Renal Tubular Necrosis After Oral Cholecystography

Acute Renal Failure due to Radio-Contrast Agents

“…Several instances of acute renal failure have been reported following ad ministration of multiple doses of bunamiodyl sodium (Orabilex) as an oral cholecystographic agent [13][14][15][16][17][18]. Excessive dosage, dehydration, and hepatic or renal disease were considered predisposing factors, although cases were subsequently reported in which renal and haptic function were normal [19].…”

“…The toxicity may be moderated by the extent and variability of intestinal absorption, alterations in blood pH resulting in dissociation of inorganic iodide [14] and the extent of hepatic removal of the media from blood [16]. Since many halogenated aromatic compounds are excreted after hepatic conjugation, a decreased clearance by the diseased liver may result in a large load of a potentially nephrotoxic agent being presented to the kidney for excretion [21], M u d g e [38], and P o stleth w a ite and K elley [39] have drawn attention to the potent uricisuric effect of iopanoic acid and meglumine iodipamide and have raised the possibility of acute urate nephropathy, especially in the setting of dehydra tion and hyperuricemia.…”

Toxic Nephropathies

“…The clinical picture varies from mild nonoliguric renal failure to severe unrelenting anuria, and the mortality rate may be as high as 40% . Nephrotoxicity has been attributed to enhanced dissociation to inorganic iodide at low urinary pH (119). Renal failure is observed only rarely with the use of iopanoic acid but was frequent with bunamiodyl (120).…”

Complications of gastrointestinal radiologic procedures: II. Complications related to biliary tract studies

“…The etiology of the renal damage caused by cholecystographic media is not clear [12][13][14][15][16][17][18][19][20][21]. Interestingly, most patients have had no underlying renal disease, as opposed to the situation with renal failure following use of the intravenous urographic agents [13,15,16,19].…”

“…Certainly factors that promote high blood levels of contrast agent would appear to be important. Other proposed mechanisms include a direct toxic effect on the renal tubules [15,20], crystalluria with intratubular block [15,16], and constriction of the preglomerular vessels with subsequent renal ischemia [13,17]. Other proposed mechanisms include a direct toxic effect on the renal tubules [15,20], crystalluria with intratubular block [15,16], and constriction of the preglomerular vessels with subsequent renal ischemia [13,17].…”