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