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 studied the clinical and pathological data for 334 patients age 65 or more who underwent renal biopsy for acute renal failure (ARF, n = 55), subacute renal failure (SRF, n = 72), chronic renal failure (CRF, n = 57), proteinuria (n = 137), and hematuria (n = 13). Tissue diagnoses were glomerulopathy (n = 252, 75.4%), acute tubular lesions (n = 18), interstitial nephritis (n = 23), vascular diseases (n = 36, including 14 with cholesterol emboli), and five miscellaneous diagnoses. Of the 55 patients with ARF, 23 had a glomerular lesion, 15 had acute tubular necrosis, and 8 had acute interstitial nephritis. Of 72 patients with SRF, 49 had a glomerulopathy, 12 had a vascular disorder, and six had acute interstitial nephritis. Hence, patients with ARF or SRF exhibited a high potential for reversible lesions. Only 11.3% of patients with CRF had potentially reversible causes. The most common causes of proteinuria were membranous glomerulopathy (34.3%), minimal change disease (14.6%), focal segmental sclerosis (11.7%), and amyloidosis (8.8%). Of the 25 patients with advanced nephrosclerosis, 24 had renal failure, 20 were hypertensive, and 13 had cholesterol emboli. Of 33 patients with diabetes mellitus, 66.7% were found to have lesions not related to diabetes. We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease. Old age alone is not a contraindication to performing a renal biopsy.
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PMID:Renal biopsy in patients 65 years of age or older. An analysis of the results of 334 biopsies. 235 29

Five hundred Ga-67 images, requested for detection or follow-up of inflammatory or neoplastic diseases, were reviewed to evaluate the incidence of delayed renal localization and the clinical significance of different degrees of uptake. Renal uptake in 48- or 72-hr images was graded as follows: 0 = background activity; 1+ = greater than background but less than spine; 2+ = close to spine but less than liver; 3+ = same as liver; 4+ = greater than liver. On the 500 images, 996 kidneys were evaluated and among them 600 (60%) had 0 uptake and 340 (34%) had 1+. These 940 kidneys were all considered to be normal. Fifty-six (6%) had 2+ or more uptake, with possible causes for uptake being: infection 27, drug-induced renal damage ten, urinary stasis or slow excretion seven, collagen vascular disease six, renal failure four, acute tubular necrosis one (ATN), and indeterminate one. Cases of renal infection or failure tended to show more or less 4+ uptake, while drug damage, ATN, or urinary stasis tended to have 2+ uptake.
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PMID:Delayed renal localization of Ga-67: concise communication. 661 59

The incidence of renal failure due to vascular diseases is increasing. Two reasons for this are the epidemic of atherosclerotic vascular disease in the aging population and the widespread use of vasoactive drugs that can adversely affect renal function. These vascular causes of renal failure include vasomotor disorders such as that associated with nonsteroidal antiinflammatory drugs, small-vessel diseases such as cholesterol crystal embolization, and large-vessel diseases such as renal artery stenosis. These causes of azotemia are less familiar to physicians than more classic causes, such as acute tubular necrosis, and are less likely to be recognized in their early stages. This article describes the various vascular diseases that impair renal function and outlines the steps necessary to identify them. Although some of these conditions, such as renal artery stenosis, can gradually impair function, the vascular causes of acute renal failure are emphasized in this article. Because the vasculitides primarily cause renal failure through secondary glomerulonephritis, they are mentioned only briefly. Extensive testing is rarely necessary because the cause is usually suspected through syndrome recognition. The diagnosis can then be confirmed by the results of one or two additional tests or by improved renal function after treatment.
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PMID:Diagnosing vascular causes of renal failure. 867 77

We studied the effect of a low-dose dopamine infusion on graft function in 60 patients undergoing transplantation with cadaveric kidneys in a prospective controlled trial. Recipients were allocated to either a control or a dopamine group, the latter receiving a 3 micrograms.kg-1 x min-1 infusion of dopamine starting intraoperatively. Evaluation of dopamine's effect was undertaken in two stages, namely, (i) initial graft function 1 wk after transplantation and (ii) graft survival at 3 mo. Initial graft function was determined by the ability of the transplanted kidney to reduce serum creatinine, and the development of acute tubular necrosis as confirmed by renal biopsy. Of the dopamine group 33.3% developed acute tubular necrosis compared to 23.3% of the control group. The second-stage evaluation was based on plasma creatinine levels and the requirement for dialysis within 3 mo of transplantation. 92.8% of the dopamine group and 76.9% of the control group had good graft function. No statistically significant difference between the two groups was found. The perioperative infusion of dopamine at 3 micrograms.kg-1 x min-1 was not shown to have any beneficial effect on the transplanted kidney in patients who do not have serious vascular disease, or who do not receive kidneys subjected to prolonged hypotension or prolonged preservation or anastomotic times.
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PMID:The effect of dopamine on graft function in patients undergoing renal transplantation. 842 17

Nephropathy as the sequences of Hansen's disease before and after the introduction of chemotherapy was compared referring to the report by Hayashi in 1943 and the summary of the autopsy reports from 1978 to 1981 at National Hansen's disease hospital Zenseien. Unlike the high rates of tuberculosis as the cause of death before the introduction of chemotherapy (41.3%) those thereafter decreased to be negligible. On the other hand the comparison of the rates of nephropathy with the same way as that of tuberculosis was impossible since the description about nephropathy by Hayashi was not sufficient to characterize each nephropathy since he included arteriolitis, glomerulonephritis and interstitial nephritis together in the term of nephritis. Death rate due to nephritis among Hansen's disease patients according to Hayashi at that time was 21.2% which was twice as many comparing to that in the other cases. According to the report about the cases of Zenseien those reported to have glomerulonephritis was 37.3% though those were not necessarily listed as the cause of death. Also the nephropathy including fibrinoid angitis with occasional microaneurysmal dilatation of afferent arteries, glomerulitis, sclerosis and stricture of efferent arteries likewise ischemic acute tubular necrosis possibly as the result of these angiopathy seemed to be present. These vascular changes partially resemble to that of microscopic periarteritis nodosa but seems to be common in the smaller arteries. In conclusion, unlike the case of tuberculosis the rate of nephritis including glomerulitis, arteriolitis and interstitial nephritis as Hayashi used as his criteria does not seem to have decreased. Therefore, the critical analysis of the nephropathy especially of that relating to the arteriolitis should be done to obtain the knowledge to suppress its occurrence.
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PMID:[Hansen's disease and nephropathy as its sequence]. 930 Dec 9

Medications cause renal disease by promoting various types of injury in the kidney. Several drugs reduce renal perfusion and cause prerenal azotemia. Vascular disease can develop following exposure to various medications through direct and indirect effects. A number of glomerular lesions have been described with therapeutic agents and illicit drugs. Acute interstitial nephritis occurs from a drug-induced allergic reaction, which promotes interstitial inflammation and tubular damage. Acute tubular necrosis is a dose-dependent process that occurs from direct drug toxicity on tubular epithelia. Other less common patterns of drug-induced tubular injury include osmotic nephropathy, crystal nephropathy and acute nephrocalcinosis. Finally, postrenal azotemia from structural or functional obstruction of the urinary tract also complicates therapy with a number of medications.
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PMID:Drug-induced nephropathy: an update. 1601 48

A number of therapeutic agents can adversely affect the kidney, resulting in tubulointerstitial, glomerular or vascular disease. Drug-induced tubulointerstitial nephritis and acute tubular necrosis are common, and are often cause by antibiotics or non-steroidal anti-inflammatory drugs. Drug-induced glomerular and vascular disease is relatively rare. This review describes the morphological patterns of drug-induced disease in the kidney. The histopathological changes are often similar to disease that is idiopathic or due to other causes, so that awareness and clinical correlation are most helpful to arrive at the aetiology.
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PMID:Renal toxicity of therapeutic drugs. 1947 53

Acute Renal Failure (ARF) in the immediate post transplant period is most commonly due to acute tubular necrosis, acute cellular rejection and calcineurin inhibitor toxicity apart from usual prerenal and post renal causes. In this report, we discuss an interesting and unusual cause of ARF due to thrombotic micro angiopathy in the immediate post transplant setting.
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PMID:Post transplant thrombotic microangiopathy causing acute renal failure. 2036 29