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)

During a one-year period, drug-associated acute renal failure (ARF) was prospectively recorded in 398 patients, registered in 58 french nephrology Units. Drugs involved were primarily antibiotics, mainly aminoglycosides, glafenine, non-steroidal antiinflammatory drugs and contrast media. Hypersensitivity reactions were reported in 69 patients. Renal biopsy, performed in 81 instances, showed acute tubular necrosis in 42 and acute interstitial nephritis in 20 patients. Hypotension, sodium depletion and/or cardiac failure were predisposing factors in 198 cases. Fifty patients died, 251 recovered fully or regained previous renal function, and in 93 permanent renal damage remained. Advanced age, oliguria, severe ARF, and preexisting cardiac, hepatic or renal insufficiency were poor prognostic factors. Prevention of drug-associated ARF should be directed to high-risk patients, particularly those receiving aminoglycosides and contrast media.
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PMID:[Acute renal failure associated with drugs or iodinated contrast media. Results of a cooperative multicentric study by the Nephrology Society]. 287 11

Combined hepatocellular injury and renal tubular necrosis developed in five alcoholic patients who were receiving acetaminophen therapeutically. Two patients were taking doses prescribed by a physician. The hepatitis was characterized by extremely high serum transaminase values that were maximal on admission. Two patients died, and autopsy disclosed hepatic centrizonal necrosis and acute renal tubular necrosis. The three who survived had clinical features typical of acute tubular necrosis. All five had measurable concentrations of acetaminophen in plasma, although measurements were requested on admission only in two patients. When an alcoholic presents with combined hepatic and renal insufficiency, acetaminophen should be considered as a possible inciting agent. This diagnosis should be considered when serum transaminase levels are markedly elevated and when renal failure is due to acute tubular necrosis.
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PMID:Combined hepatic and renal injury in alcoholics during therapeutic use of acetaminophen. 406 53

a 17-year-old gravida 1, para 0, single white girl who had undergone criminal abortion, presented at the hospital with high fever and red urine. Her vital signs were monitored and laboratory tests were performed. A total abdominal hysterectomy and salpingo-oophorectomy were performed because of gangrenous uterus and ovaries. The patient developed postoperative complications and blood transfusion was performed. The criminal abortion was induced using some type of liquid (eg., Lysol) that was injected into the uterus transvaginally. The use of Lysol, soap and detergents in criminal abortion produces an area of tissue necrosis. The compounds are also absorbed into the bloodstream. The necrotic tissue is susceptible to infection, while the part which is absorbed into the bloodstream is nephrotoxic, hepatotoxic and produces hemolysis. Common complications of septic abortion are pelvic abscesses; metastatic abscesses; tetanus; renal insufficiency; cortical necrosis; and acute tubular necrosis. Coagulation abnormalities, as well as the psychological, economic and legal aspects of septic abortion are also discussed. It is hoped that all physicians would actively support legislation which would liberalize abortion laws.
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PMID:Medical grand rounds at Yale-New Haven Hospital. Septic abortion. 550 61

Renal insufficiency occurs in some, but not all, patients with multiple myeloma and Bence Jones proteinuria. Many of these patients are found to have a distinctive renal lesion characterized by distal nephron cast formation. It has been proposed that the specific Bence Jones protein (BJP) which is produced by a myeloma tumor may play an important role in the genesis of this cast nephropathy and that patients excreting BJPs with the highest isoelectric points (pI) are those most likely to develop this cast nephropathy. We have utilized a rat model of multiple myeloma to further evaluate the relationship between Bence Jones proteinuria and the development of myeloma cast nephropathy. This model employed immunoglobulin-secreting tumors obtained from a unique strain of rats in which they spontaneously develop. These tumors were transplanted to a homologous strain of rats and the effect on renal function and morphology in these rats were evaluated. Four different kappa light chain synthesizing tumors were studied. Following transplantation of the tumors, all rats were maintained on a diet designed to produce an acid urine (pH 5.5 to 6.0) and maximal urinary concentration (2000 to 3000 mOsm/kg). Among the rats excreting BJP of pI 6.7, 17 of 18 had virtually normal renal histology. Of the 15 rats with BJP of pI 7.6, 11 also had normal renal histology. However, 12 of 12 rats excreting BJP of pI 5.2 developed a distal nephron, light chain containing cast nephropathy. In the pI 4.3 group, 6 of 12 rats developed acute tubular necrosis, and the remaining six animals sustained a less severe lesion which was characterized by the presence of bland hyaline casts. The mean serum creatinine level obtained at the time of sacrifice was elevated (compared to that found in sham-operated controls) in the pI 5.2 group (P less than 0.001) and the pI 4.3 group (P less than 0.01) but not in the pI 6.7 or 7.6 groups. These results do not support the concept that cationic BJP's are more nephrotoxic than those that carry a more negative charge and indicate that other factors must determine the nephrotoxicity of a given BJP.
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PMID:Myeloma kidney cast nephropathy in a rat model of multiple myeloma. 641 38

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.
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PMID:Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics. 649 46

To determine the nature and frequency of renal disorders in AIDS we reviewed the records of thirty-two patients hospitalized over a twenty-two month period. Group I, including all patients with AIDS who demonstrated proteinuria and/or renal insufficiency, numbered thirteen patients, in ten of whom renal tissue was available. Renal abnormalities included proteinuria in twelve patients, which exceeded two grams per day in seven. The glomerular histologic lesions included focal glomerulosclerosis, diffuse mesangial hypercellularity, diffuse proliferative glomerulonephritis, and membranoproliferative glomerulonephritis. The nonglomerular histologic lesions included acute tubular necrosis, nephrocalcinosis, focal interstitial nephritis, and one case each of intrarenal cryptococcal infection and renal cell carcinoma. Nine of these thirteen patients developed renal insufficiency, and four of them required dialysis. Their mortality by the end of the study period was eleven of thirteen patients (85 percent), significantly worse in the short term than AIDS patients without renal problems. The patients in Group I were compared to the nineteen AIDS patients without renal abnormalities in Group II. The Group I patients had a higher incidence of oral and esophageal candidiasis, other fungal infections, and infections with Mycobacterium avium-intracellulare. They also had a higher incidence of exposure to aminoglycoside antibiotics and amphotericin B, and experienced more clinical shock than their Group II counterparts. It is concluded that patients with AIDS may demonstrate renal abnormalities on the basis of immune, hemodynamic, infectious, and neoplastic derangements.
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PMID:Renal disease in patients with AIDS: a clinicopathologic study. 673 86

Forty-four cases of acute necrotic haemorrhagic pancreatitis are studied. Fourteen cases were treated medically by peritoneal dialysis, 20 were treated surgically of which 16 had been medically treated by peritoneal dialysis. Fifteen died or 34%. Forty-one patients, 93.1% presented 8 major complications on admission and 2 complications were observed during the course of medical treatment (pulmonary shock and high digestive haemorrhage). The post surgical complications are excluded from this study. We report in order of frequency; effusion of the large peritoneal cavity (37 cases : 84%), hypocalcaemia less than or equal to 8 mg% (21 cases : 47.7%), renal insufficiency defined by a creatinaemia greater than or equal 2 mg% (17 cases : 38.6%), state of shock (13 cases : 29.5%), severe neurological disorders (11 cases : 25%), peritoneal haemorrhage (3 cases : 4.5%), disseminated intravascular coagulation (1 case : 2.2%), acute rabdomyolysis (1 case : 2.2%). Certain cases are particularly derogatory : pulmonary shock : 2 cases -- 2 deaths (100%); hypocalcaemia less than or equal to 7 mg/ : 6 cases -- 5 deaths (83.3%); acute tubular necrosis : 8 cases -- 6 deaths (75%); hypocalcaemia less than or equal 8 mg% : 21 cases -- 12 deaths (57.1%); high digestive haemorrhage : 3 cases -- 1 death (33.3%); amber known brown peritoneal effusion : 27 cases -- 12 deaths (44.4%); shock : 13 cases -- 5 deaths (38.5%). When in the same patients, less than 3 complications were present, the mortality rate was 20.8%. If more than 3 signs were observed the mortality rate rose to 53.3%. Except for pulmonary shock, six major complications were needed to give 100% mortality rate.
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PMID:[Acute necrotic hemorrhagic pancreatitis. Major complications (author's transl)]. 697 50

The early use of gold in medicine and dentistry dates back to the ancient Chinese and Egyptians. The discovery in 1890 that gold salts were toxic in vitro to tubercle bacilli led to the extensive treatment of tuberculosis with gold salts in the first three decades of this century. Eventually, gold therapy was extended to arthritis and lupus erythematosus, because of the belief that these diseases were forms of tuberculosis. Because of its beneficial effect particularly on active rheumatoid arthritis, chrysotherapy has remained one of the most widely used treatments of rheumatoid arthritis for the past half century. Toxicity of gold salts includes hypersensitivity reaction of skin and mucous membranes, bone marrow depression, and nephrotoxicity. The nephrotoxic clinical manifestations are renal insufficiency, proteinuria and hematuria, and the nephrotic syndrome. The pathologic changes are tubular degeneration, acute tubular necrosis or immune complex glomerulonephritis. The justification that any of these possible changes are the result of gold therapy rests clinically upon the time relationship of gold therapy and the renal symptoms, and pathologically upon the presence of gold inclusions (aurosomes) in proximal tubular epithelial cells. Aurosomes can at times be visualized by light microscopy, are usually seen by electron microscopy, and can be identified by microprobe analysis. Their pathology will be illustrated and pathogenic mechanisms discussed.
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PMID:Gold nephropathy. 703 39

2 patients with systemic lupus erythematosus and mild renal functional impairment were treated with ibuprofen, one of the phenylproprionic nonsteroidal anti-inflammatory drugs. Within days after the onset of therapy, both developed renal insufficiency manifested by elevated serum creatinine levels, increased proteinuria, and active urinary sediments; 1 patient was oliguric. Renal biopsies disclosed mesangial proliferative lupus glomerulonephritis and acute tubular necrosis, the latter more pronounced in the oliguric patient. Renal failure resolved following discontinuation of ibuprofen and supportive therapy. It is postulated that altered blood flow, mediated through the well-known prostaglandin synthetase inhibitory effects of ibuprofen, resulted in tubular necrosis. This undesirable complication of ibuprofen therapy may be enhanced in patients with underlying renal disease, and may be a factor governing the limitation of its usage.
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PMID:Ibuprofen-induced acute renal failure with acute tubular necrosis. 718 Sep 1

Forty patients with terminal cirrhosis and 40 patients with fulminant hepatic failure-all consecutively admitted-were studied with regard to incidence, types, and prognosis of complicating renal insufficiency. Renal failure was considered present when the serum creatinine was greater than 0.20 mmol/l. Of the patients with cirrhosis 26 (65%) developed renal failure. In 15 the type was functional, in three due to acute tubular necrosis, and in eight indeterminable. Of the patients with fulminant hepatic failure 22 (55%) had renal insufficiency; of these 13 had functional renal failure, five acute tubular necrosis, and in four the type was indeterminable. In both categories of patients, renal failure was equally frequent among patients with or without gastrointestinal bleeding and with or without ascites or diuretic therapy. The biochemical tests of liver function were similar in patients with or without renal failure in both categories. The mean renal blood flow in seven unselected patients with fulminant hepatic failure was reduced in the same order as previously observed in patients with cirrhosis. In terminal cirrhosis the mortality rate was 88% in the presence of renal failure, 71% in its absence (p greater than 0.05), while the same figures in fulminant hepatic failure were 100% and 67% (p less than 0.05). The incidence, relative frequency, and prognosis of renal failure were not different in the two conditions, indicating identical pathophysiological circumstances.
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PMID:Renal failure in fulminant hepatic failure and terminal cirrhosis: a comparison between incidence, types, and prognosis. 726 32


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