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)

Recent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid-base disturbances commonly observed in these patients, and possibly in alcohol-induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti-inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol-induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.
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PMID:Alcohol misuse and renal damage. 1289 83

Boutonneuse fever is a bacterial infection caused by Rickettsia conorii. It occurs mainly in countries around the Mediterranean basin. Most cases are benign. However severe forms with major morbidity and a high mortality risk have been described. Severe forms often involve altered mental status, hepatic cytolysis, hemostatic disturbances, pneumopathy, and kidney failure. The causes of renal complications are unclear. The purpose of this report is to describe three cases of boutonneuse fever associated with acute kidney failure due to different underlying mechanisms, i.e., acute renal function failure, acute tubular necrosis, and extracapillary glomerulonephritis. While the first two mechanisms of kidney failure have been reported frequently in association with Boutonneuse fever, extracapillary glomerulonephritis has, to our knowledge, been mentioned only once. This case supports speculation that Rickettsia conorii has a toxic effect on glomeruli.
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PMID:[Acute renal insufficiency in Boutonneuse Mediterranean fever: description of three cases]. 1522 60

Renal biopsy is a fundamental tool in the diagnosis and prognostic of multiple nephrological and systemic pathologies. At our institution the first patient submitted to this technique, at 1994, showed Berger disease. Until 2002 we have performed 91 renal biopsies (57 men and 34 women) with the following annual distribution: 1994 (n=3), 1995 (n=3), 1996 (n=3), 1997 (n=15), 1998 (n=5), 1999 (n=23), 2000 (n=13) and 2001 (n=26). Ultrasound guidance was always used and in most of cases the technique was performed with Vim-Silverman (14G) needle. BARD automatic system was employed in only five patients. The clinical diagnosis that lead to renal biopsy were: nephrotic syndrome (n=27), asyntomatic urinary abnormalities (n=25), acute or rapidly progressive renal failure (n=18), chronic renal failure (n=15), hypertension (n=4) and acute nephritis (n=2). The efficacy for optic histological diagnosis was 92.3% (84/91). However, if we include seven cases of presumed IgA nephropathy that don't included fragment for immunofluorescence (IF) analysis the efficacy declined to 84.6% (77/91). The mean number of glomeruli per fragment was 18.3 -/+ 14.2 [0-80]. Histological diagnosis were the following: Berger disease (n=24), idiopathic nephrotic syndrome (n=18), lupus nephritis (n=8), mesangial proliferative glomerulonephritis without glomeruli in the IF fragment (n=6), without glomeruli (n=6), secondary nephrotic syndrome (n=4), tubulointerstitial nephritis or acute tubular necrosis (n=4), diabetic nephropathy (n=3), myeloma kidney (n=3), pauci-imune and crescentic glomerulonephritis (n=3), hypertensive nephropathy (n=2), IgM mesangial proliferative glomerulonephritis (n=2) and various (n=8). Gross hematuria appeared in 9 patients (9.9%). Only in three of these patients it was showed, by ecography, the existence of kidney haematoma. Bleeding throughout the mandrill in four cases, leaded to transfusion in only three patients. We have registered one accidental spleen puncture. Nephrectomy for incontrollable bleeding was never needed. Higher glomerulosclerosis (30% vs 8%; p<0.01) and also a greater extent of tubulointersticial lesions (100% vs 63%; p<0.01), were predictors of progression into end-stage or advanced renal failure. Concluding, renal biopsy with ultrasound guidance was valuable for diagnosis in 84.6% of our proceedings. Our serie is similar to others concerning serious complications. Nephrologists and radiologists improved progressively their coordination performing this technique, improving the results during this period of 8 years.
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PMID:[Percutaneous kidney biopsy: eight years-experience]. 1563 24

Imaging techniques, especially ultrasonography and Doppler, can give an effective assistance in the differential diagnosis of acute renal failure (ARF). An resistance Index (RI) value >0.75 is reported as optimal in attempting differential diagnosis between acute tubular necrosis (ANT) and prerenal ARF. In hepatorenal syndrome (HRS) RIs is very increased. In some renal vasculitis, as nodose panarteritis (PN), hemolytic-uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), parenchymal perfusion is reduced and RI increased. In lupus nephritis the RI values are correlated with creatinine level and normal RI are considered as a good prognostic tool. In acute primitive or secondary glomerulonephritis (GN), RI value is normal, with diffuse parenchymal hypervascularization. In acute crescentic and proliferative GN and tubulo-interstitial disease, color Doppler (CD) and power Doppler (PD) reveal a decreased renal parenchymal perfusion, which correlates with increased RI values. In acute thrombosis of renal artery, US color Doppler (DUS) reveals either an absence of Doppler signal or a tardus-parvus pulse distal to the vascular obstruction. In this situation it is possible to visualize hyperthropic perforating vessels that redirect their flow from the capsular plexus to the renal parenchyma. In acute thrombosis of the renal vein Doppler analysis of parenchymal vessels reveals remarkable RI values, sometimes with reversed diastolic flow. In postrenal ARF an adjunct to the differentiation between obstruction and non obstructive dilatation can be found through RIs. Diagnostic criteria of obstruction as reported by literature are: RI>0.70 in the obstructed kidney and, mostly, a difference in RI between the 2 kidneys >0.06-0.1.
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PMID:The US color Doppler in acute renal failure. 1578 27

The most frequent causes of glomerular diseases whose main clinical syndrome are nephrotic syndrome and acute renal failure may have several causes: acute tubular necrosis, thrombosis of renal veins, acute tubulointerstitial nephritis. Infrequently, the association between primary glomerular disease (membranous nephropathy and others) and crescentic glomerulonephritis can cause this clinical picture. We describe a young woman without systemic disease with nephrotic syndrome and acute renal failure secondary to membranous nephropathy and superimposed crescentic glomerulonephritis. She received steroids and cyclophosphamide with stabilization of renal function after two months of follow-up.
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PMID:[Membranous nephropathy and crescentic glomerulonephritis]. 1605 15

Acute renal failure is a very rare complication seen during the course of non- fulminant hepatitis A. Several mechanisms have been postulated in the pathogenesis of renal failure. Firstly, there is insufficiency of renal blood flow due to developing endotoxemia or cryoglobulinemia, secondly mesangial proliferative glomerulonephritis or interstitial nephritis occurs due to immune complexes and finally there is acute tubular necrosis caused by the direct cytopathic effect of the virus or due to immune complexes. The following case report describes a 17 year old male patient admitted with complaints of appetite loss and severe weight loss due to anorexia nervosa. During the second week of admission, he developed hepatitis A infection which was complicated by acute renal failure requiring hemodialysis therapy. Hepatorenal parameters returned to normal values by the fifth week of admission in this case of biopsy proven acute tubular necrosis. In this case, the possible negative effects of malnutrition on the liver and kidneys were not observed. The present authors emphasize that during the course of non- fulminant hepatitis A, renal functions should be closely monitored and renal biopsy should be performed if acute renal failure occurs.
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PMID:Acute oligo-anuric renal failure during the course of non-fulminant hepatitis A in a patient with anorexia nervosa. 1637 99

The paradigm that chronic rejection causes all progressive late allograft failure has been replaced by a hypothesis of cumulative damage, where a series of time-dependent immune and nonimmune mechanisms injure the kidney and lead to chronic interstitial fibrosis and tubular atrophy, representing a final common pathway of injury and its consequent fibrotic healing response. Allograft damage is common, progressive, time-dependent, clinically important and modified by immunosuppression. Early after transplantation, tubulointerstitial damage is predominantly related to ischemia reperfusion injury, acute tubular necrosis, acute and subclinical rejection and/or calcineurin inhibitor nephrotoxicity, superimposed on preexisting donor disease. Later, cellular inflammation lessens and is replaced by microvascular and glomerular injury from calcineurin inhibitor nephrotoxicity, hypertension, immune-mediated fibrointimal vascular hyperplasia, transplant glomerulopathy and capillary injury, polyoma virus and/or recurrent glomerulonephritis. Additional mechanisms of injury include internal architectural disruption of the kidney, cortical ischemia, persistent chronic inflammation, replicative senescence, cytokine excess and fibrosis induced by epithelial-to-mesenchymal transition. Current understanding of the etiology, pathophysiology and evolution of pathological changes are detailed. An approach to histological assessment of the individual failing graft are presented and a series of postulates are defined for future studies of chronic allograft nephropathy.
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PMID:Chronic allograft nephropathy: current concepts and future directions. 1653 63

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Out of which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35 years and 9 cases were below 10 years. Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for 64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstretical complications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases. Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemic syndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl, mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis, fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration of hospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, ten expired, two recovered partially, two progressed to chronic renal failure and two left against medical advice. Overall mortality was 22.2%. Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS was exclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause of acute renal failure in our country.
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PMID:Acute renal failure in a tertiary care center in Nepal. 1655 67

Acute rejection (AR) is a dominant risk factor for developing chronic allograft nephropathy (CAN) after kidney transplantation. CAN is characterized by progressive interstitial fibrosis. It has been associated with increased transforming growth factor (TGF)-beta1 expression, however, kinetic studies are absent. We investigated whether intragraft TGF-beta1 expression in various causes of early graft dysfunction may influence late renal allograft dysfunction. A total of 174 human renal biopsies were quantified for TGF-beta1 mRNA expression using real-time reverse transcriptase-polymerase chain reaction. Expression levels were correlated with the Banff histopathological grades, TGF-beta1 immunohistology, and clinical follow-up. TGF-beta1 was most markedly upregulated in AR, CAN, and acute tubular necrosis - delayed graft function compared to non-rejecting controls (P < 0.001). TGF-beta1 expression was heightened in borderline changes (P < 0.01), recurrence of glomerulonephritis, and cyclosporine toxicity (P < 0.05). There was no correlation between intragraft TGF-beta1 expression during AR and short-term outcome of a rejection episode. TGF-beta1 gene overexpression during CAN has been shown to be associated with the increased risk for renal allograft dysfunction 18 months after biopsy (odds ratios 9.9 vs 3.2, respectively). Intragraft TGF-beta1 mRNA expression is significantly upregulated in both AR and CAN. Thus, our results support the hypothesis that TGF-beta1 might play a key role in chronic allograft dysfunction.
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PMID:TGF-beta1 mRNA upregulation influences chronic renal allograft dysfunction. 1661 32

We report a 19-year-old Saudi female with nephrotic syndrome whose renal biopsy revealed findings suggestive of minimal change glomerulonephritis (MCGN). She developed oliguric renal failure requiring hemodialysis. She remained dialysis dependent for five weeks and subsequently renal function recovered fully. She remained nephrotic and responded to a six week course of corticosteroids. She was followed for two years during which she had two relapses, which responded to steroids. Acute renal failure is uncommon in MCGN and is due to acute tubular necrosis induced by hypovolemia or drugs. This patient did not have any obvious precipitating factor, which led to acute reversible renal failure.
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PMID:Idiopathic reversible renal failure in a young woman with minimal change glomerulonephritis. 1690 27


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