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.
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.
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.
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.
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.