Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphocytes from patients with neoplastic disease were tested for sensitization to encephalitogenic factor (EF) by the macrophage migration inhibition test. Sensitization to EF was demonstrated in 71% of patients with various forms of neoplastic disease. Sensitization to EF was also demonstrated for 31% of subjects with no evidence of neoplastic disease; these included patients with warts, chronic bronchitis and hernias. In contrast, healthy subjects showed no sensitization to myelin basic protein. These observations suggest that sensitization to EF may not be confined to patients with neoplastic disease. Lymphocytes from hamsters bearing a transplanted virus induced tumour were sensitized to EF prepared from both human and hamster brain. Sensitization was also seen in hamsters infected with influenza virus but not in animals with acute tubular necrosis produced by glycerol treatment. The development of an animal model system provides a method for the investigation of possible mechanisms of sensitization.
Br J Cancer 1975 May
PMID:Cellular immunity to myelin basic protein in man and in animal model systems as measured by the macrophage migration inhibition test. 5 Aug 55

A case is reported of Fanconi syndrome and nonliquric renal failure, following a brief course of cephalothin and gentamicin, in a patient with diffuse histiocytic lymphoma. These drugs, especially when used in combination, have been associated with nephrotoxicity manifested as acute tubular necrosis and altered proximal tubular function, but biochemical evidence for generalized proximal tubular dysfunction has not been accurately defined. Thus far, only two other antibiotics, degraded tetracycline and streptozotocin, have been implicated in producing an acquired Fanconi syndrome.
Cancer 1978 Feb
PMID:Fanconi syndrome associated with cephalothin and gentamicin therapy. 34 14

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

The pathologic changes induced by Cis-platinum (II) diamminedichloride (CPDD) therapy in the kidneys are described in 12 patients with solid tumors and malignant lymphomas. According to dosage of CPDD the patients were divided into two groups: 1) low-dose group--.0.5-2 mg/kg daily, for 1 to 6 days; and 2) high-dose group--single injection of 3 or more mg/kg with concommitant mannitol-induced diuresis. Pathologic changes in the kidneys were essentially similar in both groups and consisted of focal acute tubular necrosis, affecting primarily the distal convoluted tubules and collecting ducts, dilatation of convoluted tubules, and formation of casts. These changes persisted as long as 29 days post CPDD therapy. In addition, the collecting ducts exhibited significant epithelial atypia. BUN and serum creatinine levels were elevated in both groups. The mean BUN/serum creatinine values were 54/2.2 mg/100 ml and 32/2.0 mg/100 ml for low and high-dose groups, respectively. Since the nephrotoxicity of CPDD is known to be dose-related, our findings suggest that mannitol-induced diuresis has considerably decreased the renal toxic damage of CPDD therapy in these patients.
Cancer 1977 Apr
PMID:The renal pathology in clinical trials of cis-platinum (II) diamminedichloride. 85 39

One hundred and seventy-five 67Ga-citrate scans were performed to detect suspected occult inflammatory processes. None of the patients had a known malignancy. Renal activity was noted in 12 patients (6.8%) on the 48-hr image. These patients had either pyelonephritis, acute tubular necrosis, vasculitis, or a renal abscess. Since delayed 67Ga uptake in the kidneys may be the first evidence of renal disease, further investigation, including either arteriography or biopsy, is necessary. In patients with a known malignancy, tumor involvement must be considered.
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PMID:Significance of delayed 67Ga localization in the kidneys. 96 53

Cisplatin [cis-diamminedichloroplatinum (II): CDDP] is a widely used cancer chemotherapeutic agent which has been shown to cause dose-related acute renal failure. The kidney damage is histologically characterized by widespread tubular necrosis, predominantly found in the third segments (S3) of the proximal tubules. To identify the intranephron targets of CDDP more precisely, we examined alterations in ammoniagenesis (AMG) and gluconeogenesis (GLG) using rat kidney slices (for AMG and GLG), tubule suspensions (for GLG), and microdissected nephron segments (for AMG). Ultramicroassay of AMG was carried out using the enzymatic cycling method, and GLG was measured by the HK/G6PHD method. GLG obtained from kidney slices and tubule suspensions on day 3 and day 7 following CDDP treatment did not change significantly from levels in control rats. In contrast, AMG increased on day 3 in the first and third kidney slices cut from the surface inward and decreased significantly on day 7 in the third and fourth slices. Microdissected nephron segments examined on day 7 showed decreased AMG in the second segments (S2; 20.3 +/- 7.7 pmol/mm/15 min vs. 78.7 +/- 9.7 for control, P less than 0.005) and the third segments (S3; 26.3 +/- 14.4 pmol/mm/15 min vs. 79.2 +/- 7.8 for control, P less than 0.005) of the proximal tubules. Additionally, we observed morphological changes under light microscopy to examine the relationship between metabolism and morphology. On day 3 following the CDDP treatment, typical acute tubular necrosis was seen primarily localized in the outer stripe of the outer medulla, while on day 7 the lesion appeared to be recovering. Our data imply a prominent dissociation between renal metabolic and morphologic changes induced by CDDP.
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PMID:Cisplatin-induced alterations in renal structure, ammoniagenesis and gluconeogenesis of rats. 159 64

The antitumor activity and normal tissue toxicity of cis-diammine-1,1-cyclobutane dicarboxylate platinum (II) (carboplatin) in combination with whole body hyperthermia (WBH) (41.5 degrees C, 120 min.) were examined in an F344 rat model. Carboplatin data were compared with those of cis-diamminedichloroplatinum (II) (cisplatin). At 37 degrees C, carboplatin showed minimal activity against a rat fibrosarcoma, but when combined with WBH, the antitumor effect-of the drug was greatly enhanced. The major carboplatin-induced acute toxicity at both normothermic and hyperthermic temperatures was marked hypocellularity of the bone marrow. A significant decrease in peripheral blood platelet counts was caused by the maximum tolerated doses (MTD) of carboplatin alone and with WBH. While the lethal dose of carboplatin alone caused only minimal renal damage, mild acute tubular necrosis was observed at the MTD of carboplatin with WBH, although no significant increase in blood urea nitrogen occurred. Therapeutic ratios of the combined chemotherapy and WBH modalities were calculated by comparing tumor growth response at the MTD of drug alone and drug combined with WBH. The combination of the nephrotoxic cisplatin with WBH resulted in a therapeutic ratio of only 0.8, whereas when carboplatin was combined with WBH, a value of 3.0 was obtained, representing a 3- to 4-fold increase over cisplatin in the therapeutic ratio. These data indicate that the less nephrotoxic carboplatin in combination with WBH improves therapeutic gain and may provide a more promising clinical combination for cancer treatment than cisplatin combined with WBH.
Cancer Res 1991 Jun 01
PMID:Effect of carboplatin combined with whole body hyperthermia on normal tissue and tumor in rats. 203 36

The toxicity of the anti-cancer drug cis-diamminedichloroplatinum (II) (cisplatin), at 2 to 40 mg per kg, was studied in the frog, Rana pipiens. The LD50 for the drug was approximately 17 mg per kg. Major non-nervous system toxicity occurred in the kidney. Renal failure was manifested as anasarca and increasing blood urea nitrogen (BUN). Histopathological changes included acute tubular necrosis and tubular dilatation, which were more severe at higher doses. Interstitial fibrosis occurred after prolonged survival after a single dose. Ultrastructurally, there was increased electron-dense material in tubular cells, but no specific changes in mitochondria or nuclear structures were seen. Gastro-intestinal toxicity was less severe than in other species and was more prominent at higher doses. Pathological changes consisted of epithelial nuclear atypia and apoptosis. By electron microscopy, there was increased separation of cell borders, depletion of chylomicrons and mucin granules and increases in electron-dense material. Again no specific mitochondrial or nuclear changes were seen. Relatively slight changes were seen in the liver, consisting of altered distribution of rough endoplasmic reticulum and dispersion of nuclear chromatin. Minimal pathology was demonstrated in the haematopoietic system or in the gonads. Thus toxicity of cisplatin in the frog is similar to that seen in mammals, including rodents and man.
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PMID:Toxicity of cis-diamminedichloroplatinum (II) (cisplatin) in the frog, Rana pipiens. 207 54

In this study, we analyzed the incidence of complications and clinical results of 57 patients who received kidney transplants at our institution and survived with a functioning allograft for 10 years or longer. All patients received their care at our center and their clinical and laboratory data were monitored routinely at minimum monthly intervals. In this second decade, during a mean follow-up of 2.8 +/- 2.2 years (range 0.4-7.8 years), 7 patients suffered graft loss (chronic rejection 6; irreversible acute tubular necrosis from aminoglycosides 1) and 7 others died with a functioning allograft (causes: hepatic failure 2, sepsis 2, malignancy 2, and cardiac infarction 1). The cumulative patient survival was 96% at 11 years and 85% at 15 years. The corresponding graft survival rate was 92% at 11 years and 71% at 15 years. Of the 43 patients currently followed, 38 are fully rehabilitated, 4 are partially rehabilitated, and 1 is medically disabled. The complications observed were: infection in 25 patients (44%), hypertension in 24 (42%), hyperlipidemia in 23 (40%), liver disease, 22 (39%) musculoskeletal problems in 21 (37%), cataracts in 19 (33%), rejection in 15 (26%), malignancy in 9 (16%), vascular occlusive disease in 9 (16%), gastrointestinal disorders in 9 (16%), and other problems not included in the above categories in 26 (46%). Our observations suggest that renal transplant recipients experience significant morbidity and mortality even in the second decade. Continued medical follow-up is therefore essential for an early diagnosis and management of these late complications. Measures directed at prevention and therapy of these late complications may further enhance the long-term success rate of renal transplantation.
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PMID:Long-term results and complications in renal transplant recipients. Observations in the second decade. 327 61

Wistar male rats were tested for nephrotoxicity and carcinogenicity after administration of ferric nitrilotriacetate [(NTA) CAS: 139-13-9] (Fe-NTA) [No. of rats (n) = 24] and Al-NTA (n = 24). The control rats were given AlCl3 (n = 10), NTA (n = 10), and saline (n = 10). Sublethal doses of Fe-NTA [5-7 mg Fe/kg (body wt)] and Al-NTA [1.5-2.0 mg Al/kg (body wt)] were chosen and injected ip for 3 months. AlCl3 and NTA were given in equivalent doses and saline was given in equivalent volumes. All the rats given Fe-NTA or Al-NTA had a depressed weight gain, polyuria, and glucosuria from the 1st week. Histologically, acute tubular necrosis and regenerating epithelial cells were observed. Regenerative atypical epithelial cells in the renal cortex were seen at the termination of Fe-NTA or Al-NTA administration. Control rats had no remarkable changes. After 1 year, primary renal cell carcinoma and metastases to liver, lung, and peritoneum were observed only in Fe-NTA-treated rats (14 of 18 surviving rats). On the contrary, there were no tumors in Al-NTA-treated rats (none of 12 surviving rats). The results suggest that nephrotoxicity and renal cell carcinoma are two independent phenomena from Al-NTA treatment and that a long-term sublethal dose of Al-NTA is not related to renal carcinogenicity.
J Natl Cancer Inst 1986 Jan
PMID:Nephrotoxicity and renal cell carcinoma after use of iron- and aluminum-nitrilotriacetate complexes in rats. 345 33


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