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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.
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PMID:Urinary diagnostic indices in acute renal failure: a prospective study. 66 84

An 18-year-old girl developed acute renal failure 24 hr after ingestion of potassium dichromate. Laboratory data revealed associated intravascular haemolysis. Renal histology showed features suggestive of acute tubular necrosis. She went into diuretic phase after 11 days of oliguria and subsequently regained normal renal function. Both direct toxic damage by dichromate and intravascular haemolysis may have contributed to the development of acute tubular necrosis and acute renal failure.
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PMID:Intravascular haemolysis and acute renal failure following potassium dichromate poisoning. 68 12

The utilization of a hypothermic, hyperosmolar, intracellular washout solution for human kidney preservation was shown to be successful in 18 kidneys obtained from 9 heart beating cadavers. The ischemic interval ranged from 2 hrs and 57 mins to 39 hrs and 48 mins. All 18 kidneys functioned within 3 hrs of revascularization. Acute tubular necrosis with oliguria was noted in 4 of 6 patients with ischemic intervals longer than 20 hrs but not in the 12 patients obtaining kidneys preserved for 19 hrs or less. All patients with acute tubular necrosis required hemodialysis for one to 16 days post-transplantation with eventual recovery.
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PMID:Human cadaver kidney preservation using hypothermic hyperosmolar, intracellular washout solution. 78 59

Scanning with technetium-99m was used as a diagnostic aid in renal transplant patients with post-transplant oliguria. It is a safe and dependable method of determining whether the renal vasculature is still intact and can often be used to differentiate acute tubular necrosis from acute rejection.
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PMID:Dynamic scintiscanning with technetium-99m as a diagnostic aid in oliguria after renal transplant. 79 Jun 7

The renal biopsy findings in a 76 yr-old woman suffering grom anuria due to acute tubular necrosis are described. The glomeruli were normal on light- and electron microscopy. Immunofluorescent studies failed to reveal any fibrin or immunoglobulins in the glomerular capillaries. Extensive focal areas of necrosis were seen in the tubular epithelium often exposing the lumen of the tubule directly to the tubular basement-membrane. In some areas necrotic cells lay adjacent to normal or near normal cells. The proximity of the necrotic tubular epithelium to the oedematous interstitial tissue and the peritubular capillaries, together with the finding of normal glomeruli is compatible with the theory of back diffusion as a mechanism for the oliguria.
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PMID:Renal tubular necrosis due to shock: light and electron-microscope observations. 94 90

Total ureteropelvic necrosis of the transplanted kidney occurred more than one month after transplantation in 5 of 575 consecutive renal transplants performed at the University of Minnesota Hospital since 1963. Necrosis became evident long after normal renal function had been established. Histologic signs of rejection were minimal, but perinephric or periureteral hematomas were found in 3 of 5 patients: post-transplant acute tubular necorsis requiring hemodialysis occurred in all. The pathogenesis of this complication probably involves (1) a primary deficit of blood supply from the renal vessels to the pelvis and ureter, (2) a failure to develop a new ureteral blood supply because of surrounding hematoma, (3) early swelling of the ischemic ureter resulting in oliguria interpreted as acute tubular necrosis, (4) resolution of edema resulting in diuresis, and (5) late patchy ureteral necrosis and fistula formation due to ureteral ischemia.
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PMID:Late ureteropelvic necrosis after transplantation. 109 Oct 63

Thirty-four renal transplant recipients received drip infusion urograms from 2-24 days post-transplantation. Twenty-two patients exhibited changes in renal function within 1-4 days of the urogram that were indistinguishable from allograft rejection: a tender, swollen kidney, elevation of serum creatinine, oliguria, decreased urine sodium concentration, weight gain, and hypertension. Two patients developed acute tubular necrosis and required hemodialysis, but renal function in the remaining 20 patients improved after therapy for "graft rejection" with i.v. methyprednisolone sodium succinnate. Kidneys from older-age donors that were functioning suboptimally and kidneys which exhibited subsequent clinical allograft rejection were more at risk for contrast media toxicity. This suggests that occult vascular lesions may have been present in the allograft which were exacerbated when exposed to the irritant vascular effects of contrast media, producing a mild, reversible toxic nephritis. However, several kidneys with normal function and several kidneys which never exhibited rejection activity were also adversely affected by exposure to contrast media. It appears these agents should be used cautiously, if at all, in the early post-transplant period.
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PMID:Adverse effects of meglumine diatrizoate on renal function in the early post-transplant period. 110 14

Variable degrees of acute renal failure developed in three patients receiving therapy with cephalothin sodium. The course and findings were consistent with acute tubular necrosis of the oliguric and nonoliguric types. One patient had protracted oliguria, a second experienced transient oliguria, and one had normal urine output. All had urinary sediment changes consistent with tubular necrosis, and the two oliguric patients had elevated urine sodium concentrations. No other causes for renal failure could be detected, and all recovered after discontinuation of cephalothin therapy, although peritoneal dialysis was required in one patient. These observations indicate that cephalothin is capable of inducing renal damage in man.
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PMID:Nephrotoxicity associated with cephalothin administration. 113 Sep 24


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