Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proteinuria on admission, on the 3rd day of the disease, of a 15-year-old male patient with acute renal failure (vasomotor nephropathy) showed a glomerular proteinuria-predominant pattern, and had a normal activity of N-acetyl-beta-D-glucosaminidase, indicating little proximal tubular damage. During a late diuretic phase, the excretion of N-acetyl-beta-D-glucosaminidase in the urine increased in accordance with increases of sodium excretion and urine flow, and then decreased to the normal range on the 20th day of the disease. Urine during the late diuretic phase showed a tubular proteinuria pattern and finally returned to a normal pattern on the 47th day of the disease. Thus, transient proximal tubular damage was evidenced in the late diuretic phase of the patient.
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PMID:A change of urinary proteins from a glomerular pattern to a tubular pattern during a late diuretic phase of acute renal failure. 325 65

Animal studies involving concurrent pathophysiologic states, including experimental renal dysfunction, are useful for a proper understanding of the mechanisms of gentamicin nephrotoxicity and acute renal failure. This study examined gentamicin nephrotoxicity in a model of glomerular dysfunction in rats. Administration of medium molecular weight polyvinyl alcohol (PVA) produced a glomerulopathy, with characteristic accumulation of macromolecular PVA in the glomerular mesangium without altering glomerular filtration or causing proteinuria. Subsequent daily doses of gentamicin ranging from 0 to 120 mg/kg elicited a dose-response nephrotoxicity in both control and PVA-pretreated rats after 6 or 12 days of drug. Based on statistical analysis of renal clearances of creatinine, urea, sodium, and potassium; serum creatinine and urea nitrogen; urinary N-acetyl-beta-D-glucosaminidase excretion (6 days only); in vitro renal cortical transport of tetraethylammonium (TEA) (6 days); and quantified light-microscopic data (12 days), PVA induced an early (6 days) sensitivity to gentamicin nephrotoxicity. By 12 days, there were no differences in the responses of control and PVA rats to gentamicin. Single-dose gentamicin clearance, volume of distribution, and half-life were not altered by PVA and renal concentrations at 6 days were generally lower in these rats. Results of TEA transport studies tend to rule out PVA-induced metabolic lesions in the proximal tubular epithelium as the mechanism for the early sensitivity. This investigation demonstrates altered gentamicin nephrotoxicity in rats with an otherwise benign glomerulopathy and, combined with similar conclusions from a related study in subtotally nephrectomized rats, presents further evidence that the underlying pathophysiologic state of the kidney is an important factor in the renal response to nephrotoxins.
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PMID:Dose-response studies of gentamicin nephrotoxicity in rats with experimental renal dysfunction. II. Polyvinyl alcohol glomerulopathy. 402 16

A comparison of urinary alpha 1-microglobulin concentrations to the behaviour of other indicators of renal tubular disorders, beta 2-microglobulin, retinol-binding protein and N-acetyl-beta-D-glucosaminidase (NAG) has been made. In acute tubular disorders the concentrations of urinary beta 2M and RBP are highly correlated (r = 0.89) but this is less marked for alpha 1M and beta 2M (r = 0.55) and alpha 1M and RBP r = 0.48. NAG tends to run a parallel course to alpha 1M concentrations but lags behind the recovery of low molecular weight protein reabsorption following injury of the tubular cells. The concentrations of alpha 1M, and in particular its stability at low pH suggest that this protein may be useful in screening for tubular abnormalities and detecting chronic asymptomatic renal tubular dysfunction. Urinary alpha 1M greater than 15 mg/g creatinine is strongly suspicious of a proximal tubular dysfunction. The distinction between pure tubular proteinuria and mixed glomerular and tubular proteinuria requires further analysis.
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PMID:Alpha-1-microglobulin: an indicator protein for renal tubular function. 618 98

A study of the change of urinary protein excretion has been made in 26 patients followed from the time of admission to time of discharge from the Yorkshire Regional Burn Centre (7-200 days). Total protein, IgG and albumin (as indicators of glomerular function) and alpha 1-microglobulin, beta 2-microglobulin, retinol binding protein and N-acetyl-beta-D-glucosaminidase (as indicators of proximal tubular function) as well as the patterns on SDS polyacrylamide gel electrophoresis were examined. Patients were divided into three groups according to their urinary protein profiles. The first group was 3 patients who showed little or no evidence of proteinuria; the second group consisted of 7 patients who showed a mild and transient tubular proteinuria, all of whom recovered normal function within one week. The third group, 16 patients, developed moderate to severe proteinuria usually started as a mixed pattern of glomerular and tubular proteinuria, characterized by the excretion of a high level of total protein. After a few days, this pattern changed to a typical tubular proteinuria and the latter could last for as long as 200 days; in some of these patients a secondary increase of low molecular weight protein excretion occurred either due to a latent renal complication or induced by the administration of aminoglycosides. There is a close correlation between the intensity and patterns of the proteinuria and the severity and clinical progress of the burn.
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PMID:Urinary protein profiles after burn injury. 619 46

In 34 patients with multiple myeloma we have studied urinary N-acetyl-beta-D-glucosaminidase (NAG) as an index of tubular injury and related it to urinary light chain excretion and serum creatinine. Our results confirm the association of light chain proteinuria with both tubular damage and global renal impairment, but show that not all light chains are nephrotoxic. Tubular damage occurs independently of global renal impairment. Clinically, urinary NAG appears to be a useful index of early tubular damage in multiple myeloma.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase as an indicator of tubular damage in multiple myeloma. 642 24

Protection by fosfomycin of the nephrotoxicity of dibekacin was studied using Fischer 344 rats and urinary parameters such as volume, osmolality, protein, N-acetyl-beta-D-glucosaminidase, leucine aminopeptidase, lactate dehydrogenase and nucleated cells were determined as markers of nephrotoxicity. The duration of treatment was 11 d. Fosfomycin reduced polyuria, proteinuria, enzymuria and cyturia induced by dibekacin best by the concomitant administration, followed by pre-treatment, but not by post-treatment. Protection was effective in the dose ratio of dibekacin: fosfomycin = 1:2 - 1:32, regardless of administration routes. As judged from urinalysis, protection by fosfomycin (320 mg/kg) was almost complete for the experimental nephrotoxicity induced by 10 mg/kg of dibekacin, and still significant for that by 40 mg/kg. This was supported by the histo-pathological and ultrastructural improvement of proximal tubules and by suppressed blood urea nitrogen and creatinine values. Protective activity of fosfomycin was more potent than that of cephalothin, when compared on the weight basis.
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PMID:Protective effect of fosfomycin on the experimental nephrotoxicity induced by dibekacin. 715 39

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

S-(1,2-dichlorovinyl)-L-cysteine (DCVC)-induced nephrotoxicity in vivo was investigated in New Zealand White rabbits. A primary emphasis in these studies was further characterization of DCVC-induced nephrotoxicity using a variety of serum and urinary analytes, including sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Additionally, the role of oxidative injury was assessed to address the dichotomy between reports indicating that such a mechanism is important in vivo and those indicating that such mechanisms do not contribute substantially to the mechanism of effects observed in vitro. Urine was collected prior to and at 8 and 24 hr after iv administration of DCVC. Serum was collected 15 min prior to and 24 hr after DCVC administration. Rabbits were euthanized 24 hr post-DCVC administration, and kidneys were fixed in formalin and further processed for light microscopic examination. DCVC (10 mg/kg, iv) induced a 45-50-fold increase in total urinary protein excretion, a 10-15-fold increase in urinary N-acetyl-beta-D-glucosaminidase concentration, plus a marked glucosuria by 24 hr postadministration. Additionally, DCVC increased serum creatinine levels by about 2-fold, with a trend toward increased blood urea nitrogen. SDS-PAGE analysis of rabbit urine confirmed the clinical finding of marked proteinuria in DCVC-treated animals, which in contrast to previously reported data was due to the presence of both low and high molecular weight proteins. Antioxidants had no significant effect on DCVC-dependent renal injury, nor was there evidence for DCVC-induced lipid peroxidation, as measured by either thiobarbituric acid-reactive substances or a commercial assay for malondialdehyde and hydroxalkenals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-(1,2-dichlorovinyl)-L-cysteine-induced nephrotoxicity in the New Zealand white rabbit: characterization of proteinuria and examination of the potential role of oxidative injury. 750 60

We investigated the role of the vasoconstrictors endothelin-1 (ET-1) and thromboxane in renal protection by the beta 1-selective adrenoceptor antagonist, bisoprolol, in Dahl salt-sensitive rats (Dahl S) and salt-resistant rats (Dahl R). Six-week bisoprolol treatment (20 mg/kg chow) reduced systolic blood pressure (SBP) by 14% in Dahl S rats fed a high-salt (4% NaCl) diet. This BP reduction was accompanied by a decrease in aortic wall thickness. ET-1 and thromboxane released from renal cortex was significantly decreased by 17 and 30% with bisoprolol, respectively. Other prostaglandin synthesis was unaffected. Renal function such as proteinuria, N-acetyl-beta-D-glucosaminidase (NAG) excretion, and glomerular filtration rate (GFR) was not influenced by bisoprolol. Morphologic investigation showed that bisoprolol significantly improved glomerular sclerosis by 29% and attenuated arterial damage by 71%, although tubular injury was not affected. The more severe the glomerulosclerotic lesions, the greater the generation of thromboxane and ET. The arterial lesions were positively correlated to thromboxane generation. These data indicate that long-term bisoprolol treatment reduces vasoconstrictive ET-1 and thromboxane generation and that these alterations may be partly responsible for the amelioration of glomerular and arterial injury in Dahl S rats.
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PMID:Vasoconstrictors and renal protection induced by beta 1-selective adrenoceptor antagonist bisoprolol. 752 81

Lead nephropathy in adults is silent and insidious, characterized by the absence of proteinuria in its early phase. Of the early markers of nephrotoxicity, urinary N-acetyl-beta-D-glucosaminidase (NAG) appears to be the only one that is elevated in early lead nephropathy. However, the elevation in urinary NAG activity may be a response to a sharp increase in renal burden of lead. Its usefulness as a marker of chronic lead nephropathy is thus in doubt. There is a need, then, to identify a reliable early biological indicator of lead-induced kidney damage. Furthermore, there is also a need to identify suitable markers of chronic exposure to describe meaningful dose-response and dose-effect relationships. Traditionally, blood lead (PbB) was used, but the current blood lead level (PbBrec) is more an indicator of recent exposure. Time-integrated blood lead indices (PbBint) derived from repeated serial PbB measurements can be used as indices of chronic exposure. In 128 lead-exposed workers, the PbBint was the most important exposure variable in describing the variability in urinary alpha 1-microglobulin (U alpha 1 m), urinary beta 2-microglobulin (U beta 2m), and urinary retinol binding protein (URBP). U alpha 1m was the only marker that was significantly higher in the exposed group, with a good dose-response and dose-effect relationship with PbBint. The lack of dose-response and dose-effect relationships in other studies may be due to inappropriate exposure markers as well as less sensitive response markers. PbBint has a better correlation than PbBrec. Furthermore, U alpha 1m may be the most sensitive of the markers because of its higher molecular weight.
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PMID:Lead-induced nephropathy: relationship between various biological exposure indices and early markers of nephrotoxicity. 754 66


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