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)

The excretion of the enzyme gamma-glutamyl-transpeptidase and its isoenzymes into the urine was investigated in patients with renal diseases and compared with the excretion of the enzymes leucine-aminopeptidase and lactate-dehydrogenase. In animal experiments an increased excretion of these enzymes was found after autotransplantation. Increased excretion of gamma-glutamyl-transpeptidase was also found in patients with glomerulonephritis and in the polyuric phase of acute tubular necrosis, but not in cases of pyelonephritis and in the oliguric phase of acute tubular necrosis. The alterations of the isoenzyme pattern during diseases with increased enzyme excretion are in accordance with the hypothesis that the enzymes are liberated from the kidney tissue into the urine, and only a minority stems from the blood. Investigation of the excretion of gamma-glutamyl-transpeptidase and its isoenzymes into the urine seems to be of both scientific and clinical interest.
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PMID:Investigations of the excretion of gamma-glutamyl-transpeptidase into the urine. 0 55

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

Three patients having lepromatous leprosy developed acute renal failure. Two patients completely recovered and one was left with a moderate degree of renal insufficiency. Renal tissue obtained by percutaneous biopsy revealed acute tubular necrosis in two and diffuse crescentic glomerulonephritis in the third case.
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PMID:Acute renal failure in leprosy. 56 62

We report a case of renal cortical microabscesses which presented as oliguric acute renal failure. Prior to the biopsy the patient was suspected of having acute pyelonephritis with acute tubular necrosis. Biopsy was performed to rule out rapidly progressive glomerulonephritis as a cause of his renal failure. To our surprise, we found multiple small microabscesses in the renal cortiex. Renal cortical microabscesses should be considered as a reversible acute renal failure.
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PMID:Renal cortical microabscesses as cause of reversible acute renal failure. 84 81

Out of 152 cases of Acute renal failure (ARF) 32 patients (21%) were subjected to kidney biopsy. All patients had intrinsic ARF. Prerenal azotemia and obstructive uropathy were excluded. Histologic observations were: Crescentric glomerulonephritis in 7 (21.9%), acute endocapillary proliferative glomerulonephritis 5 (15.6%), acute interstitial nephritis 7 (21.9%), necrotizing vasculitis 4 (12.5%), acute tubular necrosis in 5 (15.6%) and membrano-proliferative GN with superimposed crescent in 2 (6.2%) while renal cortical necrosis was seen in 6.2% of cases. Prebiopsy diagnosis was correct in only 10 (31.25%) cases. The result of biopsy had altered clinical diagnosis in 22 (68.75%) patients and precise renal biopsy diagnosis resulted in therapeutic changes in 54.8% of patients with ARF.
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PMID:Clinical significance of kidney biopsy in acute renal failure (ARF). 129 67

Renal allograft dysfunction may be due to a variety of causes including acute and chronic rejection, acute tubular necrosis, cyclosporine A toxicity, glomerulonephritis, and surgical causes. It can be difficult to distinguish between these etiologies. Ultrasound is a relatively simple, noninvasive method for imaging the transplant kidney, and is excellent for the diagnosis of surgical complications. The features of rejection include an increase in renal volume, reduced echogenicity, indistinctness of the corticomedullary junction, and splaying of the medullary pyramids. These findings, although suggestive of rejection, cannot differentiate reliably between rejection and other causes of allograft hypofunction. Doppler studies may show an increased resistive index in a kidney undergoing rejection, but this finding may also be seen in other pathological processes and is not specific. A normal ultrasound examination does not exclude rejection. Ultrasound is useful as a baseline examination. Abnormal findings should be interpreted in the light of the clinical situation in each case. Where there is any doubt about the diagnosis, ultrasound-guided biopsy should be performed.
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PMID:Morphological appearance of renal allografts in transplant failure. 132 22

In 101 consecutive patients with renal allograft dysfunction a correlation of Duplex Doppler sonography (DDS) with histopathologic reports of simultaneously performed biopsies was made. Renal vascular impedance was estimated by calculating the resistive index (RI). A total of 290 different specific histologic diagnoses (mean 2.1 +/- 0.84 diagnoses/biopsy) was noted. With increasing time interval to transplantation, single diagnoses as cause of allograft dysfunction decreased. DDS could not reliably differentiate, exclude, or grade any of the common causes of renal allograft dysfunction like vascular and/or cellular rejection, chronic rejection, acute tubular necrosis, cyclosporin nephrotoxicity, relapse of glomerulonephritis and infection. Follow-up studies after established histologic diagnosis in 19 patients with persisting allograft dysfunction demonstrated a lack of sensitivity of DDS to significant superimposed causes of transplant malfunction. We conclude that biopsy is still necessary to direct proper therapy of renal allograft dysfunction.
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PMID:Polyetiology of renal allograft dysfunction. Does calculation of the resistive index still make sense? 138 51

261 patients who received a kidney transplant under cyclosporin-A immunosuppression were reviewed in order evaluate the benefits and the risks of renal graft biopsies. 240 graft biopsies were performed in 124 of the 261 patients. The biopsy diagnoses were 103x rejection, 90x cyclosporin-A toxicity, 8x acute tubular necrosis, 8x glomerulonephritis, 9x different biopsy results, and 12 cases of normal renal tissue. In 214 cases the clinical course was well explained by the biopsy result. The histological results led to therapeutical changes in 199 cases. 221 of the 240 biopsies were performed without any complications. There was only one biopsy with irreversible and there were 19 biopsies with reversible complications.
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PMID:Risks and benefits of graft biopsy in renal transplantation under cyclosporin-A. 139 64

From 1976 to 1987 on our Nephrological Unit, 57 patients with IgA nephropathy (IgAN) proven by renal biopsies were found. Three of those presented with acute tubular necrosis (ATN) and glomerulitis, without extrarenal predisposing cause in two; and showed, as prominent manifestation, a severe acute renal failure syndrome (ARFS), needing dialytic treatment. All three had hematuria, which was macroscopic in two and microscopic in one. Thus the prevalence of the association of glomerulitis and ATN was about 5.2%. There was complete recovery of renal functions in all three patients, but the usual symptomatology of IgAN. Two patients presented polymorphonuclear neutrophils infiltration of glomerular capillaries and in one of them, electron-dense deposits on the epithelial side of glomerular basement membrane ("humps") were observed, as well as those identified in the mesangial area. The glomerular polymorphonuclear neutrophils infiltration and endothelial cells proliferation (cases 1 and 3), the presence of "humps" (case 1), high antistreptolysin O (ASO) titers (cases 1 and 2), and low serum complement levels (case 1), suggest the possibility that antigens able to cause postinfectious glomerulonephritis (streptococcal or not) could induce in some individuals, by another immunopathogenetic route, mixed histopathological and clinical features of IgAN and postinfectious glomerulonephritis.
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PMID:IgA nephropathy: acute renal failure, acute tubular necrosis, and features of postinfectious acute glomerulonephritis. 146 4

In a prospective analysis we performed 182 colour duplex US studies in 60 patients with renal transplants to determine the effects of different causes of graft dysfunction on the resistive index (RI) and the colour imaging pattern of the transplant arteries. Allografts with normal function, cyclosporin toxicity, cytomegaly infection, acute tubular necrosis, glomerulonephritis and postoperative functional nephrotoxicity showed normal RI (less than 0.7) and normal pattern of the arteries in colour duplex. Grafts with acute and chronic rejection, obstructive uropathy and arteriolosclerosis showed significant elevated RI and in colour duplex always a characteristic blinking of the arteries and a numerical reduction of the peripheral arteries. It seems that the assessment of an increase of vascular impedance is possible also with colour duplex US.
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PMID:[Color-coded duplex sonography and the resistive index in dysfunctional kidney transplants]. 217 24


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