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)

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

Serum level of osteocalcin was measured by radioimmunoassay in 52 patients with chronic renal failure and 92 control subjects. The patients were treated by usual hemodialysis over a 3-month period. The osteocalcin level of the patients was significantly higher than that of the control subjects, but the patients with diabetic nephropathy had a lower osteocalcin level than the patients with non-diabetic nephropathy. There was a significant correlation between serum osteocalcin level and alkaline phosphatase or PTH level. On the other hand, there was no relationship between serum osteocalcin level and various parameters such as bone mineral contents, and bone cortex volume measured by the microdensitometry method. Hemodialysis affected the serum osteocalcin level. The clinical value of osteocalcin as a parameter of bone formation in chronic hemodialysis patients was discussed.
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PMID:[Clinical evaluation of osteocalcin in chronic hemodialysis patients]. 261 81

To identify early markers of the preclinical stage of diabetic nephropathy, a study was made of the activity of the specific canalicular enzymes in urine: N-acetyl-beta-D-glucosaminidase (NAG), beta-glucuronidase (beta-G1), gamma-glutamyl transferase (GGT), alkaline phosphatase (AP) and lactate dehydrogenase (LDH) in patients with diabetes mellitus without (26) and with (15) proteinuria. Patients without the clinical signs of diabetic nephropathy manifested a significant rise of excretion of lysosomal enzymes of the proximal canaliculi (NAG and beta-G1). Concomitant elevation of the excretion of several enzymes (NAG, beta-Gl, GGT and AP) was observed in 50% of cases. Patients with diabetic nephropathy demonstrated an increase of the excretion of all enzymes under study. Puncture biopsy of the kidneys was made in 4 patients without proteinuria with insignificant duration of diabetes mellitus and concomitant elevation of the excretion of a number of enzymes. Light microscopy revealed minimal changes in the glomeruli, whereas electron microscopy changes both in the glomeruli and in the canaliculi. The morphological changes in renal tissue confirm the diagnostic importance of high concomitant excretion of canalicular enzymes (NAG, beta-Gl, AP) as a marker of the preclinical stage of diabetic nephropathy.
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PMID:[Urinary enzymes as a marker of the preclinical stage of diabetic nephropathy]. 262 51

The urinary enzymes alanine amino-peptidase, alkaline phosphatase, gamma-glutamyltransferase and N-acetyl-beta-D-glucosaminidase and the two urine low-molecular mass proteins lysozyme and ribonuclease were measured in 30 healthy men and 36 insulin-dependent diabetics. 17 diabetics had "clinical proteinuria" (greater than 7.5 g/mol creatinine) and were defined as patients with manifest diabetic nephropathy. The remaining 19 diabetics were without proteinuria. The excretion rates of the two urine proteins and all enzymes except for gamma-glutamyltransferase were the highest in patients suffering from diabetic nephropathy. The excretion rates in both diabetic groups exceeded those of the control group. N-Acetyl-beta-D-glucosaminidase was more often increased than albumin in diabetics without manifest diabetic nephropathy. It is concluded that the tubular dysfunction is an early indicator of the incipient diabetic nephropathy. Thus, tubular parameters, especially the lysosomal enzyme N-acetyl-beta-D-glucosaminidase may be used in follow-up studies of diabetics.
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PMID:[Urine enzymes and low molecular weight proteins as indicators of diabetic nephropathy]. 273 55

We measured the excretion rates of six urinary enzymes that either originate from the proximal renal tubule, like alanine aminopeptidase (EC 3.4.11.2), alkaline phosphatase (EC 3.1.3.1), gamma-glutamyltransferase (EC 2.3.2.2), and N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30), or that are typical low-molecular-mass proteins, like lysozyme (EC 3.2.1.17) and pancreatic ribonuclease (EC 3.1.27.5). These rates were compared with those of total protein and albumin in urine of 36 insulin-dependent diabetic men and 30 healthy men. Seventeen of the diabetics had "clinical proteinuria," defined as excretion of more than 7.5 g of protein per mole of urinary creatinine (group B). Group A comprised the 19 diabetics without proteinuria. Except for gamma-glutamyltransferase, the excretions of enzymes and proteins were significantly higher in diabetics than in controls and were greater in group B than in group A. N-Acetyl-beta-D-glucosaminidase was the analyte most often increased in group A (89%), followed by albumin and alkaline phosphatase (each 32%). All patients in group B showed increased excretion of N-acetyl-beta-D-glucosaminidase. We conclude from the comparative data that this enzyme may be useful as an early predictor of diabetic nephropathy.
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PMID:Urinary enzymes and low-molecular-mass proteins as indicators of diabetic nephropathy. 289 6

Alterations in ouabain inhibitable Na-K ATPase activity, polyol pathway activity, and myoinositol metabolism are part of a unifying hypothesis proposed to explain the pathogenesis of the chronic complications of diabetes mellitus. Direct measurements of renal ouabain inhibitable Na-K ATPase activity in animals with streptozotocin-induced diabetes show increased or decreased activity, depending on the nephron segment examined and the duration of diabetes. While myoinositol feeding corrects depressed Na-K ATPase activity in peripheral nerve of streptozotocin diabetic rats, the effect of myoinositol feeding on altered renal Na-K ATPase activity is unknown. To assess the effect of experimental diabetes on renal ouabain inhibitable Na-K ATPase activity and test the involvement of the polyol/inositol pathway, we assayed kidneys from normal, streptozotocin diabetic, and myoinositol-supplemented diabetic rats for renal ouabain-inhibitable Na-K ATPase, alkaline phosphatase, and tau-glutamyltranspeptidase (tau-GT) activity. Ouabain inhibitable Na-K ATPase activity, expressed per milligram of protein, is increased in the inner medulla of the diabetic kidney compared with normal and, expressed per microgram DNA, is increased in both the inner medulla and cortex. Myoinositol supplementation did not affect the increase in renal enzyme activity seen with streptozotocin diabetes. These observations suggest that the regulation of renal ouabain inhibitable Na-K ATPase activity, in streptozotocin diabetes, does not depend on supplemental myoinositol. These findings do not exclude the possibility that changes in polyol or myoinositol concentrations in a specific nephron segment may have pathogenetic significance for diabetic nephropathy.
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PMID:Renal ouabain inhibitable Na-K ATPase activity and myoinositol supplementation in experimental diabetes mellitus. 289 13

In order to evaluate the differences in morbidity and mortality of diabetics on haemodialysis (HD), data on 12 patients with diabetic nephropathy and 14 non-diabetic patients have been analyzed retrospectively since 1982. The groups were matched for sex, age and duration of HD. We analyzed the differences in survival rate, the number of hospitalization days and the causes of death. Values of BUN, creatinine, calcium, phosphate, cholesterol and triglycerides, alkaline phosphatase, erythrocyte count and haemoglobin were compared throughout the dialysis period. No significant differences occurred between the two groups as regards blood chemistry values (except for creatinine) throughout the observation period. The number of hospitalization days per month of dialysis was significantly different: 1.8 days in diabetic versus 0.9 days in non-diabetic patients (p less than 0.005). This difference is due to a higher rate of vascular access complications and infections. The 3-year survival rate on HD was 73% in type I diabetics (controls 93%), while none of the type II diabetics survived for more than 24 months on HD. The most common causes of death in the diabetic patients were cardiovascular (44%) and septic (44%) complications, followed by cerebrovascular problems (12%). We conclude from our study that the reason for the poor prognosis of diabetic patients on HD is not lack of efficiency of the procedure, but progression of the multisystemic diabetic condition.
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PMID:[Results of chronic hemodialysis treatment in patients with diabetic nephropathy]. 335 18

Abnormalities in extracellular matrix degradation may play a pathogenetic role in diabetic nephropathy. Cultured renal mesangial cells are known to synthesize increased amounts of matrix proteins when incubated in high glucose media (e.g., 30 mmol/l). However, the effect of glucose loading on degradative enzymes is unknown. Primary cultures of rat mesangial cells were grown until confluent in the presence of fetal calf serum (FCS) and insulin (0.67 U/ml). Cells were then cultured for 7 days in plastic wells in either 10 or 30 mmol/l glucose media containing neither FCS nor insulin. Collagenase activity in media were determined by zymography and quantitative spectrofluorometry. Cathepsin B and D activities in cell extracts were measured by spectrofluorometry (using the fluorescent substrate Z-Arg-Arg-7-amido-4-methylcoumarin) and 125I-labeled hemoglobin digestion, respectively. Gelatin-degrading activity of live mesangial cells was also determined. mRNA levels for collagenase IV, cathepsin B, and cathepsin D were determined by Northern analysis. A major band of collagenase activity with a molecular size of 72 kDa was observed in all mesangial cell media. Exposure of cells to high glucose media resulted in significant reductions in collagenase and cathepsin B activities as well as impairment in gelatin-degrading activity. Collagenase IV and cathepsin B and D mRNA levels were also decreased by glucose loading. To exclude the possibility that glucose loading was injurious to cells, 3H-leucine uptake (as a measure of protein synthesis) and membrane alkaline phosphatase activity (as a biochemical marker of viability) were not affected by the high glucose condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased degradative enzymes in mesangial cells cultured in high glucose media. 762 99

We studied the relationship between the histomorphometric parameters of bone structure in biopsied iliac crest bone specimens and the serum biochemical parameters in 62 chronic renal failure (CRF) patients at the time of starting hemodialysis. These patients were classified into 4 groups according to Coburn's definition: 4 patients with osteomalacia, 1 with osteitis fibrosa, and 57 with mild type. Serum corrected Ca levels were significantly lower in cases with osteomalacia than those of mild type, which suggested that hypocalcemia was related to Calcification disturbance in end-stage renal failure. The bone histomorphometry revealed that in CRF patients, osteoid and bone resorption parameters were significantly higher and calcification parameters were significantly lower than those of normal controls. Osteoclast and osteoblast surfaces were significantly correlated with osteoid and bone formation parameters. In diabetic nephropathy patients, serum C-PTH levels were significantly lower than those of patients with non-diabetic nephropathies. Bone mass, osteoid and bone formation parameters were also significantly lower in diabetic nephropathy patients, which showed that low turnover bone mass decrement has already appeared at the time of starting hemodialysis. There was a significant negative correlation between serum corrected Ca levels and osteoid parameters. A significant relationship was also found between serum alkaline phosphatase levels and both osteoid and bone formation parameters. Serum C-PTH levels were significantly related to osteoid, bone resorption and bone formation parameters, demonstrating the presence of high turnover bone in secondary hyperparathyroidism. This study clarifies that morphological changes of bone structure are present at the time of starting hemodialysis in CRF patients.
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PMID:[Studies on the pathogenesis and pathophysiology of renal osteodystrophy. II. Bone histology of chronic renal failure patients at the time of starting hemodialysis]. 781 47

Urinary enzymes were determined in a controlled study including 28 type I diabetes mellitus patients. Fifteen patients had persistent microalbuminuria and were compared to 13 normoalbuminuric patients with comparable age and sex distribution. All patients had normal renal function as measured by serum creatinine. Human intestinal alkaline phosphatase (hIAP), a specific marker of the proximal tubular S3 segment, was elevated in the urine of microalbuminuric patients while human tissue non-specific alkaline phosphatase (hTNAP), indicating effects mainly at the S1-S2 segments, was not. Urinary hIAP was correlated with serum glycated haemoglobin. These results suggest that tubular alterations are present at an early stage of diabetic nephropathy, especially at the S3 segment, and that hIAP may have promise as an early marker.
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PMID:Human urinary intestinal alkaline phosphatase as an indicator of S3-segment-specific alterations in incipient diabetic nephropathy. 808 50


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