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

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

D dimer and other large fragments produced during the breakdown of crosslinked fibrin may be measured by enzyme immunoassay using monoclonal antibodies. In 91 patients with renal disease and varying degrees of renal dysfunction, plasma D dimer showed no correlation with renal function, whereas FgE antigen, a fibrinogen derivative which is known to be cleared in part by the kidney, showed a significant negative correlation with creatinine clearance. Plasma concentrations of D dimer were, however, increased in patients with chronic renal failure (244 +/- 31 ng/ml) (mean +/- SEM) and diabetic nephropathy (308 +/- 74 ng/ml), when compared with healthy controls (96 +/- 13 ng/ml), and grossly elevated in patients with acute renal failure (2,451 +/- 1,007 ng/ml). The results indicate an increase in fibrin formation and lysis, and not simply reduced elimination of D dimer by the kidneys, and are further evidence of activated coagulation in renal disease. D dimer appears to be a useful marker of fibrin breakdown in renal failure.
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PMID:Plasma D dimer: a useful marker of fibrin breakdown in renal failure. 279 64

We measured the urinary excretions of dopamine, noradrenaline and adrenaline, their conjugated metabolites, urinary excretion of sodium and creatinine clearance simultaneously in 21 patients with Type 2 (non-insulin-dependent) diabetes and 6 normal subjects. The mean (+/- SEM) value for urinary excretion of dopamine (52.4 +/- 8.8 micrograms/day) in diabetic patients with nephropathy (Group C, n = 12) was significantly lower (P less than 0.01) than in the normal subjects (Group A, 179.7 +/- 15.5 micrograms/day) and in diabetic patients without nephropathy (Group B, n = 9, 131.5 +/- 16.5 micrograms/day). The mean values for the urinary excretions of noradrenaline and adrenaline were also significantly lower (P less than 0.01) in Group C than in Groups A and B. In addition, the mean urinary excretion of conjugated metabolite of dopamine in Group C was significantly lower (P less than 0.05) than in Group A. There was a trend toward the observation that the mean 24-h urinary excretion of sodium in Group C (121.6 less than 12.9 mEq) was lower as compared with that in Group A (140.8 +/- 8.9 mEq) or B (150.7 +/- 17.9 mEq). A multiple regression analysis revealed that the 24-h urinary excretion of dopamine correlated significantly with creatinine clearance, systolic (P less than 0.01) and diastolic (P less than 0.05) blood pressures. The results indicate that synthesis or secretion of renal dopamine might decrease with a progression of diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary dopamine, noradrenaline and adrenaline in type 2 diabetic patients with and without nephropathy. 292 52

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

Glomerular hyperfiltration is thought to be of pathogenic importance in the structural abnormalities seen in diabetic nephropathy but its cause is not known. It has been suggested that the changes in the preglomerular vascular system may lead to a disturbance of glomerular blood flow in diabetes. We therefore examined the potential role of changes in the vascular system supplying the glomerulus in diabetic mice. The kidneys of 15 diabetic KK-mice (aged 2, 5 and 12 months) were studied and compared with those of 15 non-diabetic NMRI-mice. We determined vessel cross-sectional, wall and lumen areas of 408 small intrarenal arteries, 5,140 arterioles and 518 preglomerular afferent arterioles using a morphometric method. At 2 months, diabetic arteries and arterioles were considerably smaller than the controls, while preglomerular afferent arterioles were the same size. At 12 months, however, all diabetic vessels measured were much larger than the controls. This was chiefly due to an excessive increase in lumen area: in the diabetic arteries the mean (+/- SEM) lumen area at 12 months was 1,057 +/- 142 vs 616 +/- 72 sq mu in controls (P less than 0.001), in arterioles 176 +/- 7 vs 115 +/- 4 sq mu (P less than 0.001) and in preglomerular afferent arterioles (at 5 months) 131 +/- 8 vs 95 +/- 7 sq mu (P less than 0.001). The dilatation of small intrarenal arteries and arterioles in diabetic mice may result from progressive impairment of vasoconstriction and may be a cause of the glomerular hyperfiltration in diabetes.
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PMID:Renal vessel changes in diabetic KK-mice. 309 62

The renal response to volume expansion produced by water immersion to the neck at 35 degrees C was examined in eight young normotensive uncomplicated insulin-dependent diabetic subjects and in eight matched normal control subjects. Both the diabetic and normal subjects manifested a renal response of natriuresis and kaliuresis on immersion, but the natriuretic response was reduced in the diabetic group. Thus the induced excretion of sodium over the 4 h of immersion was 40 +/- 5 mmol (mean +/- SEM) in the normal group compared with 22 +/- 4 mmol in the diabetic group (P less than 0.02). In the normal subjects creatinine clearance did not change during immersion compared with pre-immersion control values while in the diabetic group it rose from pre-immersion control values of 112 +/- 11 ml/min to a mean value of 127 +/- 11 ml/min during immersion (P less than 0.01). The diabetic subjects thus excreted less sodium despite an increased filtered load during water immersion. Fractional excretion of sodium was significantly reduced in the diabetic subjects compared with the normal control subjects (P less than 0.05). The suppression of plasma renin and aldosterone was similar in normal and diabetic groups. Tubular sodium retention could be an early functional change in the diabetic kidney, and be implicated in the development of diabetic nephropathy.
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PMID:Impaired sodium excretion in response to volume expansion induced by water immersion in insulin-dependent diabetes mellitus. 353 Jun 11

The effect of continuous subcutaneous insulin infusion on renal function was studied in 12 patients with insulin-dependent diabetes mellitus. Serum creatinine was less than 110 mumol/L in all patients. Total urinary protein excretion was less than 250 mg/24 hr in seven patients (group I) and exceeded 0.5 g/24 hr in five (group II). Initial glomerular filtration rate was higher in group I compared with group II: 136.0 +/- 8.5 ml/min versus 103.2 +/- 4.6 ml/min (mean +/- SEM; p less than 0.02). After one to three months pump therapy glomerular filtration rate decreased in both groups. It remained stable during 32-36 months in group I (126.3 +/- 6.1, and 127.9 +/- 7.7 ml/min, respectively) but deteriorated in group II (98.6 +/- 4.4, and 60.0 +/- 6.8 ml/min, respectively; p less than 0.01 compared with group I). These results indicate that strict blood glucose control with continuous subcutaneous insulin infusion does not prevent deterioration of renal function in type I diabetic patients with clinical proteinuria. This suggests that other factors than metabolic control are involved in the course of diabetic nephropathy.
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PMID:The effect of continuous subcutaneous insulin infusion on renal function in type I diabetic patients with and without proteinuria. 399 67

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

Glomerular function was monitored prospectively in 13 patients with insulin-dependent diabetes and diabetic nephropathy for up to 51 months. Glomerular filtration rate, measured by 51Cr-EDTA clearance, showed a linear decline in all patients. Rates of fall ranged between 0.63 and 2.4 ml/minute per month (mean +/- SEM 1.2 +/- 0.16). Plasma creatinine concentration proved to be an insensitive marker of glomerular function, especially in the early phase of nephropathy. A good correlation was found between the rate of change of 51Cr-EDTA glomerular filtration rate and that of inverse creatinine levels when plasma creatinine concentrations exceeded 200 mumol/liter. Inverse plasma beta 2-microglobulin concentrations, however, showed a highly significant correlation (r = 0.93; p less than 0.001) with 51Cr-EDTA glomerular filtration rate over the whole range of values, making it sensitive in screening for early impairment of renal function. A significant relationship (r = 0.85; p less than 0.01) was found between the rates of change of the 51Cr-EDTA glomerular filtration rate and of inverse beta 2-microglobulin levels for plasma beta 2-microglobulin concentrations above 3 mg/liter. A progressive increase in the fractional clearance of albumin, IgG, and beta 2-microglobulin was noted as the glomerular filtration rate fell, indicating an evolving defect in the renal handling of proteins. The rate of decline of the glomerular filtration rate was unrelated to age, sex, duration of diabetes, duration of diabetes before onset of proteinuria, glomerular filtration rate, initial albumin clearance, blood glucose control, and arterial pressure, when diastolic values were below 100 mm Hg. The effect of therapeutic intervention (e.g., blood glucose, blood pressure, or diet) on the progression of diabetic nephropathy can be reliably evaluated by precise measures of rate of decline of glomerular filtration rate and changes in fractional clearance of plasma proteins. The factor(s) determining the individual rate of decline of renal function still remain obscure.
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PMID:Monitoring glomerular function in diabetic nephropathy. A prospective study. 640 24

We investigated the efficacy of polyethylene glycol (PEG) for effective and reproducible concentration of urinary type IV collagen prior to measurement by enzyme immunoassay (EIA). Human placental type IV collagen at low concentrations (5 and 10 micrograms/L) and urinary type IV collagen were readily precipitated by PEG-4000 added at a concentration of about 150 g/L in the presence of 0.5 g/L gamma-globulin. Type IV collagen measurement by EIA from PEG-concentrated urine samples showed complete recovery and good reproducibility. Analysis of size distribution by Sephacryl S-300HR gel chromatography and Western blotting following polyacrylamide gel electrophoresis confirmed that type IV collagen in PEG-concentrated urine samples was of high molecular weight comparable to that of human placental type IV collagen. After PEG concentration, type IV collagen was detectable by EIA even in the urine of healthy subjects. Significantly higher concentrations of urinary type IV collagen were found in 30 diabetic patients with nephropathy than in 20 healthy subjects [99.5 (8.9) micrograms/L, mean (SEM) versus 21.4 (2.6) micrograms/L, P < 0.0001]. Thus, urinary type IV collagen can be measured effectively by EIA following concentration with PEG. This method has potential for the assessment of the progression of diabetic nephropathy.
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PMID:A novel method for concentrating urinary type IV collagen based on precipitation with polyethylene glycol: application to its measurement by enzyme immunoassay. 753 Apr 38


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