Glomerulonephritis diuretics

Post-streptococcal glomerulonephritis is the result of infection with the nephritogenic strain of group A hemolytic streptococci. The streptococci are usually isolated from patients with a sore throat and, in developing countries, skin infection like impetigo or infected scabies is an important cause. There is no specific treatment except for antihypertensives, salt restriction and diuretics. Corticosteroids are of no value. The disease is self-limiting but, in some adults, it may progress to chronic renal failure. 

Nephrotic syndrome is characterized by proteinuria and edema due to some form of glomerulonephritis. The resulting fall in plasma protein concentration decreases vascular volume, which leads to diminished renal blood flow. This in turn causes secondary aldosteronism characterized by Na and water retention and K+ depletion. Rigid control of dietary Na is essential. Therapy of the nephrotic syndrome using a thiazide (possibly with a K -sparing diuretic) to control the secondary aldosteronism, is a useful initial approach to treatment Since nephrotic edema is frequently more difficult to control than cardiac edema, it may be necessary to switch to a loop diuretic (and spironolactone) to obtain adequate diuresis. 

The nonsalicylate NSAIDs can also affect renal function. Risk factors fc>r NSAID-induced acute renal failure include congestive heart feilure, glomerulonephritis, chronic renal insufficiency, cirrhosis, systemic lupus erythematosus, diabetes mellitus, significant atherosclerotic disease in the elderly and use of diuretics. NSAIDs can adversely affect cardiovascular homeostasis and can be a risk factor for the onset or exacerbation of heart feilure. 

Diuretic resistance may occur simply because excessive sodium intake overrides the ability of the diuretics to eliminate sodium. Other reasons exist for diuretic resistance in this population. Patients with ATN have a reduced number of functioning nephrons on which the diuretic may exert its action. Other clinical states like glomerulonephritis are associated with heavy proteinuria. Intraluminal loop diuretics cannot exert their effect in the loop of Henle because they are extensively bound to the protein present in the urine. Still other patients may have reduced bioavailability of oral furosemide. Possible therapeutic options to counteract each form of diuretic resistance are presented in Table 42-7. Combination therapy of loop diuretics plus a diuretic from a different pharmacologic class can be an effective tool in the setting of ARF. Loop diuretics increase the delivery of sodium chloride to the distal convoluted tubule and collecting duct. With time, these areas of the nephron compensate for the activity of the loop diuretic and increase sodium and chloride resorption. Diuretics that work at the... 

Glomerulonephritis Pyelonephritis Nephrotic syndrome Drug-induced renal losses Aminoglycosides Amphotericin B Cyclosporine Diuretics Digitalis Cisplatin... 

The development of an acute interstitial inflammatory reaction in the kidney related to the administration of certain classes of drugs and leading to renal failure has been recognized for almost a century [42]. Antibiotics, in particular the sulfonamides [43] and semisynthetic penicillins [44, 45], were recognized as etio-logically associated in many instances. A retrospective review of 1068 kidney biopsies from 1%8 to 1997 by Schwarz et al. yielded acute interstitial nephritis in 6.5% of cases. In the majority of instances (85%) acute interstitial nephritis was drug related. Diuretics were implicated in 7.8 % of these cases [46]. Lyons et al. noted that four patients with proliferative glomerulonephritis and nephrotic syndrome treated with sulfonamide-derivative diuretics (furosemide or thiazides) developed severe renal failure, which reversed when the diuretic was withdrawn and prednisone was adminis-... 

Treatment of oedemalous hyponatraemia is based upon two principles. The underlying condition should be treated, whether that be. for example, heart failure, glomerulonephritis or alcoholic cirrhosis. Excess sodium and water should be reduced by means of a diuretic to induce a natriuresis. and by lluid restriction. 

THERAPEUTIC USES Thiazide diuretics are used to treat edema associated with heart (congestive heart failure), liver (cirrhosis), and renal (nephrotic syndrome, chronic renal failure, and acute glomerulonephritis) disease. With the possible exceptions of metolazone and indapamide, most thiazide diuretics are ineffective when the GFR is <30-40 mL/min. 

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