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