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)

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.
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PMID:Chromium-induced kidney disease. 193 54

Male volunteers were infused with L-arginine dextran and Haemaccel. Arginine (0.5 g/kg body weight infused over 30 min) resulted in transient highly significant increases in urinary albumin (p less than 0.001), beta 2-microglobulin (p less than 0.001) and N-acetyl-beta-D-glucosaminidase [NAG] (p less than 0.001). These effects lasted less than 120 min. Dextran 40 and 70 (500 ml infused over 2 h) did not affect urinary albumin, beta 2-microglobulin or NAG excretion. Haemaccel (8 ml/kg body weight infused over 2 h) resulted in significant increases in urinary albumin (p less than 0.05) and beta 2-microglobulin (p less than 0.01) during the second hour of the infusion. It also caused a biphasic increase in urinary NAG excretion, the initial peak (p less than 0.05) coinciding with the peak of albumin and beta 2-microglobulin excretion. The second peak which was more defined (p less than 0.01) occurred 21-24 h after the beginning of the infusion. Neither arginine or Haemaccel have been reported to be nephrotoxic whereas dextran infusions are a well recognised cause of acute tubular necrosis. These data indicate that increases in urinary beta 2-microglobulin and NAG are not always reliable indicators of nephrotoxicity or renal tubular cell damage.
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PMID:The effects of arginine, dextran and Haemaccel infusions on urinary albumin, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. 242 74

Traditional methods of noninvasively evaluating patients for renal injury do not accomplish the following tasks: reliably distinguish potentially treatable forms of acute renal failure from acute tubular necrosis; provide a sensitive indicator of early allograft rejection in renal transplant recipients, particularly those in the pediatric age group; provide an early warning of incipient drug-induced nephrotoxicity; or serve as an adequate screening test for renal injury due to exposure to occupational or environmental toxins, especially heavy metals. Because of this, considerable effort has been devoted to the development of assays to satisfy these needs. Three approaches include measurement in the urine of low-molecular-weight plasma proteins such as beta 2-microglobulin; a variety of kidney-derived enzymes, such as L-alanine aminopeptidase and N-acetyl-beta-D-glucosaminidase; and specific renal antigens using immunologic detection. The first two of these have not proved to be adequately sensitive or specific, complicated by the frequent loss of activity associated with the physicochemical characteristics of the urine or the presence of pyuria. Despite this, useful information has been obtained. In particular, assays of beta 2-microglobulin urinary excretion and retinol binding protein appear to have clinical utility that should be pursued. Recent experience with a monoclonal antibody-based assay for a unique proximal tubular antigen, the adenosine deaminase binding protein, suggests that a battery of such assays, each directed against an antigen localized to a particular segment of the nephron, may be particularly useful.
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PMID:Noninvasive renal diagnostic studies. 290 37

Elevated plasma renin activity (PRA) has been documented in patients with established acute renal failure. To study the association of PRA and renal dysfunction, 53 patients who were at risk of developing acute renal failure had serial measurements of PRA, renal function, and urinary beta 2-microglobulin. Those entered for study had pneumonia, septicaemia, volume loss with hypotension, or major surgical procedures with complications. Patients were divided into groups of abnormal or normal renal function. Abnormal renal function was defined by an elevated plasma urea and/or creatinine level with a submaximal urine urea to plasma urea ratio. The mean values of PRA for the abnormal and normal renal function groups, respectively, were 29 and 5.2 ng/ml/h (p less than 0.0001) and for beta 2-microglobulin 16.2 and 6.4 micrograms/l X 10(3) (p less than 0.0005). A linear regression of the logs of PRA to beta 2-microglobulin for the total group of patients gave an r value of 0.526 (p less than 0.001). These data show an association of PRA to renal dysfunction and tubular injury/dysfunction in the prerenal phase of renal failure, suggesting an effect of the renin-angiotensin system at this phase. It is not possible, however, to conclude from our study that the renin-angiotensin system has a direct role in the development of established acute tubular necrosis, since only 3 patients fell within this category.
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PMID:Elevated plasma renin activity associated with renal dysfunction. 352 81

The determination of beta 2-microglobulin has recently been proposed as a promising diagnostic method to monitor the state of renal allografts. Elevated levels of beta 2MG in the serum and/or urine allow the substantiation of the diagnosis of an acute graft rejection and are helpful in distinguishing acute tubular necrosis from a rejection reaction. In this paper, the usefulness of beta 2MG serum levels is evaluated, not only during the immediate post-operation phase but also for the long-term prognosis of renal allografts. The immunosuppression treatment included methylprednisolone and azathioprine in all the presented patients. The data indicate that a rapid normalization of beta 2MGSL within 6 days, even if the decrease is interrupted by re-elevation due to acute rejection episodes or inflammatory diseases, represents a good long-term prognosis for kidney allografts.
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PMID:Beta 2-microglobulin: a prognostic parameter for graft survival after renal transplantation. 354 11

In a prospective study the diagnostic value of urinary thromboxane B2 (TXB2) and beta 2-microglobulin (beta MG) in renal allograft rejection was studied in 34 patients after transplantation. Twenty-four episodes of rejection were diagnosed by clinical symptoms. The clinical diagnosis of rejection was confirmed by an increase of urinary TXB2 in 21 (88%) cases. The augmented renal excretion of TXB2 proceded the clinical signs of rejection for 2.0 +/- 0.75 days. The symptoms in the remaining three (12%) cases of supposed allograft rejection without increased urinary TXB2 were caused by non-immunological events (urinary tract infection, acute tubular necrosis). No elevated TXB2 excretion was observed during urinary tract infection, sepsis, and acute tubular necrosis whereas urinary beta MG increased during these events as during transplant rejection. Urinary TXB2 was found to be an early, specific, and sensitive marker of renal allograft rejection with greater reliability than beta MG excretion or clinical signs of rejection.
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PMID:Thromboxane B2 and beta 2-microglobulin as early indicators of renal allograft rejection. 388 70

Urinary concentrations of beta 2-microglobulin (beta 2M) and creatinine were measured in normal term infants and in those born with meconium-stained amniotic fluid. None of the infants or their mothers had conditions known to modify beta 2M excretion. Measurements of beta 2M were made on urines collected by bagging; urines obtained from diapers were not satisfactory. Urinary beta 2M concentrations increased significantly (P less than .02) in the normal infants from the first day (0.36 +/- 0.29 mg/L: n = 29) to the third day (0.60 +/- 0.43 mg/L: n = 21) postpartum. Compared with the normal infants, values for the infants with meconium-stained amniotic fluid were increased significantly on days 1 (1.64 +/- 2.16 mg/L: n = 25: P less than .005) and 3 (2.12 +/- 2.04 mg/L: n = 23: P less than .005). Levels exceeded two standard deviations above the normal mean in 12 of the 26 infants with meconium-stained amniotic fluid on postpartum day 1, and 12 of the 23 infants with meconium-stained amniotic fluid on day 3. Urinary creatinine levels were similar in both the normal infants and those with meconium-stained amniotic fluid. All infants with meconium-stained amniotic fluid with a one-minute Apgar score of 6 or less had an elevated urinary beta 2M concentration. The elevated levels of urinary beta 2M in infants with meconium-stained amniotic fluid indicate the existence of tubular dysfunction, probably mild acute tubular necrosis secondary to hypoxia.
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PMID:Urinary beta 2-microglobulin in full-term newborns: evidence for proximal tubular dysfunction in infants with meconium-stained amniotic fluid. 390 50

Immunoreactive thromboxane B2 (i-TXB2) was measured in daily urine samples from twelve patients after renal transplantation. In 21 of 30 rejection episodes, the increase in i-TXB2 preceded both the increase in serum beta 2-microglobulin (beta 2-MG) and the clinical diagnosis of rejection. In 26 of 30 rejection episodes, the increase in urine i-TXB2 preceded the increase in serum creatinine. The degree of change in i-TXB2 is greater than that of either serum beta 2-MG or creatinine. Urinary i-TXB2 was very high in one patient with deep venous thrombosis, but it did not rise in patients with urinary tract infection, pneumonia, or acute tubular necrosis. Thus, urinary i-TXB2 seems to be an early indicator of clinical renal allograft rejection.
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PMID:Urine i-TXB2 in renal allograft rejection. 611 99

Tubulo-interstitial nephropathy or nephritis is suggested if renal function is deteriorated and urinary findings are slight. In most cases, the daily urinary protein excretion is less than 1 g and macrohematuria is not present. Urinary excretion of N- acetyl-beta-glucosaminidase and beta 2-microglobulin is a good indicator for tubulo-interstitial damage. Acute renal failure is caused either by acute tubulo-interstitial nephritis or acute tubular necrosis. In either case, renal biopsy is essential for diagnosis and to characterize the renal damage. In the interstitium, edema and fibrosis are seen and lymphocytes, plasma cells, polymorpholeukocytes, and/or eosinophils infiltrate. Tubular basement membrane is sometimes disrupted and lymphocytes have infiltrated inside (tubulitis).
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PMID:[Renal biopsy for diagnosis of interstitial nephritis]. 756 31

Hemolytic uremic syndrome (HUS) in childhood is recognized as the most frequent cause of acute renal failure and is greatly associated with verotoxin-producing E. coli (VTEC) infection. Most of the prodromal feature in HUS associated with VTEC infection is hemorrhagic colitis (HC). HC progresses to HUS in several days. So it is important to detect whether the patient with bloody diarrhea is associated with VTEC infection or not. From 1992 to 1996 we analyzed clinical findings of 80 HUS and 29 HC patients. High level of beta 2-microglobulin (BMG) and N-acetyl-D-beta-glucosaminidase (NAG) in the urine were observed in the early stage of the disease. We went on to examine verotoxin (VT2)-binding in mouse (ICR) renal sections by enzyme immunoassay. Specific binding of VT2 to tubules was seen in mouse kidney, and intravenous injection of VT2 to mice caused acute tubular necrosis in 15 h whereas glomeruli were intact. These data suggest that the primary target cell of VT2 was tubules in the kidney of the HUS patients with VTEC infection.
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PMID:[Primary tubular impairment by verocytotoxin in hemolytic uremic syndrome]. 908 88


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