Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:The effects of arginine, dextran and Haemaccel infusions on urinary albumin, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. 242 74

Intestinal-type alkaline phosphatase (IAP) has been localized to the S3 segment of the renal tubule in previous studies, a site believed to be particularly vulnerable to toxic and ischaemic damage. During a 17-month period a pilot study of the value of urinary enzyme measurements (IAP and tissue non-specific alkaline phosphatase--TNAP, using monoclonal antibody-based immunoassays, and N-acetyl-beta-glucosaminidase--NAG, using colorimetric assay) in 50 prospectively followed cases of acute renal failure (ARF) was performed. Urinary enzymes were measured at initial evaluation ('start'), and then each day for 14 days, with the highest enzyme value ('peak') also used for analysis. Patients were divided into prerenal (n = 16), renal (n = 28), postrenal (n = 6) categories according to standard criteria. Of the renal ARF patients 23 of 28 had acute tubular necrosis (ATN), 3 of 28 acute interstitial nephritis (AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50 had a fatal outcome and 1 of 50 was dialysis-dependent at discharge ('poor' prognosis group), while 31 of 50 survived hospital without becoming dialysis-dependent ('good' prognosis group). Median enzyme concentration were increased in 'poor' compared to 'good' prognosis patients: start IAP 3.2 versus 2.2 U/g creat (NS), start NAG 48.6 versus 13.7 (P < 0.01), start TNAP 3.5 versus 0.9 (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Urinary enzymes in acute renal failure. 839 30

During the first month after bone marrow transplantation, approximately 15% of patients develop acute renal failure (ARF). This usually occurs in the setting of hepatic veno-occlusive disease (VOD). Prior clinical data have suggested that this form of ARF has a hemodynamic basis, analogous to the hepatorenal syndrome (HRS). If so, then proximal tubular injury would not be expected. To directly test this hypothesis, enzymuria (N-acetyl-beta-D-glucosaminidase [NAG]) was quantitated in the following groups of patients within the first 35 days after BMT: (1) VOD+ARF (serum creatinine level > 1.5 mg/dL; N = 10); (2) VOD with relatively normal renal function (serum creatinine level < 1.5 mg/dL; N = 11); and (3) patients without hepatic or renal complications (BMT controls; N = 12). For comparison, NAG was also quantitated in the following groups of non-BMT patients: (1) toxic/ischemic acute tubular necrosis (ATN) (N = 10); (2) jaundice without azotemia (N = 5); and (3) HRS (N = 6). Urine samples from eight healthy subjects established normal NAG concentrations (2.5 +/- 0.5 microU/mg urinary creatinine; mean +/- SE). All non-BMT patients with ATN had markedly elevated NAG levels (61 +/- 12; P < 0.001), validating the test as a marker of tubular damage. NAG concentrations were significantly elevated in all of the control BMT patients (24 +/- 3; P < 0.01), and the presence of VOD was associated with further striking increments (approximately 50 times normal). However, the degree of enzymuria was virtually identical for VOD patients with (125 +/- 27) and without (122 +/- 17) ARF. Jaundice in a non-BMT setting was associated with only mild NAG elevations (11 +/- 2). However, striking enzymuria was noted in all HRS patients (61 +/- 20), equaling the levels seen with ATN. The following conclusions were derived: (1) subclinical tubular injury, as defined by enzymuria, appears to be ubiquitous after BMT; (2) VOD dramatically increases the extent of enzymuria; (3) the degree of enzymuria in VOD patients is not correlated with renal dysfunction, implying that the associated ARF has a large hemodynamic component; and (4) HRS and ATN manifest comparable degrees of enzymuria, suggesting that substantial tubular damage exists in both of these forms of ARF.
 ...
PMID:Marked enzymuria after bone marrow transplantation: a correlate of veno-occlusive disease-induced "hepatorenal syndrome". 874 94