Glomerulonephritis

In Glomerulonephritis (GN), there's inflammation that causes damage to the glomerulus, basement membrane and capillaries.

Interstitial nephritis is inflammation of the space between the cells and tubules. Glomerulosclerosis is the scarring of the glomerulus, which can be due to GN, obstructive uropathy, and focal segmental glomerulosclerosis.

Causes:

• Infection e.g. Group A Strep, Hep B and C

• Systemic inflammation e.g. SLE, RA

• Drugs e.g. NSAIDs

• Metabolic disorders e.g. DM, HTN

• Malignancy

Clinical features:

• Haematuria

• Oliguria

• Proteinuria (< 3g/24hrs, which is the hallmark after which it becomes nephrotic syndrome)

• Oedema

• HTN

Most types of GN are treated with Steroids and ACEi/ARBs (controls BP and decreases proteinuria).

IgA Nephropathy - Typically occurs days post-infection. Histology shows IgA deposits and glomerular mesangial proliferation.

• Here, the IgA-IgG complexes deposit in the mesangium (cells within glomerular matrix), causing the activation of the complement pathway → glomerular injury

Membranous GN - Histology shows IgG and complement deposits on the basement membrane.

Post-streptococcal GN - Typically occurs weeks post-infection e.g. tonsillitis or impetigo.

Goodpastures Syndrome - Also known as Anti-GBM (glomerular basement membrane) Disease. With this, Anti-GBM attack the kidneys and lungs, causing glomerulonephritis and pulmonary haemorrhage, therefore presenting with acute kidney failure and haemoptysis. Patients are treated with High-dose steroids and Cyclophosphamide.