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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured in patients with hyperthyroidism. The value of urinary NAG in these patients was higher than that in normal subjects and diabetic patients without diabetic nephropathy. This high level of urinary NAG in patients with hyperthyroidism decreased to the level of normal subjects after treatment of hyperthyroidism. Why urinary NAG increases in the patients with hyperthyroidism remains unknown. On the occasion of estimating the significance of the high level of urinary NAG, however, the possibility of the existence of hyperthyroidism has to be considered in addition to renal damage or hyperglycemia which have already been found to increase urinary NAG.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in the patients with hyperthyroidism. 279 65

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

To examine whether plasma and urine concentrations of human atrial natriuretic peptide (hANP) are altered in patients with diabetes mellitus (DM), plasma and urine hANP concentrations were evaluated in 86 patients with diabetes mellitus using an extraction procedure. The mean recovery rate of extraction was 71.8 +/- 0.6% (mean +/- SEM). The major immunoreactive component of hANP in extracted plasma and urine appeared to be identical to synthetic alpha hANP as judged by reverse-phase high-performance liquid chromatography (HPLC). The patients were divided into three groups according to their renal complications. The patients in group 1 had no apparent abnormality in serum creatinine, serum or urine beta 2-microglobulin (beta 2-MG), or urine N-acetyl-beta-D-glucosaminidase (NAG); those in group 2 showed either beta 2-MG or NAG abnormality but no creatinine abnormality. The patients in group 3 were though to have an established diabetic nephropathy and showed a serum creatinine increase. Plasma ANP concentrations in groups 1, 2, and 3 were 10.7 +/- 2.1, 19.9 +/- 5.6, and 39.2 +/- 9.9 fmol/ml, respectively. These values in groups 2 and 3 were significantly higher than the control values (p less than 0.05 or p less than 0.01 versus 6.2 +/- 0.7 fmol/ml). Urine ANP concentrations in group 1 were also within normal range, though those in groups 2 and 3 markedly increased in comparison with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma and urine concentrations of atrial natriuretic peptide in patients with diabetes mellitus. 297 69

The effect of imidazole-2-hydroxibenzoate on urinary excretion rates of glycosaminoglycans and albumin in 22 insulin-dependent diabetics with albumin excretion rates under 300 mg/day was evaluated in a 165-day double blind crossover study. Unlike placebo, the drug reduced glycosaminoglycan and albumin excretion rates significantly after 40 and 60 days of treatment, and the effects were significantly intercorrelated. Moreover, a parallel reduction in urinary excretion of N-acetyl-beta-D-glucosaminidase was also observed. These pharmacological effects may have a positive impact on the subsequent natural history of diabetic nephropathy.
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PMID:Effects of imidazole-2-hydroxibenzoate on glycosaminoglycan and albumin urinary excretion in type 1 diabetic patients. 317

Urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) has been suggested as a marker for diabetic nephropathy. In this study, urinary activity of NAG was measured with an interval of 5 yr in 36 insulin-dependent diabetic subjects to evaluate its predictive value for development of diabetic nephropathy. During the observation period, 9 patients developed detectable signs of diabetic nephropathy. In these patients, urinary albumin concentration had increased to 503 +/- 185 mg/L, compared to 16 +/- 1 mg/L in patients without nephropathy (P less than .01; means +/- SE), and the fractional albumin excretion rate was 0.21 +/- 0.07 X 10(-3), compared to 0.01 +/- 0.00 X 10(-3) (P less than .01). However, the activity of urinary NAG was not different in these patients compared with the patients without nephropathy (0.69 +/- 0.15 and 0.61 +/- 0.09 U/mmol creatinine, respectively). Furthermore, no increase in the activity of urinary NAG was seen during the observation period in either group. We concluded that the urinary activity of NAG is not related to the development of microalbuminuria and therefore cannot be used as a predictor for the development of diabetic nephropathy.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase activity does not predict development of diabetic nephropathy. 367 79

Tubular function was investigated in patients with diabetic ketoacidosis and those with poorly controlled type I diabetes. Urinary excretion of beta 2 microglobulin and that of certain enzymes: gamma glutamyltransferase, leucine aminopeptidase, and N-acetyl-beta-D-glucosaminidase activities were significantly raised during ketoacidosis in 11 patients compared with healthy controls. In 13 poorly controlled diabetics, tubular electrolyte transport was studied and a significant reduction in tubular phosphate and sodium reabsorption was found. Tubular dysfunction occurring during diabetic ketoacidosis and in poorly controlled diabetics may contribute to the development of diabetic nephropathy.
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PMID:Tubular dysfunction in type I diabetes mellitus. 393 37

Urinary N-acetyl-beta-D-glucosaminidase (NAG), a proximal tubule lysosomal enzyme, has been used as an indicator of subtle renal injury. Since it has been positively and significantly correlated with hemoglobin A1c and microalbuminuria, it has been suggested that this enzyme may also reflect metabolic control. Albumin excretion is exacerbated in adult diabetic individuals during exercise; such exercise-induced albuminuria may be a forerunner of diabetic nephropathy. Metabolic control, degree of exertion, and duration of diabetes have been suggested to influence this increase in albuminuria during exercise. Studies of children are few and have produced inconsistent results. Thus we studied 28 insulin-dependent diabetic children ranging in age from 5 yr to 16 yr and 27 age-matched controls using treadmill exercise; two exercise periods consisting of (1) graded increases in speed and grade at 3-min intervals until exhaustion and (2) a constant speed and grade necessary to produce 2/3-3/4 maximal heart rate for 30 min were performed. Capillary blood glucose, urinary NAG/creatinine (cr) ratios (UNAG/Ucr) and urinary albumin/creatinine ratio (Ualb/Ucr) were measured before and after each exercise period; hemoglobin A1c was also measured. The latter averaged 11.8 +/- 0.6% (mean +/- SEM); contrary to previous studies, this was not correlated with pre- or postexercise UNAG/Ucr. During both exercise periods, blood glucose dropped 271 +/- 19 mg/dl to 213 +/- 21 mg/dl (period 1) and 230 +/- 22 mg/dl to 157 +/- 21 mg/dl (period 2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of exercise on urinary N-acetyl-beta-D-glucosaminidase activity and albumin excretion in children with type I diabetes mellitus. 405 33

Excretion of urinary N-acetyl-beta-D-glucosaminidase has been found to be elevated in diabetic humans and rats. This urinary glycosidase may reflect blood sugar control over time, since it has been significantly and positively correlated with hemoglobin A1 in children with insulin-dependent diabetes. Other studies have suggested that urinary NAG may predict diabetic nephropathy. In order to more carefully define the relationship between urinary NAG excretion and blood and urine sugars, hemoglobin A1, and microalbuminuria, 48 rats were made diabetic by the use of streptozotocin. All rats were uninephrectomized at 3 weeks. Of these, 23 were treated with daily insulin injections, 25 were untreated, and both groups were compared to 13 control, nondiabetic rats. Urine volume, glucose, albumin, and blood sugar were all significantly (P less than 0.05) elevated in the untreated rats compared to the treated and control groups. Urinary NAG:UCr was significantly (P less than 0.01) elevated in the untreated group with lower but still elevated levels (P less than 0.05) in the treated rats. To further define the time course of the increase in UNAG:UCr 12 rats were followed serially at 12-hr intervals for 92 hr after streptozotocin. Urinary NAG increased significantly (P less than 0.05) at 12 hr after streptozotocin injection and reached a plateau at 36 hr while hemoglobin A1 did not rise until 2 weeks after onset of hyperglycemia. Urinary NAG increases more rapidly than hemoglobin A1 after onset of hyperglycemia and glycosuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in streptozotocin-induced diabetic rats. 647 35


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