A diffuse proliferative type of glomerulonephritis
Most common cause of acute nephritis worldwide
Group A strept (strept. Pyogens)
Occurs 1–12 weeks after a sore throat or skin infection (streptococcal antigen deposited on the glomerulus à host reaction and immune complex formation)
Presentation of post-streptococcal glomerulonephritis
Diagnosis of post-streptococcal glomerulonephritis
Findings of acute nephritis + demonstration of a recent GAS infection (positive throat or skin culture or serologic tests [anti-streptolysin titer ASOT), low complement, RBC casts
Renal biopsy findings in post-streptococcal glomerulonephritis
Management of post-streptococcal glomerulonephritis
Supportive, >95% recover normal renal function
Antibiotic therapy is given to those who have still have a streptococcal infection at the time of diagnosis
Anti-GBM (Goodpasture syndrome)
Caused by autoantibodies to type IV collagen, which is highly expressed in the GBM and alveoli
Usually presents with rapidly progressive glomerulonephritis: acute renal failure (may occur within days), nephritic urine sediment, and non-nephrotic proteinuria
Pulmonary involvement (alveolar hemorrhage à hemoptysis & dyspnea) is present in 40 to 60% of patients, especially in smokers
Diagnosis of Anti-GBM (Goodpasture syndrome)
Demonstration of anti-GBM antibodies, so kidney biopsy is required: Linear deposits of IgG along the GBM is diagnostic
Treatment of Anti-GBM (Goodpasture syndrome)
Plasma exchange to remove the autoantibodies, steroids ± cyclophosphamide
If treatment is started early, full recovery is possible, and relapses are rare
Renal prognosis is poor if dialysis-dependent at presentation
IgA nephropathy (HSP)
Most common cause of chronic glomerulonephritis in developed countries
Common cause of mild recurrent hematuria
Most patients present with either gross hematuria (single or recurrent), usually accompanying an upper respiratory infection or after exercise, or microscopic hematuria with or without mild proteinuria incidentally detected on a routine examination
Occasionally they might present with rapidly progress glomerulonephritis & nephritic syndrome
lgA production is increased during infections à forms immune complexes and deposits in mesangial cells
When accompanied by extra-renal symptoms: purpuric skin lesions, abdominal pain, arthralgia à Henoch-Schoenlein purpura
Renal biopsy findings in IgA nephropathy
Treatment of IgA nephropathy
Supportive
ACEI should be given to all patients
Steroids/immunosuppression may slow decline of renal function if persistent proteinuria
Prognosis of IgA nephropathy
Investigations for nephritic syndrome
Urine microscopy for red cells and casts
RFT (Serum urea and creatinine raised)
Creatinine clearance (low)
24-hour urine protein (raised)
C3 and C4 (low), Normal complement in IgA nephropathy & anti-GBM
Chest X-ray for pulmonary edema
Renal imaging (normal size)
Renal biopsy if needed
Diagnostic tests for specific causes: Throat swab, Antistreptolysin O titer, ANCA, Anti-GBM antibody, Cryoglobulins
General management of nephritic syndrome
Daily weight checks
Fluid balance chart
Antihypertensive & BP monitoring
Salt restriction
Fluid restriction
Diuretics
Dialysis if needed
Specific treatment for each cause if needed
Alport syndrome
Congenital defect of collagen IV à glomerular disease