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)

The beta-2-microglobulin (B2M) level of the serum and urine was determined in 61 diabetics and 15 control patients by enzyme-immunoassay, to asses the value of B2M in clinical diagnosis. In patients with daily protein excretion exceeding 300 mg there was a significant positive correlation between serum creatinine, daily (24-hour) protein excretion, and B2M level of the serum and urine. In patients with less than 300 mg and in those with more than 300 mg daily protein excretion the B2M levels of the serum and urine were significantly higher than in the controls. Serum creatinine level underwent a significant rise only in patients with more than 1000 mg daily protein excretion. Determination of the B2M level is a sensitive method in the diagnosis of diabetic nephropathy. Simultaneous measurement of B2M level in the serum and urine detects nephropathy at an early stage and thus it may be of value in the prevention of the disease.
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PMID:[Clinical significance of beta-2-microglobulin in diabetes mellitus]. 264 8

Plasma inactive renin concentration (IRC) was determined in 92 diabetic patients with or without chronic diabetic complications, 23 non-diabetic patients with renal failure and 36 normal subjects. IRC of the diabetics was higher than that of normal persons. With the Pearson's correlation analysis, IRC of the diabetics correlated with duration of diabetes, degrees of chronic complications (nephropathy, retinopathy and neuropathy), but not with age of patient, HbA1c or mean blood pressure. The stepwise logistic analysis revealed the relation of neuropathy to mean blood pressure, serum creatinine concentration and duration of diabetes, retinopathy to mean blood pressure, duration of diabetes and serum beta 2-microglobulin and nephropathy to IRC and urinary NAG/Cr ratio. In addition, IRC was dependent on nephropathy but not on retinopathy or neuropathy. IRC in diabetics was high even in diabetics without albuminuria (group I) and significantly increased in diabetics with albuminuria but without increased serum creatinine level (group II) and more marked high levels were observed in diabetics with increased serum creatinine concentrations (group III). However, IRC of the non-diabetic patients with renal failure was not elevated, therefore, the increased IRC in nephropathy is likely to be specific to diabetic nephropathy. The correlation of other factors to increased IRC level seem to be due to nephropathy concomitant to these factors. Therefore, the increased level of IRC in diabetics is intimately connected to renal change in diabetes but whether it is the cause or result of nephropathy remains to be elucidated. It is concluded that the determination of IRC in diabetic patients was an effective means of assessment or forecast of nephropathy.
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PMID:[A study on inactive renin in the plasma of patients with diabetes mellitus]. 267 Jul 25

We studied the effect of perindopril, administered for a period of 9 months, on renal function, albuminuria and glycemic control of diabetic subjects with mild-to-moderate hypertension. After 1 month of placebo, 40 insulin-treated patients were divided into 3 groups based on the level of albuminuria. Group I had normal albuminuria (less than 15 mg/24 hr), group II had pathological microalbuminuria (15-150 mg/24 hr) and group III had macroproteinuria (greater than 150 mg/24 hr). They were given perindopril (4 or 8 mg) once daily. Diastolic blood pressure was normalized within the first 3 months in 80% of the patients. Twenty-nine of these patients (13, 9 and 7 from groups I, II and III, respectively) were followed for a total treatment period of 9 months. They were matched for age, duration of diabetes and hypertension, daily insulin dose, systolic and diastolic blood pressures and quality of glycemic control. Diastolic blood pressure was decreased by 14 and 17% at 1 and 9 months, respectively. Heart rate was not significantly modified. At 3 months, the angiotensin converting enzyme activity was markedly inhibited, while plasma renin activity was increased. In patients in group II, microalbuminuria was reduced from 59 +/- 13 to 32 +/- 6 mg/24 hr after 1 month and this effect was maintained at 9 months. Despite similar decreases in blood pressure, no significant change in the albumin excretion rate was observed in patients in groups I and III. Creatinine clearance remained stable and glycemic control did not change throughout the study in the 3 groups. We conclude that perindopril normalizes blood pressure in a large majority of hypertensive diabetic patients without affecting the quality of diabetes control. It also induces a marked and sustained reduction in microalbuminuria in patients at risk of developing diabetic nephropathy.
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PMID:Renal function, glycemic control and perindopril in diabetic patients. 269 Nov 28

A double-blind urographic and angiographic study was done with the ionic contrast medium meglumine metrizoate and the non-ionic iohexol in 90 patients with diabetes mellitus. Twenty patients were insulin dependent, and 70 non-insulin dependent diabetics. Diabetic patients with decreased as well as normal renal function prior to the examination sustained a reversible and small increase in the plasma creatinine level postexamination. The small increase caused by meglumine metrizoate was significantly higher than the increase caused by iohexol. There was also a significantly higher increase in plasma creatinine among the patients with diabetic nephropathy compared with those without nephropathy.
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PMID:Nephrotoxicity of contrast media in patients with diabetes mellitus. A comparative urographic and angiographic study with iohexol and metrizoate. 269 66

Recent clinical studies have demonstrated the potential benefit of the T-cell-specific immunosuppressant, cyclosporine, in the treatment of Type I insulin-dependent diabetes. In the present study, steady-state cyclosporine pharmacokinetics, fasting glucose and insulin levels and renal function were examined in stable insulin-dependent diabetic rats and compared to non-diabetic rats. Mean creatinine clearance 30 days following diabetes induction was not significantly different from saline controls. Cyclosporine treatment (5 mg/kg/day i.v. for 13 days) did not significantly alter creatinine clearance in either group; however, renal function of vehicle-treated diabetic rats was markedly reduced compared to other groups. Serum insulin concentrations were significantly greater in diabetic rats treated with cyclosporine compared to the control group (35.1 +/- 22.7 vs. 16.0 +/- 8.1 microU/ml; P less than 0.05). Glucose levels were proportionately reduced in diabetic rats treated with cyclosporine. Area under the concentration-time curve, half-life and volume of distribution of cyclosporine were significantly reduced in diabetic rats compared to non-diabetic controls. In summary, the pharmacokinetics and pharmacodynamics of cyclosporine were significantly different in the insulin-dependent diabetic rat model compared to normal controls. Furthermore, short-term cyclosporine therapy reduced the extent of experimental diabetic nephropathy observed in this model.
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PMID:Cyclosporine pharmacokinetics and effect in the type I diabetic rat model. 269 89

Diabetic nephropathy develops in less than half of all patients with diabetes. To study heredity as a possible risk factor for diabetic kidney disease, we examined the concordance rates for diabetic nephropathy in two sets of families in which both probands and siblings had diabetes mellitus. In one set, the probands (n = 11) had no evidence of diabetic nephropathy, with normal creatinine clearance and a urinary albumin excretion rate below 45 mg per day. In the other set, the probands (n = 26) had undergone kidney transplantation because of diabetic nephropathy. Evidence of nephropathy was found in 2 of the 12 diabetic siblings of the probands without nephropathy (17 percent). Of the 29 diabetic siblings of probands with diabetic nephropathy, 24 (83 percent) had evidence of nephropathy (P less than 0.001), including 12 with end-stage renal disease. No significant differences were noted between the sibling groups with respect to the duration of diabetes, blood pressure, glycemic control, or glycosylated hemoglobin levels. Logistic regression analysis found nephropathy in the proband to be the only factor significantly predictive of the renal status of the diabetic sibling. We conclude that diabetic nephropathy occurs in familial clusters. This is consistent with the hypothesis that heredity helps to determine susceptibility to diabetic nephropathy. However, this study cannot rule out the possible influences of environmental factors shared by siblings.
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PMID:Familial clustering of diabetic kidney disease. Evidence for genetic susceptibility to diabetic nephropathy. 277 Aug 29

Low-protein diets in nondiabetic renal failure may slow the progressive loss of renal function in some patients, but few studies have detailed the nutritional consequences of these diets in patients with diabetic nephropathy. We studied 7 patients with insulin-dependent diabetes mellitus and chronic renal insufficiency [mean +/- SEM creatinine clearance (S, U): 28.3 +/- 6.5 ml/min (0.47 +/- 0.11 ml/s x 1.73/A)] for 15 weeks who were prescribed a diet of 0.6 g protein/kg ideal body weight. Midarm muscle circumference (24.1 +/- 1.8 at onset vs. 24.5 +/- 1.5 cm at completion), triceps skinfold thickness (21.6 +/- 3.1 vs. 21.0 +/- 1.5 mm), body weight (71.8 +/- 4.1 vs. 71.2 +/- 4.6 kg), and serum albumin [3.0 +/- 0.1 vs. 3.2 +/- 0.1 g/dl (30 +/- 1 vs. 32 +/- 1 g/l)] remained stable. Based on urinary nitrogen excretion, diet diaries overestimated the degree of dietary protein restriction; there was good adherence to the diet as evidenced by a reduction in urinary urea nitrogen (average 32%). Blood glucose control was maintained despite increased carbohydrate intake. On average, creatinine clearance did not change significantly, but proteinuria diminished slightly (1.8 +/- 0.2 vs. 1.5 +/- 0.6 g/day). These results indicate that 0.6 g/kg/day protein diets did not cause protein depletion in insulin-dependent diabetic patients. Longer-term studies are indicated to assess more fully the efficacy of these dietary regimens in reducing proteinuria or benefiting diabetic nephropathy.
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PMID:Protein-restricted diets in diabetic nephropathy. 271 Feb 67

Microalbuminuria has been established as a marker strongly predictive of diabetic nephropathy. The appearance of microalbuminuria (30-150 micrograms/min) is considered to herald incipient nephropathy, and the progression to clinical proteinuria (greater than 200 mg/24 h) is believed to reflect a shift from reversible to irreversible renal damage in diabetic patients. Periodic monitoring of albumin excretion could thus detect diabetic renal disease at an early, potentially reversible stage. However, this is not routinely done, largely due to cumbersome collection and methodologic constraints. We therefore have developed a simplified competitive immunoassay (ELISA) that is sensitive to 10 ng and reproducibly quantifies urinary albumin levels between 0.1-10 micrograms/ml, a range appropriate to that demarcating normal from microalbuminuric patients. Examination of results obtained with aliquots of 24 h and fractional urine collections, without and with correction for creatinine (albumin: creatine ratio), in basal and post-exercise states indicates that (a) this assay can effectively measure urine albumin concentration in single void specimens, and albumin excretion rates in fractional collections, and (b) conversion to albumin:creatinine ratio is not necessary to discriminate normal from microalbuminuric states.
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PMID:Improved competitive enzyme-linked immunoassay (ELISA) for albuminuria. 271 96

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 studied kidney glomerular structure and function in two groups of type I (insulin-dependent) diabetic subjects with 14-16 yr (group 1, n = 16) and 24-26 yr (group 2, n = 13) duration of diabetes and compared them to a group of 18 nondiabetic subjects with similar age ranges. Within each diabetic group, subjects were selected for normal kidney function (urinary albumin excretion less than 40 mg/24 h, normal blood pressure, creatinine clearance greater than 90 ml.min-1.1.73 m-2) or for nephropathy (urinary albumin excretion greater than 200 mg/24 h). Morphometric analysis of glomeruli revealed a significantly larger mean glomerular volume in subjects with nephropathy (group 2). Mesangial volumes were significantly greater in the nephropathic than the normoalbuminuric diabetic subjects in each group, but filtration surface per glomerulus was constant among all subjects. The percentage of sclerosed glomeruli was also significantly increased in the nephropathic subjects compared with the subjects with normal kidney function, in whom sclerosed glomeruli did not exceed 8%. In addition, there was a significant correlation between percentage of globally sclerosed glomeruli and glomerular volume in group 2 (rs = .79, P less than .01) but not group 1 (rs = -.20, NS) subjects. Thus, glomerular size or individual capacity for glomerular expansion may determine the rate of progression of the loss of kidney function in subjects destined to develop diabetic nephropathy.
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PMID:Mean glomerular volume and rate of development of diabetic nephropathy. 276 38


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