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

Recent advances in prenatal and neonatal care have increased the number of live births and extended the life expectancy of critically ill premature infants. These infants represent a formidable therapeutic challenge in that multisystem involvement and previously uncommon conditions, such as intravascular coagulation, acute tubular necrosis, and acute cortical necrosis are now seen with increased frequency. This review begins with a discussion of the development of renal function in the neonate followed by a description of the more common causes of acute renal failure (ARF) in this age group. Finally, the pathophysiology, diagnosis, and management of this condition are discussed.
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PMID:Acute renal failure in the newborn. 40 50

The usefulness of the renal scan in diagnosing technical complications in the transplant patient is well established. However, the ability of the renal scan to differentiate between acute rejection and acute tubular necrosis has remained uncertain. We have evaluated the effectiveness of the 99mTc DTPA computer-derived time-activity curve of renal cortical perfusion, as well as data obtained from scintillation camera images, in making such diagnoses. Fifteen patients with a clinical diagnosis of either acute rejection or acute tubular necrosis, or both, were studied retrospectively. Technetium scan diagnoses did not agree with the clinical assessment in nine of the patients. Thus selection of a course of treatment should not be based on data obtained from the scan alone.
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PMID:Differentiation between renal allograft rejection and acute tubular necrosis by renal scan. 40 93

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

A patient with nonoliguric acute renal failure secondary to acute tubular necrosis in conjunction with anorexia nervosa is described. Parenteral feeding at a critical time has salutory effects on the biosynthesis of new protein and thereby reduces many of the hazards of azotemia. The technique of estimating endogenous acid production is applied for the first time in a severely malnourished subject and documents the retention of dietary sulfur which presumably is retained in the formation of new tissue in the recovery phase.
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PMID:Anorexia nervosa with acute tubular necrosis treated with parenteral nutrition. 40 63

Studies were undertaken to determine whether a hypotensive episode under variable conditions is capable of inducing experimental acute renal failure in rats. Animals were subjected to hypovolemic shock by withdrawing volumes of blood necessary to maintain a systolic pressure of 30-40 mm Hg for 105-110 min. The blood was then reinfused and the animal was allowed to recover for 48 h prior to sacrifice. In an attempt to increase the injury, a second group of animals was salt-depleted prior to injury, a third group was volume-depleted by being deprived of H2O for 72 h prior of injury, a fourth group received 7.5 mg/kg indomethacin 30 min prior to injury, and a fifth group had 30% of the blood which was removed to produce shock hemolyzed and returned following the injury. In all groups examined, light microscopy revealed a moderate to severe acute tubular necrosis localized mainly in the outer stripe of the outer zone as defined by Peter (1909). Tubular damage was confined to the medullary pars recta of the proximal tubule and only in the most severe cases did injury involve the cortical pars recta and pars convoluta. Casts were present in the distal tubules and collecting ducts. Despite these significant histologic alterations, BUN values from all experimental groups remained within control levels. These studies clearly show that extensive necrosis of the medullary pars recta can be dissociated from the development of acute renal failure.
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PMID:Hypovolemic models of acute tubular necrosis in the rat kidney. 41 58

Twelve Rhesus monkeys were inoculated intravenously with about 500 000 malaria parasites, Plasmodium knowlesi. Acute hemolysis occurred 5 days later, and all animals died on the 6th or 7th day after inoculation. All organs were gray-green to gray-brown because of deposition of hemoglobin and malaria pigments. This deposition was particularly striking in the lung, brain, abdominal fat and serous surfaces. Microscopic changes indicative of acute hypoxia were found in the liver (centrilobular necrosis) and kidneys (acute tubular necrosis). Terminal intravascular coagulopathy was evidenced by widely distributed, recently formed, fibrin thrombi.
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PMID:Plasmodium knowlesi malaria in the Rhesus monkey. 41 5

The course of nonoliguric acute renal failure (ARF) in 11 patients was analyzed. The possible etiology of the renal failure was multiple in all cases and did not differ from that seen in oliguric acute tubular necrosis (ATN). Other than the urine volume, which ranged from 510 to 2,325 ml/day, there was no major clinical or biochemical difference between these cases of nonliguric ARF and those described for oliguric ATN. Creatinine clearance, however, was higher than anticipated in oliguric ATN and ranged from 2.8 to 15.0 ml/min. There was a direct relationship between creatinine clearance and daily urine volume. The essential difference between oliguric and nonoliguric renal failure appears to be the lesser degree of renal damage in the nonoliguric form.
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PMID:Nonoliguric acute renal failure. 42 44

Five patients with severe jaundice resulting from amoebic liver abscess are described. All had features of hepatic parenchymal damage and cholestasis, and 1 patient developed hepatic coma. In addition, acute tubular necrosis and renal failure occurred in 3 patients. Four patients in the series survived. The importance of early recognition and treatment of amoebic liver abscess in patients presenting with jaundice is emphasized, so that the serious and often fatal complications of hepatic and renal failure can be prevented.
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PMID:Amoebic liver abscess in patients presenting with jaundice. A report of 5 cases. 42 69

Regeneration of the ray kidney was observed for six days after inducing acute tubular necrosis of the proximal pars recta with d-serine (80 mg/100 g body weight. Regenerating cells appear by two days post-treatment, and re-epithelialization of the nephron is completed within six days, with the most mature cells approaching normal morphology. Regeneration originates from viable cells adjacent to the necrotic zone which divide and follow a template provided by the intact basement membrane. Transient, cytoplasmic regenerative activity among developing tubular cells is characterized by the presence of large, irregularly shaped nuclei, prominent nucleoli, abundant ribosomes and lysosomes, and abnormal mitochondrial configurations. Microfilaments appear to be involved in the formation of apical microvilli and the basal labyrinth of plasmalemmal convolutions. These data suggest that d-serine induced acute tubular necrosis of the proximal pars recta may be followed by rapid, patterned regeneration along an intact basement membrane, and that microfilaments are involved in differentiation of cellular morphology.
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PMID:Renal regeneration following d-serine induced acute tubular necrosis. 42 2

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


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