomerular care.
  • NICE NG203 chronic kidney diseaseKidney function, proteinuria, haematuria and specialist referral framework.
  • UKKA acute hyperkalaemia guidelineTime-critical potassium assessment and treatment during RPGN.
  • BNF cyclophosphamide prescribing monographCurrent specialist dosing, fertility, marrow and bladder safeguards.
  • NICE NG253 suspected sepsis in people aged 16 or overRecognition and immediate treatment when infection mimics or triggers GN.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom