abrupt onset of glomerular haematuria (RBC casts or dysmorphic RBC) non-nephrotic range proteinuria Oedema hypertension transient renal impairment.
This is due to the immunologic response which triggers inflammation and proliferation of glomerular tissue that results in damage to the glomerular layers.
Post-streptococcal glomerulonephritis Non-streptococcal post-infectious glomerulonephritis, e.g. staphylococcus, pneumococcus, Legionella, syphilis, mumps, varicella, hepatitis B and C, echovirus, EpsteinBarr virus, toxoplasmosis, malaria, schistosomiasis, trichinosis Infective endocarditis Shunt nephritis Visceral abscess Systemic lupus erythematosus HenochSchnlein syndrome Cryoglobulinaemia Disease Most Frequent Clinical Presentation Pathogenesis Age Group Affected Treatment and Outcome Acute (Post- Streptococcal) Glomerulo nephritis Acute nephritis Abrupt oliguria, hematuria, facial edema, hypertension. Immune-complex mediated Occurs after Streptococcal pharyngitis or Hepatitis-B High ASO-titer, low C3 Common renal disease in childhood -Return to normal in 8 weeks. Complete recovery without treatment (especially in kids) within 3 years. Disease Most Frequent Clinical Presentation Pathogenesis Age Group Affected Treatment and Outcome Focal Segmental Glomerulo nephritis IgA Nephropathy (Berger's Disease): Most common primary Glomerulo nephritis Circulating IgA + fibronectin (due to chronic liver disease) Young men 15-30
Disease Most Frequent Clinical Presentation Pathogenesis Age Group Affected Treatment and Outcome Endocarditis S. Aureus Subepithelial immune deposits Kidney disease resolves when infection is cured. Rapidly Progressive Crescentic Glomerulo nephritis Wegener's: kidney + upper respiratory tract. Anuria Oliguria Inflamed glomerular capillaries ANCA (+) Must be treated or it will go to renal failure within weeks. POSTINFECTIOUS ACUTE GLOMERULONEPHRITIS is due to immune attack on the infecting organism in which there is cross-reactivity between an antigen of the infecting organism and a host antigen. Lancefield group A -haemolytic streptococcus of a nephritogenic type. The result is deposition of immune complexes and complement in glomerular capillaries and the mesangium. Symptoms and signs typically occur 710 days after onset of the acute pharyngeal or cutaneous infection and resolve over weeks after treatment of the infection. This is diagnosed by evidence of a recent streptococcal infection (culture of the organism, raised ASO titre) and low complement C3 levels that return to normal after 3-4 weeks. Long-term prognosis is good.
Renal function begins to improve spontaneously within 10-14 days, and management by fluid and sodium restriction and use of diuretic and hypotensive agents is usually adequate. Remarkably, the renal lesion in almost all children and most adults seems to resolve completely despite the severity of the glomerular inflammation and proliferation seen histologically. GENERAL MEASURES Fluid balance : strict input/output if oliguria is present, daily weight measurement. Diet : restriction of sodium intake in all children with edema or hypertension, restriction of foods high in potassium until oliguria resolves Bed rest: if hypertension, edema or cardiac failure are present
Drug treatment: Eradication of streptococcal infections using penicillin or alternatively erythromycin. Intravenous furosemide(1mg/kg) for edema and circulatory congestion For hypertension, the use of vasodilators (hydralazine, nifedipine, ACEI) may be effective A small number of adults develop hypertension and/or renal impairment later in life. Therefore in older patients, an annual blood pressure check and measurement of serum creatinine are required. Evidence in support of long-term penicillin prophylaxis after the development of glomerulonephritis is lacking. In non-streptococcal post-infectious glomerulonephritis, prognosis is equally good if the underlying infection is eradicated. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS RPGN is a syndrome with glomerular haematuria (RBC casts or dysmorphic RBCs), rapidly developing acute renal failure over weeks to months and focal glomerular necrosis with or without glomerular crescent development on renal biopsy. The crescent is an aggregate of macrophages and epithelial cells in Bowmans space . RPGN can develop with immune deposits (anti-GBM or immune complex type, e.g. SLE) or without immune deposits (pauciimmune, e.g. anti-PR3 and or anti-MPO-ANCA positive vasculitides). It can also develop as an idiopathic primary glomerular disease or can be superimposed on secondary glomerular diseases such as IgA nephropathy, membranous GN and postinfective GN. plasma exchange is used to remove circulating antibodies, steroids to suppress inflammation from antibody already deposited in the tissue, and cyclophosphamide to suppress further antibody synthesis. The prognosis is directly related to the extent of glomerular damage (measured by percentage of crescents, serum creatinine and need for dialysis) at the initiation of treatment. When oliguria occurs or serum creatinine rises above 600 700 mol/L, renal failure is usually irreversible. Once the active disease is treated, this condition, unlike other autoimmune diseases, does not follow a remitting/ relapsing course. Furthermore, if left untreated, autoantibodies diminish spontaneously within 3 years and autoreactive T cells cannot be detected in the convalescent patients. Disease Most Frequent Clinical Presentation Pathogenesis Age Group Affected Treatment and Outcome SLE Nephropathy Degree of kidney involvement correlates with prognosis in SLE. Anti ds-DNA antibodies.