Management And Special Types Of Acute Nephritic Syndrome (Goodpasture’s Syndrome)
Special Types Of Acute Nephritic Syndromes
A General Overview
Complications arising during the course of the disease, such as hypertensive encephalopathy, cardiac failure with pulmonary edema, hyperkalemia and uremia demand active intervention.
The hypertension occurring in acute nephritic syndrome is often self-limiting and in most cases does not require any special treatment. If the blood pressure is high (diastolic above 110-120) and hypertensive complications are imminent, hydrallazine, methyl dopa or propranolol have to be used in adequate doses. If blood pressure rises rapidly or hypertensive encephalopathy occurs, parenteral reserpine 0.5- 1mg intramuscularly or diazoxide 100-200mg intramuscularly may be given. If convulsions continue in spite of antihypertensive therapy, lumbar puncture to release a small quantity of CSF may help in controlling seizures. This procedure is seldom resorted to these days.
Pulmonary edema is to be treated on the usual lines of left ventricular failure. Sedation with diazepam 10mg given intramuscularly or intravenously, oxygen inhalation, furosemide in large doses (often 100-200mg given intravenously) and slow intravenous injection of aminophylline may be helpful. If the diuretic does not bring about dieresis, pulmonary congestion can be effectively relieved by physiological venesection by applying tourniquets to the proximal parts of the limbs to prevent venous return. Open venesection in which 250-400ml of blood is removed from the antecubital vein can also be tried if facilities for more effective therapy are not available. Dialysis or ultrafiltration may be employed to removed the excess of fluid in these cases. Digitalisation has to be determined, based on the individual case. A course of penicillin is indicated if there is active infection by streptococcus.
Good Pasture's Syndrome In Diagram
This is a typical example of anti-GBM-antibody mediated glomerulonephritis. Antibodies against the glomerular basement membrane (GBM) and pulmonary capillary basement membrane are produced. These attach to the respective basement membranes and set up inflammatory reaction. In the glomerular capillary basement membrane, the antibody appears as a linear deposit on immunofluoresence microscopy. This stands out in sharp contrast to the granular deposit of immune complexes seen in post-streptococcal acute glomerulonephritis. Renal histology shows proliferation of the epithelial cells of the Bowman’s capsule giving rise to the appearance of crescents. The disease presents with pulmonary symptoms such as hemoptysis and features of acute glomerulonephritis. The prognosis is generally unfavourable. Large doses of corticosteroids and immunosuppressive drugs have been tried but the results are not uniformly good.
Systemic lupus erythematosus, polyarteritis nodosa, Henoch-Schonlein syndrome, and infective endocarditis may give rise to acute nephritic syndrome during their course. Other evidence of the underlying disease is generally present. Treatment is for the primary disorder. Renal manifestations usually subside with the underlying condition.
© 2014 Funom Theophilus Makama