Nephritic Syndrome

Nephritic Syndrome (often referred to as Acute Glomerulonephritis) is a syndrome rather than a single disease, representing an inflammatory process within the glomeruli. This inflammation allows red blood cells to leak into the urine and causes a decrease in GFR. The classic presentation includes: 1. Haematuria (microscopic or macroscopic 'cola-coloured' urine). 2. Hypertension (due to salt/water retention). 3. Oliguria. 4. Mild-to-moderate proteinuria (<3.5g/day). Common causes include IgA Nephropathy (Berger's disease), Post-streptococcal glomerulonephritis (PSGN), and vasculitides like ANCA-associated vasculitis (GPA/MPA) or Anti-GBM disease (Goodpasture’s). A critical variant is Rapidly Progressive Glomerulonephritis (RPGN), which presents with a rapid decline in renal function and 'crescents' on biopsy; this requires urgent immunosuppression. Unlike nephrotic syndrome, which is a basement membrane 'leak', nephritic syndrome is an 'inflammatory' insult that impairs the filter itself, leading to uraemia and hypervolaemia. Diagnosis is confirmed by renal biopsy, and management depends on the specific immunological cause, often involving steroids and plasmapheresis.

The primary pathology is inflammation of the glomerulus. This can be triggered by immune complex deposition (IgA in the mesangium for IgA nephropathy) or by autoantibodies (anti-GBM antibodies attacking the type IV collagen in the basement membrane). The resulting inflammatory cascade leads to the infiltration of leucocytes, proliferation of glomerular cells, and necrosis. This damage breaks the capillary wall, allowing RBCs to pass into the Bowman's space (forming RBC casts in the tubules). The global inflammation reduces the surface area available for filtration, causing a drop in GFR, leading to salt and water retention and uraemia. In RPGN, the proliferation of parietal epithelial cells and monocytes in Bowman’s space creates a 'crescent' shape that physically compresses the capillary tuft, leading to rapid renal failure.

Patients typically present with visible haematuria or 'smoky/cola-coloured' urine. Physical examination reveals hypertension and varying degrees of oedema (though less severe than nephrotic syndrome). If associated with a systemic vasculitis, there may be a purpuric rash, joint pains, or epistaxis. Importantly, in Goodpasture's or ANCA-vasculitis, patients may present with 'Pulmonary-Renal Syndrome', combining AKI with haemoptysis (coughing up blood). Post-streptococcal GN is classic in children following a sore throat, whereas IgA nephropathy often occurs *during* an illness. Complications include hypertensive emergency, acute heart failure due to fluid overload, and progression to end-stage renal failure (especially in RPGN).

Bedside: Urinalysis (Haematuria, Proteinuria); BP. Bloods: U&Es (rising creatinine), FBC, CRP, ESR. Immunological screen (vital): ANA (SLE), ANCA (Vasculitis), Anti-GBM (Goodpasture's), Complements C3/C4 (low in PSGN, SLE), ASOT (Streptococcal infection). Urine: Microscopy for RBC casts (pathognomonic for GN). Imaging: Renal ultrasound. Gold Standard: Renal Biopsy (to assess for crescents or specific immune deposits).

Medical: 1. General: Control hypertension (often with ACEi/ARBs) and fluid balance. 2. Steroids: High-dose IV Methylprednisolone is often used in acute presentations. 3. Immunosuppression: Cyclophosphamide or Rituximab for vasculitis. 4. Plasmapheresis: Essential in Anti-GBM disease and severe ANCA-vasculitis to remove circulating antibodies. 5. Specific: PSGN is usually supportive; IgA nephropathy focus is long-term BP control with ACEi. Surgical: None directly; however, patients may require urgent Renal Replacement Therapy (dialysis) if AKI is severe.