Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although acute renal artery obstruction causes cessation of kidney function, the viability of the nephron is often maintained by collateral circulation. When renal artery blood flow is restored, filtration is resumed and the resulting acute tubular necrosis is gradually resolved as renal tubular cells regenerate. We have observed several different mechanisms of acute renal artery obstruction resulting in anuric renal failure: temporary suprarenal placement of an aortic clamp during absominal aneurysmectomy, resulting in bilateral renal artery occlusion; embolus, presumably of cardiac origin, to a solitary kidney; and thrombosis of the distal aorta extending to a level proximal to the renal arteries. There is no correlation between the duration of renal artery occlusion and the viability of kidney parenchyma. Viability of the kidney can only be determined by visual inspection at operation and response to revascularization. When vascular obstruction is a possible cause of acute anuric renal failure, immediate angiography is indicated. If a correctable vascular lesion is identified, operative intervention is mandatory.
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PMID:Revascularization of the ischemic kidney. 62 86

The effects of intramuscular glycerol on ischemic acute renal failure was investigated in dogs. Anesthetized dogs received a bilateral 120-min renal artery obstruction (RAO) alone, RAO plus 5 ml/kg of 50% glycerol or RAO plus 5 ml/kg of 75% glycerol. Control groups received the glycerol injection, but not RAO. Renal histopathology was minimal in dogs receiving glycerol alone. In RAO dogs, those receiving 50% glycerol showed diffuse acute tubular necrosis (ATN), while those receiving 75% glycerol had severe ATN with extreme mortality. Changes in serum creatinine, creatinine clearance, and fractional excretion of sodium were consistent with the histopathologic changes. We conclude that myoglobinuria, of a degree insufficient to cause renal failure itself, can interact with renal ischemia to significantly exacerbate the renal damage produced.
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PMID:Myoglobinuria exacerbates ischemic renal damage in the dog. 279 46

Splenectomy (SPLX) prevents ischemic acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion. This study attempts to reverse the protective effect of splenectomy in the ischemic model of ATN by increasing hematocrit before inducing ATN. Sham-SPLX, SPLX, and SPLX dogs given packed red cells to elevate hematocrit by 30% (SPLX-high hematocrit) received bilateral renal artery obstruction (RAO) for 120 minutes. Renal function was tested for 6 days post-RAO. Hematocrit in the SPLX-high hematocrit group was greater (p less than .05) than the SPLX-RAO group but did not differ from the non-SPLX group. All groups had different (p less than .05) serum creatinine levels for 48 hours post-RAO, and untreated animals differed from all the others at 144 hours. Serum creatinine was highest in untreated, lowest in SPLX-high hematocrit, and intermediate in noninfused SPLX animals. The same pattern was observed in blood urea nitrogen, creatinine clearance and renal histopathology. Fractional excretion of sodium in the SPLX groups was six times that in the intact animals (p less than .05), irrespective of hematocrit level. We conclude that increased hematocrit is protective in ischemic ATN, and does not promote PTC congestion or ATN in the SPLX animal. In addition, the protective effect of splenectomy may be mediated, in part, by mechanism(s) that alter sodium transport or osmolar excretion.
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PMID:Increased hematocrit mitigates ischemic renal damage in the splenectomized dog. 292 39

Two prior reports have described a cortical rim sign associated with renal infarction from acute renal artery obstruction. This paper adds four additional cases of a thin outer (subcapsular) cortical nephrogram due to renal vein thrombosis (two cases), acute tubular necrosis (one case), and renal artery embolization (one case). An acute vascular compromise from differing etiologic mechanisms appears to be the common denominator of the rim nephrogram. The nephrogram probably represents an intact subcapsular renal cortex (2-4 mm thick) perfused by the perirenal capsular collateral circulation. To date, the rim nephrogram has been visible only on high dose nephrotomography. Its smooth inner margin is sufficiently distinct to differentiate it from the shell nephrogram of severe hydronephrosis.
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PMID:Renal subcapsular rim sign: new etiologies and pathogenesis. 697 11

A case involving immediate postoperative prolonged warm ischemia in a transplanted kidney from a living related donor is presented. Repair of the renal artery after 3 hours 15 minutes of complete occlusion resulted in an 18-day course of acute tubular necrosis followed by full return of normal renal function. Significant collateral circulation has been present in all previously salvageable cases of transplant renal artery obstruction. This case demonstrates that a kidney from an optimally prepared donor can withstand more than 3 hours of posttransplant warm ischemia despite the absence of collateral circulation. An aggressive surgical approach to restoring circulation is indicated.
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PMID:Successful revascularization of early posttransplant renal arterial occlusion. 703 93