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

Acute renal failure or its equivalent, acute tubular necrosis, was induced in rhesus monkeys by a combination of dehydration, hemorrhagic hypovolemia, and packed cell transfusion. Clinicopathologic changes were studied at different time intervals. Increasing edematous swelling and disintegration of the epithelial cells in the convoluted tubules, thick loops of Henle, and collecting tubules during the first four hours were conspicuous. As a result, intratubular cellular detritus, red blood cells, and various types of casts were increased progressively between one and four hours, and decreased thereafter. As the time progressed, edema was subsiding but the absorption granules and fat droplets were increased in size and number from one to twenty-four hours. These findings would indicate widespread cellular degeneration and necrosis. Consequently, tubular integrity was impaired leading to necrosis, denuded tubular basement membranes, and occasional tubulorrhexis. Concurrently, some dilated peritubular or interstitial capillaries were ruptured releasing red blood cells and cellular debris, which eventually were picked up by the damaged tubules. Although the regeneration of the renal parenchyma was in progress after sixteen hours, groups of subcapsular tubules were dilated showing flattened epithelial cells. The glomerular capillaries were either dilated or engorged, empty or collapsed during the experiment. Bowman's spaces contained red blood cells and varying amounts of cellular debris. Although the clinicopathologic changes reported here may be attributed to one or more of the following factors, hypoxia, toxic effects and dehydration, most of the changes were apparently due to hypoxia.
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PMID:Experimental acute renal failure in primates. Clinical and histopathologic evaluation in light and electron microscopy. 10 71

A renal transplant patient in whom acute pancreatitis developed 2 1/2 years after surgery is presented. Pancreatisis was accompanied by hyperlipaemia, diabetes mellitus and acute renal failure possibly due to acute tubular necrosis. Pancreatic abscesses necessitated subtotal pancreatectomy 2 months later. Because of generalized tuberculosis finally the patient succumbed 6 weeks thereafter. As aetiological factors cytomegalovirus disease, disorders in lipid metabolism and immunosuppressive therapy must be discussed. It is concluded that prophylactic measures as well as early diagnosis, intensive care and therapy are necessary for reducing the high risks of pancreatis in renal transplant recipients.
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PMID:[Pancreatitis after renal transplantation (author's transl)]. 20 57

In cirrhosis and fulminant hepatic failure acute renal failure may occur both without ("functional renal failure") and with tubular necrosis, the two probably being the ends of a spectrum. The underlying pathophysiological change is an intense renal and intra-renal vasoconstriction. Evidence is presented that this is due to systemic endotoxaemia resulting from failure of the liver to filter endotoxins absorbed from the gastrointestinal tract. Acute renal failure complicating obstructive jaundic has also been related to endotoxaemia, but in contrast to cirrhosis and fulminant hepatic failure this is usually due to an associated gram-negative infection and the renal failure almost invariably has the features of acute tubular necrosis. Endotoxins have two major effects on the kidney: (i) renal vasoconstriction, and (ii) glomerular and peritubular fibrin deposition. The nature of the renal failure depends on the balance between these variables which may be profoundly altered by the underlying liver disease.
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PMID:[Renal failure during liver disease--The significance of endotoxins (author's transl)]. 33 83

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
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PMID:Drug-induced renal disease. 38 1

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

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

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

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

In a study of 1729 consecutive autopsies, the histopathologic diagnosis of disseminated intravascular coagulation (DIC) confirmed by the presence of microthrombi in more than two organs was made in 51 cases. Among them, 38 cases (74.5%) were clinically not suspected of having DIC. Microthrombi were most frequent in the kidneys, followed by the lungs, spleen, adrenals, heart, brain, and liver, in descending order of frequency. Furthermore, a wide variety of visceral lesions was another important histologic feature of DIC. Kidney lesions assumed a position of prime importance, and special attention was given to the high frequency of acute renal failure due to so-called acute tubular necrosis and bilateral renal cortical necrosis. Infections, often associated with shock, and malignancies were the most common underlying causes of DIC. DIC is a frequent, often fatal pathophysiologic condition complicating many disorders. The true incidence of DIC at autopsy may be higher. It should be noted that demonstration of microthrombi and visceral alterations related to intravascular clotting is important for the evaluation of cases suspected of having DIC.
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PMID:Disseminated intravascular coagulation in autopsy cases. Its incidence and clinicopathologic significance. 53 Aug 89


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