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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

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

During the last 6 years, 7 healthy individuals who were reasonably well acclimatised to physical exertion came under observation with acute renal failure due to exercise induced myoglobinuria. Their mean age was 20 years, and renal failure resulted after cross country run of 10-15 km in 6 cases and long route march of 90 km in 3 days in one case. There was no evidence of effects of heat, dehydration or hypotension. Apart from myoglobinuria and significant urinary sediments, serum aldolase (mean 69.0 SL u/ml) and serum creatinine phosphokinase (mean 120.0 Sigma u/ml) were also elevated. Maximum blood urea and creatinine were 224 mg/dl and 13.9 mg/dl respectively. Hypocalcaemia was noticed in 3 cases, hyperkalaemia in 4 cases and hyperuricaemia in one case during the oliguric phase. One case had features of non-oliguric acute renal failure. All cases recovered though 4 cases required dialysis support. Kidney biopsy in 3 cases showed recovering acute tubular necrosis with eosinophilic material in tubules. Lactate studies in the convalescent period revealed normal response and repeat physical exertion of same severity after 6 months did not reproduce the syndrome. It is concluded that exertional rhabdomyolysis unassociated with heat stress is a rare entity, and with prompt diagnosis and energic management results are rewarding.
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PMID:Acute renal failure in severe exertional rhabdomyolysis. 824 Apr 94

Few studies have assessed the prevalence and outcome of acute renal failure (ARF) in the elderly. Among 437 ARF cases prospectively studied during a nine-year period in a nephrology department, 152 (35%) occurred in patients over 70 years of age (Group 1). Patients over 70 account for only 10.5% of all hospital admissions in our country, and prevalence of ARF was 3.5 times higher in these patients than in younger people. Acute tubular necrosis (ATN) was diagnosed in 40% of Group 1 and 52% of the younger patients (Group 2) (P less than .05), whereas prerenal ARF was found in 47% and 32%, respectively (P less than .001). Dehydration was the most frequent cause of prerenal ARF in the elderly (51%). The etiological distribution of ATN was similar in both groups, being of multifactorial origin in most cases. Oliguria was present in 49% of ATN in Group 1 and in 66% of Group 2 (P less than .05). There were no significant differences in dialysis needs. Mortality was higher in the elderly in all types of ARF, although differences did not reach statistical significance. Need for dialysis, mechanical respiration, decreased level of consciousness, and hypotension were associated with poor prognosis in both groups. Total recovery from ARF in older persons was less frequent and slower than in younger patients. It may be concluded that patients over 70 years of age are at high risk for developing ARF; nevertheless, age should not be used as a discriminating factor in therapeutic decisions concerning ARF.
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PMID:Incidence and prognosis of acute renal failure in older patients. 229 66

This patient had severe dehydration and renal failure presumed to be extrarenal. After volume replacement, the course was not typical for simple extrarenal azotemia or acute tubular necrosis. Tubular handling of salt and water may not provide adequate criteria to evaluate the cause of reduced glomerular filtration rate.
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PMID:Acute renal failure: a diagnostic dilemma. 685 13

Accepted causes (acute insults) and risk factors for the development of acute renal failure were defined, quantitatively assessed, and tested for statistical significance in 143 patients with acute tubular necrosis. Sixty-two percent of patients had more than one acute insult, and 48 percent had more than one suspected risk factor. Hypotension, excessive aminoglycoside exposure, pigmenturia, and dehydration were identified as highly significant acute insults, while it was concluded that sepsis and administration of radiocontrast material could not be incriminated as causes of acute tubular necrosis. An additive interaction between acute insults was demonstrated, and the severity of acute renal failure was related to the number and severity of acute insults. Patients with oliguric renal failure had more severe acute insults than patients with nonoliguric renal failure. Preexisting renal disease and chronic hypertension were significant risk factors, the latter only when hypotension had been one of the acute insults. An age of more than 59 years, gout and/or chronic hyperuricemia, diabetes, and long-term diuretic administration were not found to be significant risk factors.
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PMID:Acute renal failure. Multivariate analysis of causes and risk factors. 711 78

Renal failure secondary to CDDP is due to acute tubular necrosis and is usually reversible. We report 4 cases of definitive renal failure secondary to administration of cisplatin (CDDP). Three women and one man, mean age 40 +/- 8 years (24 to 64 years), at onset of dialysis are reported. They had received 1 to 4 courses of CDDP for an endometrial carcinoma (n = 2), a breast carcinoma or a thymoma. The mean total dose of CDDP was 447 +/- 169 mg (160 to 900 mg). There was no additional nephrotoxic drug. Before treatment serum creatinine concentration was normal (77 +/- 7 mumol per liter) in all patients. In 2 cases dehydration (due to vomiting and use of mannitol) occurred during CDDP treatment. One patient was treated 30 days after a nephrectomy. At the onset of dialysis, renal ultrasound was normal. In 3 cases dialysis was necessary within 15 days following chemotherapy. In one case renal function deteriorated progressively to end stage renal failure 12 months after CDDP treatment. Dialysis was performed in 3 cases by hemodialysis and in one patient by peritoneal dialysis. All patients remained more than 6 months on dialysis. Three patients died from their cancer. One patient, being considered cured from his thymoma, is currently being evaluated for a kidney transplantation. Our observations outline the potential severity of CDDP nephrotoxicity. Systemic hydration with serial serum creatinine measurements are mandatory during and after CDDP administration these patients.
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PMID:[Definitive end-stage chronic kidney failure after cisplatin treatment]. 815 52

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

The development of heterotopic ossification (HO) as a complication of toxic epidermal necrolysis (TEN) has not been previously reported. TEN, also known as Lyell's syndrome, is a rare but serious skin disorder that typically occurs after the administration of drugs, especially sulfonamides, barbiturates, phenytoin, and nonsteroidal anti-inflammatory agents. TEN is characterized by the development of large fluid-filled bullae with separation of large sheets of skin. Complications of TEN can include extensive denudation of skin with dehydration and electrolyte abnormalities, gastrointestinal hemorrhage, acute tubular necrosis, secondary infection of denuded skin, pneumonia, bacterial conjunctivitis, keratitis, and septic infarcts of internal organs. We report a case of HO in a patient with TEN after treatment with trimethoprim-sulfamethoxazole. A 49-year-old man developed an erythematous rash, bullae, fever, and extensive skin loss consistent with a diagnosis of TEN. He was intubated for complications of TEN (pneumonia) and maintained on bed rest for several weeks. In addition, he developed HO that resulted in multiple joint contractures. He was treated with aggressive range of motion by physical therapy, surgical resection of the HO followed by radiation to both elbows, right hip, and right knee. Postoperative outpatient rehabilitation enabled improved function in his mobility and activities of daily living. HO is known to occur after spinal cord and brain injuries and burns. It has not been reported to occur after TEN. Our experience with this case suggests that HO may merit inclusion into the list of complications of TEN.
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PMID:Heterotopic ossification as a complication of toxic epidermal necrolysis. 922 83

NSAID use is pervasive in our society. Existing NSAIDs pose little risk to patients who tolerate them early during their administration. Among persons with normal renal function who have no other risk factors (dehydration) for an acute hemodynamic effect, there is no risk. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. This acute hemodynamic effect is the most common renal syndrome caused by NSAIDs. With careful monitoring, this effect is readily detected with routine clinical laboratory tests (serum creatinine and/or blood urea nitrogen concentrations). However, patients who continue administration of NSAIDs in this setting risk acute tubular necrosis and permanent damage to the kidney. Newer NSAIDs that selectively inhibit cyclooxygenase-2: cyclooxygenase-1 ratio may provide a more favorable risk profile for patients who cannot tolerate existing drugs.
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PMID:Effects of NSAIDs on the kidney. 938 87


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