Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess whether urinary N-acetyl-beta-D-glucosaminidase (NAG) could be used as a predictor of diabetic nephropathy, renal tubular enzymes such as NAG and gamma-glutamyl transpeptidase (gamma GTP), albumin, total protein and beta 2-microglobulin (BMG) in urine and/or serum were measured in various stages of diabetic nephropathy. As a predictor of diabetic nephropathy, urinary NAG was the most useful indicator among of them. Urinary gamma GTP had no clinical benefit on early detection of diabetic nephropathy although in cis-platin induced nephrotoxicity both urinary gamma GTP and NAG increased in parallel. Increase of urinary NAG appeared in diabetic patients prior to clinical proteinuria. With appearance of proteinuria, urinary NAG more increased. Urinary NAG correlated significantly with HbAlc and BMG in serum (sBMG). It is therefore needed for clinical application of urinary NAG as a predictor of diabetic nephropathy that control states of blood glucose in the patients should be considered. However, the results of sequential measurements of urinary NAG, sBMG and HbAlc in 78 diabetic patients for 18-month period showed that only urinary NAG was a responsible factor for elevation of sBMG known as an indicator of deterioration of renal function. These results indicate that renal tubular damage may already exist in early-stage of diabetic nephropathy, and that increase of urinary NAG activity is a useful predictor of diabetic nephropathy.
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PMID:[Clinical evaluation of N-acetyl-beta-D-glucosaminidase on prediction of diabetic nephropathy]. 135 Jul 71

The diagnostic significance of urinary sialic acid (SA) determinations was evaluated in relation to the histological findings of renal biopsy specimens. The subjects enrolled in this study comprised 82 diabetics. They were divided into 4 groups according to Gellman's criteria, namely D0, DI, DII and DIII approximately IV. Thirty non-diabetic healthy volunteers were used as controls. The urinary SA was measured by high performance liquid chromatography, and the urinary albumin excretion was estimated by solid phase radioimmunoassay. In addition, urine samples were assayed for N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2MG). The urinary level of total SA (under conditions of hydrolysis) was significantly increased in the DII and DIII approximately IV groups as compared to the controls; however, a similar value was observed in the D0, DI and control groups. The urinary level of glycoprotein-bound SA was significantly increased in all diabetics as compared to the control group, and was significantly higher in the DII and DIII approximately IV groups than in the D0 and DI groups. The bound-SA/total-SA ratio (B/T ratio) showed a significant increase with respect to the progress of diffuse lesions. A weak correlation was noted between the B/T ratio and urinary protein excretion. However, there was no correlation between the B/T ratio and other indices. The urinary SA is considered to represent a useful indicator for estimating diabetic nephropathy.
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PMID:Diagnostic significance of urinary sialic acid in diabetic nephropathy. 159 1

To determine whether or not urinary Alanine aminopeptidase (AAP) could be used as an early marker for diabetic nephropathy, urinary AAP, microalbumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in 132 diabetic patients and 59 normal subjects. Urinary AAP, microalbumin and NAG in the diabetic patients and the normal subjects were 15.5 +/- 11.7 U/g. Cr and 9.1 +/- 6.9 (P less than 0.01), 27.4 +/- 35.5 mg/g. Cr and 8.4 +/- 4.4 (P = 0.0001), 10. 3 +/- 9.5 U/g. Cr and 3.9 +/- 2.1 (P = 0.0001), respectively. AAP had a moderate correlation with NAG (r = 0.58, P = 0.0001). AAP, microalbumin and NAG showed a slight positive correlation with age (AAP: r = 0.25, P less than 0.01, microalbumin: r = 0.32, P less than 0.01, NAG: r = 0.21, P less than 0.05), although it is significant, and AAP had a positive correlation with urinary protein concentration (r = 0.45, P = 0.0001) in diabetic patients. However, AAP in diabetic patients without proteinuria was higher than that in age-matched normal subjects. Urinary AAP was correlated with the indices of renal tubular damage like NAG, alpha 1-microglobulin and beta 2-microglobulin, so it seemed to be tubular origin but in the patients with clinical proteinuria, it might be partially glomerular origin. Since urine AAP increased in some patients without microalbuminuria and was not influenced by control of blood sugar, AAP could be used as an early marker of diabetic nephropath y in addition to microalbumin and NAG, but the effect of age should be considered in its estimation as in the case of NAG.
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PMID:[Clinical evaluation of urinary alanine aminopeptidase in the patients with diabetes mellitus-comparison among AAP microalbumin and N-acetyl-beta-D-glucosaminidase]. 168 Jul 83

Urinary enzyme activities (N-acetyl-beta-D-glucosaminidase [NAG], alkaline phosphatase [ALP], leucine aminopeptidase [LAP], gamma-glutamyl transpeptidase [gamma-GTP]) were investigated to determine their clinical significance in diabetic nephropathy. There were correlations among ALP, LAP, and gamma-GTP, though no correlation existed between NAG and the other three enzymes. Activities of NAG isozymes (both A and B) were higher than in normal controls. It has been reported that NAG isozyme A might be associated with glomerular diseases, and isozyme B might be associated with proximal tubular damage. The results of our study suggest that NAG reflects lysosomal dysfunction of both glomerular and proximal tubular epithelial cells, which may be caused by poor glycemic control, and that ALP, LAP, and gamma-GTP reflect brush border damage of proximal tubules, which may be caused by diabetic nephropathy.
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PMID:Clinical significance of urinary enzymes in diabetic nephropathy. 168 60

Glomerular and tubular microproteinuria precede the development of overt nephropathy in Type 1 diabetes mellitus. However, in Type 2 diabetes urinary protein excretion and its relationship to diabetic nephropathy has not been clearly characterized. Twenty consecutive, newly diagnosed patients with Type 2 diabetes, whose urine was Albustix-negative and sterile on culture, were studied. Two timed overnight urine samples were collected at diagnosis, and after 2 months and 2 years, and excretion rates of albumin, alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase were calculated. HbA1c fell from 12.1 +/- 2.4% at diagnosis to 9.5 +/- 1.5% at 2 months and 9.6 +/- 2.2% at 2 years. Albumin excretion rate fell marginally from 6.5 (2.1-242.5) micrograms min-1 at diagnosis to 5.5 (1.7-274.0) micrograms min-1 at 2 months (p less than 0.05) rising again to 6.1 (1.9-201.7) micrograms min-1 at 2 years. alpha-1-Microglobulin excretion rate fell from 13.5 (3.6-59.9) micrograms min-1 at diagnosis to 8.4 (2.9-16.1) micrograms min-1 at 2 months and 8.8 (1.8-54.1) micrograms min-1 at 2 years (both p less than 0.05). Albumin excretion rate was found to correlate significantly with creatinine clearance at diagnosis (rs = 0.61, p less than 0.005), though not subsequently. In contrast, excretion rates of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase correlated with HbA1c (rs = 0.68 and 0.66, respectively, p less than 0.005 at diagnosis and rs = 0.57 and 0.53, p less than 0.05 subsequently in both cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microproteinuria in type 2 diabetes mellitus from diagnosis. 169 21

The urinary concentrations of laminin fragment P1 (L-P1), a major component of laminin, were determined in diabetic patients without diabetic nephropathy and healthy controls. In the control subjects, urinary L-P1 increased with age, especially over 60 years of age. A significant increase of urinary L-P1 was observed in diabetics aged less than 50 years. Neither urinary albumin nor N-acetyl-beta-D-glucosaminidase correlated to the urinary L-P1 level. We used immunohistochemistry to locate L-P1 in the cortex of human kidneys. In non-diabetic kidneys, the glomerular and tubular basement membranes, mesangium, and Bowman's capsule were stained. In the diabetic kidney, more was stained, including the mesangial expansion and the thickened capillary basement membranes.
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PMID:Clinical significance of urinary laminin P1 in diabetic patients. 177 46

Pravastatin, a novel inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, was administered to nine hypercholesterolemic patients with diabetes mellitus to examine its effects on diabetic nephropathy. Pravastatin treatment resulted in lowering serum total cholesterol by 22.1% on the average (p less than 0.001), and led to a significant reduction in urinary excretion of albumin and beta 2-microglobulin in patients with an elevated urinary protein excretion rate at the baseline period. But glycemic control, blood pressure, urinary excretion of creatinine and that of N-acetyl-beta-D-glucosaminidase showed no significant change during the study. These results suggest that reduction of atherogenic lipids and lipoproteins with pravastatin could alleviate diabetic glomerular injury.
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PMID:Amelioration of proteinuria with pravastatin in hypercholesterolemic patients with diabetes mellitus. 212 49

While microalbuminuria indicates the glomerular damage of early diabetic nephropathy, tubular abnormalities also occur at an early stage of diabetic renal disease. Urinary excretion of beta-thromboglobulin (BTG) and N-acetyl-beta-D-glucosaminidase (NAG) was measured in 132 normotensive Type 1 (insulin-dependent) diabetic patients with no evidence of overt renal disease, of whom 35 had microalbuminuria and the remainder had normal urinary albumin excretion. Of 21 patients in whom there was a detectable urinary BTG concentration, only 8 (38%) had a concurrently abnormal urinary albumin excretion. NAG excretion was elevated in 22 (63%) of the 35 patients with microalbuminuria; significant associations were also identified between urinary NAG excretion and smoking habit (x2 = 12.7, p less than 0.001) and glycated haemoglobin (r = 0.49, p less than 0.01). It is concluded that measurement of urinary BTG is not of sufficient sensitivity to be of value in the detection of early diabetic renal disease, but measurement of urinary NAG may be of value in the detection of diabetic nephropathy at a potentially reversible stage.
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PMID:Urinary excretion of beta-thromboglobulin and N-acetyl-beta-D-glucosaminidase in type 1 diabetes: potential indicators of early nephropathy? 215 50

In the second morning urine of 51 patients with diabetes mellitus (type I/II) albumin, N-acetyl-beta-D-glucosaminidase (NAG), alpha 1-microglobulin (alpha 1-M/U), creatinine (reference parameter) as well as serum alpha 1-microglobulin and creatine were determined. Following an international expert recommendation, three groups were formed depending on albumin excretion: group 1: albumin less than 24 mg/g creatinine (normal range) group 2: albumin greater than 24 mg/g creatinine and less than 200 mg/g creatinine (so called microalbuminuria) group 3: albumin greater than 200 mg/g creatinine (manifest proteinuria) The urinary tubular parameters NAG and alpha 1-microglobulin were above normal range in 17 and 21% respectively in group 1. For group 2 the results were abnormal in 94 and 69% and for group 3 in 100% of patients. Albuminuria correlated with NAG activity, but not with alpha 1-microglobulin excretion. These results indicate, that measuring NAG and alpha 1-microglobulin as markers for tubular dysfunction can give additional diagnostic informations about type and degree of diabetic nephropathy.
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PMID:[Urinary proteins in patients with diabetes mellitus]. 247 8

There is evidence that increased excretion of urinary enzymes and low-molecular mass proteins indicate impaired tubular function. The excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, and ribonuclease in Type I diabetic patients with (n = 19) and without (n = 17) persistent proteinuria (urinary protein excretion greater than 0.5 g/day) was investigated and compared with this excretion in 30 weight- and gender-matched nondiabetic subjects without renal disease. Urinary NAG excretion was significantly higher in diabetic patients with and without persistent proteinuria (1.16 +/- 0.09 and 3.19 +/- 1.2 Umol/L creatinine, respectively) compared to controls (0.37 +/- 0.03 Umol/L creatinine p less than 0.01). In addition, the urinary excretion of lysozyme and ribonuclease was significantly increased in diabetic patients. Urinary NAG was found to correlate positively with albuminuria and proteinuria (r = 0.95 and 0.93, respectively), as well as with ribonuclease and lysozyme (r = 0.93 and 0.60; p less than 0.01) in patients with persistent proteinuria. Furthermore, NAG excretion was significantly related to the duration of diabetes (r = 0.36; p less than 0.05). No relationship existed between urinary NAG and serum creatinine, beta-2-microglobulin, and degree of metabolic control (HbA7). The lysozyme excretion, but not NAG excretion, was significantly related to hypertension in patients with clinical proteinuria. In conclusion, our results suggest a relationship between the development of tubular dysfunction and the impairment of glomerular function in diabetic nephropathy. An increased excretion of NAG and low-molecular mass proteins may indicate early nephropathy
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PMID:Further evidence for tubular dysfunction in insulin dependent diabetes. 252 61


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