Use of a Pteridine Diuretic (Triamterene) in Treatment of Hepatic Ascites

The use of amiloride hydrochloride in the correction of hypokalaemic alkalosis induced by diuretics

“…Gynaecomastia may be troublesome (Senewiratne & Sherlock, 1968), and it is not always effective without additional K+ supplement (Rosse, 1961). Triamterene has a shorter latent period but a rise in blood urea has been noted (Ginsberg, Saad & Gabuzda, 1964) especially when given in combination with a benzothiadiazine diuretic (Shaldon & Ryder, 1962).…”

Triamterene and the Kidney

“…The observed declines in renal function have occurred in normal volunteers [56,68], hypertensive subjects [18,21,30], edematous individuals [3,29,[57][58][59]62] and diabetics [56], and would suggest that TA manifests intrinsic nephrotoxicity independent of an underlying disease state.…”

“…can result in substantial deterioration in renal function which may prove to have very slow and limited reversibil ity [59,62]. The genesis of this form of acute renal failure, although not readily apparent from early studies, would seem not to be related to excessive diuresis alone [59].…”

“…A variety of indices of renal function have been em ployed as markers for TA's nephrotoxicity including increases in serum creatinine [18,21,58] or blood urea nitrogen [3,57,59,62] or decreases in creatinine clearance [56,68] and/or renal blood flow [30,58], with the latter most commonly attributed to the decline in cardiac out put [67] accompanying the administration of high doses of TA. Typically, the observed declines in glomerular filtration rate and renal blood flow with TA have oc curred in the dose range of 100-200 mg/day with or without concurrent administration of HCT.…”

“…Renal Failure TA has been frequently associated with transient de clines in renal function [3,30,[56][57][58][59][60][61][62] as well as with the development of frank acute renal failure. The latter can occur relative to several different causal mechanisms including interstitial nephritis [47-50], intrarenal ob struction secondary to crystalline deposits [63], and hem odynamic events which accompany the coadministration of TA with an NSAID [52- 55,64],…”