Glomerulonephritis

• Common form of end stage renal failure along with diabetes and hypertension
• Group of disorders where there is damage to the glomerular filtering apparatus
• This causes a leak of protein +/- blood into the urine depending on the disease
• Patients may present with;
  • Haematuria
  • Proteinuria
  • Nephrotic syndrome
  • Nephritic syndrome
  • Renal failure
  • Hypertension

Tests

• Bloods – FBC, U&Es, LFts, CRP, immunoglobulins, electrophoresis, complement (C3, C4), autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM), blood culture, anti-streptolysin O titre, HbSAg, anti-HCV
• Urine – RBC casts, microscopy and culture and sensitivity, Bence-Jones proteins
• 24hr urine protein
• CXR, renal ultrasound +/- renal biopsy

General management

• Refer to a nephrologist
• Keep BP <130/80 or 125/75 if proteinuria >1g/day
• Include an ACEI or ARB

Thin basement membrane nephropathy

• Genetic – autosomal dominant
• Causes persistent microscopic haematuria
• Biopsy – thin BM via EM
• Usually benign – small risk of CRF

Minimal change glomerulonephritis

• Commonest cause of nephrotic syndrome in children
• Thought to be T cell mediated
• Associated with Hodgkin’s lymphoma and drugs
• Causes a selective proteinuria – only small proteins are leaked out e.g. albumin
• Renal biopsy – fusion of podocytes on EM
• 95% of children and 70% of adults undergo remission with corticosteroids but are prone to relapse

Membranous nephropathy

• Accounts for 20-30% of nephrotic syndrome in adults and 2-3% in children
• Unknown cause
• Associations – malignancy, drugs (gold, penicillamine, captopril), autoimmune disease (RA, SLE, thyroid disease), infections (HBV, syphilis, leprosy, filiariasis)
• Usually presents with nephrotic syndrome
• Biopsy shows diffuse thickened glomerular BM, IF shows IgG and C3 subepithelial deposits
• Treat with corticosteroids or cyclophosphamide

Focal segmental glomerulosclerosis

• May be primary (idiopathic) or secondary (due to reflux or IgA nephropathy, Alport’s syndrome, vasculitis, sickle cell disease or heroin use
• Presents with nephrotic syndrome or proteinuria
• Biopsy – some glomeruli have scarring of certain segments (focal sclerosis) IF IgM and C3 deposits in affected areas
• 30-50% proceeds to end stage renal failure

IgA nephropathy (Berger’s disease)

• Commonest GN in the developed world
• Most present with macro or microscopic haematuria
• Typically the patient is a young male with episodic macroscopic haematuria occurring a few days after URTI. Recovery is rapid between attacks
• There is overproduction of IgA possibly due to infection which forms IC and deposits in mesangial cells

Henoch-Schonlein purpura

• Systemic form of IgA nephropathy causing a small vessel vasculitis
• Causes a purpuric rash on the extensor surfaces – most commonly the legs, flitting polyarthritis, abdominal colic and GN
• Diagnosis is usually clinical but IF on the renal or skin biopsy is positive for IgA and C3

Proliferative GN

• Chief cause is post-streptococcus GN – streptococcal antigen is deposited on the glomerulus cuasing a host reaction and IC formation
• Usually presents with a nephritic syndrome
• 95% recover renal functions

Mesangiocapillary glomerulonephritis

• Rare
• Most commonly presents with nephritic syndrome
• Biopsy shows large glomeruli, mesangial deposits and thickened capillary walls – tramline appearance of double BM
• There are 2 types;
  • Type 1 – subendothelial immune deposits, associated with classical complement activation. Associated with  HCV, endocarditis, visceral abscesses, infected arteriovenous shunts
  • Type 2 – intramebranous deposits sometimes with partial lipodystrophy (gaunt facial appearance)

Rapidly progressive GN

• The most aggressive GN with potential to cause end stage renal failure over days
• Biopsy finding of crescents affecting most glomeruli (proliferation of parietal epithelial cells and macrophages in Bowman’s capsule)
• Causes; microscopic polyangiitis, Wegener’s granulomatosis, Goodpasteur’s disease
• Treat with aggressive immunosuppression