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)

We analyzed 432 patients with acute tubular necrosis, dialyzed at the University of Minnesota Dialysis Unit between 1968-1979. Only 135 patients or 31% survived. The median time to death was 5 days and to recovery of renal function was 12 days. Serum creatinine continued to fall for one month after the last dialysis and then stabilized. Ultimate serum creatinine level was directly related to age of patient but not duration of need for dialysis. One-fourth of the patients were left with moderate renal insufficiency (creatinine 1.5-3 mg/dl). Eight of 82 (10%) of the patients with long term (greater than 1 mo follow-up) had severe renal failure (creatinine over 3 mg/dl) and 4 other patients never recovered renal function but needed chronic hemodialysis. Acute renal failure is numerically important but not very time demanding on the capacity of dialysis units. The majority of the patients have no clinical problem of renal dysfunction if they survive their basic disease leading to acute tubular necrosis.
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PMID:Time of death, recovery of renal function, development of chronic renal failure and need for chronic hemodialysis in patients with acute tubular necrosis. 733 Nov 11

Thirty patient suffering from acute necrotic hemorrhagic pancreatitis and treated from admission by peritoneal dialysis were studied. According to developments, 4 groups are defined. The first group consisted fo 14 patients treated only by peritoneal dialysis, 3 died. The second group consisted of 7 patients whose peritoneal dialysis was interrupted during hospitalization and who underwent differed surgery. The third group consisted of 5 patients who were operated during the period of peritoneal dialysis, all died. Finally, the fourth group consisted of 4 patients who were dialysed for a short period before emergency surgery, there were no deaths. Peritoneal dialysis, associated with other therapeutic measurements resulted in early improvement of abdominal and toxaemic signs such as shock and functional renal insufficiency. Acute tubular necrosis, observed in 5 patients was reversible in two. Six out of eleven were weaned from assisted ventilation. This allowed the spontaneous resorption of peripancreatic necrotic masses in four cases. Nevertheless it did not prevent the development of new necrotic masses in 5 other cases nor peritoneal infection, seen in 4 cases. It is ineffective in the development of shock lung which followed in 2 cases, during the course of treatment. In all, 11 patients survived by medical peritoneal dialysis only. Of the 30 patients, 19 survived or 63.4%. If the period between the first digestive signs and the installation of the peritoneal dialysis is less than or equal to 7 days, as seen in 21 cases, 15 patients survived or 71.5%.
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PMID:[Peritoneal dialysis treatment for acute necrotic hemorrhagic pancreatitis (author's transl)]. 733 48

The renal insufficiency which has been described in some of Legionnaires' Disease, has not been characterized. We describe a patient who developed severe oligoanuric renal failure associated with Legionnaires' Disease. Renal biopsy revealed acute tubular necrosis.
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PMID:Acute renal failure in legionnaires' disease: report of a case. 737 63

Calcium antagonists block calcium entry into cells, resulting in relaxation of smooth muscle and limitation of the cytotoxic effects of ischaemia in various organ systems. They are most frequently used for clinical conditions requiring vasodilatation, i.e. hypertension and Raynaud's phenomenon, and this also suggests that the most common adverse effect of these drugs for noncardiovascular indications is an unwanted decline in blood pressure. Other uses include treatment of supraventricular arrhythmias and angina. There is some evidence that these drugs retard the development of atherosclerosis. Calcium channel blockers also improve renal reperfusion and may reduce renal insufficiency due to various nephrotoxins, and are particularly useful in renal transplantation for protection against cyclosporin toxicity and post-transplant acute tubular necrosis. These drugs are also useful in pregnancy-induced hypertension and unwanted uterine contraction. Affective disorders and malignancies may be other conditions which benefit from calcium antagonist therapy. Calcium antagonists, in particular nimodipine which is most selective for the cerebral vasculature, have been approved for treating vasospasm after subarachnoid haemorrhage. They are probably also effective for treatment of migraine. Calcium channel blockers may be effective for treating acute cerebral infarction, but results of clinical trials to date have been equivocal, largely because it has been difficult to recruit patients within the short interval after the onset of stroke when these drugs would be most effective, and because of the unwanted hypotensive effect of high doses.
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PMID:New uses for calcium channel blockers. Therapeutic implications. 751 Jun 13

Three children treated for appendicitis developed anuria and acute renal insufficiency several days after appendicectomy. Associated hydronephrosis or hydroureters were present in two. At cystoscopy, marked swelling of the trigonum and ureteric orifices was seen. One patient developed unilateral acute tubular necrosis, a complication not reported before. Recognition of this rare complication of acute appendicitis, which need not be accompanied by hydronephrosis, should lead to prompt decompression by the introduction of ureteric stents.
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PMID:A rare complication of acute appendicitis: complete bilateral distal ureteral obstruction. 798 Jul 94

Acute renal insufficiency developed in four idiopathic nephrotic patients with minimal change or mild proliferative glomerulonephritis. The reduction in glomerular filtration rate (CInulin) was not in proportion to the renal plasma flow (CPAH) as evidenced by a low filtration fraction. Diuretic therapy failed to reverse renal insufficiency, and renal biopsy showed no evidence of interstitial nephritis, acute tubular necrosis or interstitial edema. Corticosteroid therapy induced a recovery of renal function with a decrease in proteinuria. These observations suggest that acute renal insufficiency in the idiopathic nephrotic syndrome might be caused by impaired glomerular permeability.
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PMID:Reversible acute renal failure in idiopathic nephrotic syndrome. 849 41

Although the therapeutic administration of lithium in the psychiatric setting has been associated with various renal side effects, only a few reported cases have suggested a possible link to glomerular disease. We report two patients who, while taking lithium, developed heavy proteinuria caused by minimal change disease and acute renal insufficiency attributable to acute tubular necrosis. These clinical findings resolved on discontinuation of the drug, suggesting a role for lithium in their development. We also postulate that lithium, with its unique properties as a modulator of the phosphoinositol pathway, may play a key role in the pathogenesis of minimal change disease.
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PMID:Nephrotic syndrome and renal insufficiency associated with lithium therapy. 862 33

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

Cellular stress, particularly in response to toxic and metabolic insults that perturb function of the endoplasmic reticulum (ER stress), is a powerful inducer of the transcription factor CHOP. The role of CHOP in the response of cells to injury associated with ER stress was examined in a murine deficiency model obtained by homologous recombination at the chop gene. Compared with the wild type, mouse embryonic fibroblasts (MEFs) derived from chop -/- animals exhibited significantly less programmed cell death when challenged with agents that perturb ER function. A similar deficit in programmed cells death in response to ER stress was also observed in MEFs that lack CHOP's major dimerization partner, C/EBPbeta, implicating the CHOP-C/EBP pathway in programmed cell death. An animal model for studying the effects of chop on the response to ER stress was developed. It entailed exposing mice with defined chop genotypes to a single sublethal intraperitoneal injection of tunicamycin and resulted in a severe illness characterized by transient renal insufficiency. In chop +/+ and chop +/- mice this was associated with the early expression of CHOP in the proximal tubules followed by the development of a histological picture similar to the human condition known as acute tubular necrosis, a process that resolved by cellular regeneration. In the chop -/- animals, in spite of the severe impairment in renal function, evidence of cellular death in the kidney was reduced compared with the wild type. The proximal tubule epithelium of chop -/- animals exhibited fourfold lower levels of TUNEL-positive cells (a marker for programmed cell death), and significantly less evidence for subsequent regeneration. CHOP therefore has a role in the induction of cell death under conditions associated with malfunction of the ER and may also have a role in cellular regeneration under such circumstances.
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PMID:CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum. 953 36

We describe here the broad spectrum of acute renal insufficiency occurring in the course of human immunoinsufficiency virus infection. In our renal unit in Tenon hospital, 90 human immunoinsufficiency virus-infected adult patients were admitted for acute renal insufficiency between June 1988 and December 1996. Sixty out of them had a pathological diagnosis. The remaining patients did not have renal biopsy because of obstructive renal failure (n = 2), bleeding risk (n = 11), or clinically evident hypovolemic and/or sepsis-related acute tubular necrosis (n = 17). Nine different causes of acute renal insufficiency were listed. Human immunoinsufficiency virus-associated nephropathy, the most specific human immunoinsufficiency virus-related renal disease, which was diagnosed in 14 patients, is characterized by focal and segmental glomerulosclerosis with an important hyperplasia and/or proliferation of podocytes and huge tubular distension. The rapid progression to end-stage renal failure was not a constant feature since 10/14 patients had a partial renal recovery. Hemolytic-uremic syndrome was the other major cause of acute renal failure in these patients (32 cases) and was found to be associated with active cytomegalovirus infection. Cytomegalovirus-infected cells were present in half of the renal biopsies performed in this group of patients. Furthermore, these patients had an increased plasma tissue-type plasminogen activator activity whereas its type 1 inhibitor was not significantly increased, as opposed to non human immunoinsufficiency virus-associated hemolytic-uremic syndrome. Half of the patients had a complete renal recovery. The other causes of acute renal insufficiency were 1) intratubular deposition of either drugs (Adiazine, Foscavir, Indinavir) in 13 patients, or monoclonal light chain in one patient with B cell-lymphoma; 2) lupus-like glomerulonephritis characterized in one case by a complete clinical remission after 6 month-treatment by antiproteases; 3) acute tubular necrosis. In this setting, rhabdomyolysis could reveal HIV infection. The heterogeneity of renal diseases could be explained by the variation of human immunoinsufficiency virus-associated infections along time and by the different drugs which permit a better survival. We can hypothesize that new HIV-associated diseases will occur with the long term use of antiproteases.
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PMID:[Human immunodeficiency virus and acute renal insufficiency]. 961 98


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