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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary excretion of the lysosomal hydrolases cathepsin B and beta-N-acetylglucosaminidase (beta-NAG) was compared with the tubular activities of these enzymes in remnant kidneys 16 weeks after subtotal nephrectomy (5/6 NX) or unilateral nephrectomy (UNX), as well as in kidneys from diabetic rats. In addition, the urinary excretion of the low-molecular weight protein cystatins, inhibitors of lysosomal cathepsins, was also followed in these animals. The urinary excretion of cathepsin B and beta-NAG was significantly enhanced in all three models of renal disease. The highest excretion rates for these enzymes were found in diabetic animals (cathepsin B: 4-fold; beta-NAG: more than a 10-fold increase over respective controls). In terms of tubular enzyme activities, tissue activities of both hydrolases were reduced in the remnant kidney after 5/6 NX, while in UNX and diabetes only cathepsin B activity was decreased. The urinary excretion of cystatins was enhanced in all three animal models, particularly in 5/6 nephrectomized rats, where a 40-fold increment over control animals was observed. Taken together, these findings indicate that there was severe tubular damage in the remnant kidney after 5/6 NX (reduced tubular enzyme activities, enzymuria and severely compromised tubular protein reabsorption). Furthermore, considerable enzymuria and disturbed protein reabsorption in early diabetes suggest tubular dysfunction before signs of glomerular damage become evident.
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PMID:Urinary excretion of cathepsin B and cystatins as parameters of tubular damage. 786 75

Pancreatic elastase has been shown to inhibit the thickening of glomerular basement membranes in experimental diabetic animals. We explored the clinical significance of the prolonged administration of pancreatic elastase on diabetic nephropathy, in patients whose blood glucose levels and blood pressure were controlled. Pancreatic elastase was administered for 12 months. Body weight levels, blood glucose levels, HbA1c values and blood pressure remained unchanged. Administration of 10,800 U of pancreatic elastase caused a significant decrease in albuminuria (before administration, 512.4 +/- 79.8 mg/g creatinine vs. 12 months after administration, 284.1 +/- 61.9 mg/g creatinine, P < 0.01, n = 28). In the contrast group (n = 18), no significant changes in albuminuria were observed after administration of 300 mg of dilazep dihydrochloride. Serum levels of creatinine and urinary levels of NAG and beta 2 MG were not affected by pancreatic elastase. The present study indicates a significant inhibitory effect of pancreatic elastase on increased albuminuria in diabetic patients.
Diabetes Res Clin Pract 1994 Jul
PMID:The effect of pancreatic elastase on diabetic nephropathy. 798 47

To evaluate the renal structural changes in non-insulin-dependent diabetes mellitus (NIDDM), we studied the renal histological findings and urinary albumin excretion in 75 patients with NIDDM. They were divided into two groups according to excretion of urinary albumin: 40 cases of normoalbuminuria and 35 cases of microalbuminuria. Renal biopsy specimens were evaluated by light microscopy. Diffuse glomerular lesions were graded on a scale of D0 through DIV (Gellman's criteria). The incidence of microalbuminuria was 19.2% in D0, 53.3% in DI, 61.5% in DII and 100% in DIII. Grade IV lesions were not present in either group. Creatinine clearance differed significantly between the groups with and without microalbuminuria. There was no difference between the groups with normoalbuminuria and microalbuminuria in the incidence of retinopathy and hypertension, or in the urinary excretion of beta 2MG and NAG. We conclude that microalbuminuria in NIDDM indicates the early morphological changes of glomerular lesions.
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PMID:Glomerular lesions in patients with non-insulin-dependent diabetes mellitus and microalbuminuria. 801 66

In an in-depth examination to better define the renal effects of mild hypertension, we used urinary proteins to indicate damage to the glomerulus (albumin), tubular reabsorption capability (retinol-binding protein), and turnover of tubular tissue (alanine aminopeptidase and N-acetyl-beta-D-glucosaminidase) in a group of 18 people with mild hypertension not associated with diabetes and a control group (n = 12). The participants' activity was controlled on a high normal salt diet for 3 days followed by a low salt diet for 4 days. Two distinct patterns of albumin excretion were evident in the hypertensive group: 22% had elevated, highly variable excretion patterns, and the rest had tightly grouped values below 16 mg/g creatinine, 16 micrograms/min, or 16 mg/L, with the lowest within-person biological variability given by albumin calculated as a ratio to creatinine. Albumin and NAG excretion primarily correlated with systolic blood pressure and the best correlations were given by ratios to creatinine. A marked decrease in salt excretion of 71% (to 50.8 mEq/day) resulted in significant (P < .0005) decreases in systolic (13.9 mm Hg), diastolic (6.4 mm Hg), and mean arterial pressures (8.9 mm Hg) only in the group with mild hypertension. However, albumin excretion did not decrease when dietary salt content was lowered. The group with hypertension also had higher urinary excretion of lysosomal N-acetyl-beta-D-glucosaminidase (P < .01), and whites in the group had a higher excretion of retinol-binding protein than did whites in the control group (P < .02). Retinol-binding protein values, however, were within the normal range, indicating that the elevated albumin values were the result of changes in selectivity of the glomerulus.
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PMID:An in-depth examination of the excretion of albumin and other sensitive markers of renal damage in mild hypertension. 855 30

The aim of this study was to assess the relationship between markers of tubular function, markers of glycaemic control and erythrocyte sodium-lithium countertransport activity (SLC) in 40 normotensive, normoalbuminuric insulin-dependent diabetic (IDDM) subjects and 11 normal control subjects. Nine IDDM subjects had SLC > 0.40 mmol lithium h-1 litre RBC-1. Glomerular filtration rate (GFR) and the excretion rate of retinol-binding protein (RBP), N-acetyl-beta-D-glucosaminidase (beta-NAG) and glucose were significantly higher in IDDM subjects compared to control subjects (Mann-Whitney test, p = 0.02, < 0.001, < 0.001 and < 0.001, respectively), whilst the two groups had similar SLC and TmPO4 levels. There was no significant relationship between SLC and the other variables in IDDM subjects, even when comparing IDDM subjects with normal and high SLC. beta-NAG excretion rate was correlated to urinary glucose (rs 0.47, p = 0.001) and, weakly, to the other markers of glycaemic control (fasting blood glucose rs = 0.31, p = 0.03, fructosamine rs 0.28, p = 0.04, HbA1 rs 0.27, p = 0.04). RBP excretion rate was correlated to the excretion rate of beta-NAG (rs 0.38; p = 0.007) and albumin (rs 0.45; p = 0.002); the excretion rates of beta-NAG and albumin were significantly associated (rs 0.37, p = 0.009). Diabetes duration did not correlate to any of the aforementioned variables. In this study, beta-NAG and RBP overnight excretion rates were higher in normoalbuminuric IDDM subjects compared to control subjects but no relationship was present between SLC and tubular function in IDDM patients without complications. Excretion rates of different proteins appear to be interrelated and, in IDDM, beta-NAG excretion is associated with glycaemic control.
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PMID:Measures of tubular function in normoalbuminuric insulin-dependent diabetic patients and their relationship with sodium lithium countertransport activity. 885 60

To investigate the extra susceptibility of diabetics to some nephrotoxic agents, adult normal and diabetic Chinese hamsters (6-7 animals in each group) were injected subcutaneously with different doses of cadmium-metallothionein (Cd-MT) equivalent to 0.0, 0.1 or 0.25 mg Cd/kg body weight and the first 24 hr urinary outputs were collected. Several days prior to exposure to the Cd-MT the diabetic hamsters were hyperglycaemic, and plasma insulin levels and body weights were elevated in some of the diabetics. The higher dose of Cd-MT caused significant spillage of N-acetyl-beta-glucosaminidase (U-NAG) activity and protein into the urine of both normal and diabetic animals. The higher dose of Cd-MT was more toxic to the diabetic kidneys because U-NAG levels were higher in the diabetics (2.5-fold higher than normal). U-Cd levels were proportional to the injected Cd-MT dose. U-Zn levels were not consistently affected by the injected Cd-MT although it had contained small amounts of Zn. Therefore, genetic diabetes in the Chinese hamster appears to increase susceptibility to acute cadmium-MT nephrotoxicity. The mechanisms underlying this need to be further investigated.
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PMID:Cadmium-metallothionein nephrotoxicity is increased in genetically diabetic as compared with normal Chinese hamsters. 888 66

The paper discusses the results of the studies conducted with a group of patients with type II diabetes without clinical nephropathy. The aim of the study was to attempt to determine the markers for early stages of diabetic nephropathy in NIDDM patients. The following examinations were carried out: the level of selected microproteinuric components, 24 h monitoring of arterial blood pressure, and electrocardiogram (ECG). Among the patients examined, the level of alfa-1-microglobulin, albumin and immunoglobulin G (IgG) in diabetic patients was higher than in the control group, and the increased activity of beta NAG was observed. The 24 h profile of blood pressure and the ratio afternoon/night of albumin excretion flattened in the majority of diabetic patients. The results of the study suggest that the proximal tubules and the membranes of renal glomeruli are damaged as early as during the period of subclinical diabetic nephropathy.
Diabetes Res Clin Pract 1996 Aug
PMID:Day/night ratio of microproteinuria and blood pressure rhythm in type II diabetes. 892 38

Insulin resistance and hyperinsulinemia cluster with microalbuminuria in both diabetic and nondiabetic subjects, but the mechanism underlying this association is unknown. To test the hypothesis that insulin influences protein permeability, we measured the albumin transcapillary escape rate (TER) by the (131)I-labeled albumin technique in 12 healthy volunteers and 12 normoalbuminuric NIDDM patients (fasting plasma glucose, 10.9 +/- 1.3 mmol/l) during 4 h of isoglycemia with high (1.1 mU x min(-1) x kg(-1)) or, on a different day, low (0.1 mU x min(-1) x kg(-1)) insulin infusion. In both patients and control subjects, high insulin was associated with a 7% decrease in blood volume (P = 0.006) and a 6% decrease in diastolic blood pressure (P < 0.02), these two changes being related to one another (r = 0.56, P < 0.01). Basal albumin TER was similar in patients (8.4 +/- 0.5% x h(-1)) and control subjects (7.7 +/- 0.7% x h(-1)) and was not significantly changed by high insulin in either group (patients vs. control subjects, 7.3 +/- 0.9 vs. 6.2 +/- 0.4% x h(-1); NS vs. low insulin). In contrast, high insulin increased renal albumin excretion (from 3.6 +/- 0.8 to 5.4 +/- 1.1 microg/min, P < 0.01) and clearance rate (0.09 +/- 0.02 to 0.13 +/- 0.03 microl/min, P < 0.001) in patients but not in control subjects. To localize the effect of insulin along the nephron, we measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (beta-NAG), released by the proximal tubule; retinol-binding protein (RBP), reabsorbed by the proximal tubule; and Tamm-Horsfall protein (THP) and epidermal growth factor (EGF), both secreted by the distal tubule. For both beta-NAG and RBP, but not EGF or THP, insulin enhanced urinary excretion (diabetics vs. controls: beta-NAG, 0.48 vs. -0.15 microU/min [P = 0.03]; RBP, 78 vs. -32 ng/min [P = 0.05]). In conclusion, physiological hyperinsulinemia does not affect systemic albumin permeability in healthy subjects or normoalbuminuric NIDDM patients. In contrast, in NIDDM patients, but not in healthy subjects, insulin increases the urinary excretion of albumin and protein markers of proximal tubular function. The significance of this finding for the pathogenesis of diabetic nephropathy remains to be established.
Diabetes 1997 May
PMID:Effect of insulin on systemic and renal handling of albumin in nondiabetic and NIDDM subjects. 913 57

Curcumin, the coloring principle of the commonly used spice turmeric (Curcuma longa) was fed at 0.5% in the diet to streptozotocin-induced diabetic Wistar rats for 8 weeks. Renal damage was assessed by the amount of proteins excreted in the urine and the extent of leaching of renal tubular enzymes: NAG, LDH, AsAT, AlAT, alkaline and acid phosphatases. The integrity of kidney was assessed by measuring the activities of several key enzymes of the renal tissue: glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, and LDH (Carbohydrate metabolism), aldose reductase and sorbitol dehydrogenase (polyol pathway), transaminases, ATPases and membrane PUFA/SFA ratio (membrane integrity). Data on enzymuria, albuminuria, activity of kidney ATPases and fatty acid composition of renal membranes in diabetic condition suggested that dietary curcumin brought about significant beneficial modulation of the progression of renal lesions in diabetes. These findings were also corroborated by histological examination of kidney sections. It is inferred that this beneficial ameliorating influence of dietary curcumin on diabetic nephropathy is possibly mediated through its ability to lower blood cholesterol levels.
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PMID:Amelioration of renal lesions associated with diabetes by dietary curcumin in streptozotocin diabetic rats. 956 45

In 32 published reports in surgical patients, the preponderance of evidence from standard clinical measures of renal function (BUN and Cr) indicates the absence of renal toxicity following sevoflurane anesthesia. Studies of surgical patients receiving intermediate-duration sevoflurane with high or low fresh gas flow and long-duration sevoflurane with high fresh gas flow included sensitive measures of renal function and/or injury, which also indicate the absence of renal toxicity following sevoflurane anesthesia. Studies of surgical patients receiving long-duration sevoflurane with low fresh gas flow did not include sensitive measures. Seven studies in volunteers are not directly relevant to clinical practice but do raise the issue of whether it is important to apply sensitive measures of renal function and/or injury such as urine concentrations and/or excretion of NAG, beta 2M, alpha 1M, AAP, alpha GST, pi GST, gamma GTP, albumin, protein, and glucose and Cr clearance. Two studies of volunteers receiving prolonged sevoflurane anesthesia with fresh gas flow no greater than 2 L/min concluded that the potential for adverse renal effects of sevoflurane may exist. The other studies of volunteers did not. In 14 published reports of surgical patients in special conditions, the preponderance of evidence from standard clinical measures of renal function indicates the absence of renal toxicity. Studies with sensitive measures have been reported for some conditions where the kidney may be at increased risk (e.g., sevoflurane-induced hypotension, advanced age, and renal insufficiency and failure), are incomplete in others (e.g., hypertension and ischemic heart disease), and are missing in others (e.g., morbid obesity). Studies with sensitive measures of renal function and/or injury are also missing in an important group where the kidney may not be at increased risk--pediatric patients. Studies of other risk conditions, such as temporary ischemia, hemorrhagic hypotension, nephrotoxic antibiotics, kidney transplantation, and diabetes may provide additional information about the renal effects of sevoflurane.
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PMID:Renal effects of sevoflurane during conditions of possible increased risk. 980 93


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