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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 mechanism by which amino acid infusion stimulates membrane physpholipid biosynthesis during renal regeneration after mercuric-chloride-induced acute tubular necrosis was studied in the rat. Amino acids can act directly on regenerating renal tissue to enhance net phospholipid synthesis because preincubation of cortical slices with amino acids induced an increase in [14C]-choline incorporation into phospholipid without altering the rate of breakdown. This amino acid stimulation of phospholipid biosynthesis was studied further by measuring [14C]-choline accumulation and its sequential conversion to phosphorylcholine, cytidine diphosphocholine (CDP-choline), and phosphatidylcholine via the Kennedy pathway in regenerating renal tissue. [14C]-Choline accumulation was increased after amino acid infusion, compared to glucose infusion. There were also increments in the Vmax of the choline kinase reaction, which converts entering [14C]-choline into [14C]-phosphorylcholine, and of the cholinephosphotransferase reaction in which [14C]-CDP-choline is incorporated into [14C]-phosphatidylcholine, whereas the apparent Km of each reaction was unchanged. Thus, amino acids infused after tubular necrosis can act directly on regenerating renal cells to increase precursor availability and augment two reactions of the phospholipid biosynthetic pathway.
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PMID:Amino acid-mediated stimulation of renal phospholipid biosynthesis after acute tubular necrosis. 48 Jul 86

The Comrades Marathon is a gruelling test of man's stamina and only trained athletes participate. It is surprising that of over 2,000 contestants each year on a 90-km (56.25-mile) course, severe cardiac and renal damage does not occur more often. We are able, however, to report 10 cases over 9 years when renal damage did occur. 3 cases required haemodialysis; 1 had peritoneal dialysis; 2 patients had renal biopsies. Possible idiosyncratic factors are discussed as is the pathogenesis of acute tubular necrosis.
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PMID:Acute renal failure in marathon runners. 50 65

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

The essential pathologic lesion in Rocky Mountain spotted fever (RMSF) is a vasculitis that may involve the kidneys as well as the heart, brain, skin, and subcutaneous tissues. Histopathologic information concerning the response of the kidneys in RMSF is rather limited, however. In this study renal tissue from 17 children who died of RMSF was examined by light, electron, and immunofluorescence microscopy. A lymphocytic or mixed inflammation, or both, involving vessels and interstitium of the kidney was found in all patients. In addition, 10 patients had histologic evidence of acute tubular necrosis, and another 3 had glomerular lesions consisting of focal segmental tuft necrosis or increased cellularity secondary to neutophilic infiltration, or both. Immunofluorescence- and electron-microscopic studies failed to demonstrate immune-complex deposition within glomeruli, a finding that suggests that immunoglobulin and classic immune complexes were not involved in the pathogenesis of the renal lesions at the time of death. These findings suggest the possibility that the pathogenesis of the renal lesion in RMSF may be due to a direct action of the organism (Rickettsia rickettsii) on the vessel wall.
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PMID:Kidney lesions in Rocky Mountain spotted fever: a light-, immunofluorescence-, and electron-microscopic study. 52 76

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

In one case of fulminant hepatic failure by acute alcoholic hepatitis, renal failure seemed to be related to active renal vasoconstriction by systemic endotoxemia due to impaired hepatic clearance of toxins, associated with or complicated by a located intravascular coagulation with acute tubular necrosis. The associated thiamin deficiency may have accentuated this renal vasoconstriction.
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PMID:[Acute tubular necrosis in acute alcoholic hepatitis with cardiac beriberi (author's transl)]. 55 56

Three patients having lepromatous leprosy developed acute renal failure. Two patients completely recovered and one was left with a moderate degree of renal insufficiency. Renal tissue obtained by percutaneous biopsy revealed acute tubular necrosis in two and diffuse crescentic glomerulonephritis in the third case.
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PMID:Acute renal failure in leprosy. 56 62

Intravesical instillation of formalin in a patient with transitional cell carcinoma of the bladder and radiation cystitis was followed by acute renal failure due to acute tubular necrosis. Formic acid, which is a metabolic product of formalin, has been postulated as the pathogenetic agent responsible for acute tubular necrosis.
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PMID:Acute tubular necrosis following intravesical instillation of formalin. 56 92

Fatal acute tubular necrosis occurred in 1 patient in whom intravesical formalin was used to control massive persistent hemorrhage from radiation cystitis. A suggestion is made to monitor blood formic acid levels and institute prompt dialysis whenever these exceed 80 mg. per 100 ml. to avert such a catastrophe. Intravenous sodium bicarbonate appears to be indicated prophylactically in combating the associated metabolic acidosis due to absorbed formic acid.
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PMID:Fatal complication of intravesical formalin during control of intractable hemorrhage from radiation cystitis. 56 77

Acute renal failure due to intravascular hemolysis is a common clinical problem in North Indian patients. It constituted 21.5 percent of 325 patients dialyzed for acute renal failure over an 11-year period at Chandigarh. Thirty patients had developed acute intravascular hemolysis in association with erythrocyte glucose-6 phosphate dehydrogenase (G-6PD) deficiency, 17 due to copper sulphate intoxication and 8 due to envenomation by snakes. Less frequent causes were insect stings, incompatible blood transfusion, intake of anti-leprosy drug--dapsone in non-G-6PD-deficient patients, and mercuric chloride toxicity in two patients each; naphthalene poisoning in one; and uncertain causes in six patients. Renal histology was available in 55 patients. Acute tubular necrosis was seen in 54 and bilateral diffuse cortical necrosis in one patient. Fifty patients (71.43 percent) survived and 20(28.6 percent) diet. G-6PD erythrocyte deficiency, which is present in 4.5 percent of the North Indian population, was the most frequent cause of acute renal failure in this group.
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PMID:Acute renal failure due to intravascular hemolysis in the North Indian patients. 60 54


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