Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary N-acetyl-beta-D-glucosaminidase (NAG) activities were measured in 181 patients with renal allografts during a 15-month period. Activities were high immediately after transplantation but decreased rapidly in the absences of complication. Urinary NAG activities increased by 50% or more in relation to 33 of 36 (92%) episodes of acute rejection diagnosed and treated by clinicians during the first 90 days after transplantation. The increase preceded clinical diagnosis in 70% of the cases, the median interval being 1.5 days. NAG activities decreased after treatment of rejection in 90% of the cases. Chronic rejection, renal vein thrombosis, renal artery stenosis, oliguria, hypotension, and the administraion of gentamicin may also cause increased NAG activity. Urinary NAG assay is simple and inexpensive, and is a useful aid to the early diagnosis of rejection of renal transplants. Results must, however, be interpreted by the clinician, bearing in mind other causes for increased activity.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase assay in renal transplant recipients. 36 24

Renal failure in sepsis often occurs without other organ failure such as cardiovascular or pulmonary dysfunction. An endotoxin-induced renal insufficiency model using rabbits, which does not complicate other organ failure, was developed. To selectively damage kidneys endotoxin (40 micrograms/kg/h, 3 h) was infused through a cannula placed into the abdominal aorta just distally to the take-off of the superior mesenteric artery after ligation of the aorta below the junction of renal arteries. The following manifestations of renal insufficiencies were observed with high reproducibility: oliguria, increase in plasma creatinine (from 1.1 to 1.6 mg/dl) and urine N-acetyl-beta-D-glucosaminidase (from 7.9 to 23.7 U/l), decrease in effective renal plasma flow (33%) and glomerular filtration rate (35%), and an apparent renal ischemic change in the histological examination. On the other hand, blood pressure, heart rate, respiration rate, body temperature and hematocrit were not significantly altered. The present model is useful for studying the effects of drugs on renal insufficiency in sepsis or endotoxemia and its pathogenesis. Most renal insufficiencies in clinical sepsis may be caused by endotoxin-induced renal ischemic change due to neither low blood pressure nor renal microthrombi.
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PMID:Renal insufficiency induced by locally administered endotoxin in rabbits. 208 49

N-acetyl-beta-D-glucosaminidase (NAG) activity in urine was measured as an indicator for detecting the onset of renal damage in patients receiving aminoglycoside and cephalosporin drugs. The studies reveal that gentamicin appears to be most nephrotoxic of the aminoglycoside antibiotics. Polyuria, not oliguria, is the first clinical symptom observed in patients with marked elevation of urinary NAG activity more than 10 mM/hr/day and moderate proteinuria and disturbance of renal function are followed in some cases. Although immediate recovery from these nephrotoxic effects of aminoglycosides and the elevation of urinary NAG activity occurs on prompt withdrawal of the drugs, two autopsied cases receiving prolonged administration of gentamicin, followed marked NAG elevation, show necrosis and exfoliation of tubular epithelial cells with little glomerular injury. The other aminoglycosides, such as amikacin, tobramycin and dibekacin are less nephrotoxic, and the administration of cephalosporin developed no nephrotoxic symptoms nor marked elevation of urinary NAG activity. The results indicate that measurement of urinary NAG activity is useful for the early diagnosis and monitoring of nephrotoxic reactions due to aminoglycosides.
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PMID:Clinical evaluation of urinary N-acetyl-beta-D-glucosaminidase activity in patients receiving aminoglycoside and cephalosporin drugs. 722 Nov 85

Nephrotoxicity of free hemoglobin (Hb) based blood substitutes still awaits full elucidation. Previous reports attributed Hb passage through the renal glomeruli to a tendency of the Hb tetramer to dissociate into dimers. Now it has become more evident that the Hb tetramer is able to extravasate. It appears that the electrical charge of proteins plays an important role, with electronegativity and a low isoelectric point favoring intravascular persistence. This effect was utilized in the development of an improved blood substitute, comprising Hb reacted with o-ATP and o-adenosine, to form an intra- and intermolecularly cross linked product, which is reduced with glutathione. The modification reagents possess the desired pharmacologic activities and produce an increase in the electronegative charges on the Hb surface. All Hb polymers and chemically modified tetramers present in this solution have a uniform electronegative charge, with a pl of 6.1-6.2. In this present study, unmodified bovine Hb and an improved blood substitute were used for the replacement of 40% of the total blood volume in rats. The nephrotoxic effect was investigated by the determination of urinary output, glomerular filtration rate (GFR), fractional excretion of sodium (FENa), potassium (FEK), and chloride (FECl), urine/plasma osmolality ratio, and urine N-acetyl-beta-D-glucosaminidase (NAG) level. The free Hb and non heme protein contents in the urine were analyzed by using isoelectric focusing and size exclusion liquid chromatography methods. The results indicate that unmodified Hb is nephrotoxic. An initially elevated urinary output was followed by a significant oliguria associated with decreased GFR, FEK, and FECl and elevated FENa and NAG. Severe hemoglobinuria was associated with proteinuria. Analysis of urine from unmodified Hb treated rats revealed the presence of Hb tetramers. Histopathological examination of the kidneys showed cytoplasmic vacuolization of proximal tubular epithelium. On the contrary, an improved blood substitute did not produce any nephrotoxic reactions. It was found that this Hb solution did not pass through the renal glomerular barrier and was not present in urine samples. In conclusion, such a chemical and pharmacological alteration of Hb molecules reduced their interaction with renal glomeruli and suspended nephrotoxicity.
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PMID:An improved blood substitute. In vivo evaluation of its renal effects. 936 Jan 40

When cyclophosphamide (CY) (100-120 mg kg(-1)) was administered intravenously (i.v.) to normal F-344 rats, oliguria occurred over the 5-day observation period. Conversely, in rats bearing matrix metalloproteinase-9 (MMP-9) producing 13762NF mammary adenocarcinoma (MTLn3 clone), polyuria occurred chiefly during the first 24 h after CY treatment. In parallel with urine volume, a decrease in the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was observed during the first 5 days after CY treatment in normal rats, but it increased in MTLn3-bearing rats. No elevation in blood urea nitrogen (BUN) or serum creatinine (Cr) values was observed for either group. Both urine volume and urinary excretion of NAG after CY treatment were lower in rats bearing the MTC clone (lower production of MMP-9) than for those bearing the MTLn3 clone. In the case of treatment with cisplatin (CDDP, 4-6 mg kg(-1)), urine volume, urinary NAG excretion and BUN and serum Cr values all increased in normal rats and were all found to be higher in MTLn3-bearing rats than in normal rats. The diuretic response to these drugs in tumour-bearing (TB) rats may be associated with MMP-9 produced by the tumour cells. This report suggests that the nephrotoxicity due to anti-cancer drugs may change when the drugs are used for the treatment of patients bearing a MMP-9-producing tumour.
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PMID:Diuretic response to cyclophosphamide in rats bearing a matrix metalloproteinase-9-producing tumour. 979 46