Diffuse endothelial proliferate glomerulonephritis - Light microscopy reveals hypercellular glomerular tufts

deposits and C3 (type I) or electron dense material incorporated into the membrane (type II, dense deposit disease). 4. Diffuse endothelial proliferate glomerulonephritis - Light microscopy reveals hypercellular glomerular tufts with proliferation of endothelial and mesangial cells which have neutrophilic and mononuclear cell infiltrate and perhaps crescent formation. IgG containing complexes seen on immunofluorescence along the GBM and in the mesangium. The lesion often occurs in association with acute infections, producing an acute nephritic illness (e.g. post-streptococcal GN) but healing completely .5. Anti-GBM disease - Linear deposition of IgG along GBM with variable inflammatory response Most destructive, hence neutrophilic cell infiltration, heavy fibrin deposition and extensive epithelial crescent formation Circulating anti-GM antibody attaches to the basement membrane and initiates damage. Goodpasture's syndrome - Anti-GBM disease associated with pulmonary hemorrhage. It is strongly associated with cigarette smoking G Crescentic glomerulonephritis - results from proliferation of epithelial cells. It may occur particularly in SLE, anti-GBM disease and the vasculitides (Wegner's granulomatosis and microscopic polyarteritis), but often occurs in absence of underlying disease. This pathological term is used synonymously with classical term 'rapidly progressive glomerulonephritis' Investigations in glomerular disease: Baseline measurements: 1. Glomerular filtration 2. 24-hr protein excretion 3. Plasma albumin and creatinine Diagnostically important tests: 1. Urine - RBC casts indicate glomerular disease 2. Anti-DMA antibodies - positive in SL E 3. Antinuclear factor - positive in SLE 4. Blood glucose - excludes diabetes 5. CXR -detects pulmonary oedema, malignancy, pulmonary hemorrhage, cavitation in Wegner's granulomatosis G Hepatitis B antigen -excludes hepatitis B 7 Rheumatoid factor - positive in RA 8. Serum and urine electrophoresis - excludes paraprotein 9 Anti-neutrophil cytoplasmic antibodies - positive in most cases of microscopic polyarteritis and Wegner's granulomatosis 10. Anti-glomerular basement membrane antibodies - Diagnostic of antiglomerular basement membrane disease 11. Serological tests for syphilis - excludes syphilis Clinical manifestations ACUTE NEPHRITIC SYNDROME Definition - A disease most common in children, characterised pathologically by diffuse inflammatory changes in the glomeruli and clinically by usually abrupt onset of macroscopic hematuria, proteinuria (usually moderate), oedema, hypertension and impaired renal function with or without oliguria Not all features may be present at the same time. Causes - 1. Infective agents - (a) Viral- Hepatitis, HIV, mumps, echovirus, varicella, cytomegalovirus, (b) Bacterial - Hemolyic streptococcus, pneumococcus, klebsiella, staphylococcus spp , salmonella, brucella, gonococcus, yersinia, syphilis, tuberculosis, leprosy. (c) Parasitic - Malaria, filaria, schistosomiasis, mycoplasma 2 Multisystem diseases - SLE, polyarteritis, Henoch-Schonlein purpura, Goodpasteur's syndrome, hemolyticuremic syndrome 3 Primary glomerular disease - Membranoproliferative glomerulonephritis, Berger's disease, mesangial proliferative glomerulonephritis. 4. Miscellaneous - Acute inflammatory demyelinating polyneuropathy, serum sickness, irradiation of Wilrrfs tumour Clinical features - Modes of onset - (a) Oedema - puffiness of face. (b) Urinary symptoms - Scanty and smoky orfranky bloody urine. (c) Symptoms of acute infection - Fever, bodyache, vomiting. (d) Cerebral symptoms - Headache, convulsions (e) Insidious onset - Weakness, pallor, loss of appetite. (f) Accidental discovery - on routine urine examination SYMPTOMS AND SIGNS -. 1. Oedema - may come on suddenly or gradually. Puffiness of face and whitish pallor constitute "nephritic fades", swelling of face usually in morning Generalised anasarca may occur. Oedema may be absent in mild cases and also in very severe cases. 2. Hypertension - occurs in majority of cases, the diastolic pressure being 90 to 120 mm usually, and as a rule persists for at least one week, returning to normal a few days after patient has had diuresis In 5 to 10 per cent cases hypertensive encephalopathy develops, the clinical features being severe headache, vomiting, fits, hemiparesis and other focal signs such as aphasia Associated mental changes such as confusion, disorientation and coma. The rise of pressure may give rise to pulmonary oedema. JVP is commonly elevated and with peripheral oedema presents a picture of CCF Renal retention of salt and water is responsible for the circulatory disturbance in acute nephritis. 3. Impaired renal function - Oliguria. Acute renal failure develops in some. Laboratory findings - 1. Urine -Volume reduced, dark in colour or smoky when fresh, tea-coloured after haemolysis. Proteinuria variable, rarely more than 2. 5 gm per day. Red cells and red cell casts. Also white cells, white cells casts and granular casts. 2. Evidence of streptococcal infection - in post-streptococcal GN. Demonstration of presence of A beta-haemolytic streptococcus of nephritogenic M-protein type in throat or skin lesion, and of an immune response to one or more of streptococcal exoenzymes. 3. Haematology - Polymorphonuclear leucocytosis, raised ESR 4. Biochemical - Blood urea and