| ID | 397 |
|---|---|
| Name | ACUTE GLOMERULONEPHRITIS SYNDROME |
| Cause | The acute disease may be caused by infections such as strep throat. It may also be caused by other illnesses, including lupus, Goodpasture's syndrome, Wegener's disease, and polyarteritis nodosa. Early diagnosis and prompt treatment are important to prevent kidney failure |
| Signs Symptoms | Pink or cola-colored urine from red blood cells in your urine (hematuria) Foamy or bubbly urine due to excess protein in the urine (proteinuria) High blood pressure (hypertension) Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen. Urinating less than usual. Nausea and vomiting. |
| Diagnosis | Diagnosis: 1. Urine- R/E (findings- high coloured, R.B.C, RBC cast, albumin). Presence of RBC cast is a diagnostic feature of AGN. 2. Blood- routine counts. 3. Blood biochemistry-Blood urea or blood urea nitrogen increased S. creatinine- increased S. electrolytes- Na+ decreased K+ increased S. total protein- decreased Albumin/globulin ratio- decreased S. cholesterol- may increased 4. Serology- ASO litre- increased (but it rarely rises after skin infection) Complement component C3 + (C4)- decreased 5. Isolation of orgaism (streptococci)- if in carrier state or active infection-Throat swab- C/S Skin lesion (if present)- C/S 6. Renal ultrasound- enlarged kidney. 7. Renal biopsy- to exclude ARF, N. syndrome, SLE or Ch. glomerulonephritis. 8. X-ray chest-any evidence of cardiomegaly or pulmonary oedema. 9. E.C.G- evidence of cardiomegaly or effect ofhyperkalemia. |
| Investigations | Urine test: This test will determine if you have protein or blood in your urine. Blood test: This test will measure the level of creatinine (waste product filtered by the kidneys) in a sample of your blood |
| Management | Management: Management depends on the clinical manife-stations of the disease. 1. In mild or initial stage (i.e oliguria with normal blood pressure)-a. Careful monitoring of blood pressure & fluid intake, b. Restriction of potassium intake, c. Diuretics can be given if oedema is present. d. Inj. Crys. penicillin should be given if pharyngitis or pyoderma is present-1 lac unit/kg/ day divided in 6 hourly doses for 7 days, (to kill any surviving streptococci, but has no effect on the course of renal disease). 2. Acute renal insufficiency a. Fluid restriction to an amount equal to insensible water loss (about 400ml/m2/24 hours), plus urinary output, and also loss in stool, vomitus & suction, b. Adequate calories at least 400 kcal/m2/24 hours in the form of carbohydrate & fat to minimize endogenous tissue catabolism. Total 60-100 kcal/kg/day, or more can be given. Protein should be restricted, c. Electrolyte and acid base abnormalities: i. Metabolic acidosis: should be corrected by i.v sodi-bi-carbonate. ii. Hyperkalemia: can profoundly affect cardiac depolarisation. If there is evidence of cardiac effects of hyperkalemia, measures should be taken immediately- viz. i.v glucose & insulin- 4gm glucose/kg with 1 unit soluble insulin/4gm glucose to be given slowly over 90 mins. Or, sodi-bi-carbonate 7.5% 2-3mmol/kg to be given i.v slowly. Both cause shifting of potassium into the cells within short time. iii. Hyponatremia: restriction of fluid alone is usually enough. 3% sodium chloride solu-tion can be used i.v over 15-60 minutes in an amount calculated to achieve a half-correction of the serum sodium concentration (if concentration of sodium is less than 120mEq/l). Normal saline can also be used. Frusemide l-2mg/kg i.v may also be of value. 3. Acute hypertension In AGN with hypertension, the aim of treatment is to keep the diastolic pressure below 90 mmHg & systolic below 140 mmHg. a. When hypertension is associated with- i. Evidence of hypertensive encephalopathy such as seizures, drowsiness or headache; ii. Signs of circulatory congestion and pulmonary oedema. Standard therapies for treating acute hypertension include- calcium channel blockers, vasodilators or angiotensin-converting enzyme (ACE) inhibitors. Diazoxide 5 mg/kg i.v rapidly in less than 15 sec. (acts in 3-5 mins; max effect up to 10 mins; duratio 6-24 hr). This dose may be repeated if a satisfactory drop in BP is not achieved within one hour. A dose of 5mg/kg may be given up to 4 times in 24 hours if necessary. As repeated administration leads to sodium retention, i.v. frusemide (0.5-Img/kg) is recommended if more than 2 doses of diazoxide are given. If diazoxide is not available, other vasodilator intravenous preparation can be given to control severe hypertensive crisis. Propranolol 1.5mg/kg/24 hrs, or methyldopa 10-50mg/kg/24 hrs in divided doses should be commenced after the first dose of diazoxide. Usually the lower dose is used first; dosage is then increased if blood pressure is not controlled. Nifedipine 0.2mg/kg/day can also be used with caution. Frusemide Img/kg/dose i.v. if circulatory congestion is present b. Diastolic BP > 100 mmHg with no other signs or symtoms-Hydralazine 0.15-0.3mg/kg/dose i.m. &/Or, Methyldopa 10-50mg/kg/24 hour. c. Diastolic BP > 80mm Hg but < 100 mmHg-Phenobarbitone 5mg/kg/24 hour. Frusemide Img/kg/dose i.v may also be given. 4. Left ventricular failure The child should be propped up. Frusemide 5mg /kg is often very effective. Digitalisation may be needed (dosage- see ‘common clinical problems’), the first one or two doses should be given i.m. Morphine 0.02mg/kg dose can be given to relieve restlessness. Hypertension should be controlled. 5. Circulatory congestion May pose a serious problem because of pulmonary edema and cardiac decompensation. Treatment consists of restriction of sodium and fluid intake, control of hypertension, relief of congestion with i.v frusemide, and in refractory and progressive cases phlebotomy or dialysis (with hypertonic dialysate) to reduce intravascular volume. Bed rest should be allowed during the oliguric hypertensive phase (upto first 1 or 2 weeks), ambulation with return to normal activities can be permitted after diuresis has started, and when ESR returns to normal. |
| Introduction | Acute glomerulonephritis is a glomerular disease characterised anatomically by inflammatory alteration in the glomeruli & clinically presents with hematuria, 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 tereptococcal (group-A p-hemolytic streptococus) or other infection (which may be slight or even pass unnoticed) |
| History | |
| Etiology | Infections such as strep throat. It may also be caused by other illnesses, including lupus, Goodpasture's syndrome, Wegener's disease, and polyarteritis nodosa. Early diagnosis and prompt treatment are important to prevent kidney failure |
| Clinical Features | Clinical features: 1. Age group- most common is children of school age, rare before the age of 3 years. 2. History of pharyngitis or impetigo (usually 1-2 wks. or 3 wks. following streptococcal sore throat or skin infection). Clinical features may vary from minimal to a very severe degree. 3. Onset- usually abrupt. 4. Oliguria with high coloured urine 5. Initially oedema of eyelids & face followed by oedema legs or limbs. 6. Hematuria (microscopic or macroscopic) 7. Hypertension with headache or vomiting- (in 50% cases) 8. Proteinuria (30-100mg/dl to over l000mg/dl) 9. Circulatory congestion or overload with dyspn-oea & tachypnoea 10. Abdominal or flank pain. 11. Irritability. 12. Low grade fever & general malaise. 13. Anorexia- sometimes associated with vomiting and upper abdominal pain. Acute phase lasts usually 4-10 days; increased B.P & BUN may persist for 2 weeks. Gross hematuria for 1 week; microscopic hematuria for 1-2 months. |
| Preventions | |
| Treatment | Prednisolone. Steroids are used to reduce swelling and suppress your immune system. Once your kidneys have started to recover, your dose of steroids will usually be lowered |
| Complications | Complications of AGN: 1. ARF with complete anuria, leading to- - uremia - hyperkalemia - metabolic acidosis. 2. Circulatory congestion, hypertension & left ventricular failure. 3. Hypertensive encephalopathy. (c/f- headache, vomiting, mental confusion, convulsion or coma). 4. Severe anemia. 5. Fits- febrile, hypertensive or due to sodium retention. |
| Prognosis | Course & prognosis of AGN: 1. Acute phase lasts usually 4-10 days; increased BP. & BUN may persist for, 2 wks; Gross hematuria for 1 week microscopic hematuria for 1-2 mons. 2. Complete recovery can be expected in about 90-95% cases. 3. A few patients (1-2%) die in the acute stage from anuria, cardiac failure or hypertensive encephalopathy. 4. A few enter a rapidly progressive phase with persisting proteinuria, hematuria and azotemia; death occurs few months from the onset. 5. About 10% of cases enter into a latent phase during which they feel well but continue to have persistent proteinuria with red cells and casts in the urine and a raised Addis count. These patients ultimately enter the terminal stage of chronic glomerulonephritis. Ultimately death from ure-mia & metabolic acidosis. 6. Recurrences are extremely rare. Note: 1. During diuretic phase fluid, protein, sodium and potassium content of diet should be increased, and soon be returned to normal. 2. Gross hematuria seldom persists beyond the 1st week, but microscopic hematuria and customarily persist for 1-2 months. 3. Blood pressure, weight, pulse, respiration and intake-output charts should be maintained. |
| Types | Nephritic Glomerulonephritis IgA nephropathy. Henoch Schonlein purpura (HSP)[7] Post streptococcal glomerulonephritis. Anti-glomerular basement membrane disease. Rapidly progressive glomerulonephritis. Granulomatosis with polyangiitis. Eosinophilic granulomatosis with polyangiitis. Polyarteritis nodosa |
| 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 & ‘fixed’ or planted antigen. 4. Circulating ‘primed’T cells in association with macrophages. |
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