Patients with chronic renal failure retain Na+ and H2O, and they retain K+ and acid. This disordered homeostasis results in hypertension, edema, hyperkalemia and acidosis. Diuretics may be used to favorably modify these disturbances. However, because of the limited filtered load of water and electrolytes, and the low renal blood flow, measures need to be taken to maximize the response to diuretics. These measures include: (a) the use of the most bioavailable drug, torasemide, when using the oral route; (b) the use of the drug with the least hepatic elimination, furosemide, when using the intravenous route; (c) the use of combinations of loop- and distal tubule-acting diuretics; (d) the use of the maximum effective diuretic dose; and (e) the use of repeated doses or constant infusion. In benefiting hypertension, vascular congestion and hyperkalemia diuretics appear to exert their effects not only on the kidneys but also on extrarenal sites, such as the vascular tree and the gastrointestinal tract. The use of diuretics, however, is not without complications, which include: intravascular volume depletion and azotemia, ototoxicity (when using loop-acting diuretics), hyperlipidemia, acute pancreatitis, hyperkalemia (when using K+-sparing agents), and acidosis (when using carbonic anhydrase inhibitors).
|Original language||English (US)|
|Journal||Kidney International, Supplement|
|State||Published - Jan 1 1997|
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