| ID | 136 |
|---|---|
| Name | ACUTE GLOMERULONEPHRITIS (Acute Nephritis) |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. Blood shows leukocytosis with increased polymorphs, high E.S.R. 2. Urine: colour smoky or coffee colour or cola coloured. Albumin (typically not in nephrotic range), RBC & RBC cast may be present. 3. Renal function test: Blood urea is raised & creatinine value changed. 4. Amount of urine: 300-600ml in 24 hours. 5. ASO litre is raised. 6. Throat swab for C/S is usually positive. 7. CXR: May be normal or may show sign of pulmonary oedema. |
| Management | |
| Introduction | Acute glomerulonephritis is a glomerular disease characterised anatomically by inflammatory alteration in the glomeruli & clinically presents with haematuria, proteinuria, oliguria & hypertension, with evidence of renal salt and water retension. Not all features may be present simultaneously. In some cases the condition develops 7-20 days after a stereptococcal (group-A-haemolytic streptococcus) or other infection (which may be slight or even pass unnoticed) |
| History | |
| Etiology | |
| Clinical Features | Clinical features: In children: 1. History- commonly a preceding infection (e.g sore throat,, skin infection). 2. Generalised oedema- salt and water retention producing oedema most marked around the eyes and puffy face. 3. Breathlessness- due to pulmonary oedema and in severe cases pleural effusion. 4. Fever (low grade). 5. Anorexia- sometimes associated with vomiting and upper abdominal pain. 6. Hypertension- rarely hypertensive encephalopathy. 7. Fits- febrile, hypertensive or due to sodium retention. 8. Urinary abnormalities- oliguria, haematuria and proteinuria < 3gm/day. In adults: 1. History- in many there is no history of preceding infection. 2. Oedema- not a marked feature. 3. Hypertension- variable 4. Urinary abnormalities- reduction in volume, haematuria (characteristically described as smokey), proteinuria < 3gm/day. |
| Preventions | |
| Treatment | Treatment: It is a self-limiting disease, so treatment is mainly for complications. 1. Hospitalization of the patient in case of oliguria, acute renal failure, heart failure or severe hypertension. 2. Rest of the patient till odema, hypertension, renal failure, heart failure is controlled. Proteinuria may continue for several years. RBC may or may not disappear at all. 3. If oedema is present, restriction of the fluid in first 24 hours upto 1/2 litre then fluid should be given after maintaining intake output chart. Fluid should be given = 24 hours (previous day) output + 500ml (or 2 glass of water as insensible loss). 4. Diet: Salt and protein restriction upto 20-40mg/day to be given. When blood urea becomes normal, food should be in normal quantity. Fruit and fruit juice should be restricted if there is hyperkalaemia. 5. For active strepto or staphylococcal infection: i. Inj Crystalline penicillin 5 lack unit i.m 6 hourly for 7 days. ii. Treatment for infected tonsil or other septic foci should be given. 6. For hypertension: Methyldopa, hydralazine or b-blocker may be given, but avoid propranolol if heart failure is present. Nifedipine is useful in acute hypertensive crisis. 7. Dialysis is indicated: When blood urea 200mg or above. Serum creatinine 10mg or above. Creatinine clearence- below 5ml. 8. Follow up: a. Urine examination (every 15 days or 1 month), b. Blood for serum creatinine and blood urea level. |
| Complications | Complications: 1. Hypertensive encephalopathy 2. Pulmonary oedema &/or pleural effusion 3. Severe uraemia 4. Fits (febrile, or hypertensive). |
| Prognosis | |
| Types | |
| Classification | |
| Observation | |
| Pathology | Pathogenesis: 1. In AGN the pathogenesis starts with diposition of immune complexes within the glomerulus which develops due to a modified immune response when a ‘specific glomerular basement membrane antigen’ excites antibody formation resulting in a relative antigen excess or antigen-antibody equivalence. 2. Trapping” of circulating small soluble immune complexes in the glomerular capillary wall. 3. ‘In situ’ formation of immune complexes in the glomerular capillary and/or mesangium from circulating antibody and ‘fixed’ or planted antigen. 4. Circulating ‘primed’T cells in association with macrophages. |
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