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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

Eleven patients with insulin-dependent diabetes, advancing renal insufficiency, and proteinuria were placed on a diet containing 0.6 g/kg per day of high-biologic-value protein. Selected clinical variables were observed over a 2-year interval. The rate of decline in renal function was significantly decreased during the intervals of protein restriction. The rate during the second 12 months of the study, however, was increased, when compared with the first 12-month interval. Urinary protein excretion decreased significantly, from 2.27 +/- 0.49 g/d to 0.57 +/- 0.40 g/d after the first 12 months of the study, but increased to 1.43 +/- 0.63 g/d after the second 12 months of the study. The dietary protein intake estimated from urea nitrogen excretion in urine samples correlated significantly with urinary protein excretion. These findings suggest that dietary protein restriction has a sustained beneficial effect on the course of diabetic nephropathy, if compliance to the diet can be maintained.
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PMID:Prolonged dietary protein restriction in diabetic nephropathy. 271 6

We examined clinical and laboratory features retrospectively in 402 patients at the start of chronic hemodialysis in order to define better the "uremic syndrome" in the dialysis era. The information gathered included demographic data, renal diagnoses, uremic symptoms, biochemical values, and prevalences of hypertension (69%), diabetes mellitus (23%) and ischemic heart disease (16%). Unexpected findings were the wide ranges of serum creatinine levels (3.5 to 35 mg/dl) and blood urea nitrogen levels (35 to 345 mg/dl), and the frequency of hyponatremia (27%), hypoalbuminemia (52%), and anion gaps above 25 mg/dl (5%). There were higher hematocrits in males and diabetics, lower serum creatinine levels in females, diabetics and older patients, and lower blood urea nitrogen levels in blacks. The time interval from diagnosis of diabetes mellitus to initiation of dialysis in patients with diabetic nephropathy due to juvenile-onset diabetes mellitus (20.6 +/- 6.8 years) was twice that in adult onset diabetes mellitus (10.3 +/- 8.3 years).
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PMID:Clinical and laboratory features of patients with chronic renal disease at the start of dialysis. 292 Apr 71

The suggested harmful effect of dietary protein on renal function in diabetic nephropathy was tested in three groups of insulin-dependent diabetic patients: 1) 10 patients without signs of nephropathy in spite of at least 30 years of diabetes; 2) 11 patients with nephropathy and reduced but stable glomerular filtration rate (GFR) (decline less than 4 ml/min per year [mean 1.8] during the last 2 years); 3) 10 patients with progressive nephropathy with GFR declining by an average of 11 ml/min per year. Dietary protein intake was estimated from a dietary history interview, as well as from urinary excretion of nitrogen (mean = 4.7 samples). Both methods showed a wide range of protein intake in all three groups of patients (0.6-2.3 g/kg body weight [BW]). The mean values did not differ between the groups, 1.30, 1.34, and 1.24 g/kg BW by interview, and 1.20, 1.10, and 1.13 g based on urinary nitrogen levels. There was no correlation between rate of decline of GFR and protein intake, even in those patients with no or minimal decline. These results do not support the hypothesis that dietary protein is a factor of importance in the development or progression of human diabetic nephropathy.
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PMID:Diabetic nephropathy: is dietary protein harmful? 296 99

Some cardiovascular (heart rate and mean arterial pressure), and renal (glomerular filtration rate-GFR; renal plasma flow-RPF; filtration fraction-FF; blood urea nitrogen-BUN and albuminuria) parameters, coupled with morphologic examination, was undertaken in early (2 months) and late (6 months) stage of streptozotocin-induced diabetes mellitus in rats. The results showed a temporally (early) bradycardia and gradually increase of blood pressure with morphologic changes typical for diabetic cardiopathy. The increased GFR (by 92%), associated with significantly decreased RPF (by 37%), increased FF (by 133%), increased kidney weight/body weight ratio (by 88%), increased BUN (by 52%) and distinct albuminuria (13.53 +/- 2.08 mg/24 h/100 g b. w.), together with typical morphologic changes, suggested the development of diabetic nephropathy which was progressive with the duration of the disease.
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PMID:Pathogenesis of cardiovascular disorders in streptozotocin-induced diabetes in rat. I. Cardiovascular, renal and morphologic changes in different stages of diabetes. 306 11

The aim of the study was to evaluate risk factors for the development and progression of diabetic nephropathy. For this purpose, a reliable method of monitoring renal function is necessary. Five different methods of estimating renal function (plasma and renal clearance of 51Cr EDTA, serum creatinine, plasma beta-2-microglobulin and endogenous creatinine clearance) were compared. The risk factors studied were hyperglycaemia, smoking, diabetic cystopathy and dietary protein. All patients were treated for hypertension. The metabolic control was evaluated by assay of HbA1c and repeated estimation of blood glucose. A careful interview about previous and current smoking habits was used for evaluation of the role of smoking. Presence of residual urine, registered with an isotope technique using 131I-Hippuran, was used as the criterion of diabetic cystopathy. Dietary protein intake was studied with a dietary history interview and by measuring the urinary excretion of nitrogen. All five renal function tested evaluated have disadvantages. The most reliable information is given by the combined measurement of plasma clearance and renal clearance of 51Cr EDTA. Hypertension is the most important factor for progression but metabolic control also has an impact, which can be shown when hypertension is adequately controlled. Diabetic patients with nephropathy have smoked more and still smoke more than patients without nephropathy. Diabetic cystopathy is common but with instructions it can be kept constant for several years. Although a correlation of cystopathy to progression is likely, it could not be demonstrated. The study of protein intake does not support the theory of a harmful effect of dietary protein on the development or progression of diabetic nephropathy. By intervening against risk factors, it is possible to achieve a very low progression rate or even to arrest the progression for several years.
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PMID:Diabetic nephropathy. A clinical study of risk factors in type-I diabetes mellitus. 322 21

Hematuria is not described as a common finding in diabetic nephropathy, and may suggest nondiabetic renal disease. We reviewed the records of 59 children and adolescents with insulin-dependent diabetes mellitus referred to the Children's Kidney Center from 1983 to 1992. Fifty-two patients had clinical and/or biopsy evidence of diabetic nephropathy; 18/52 (35%) had microscopic hematuria at the time of referral. Patients with hematuria on presentation were referred for: hypertension (61%), proteinuria (61%), and decreased glomerular filtration rate (GFR) (11%). For patients without hematuria on presentation, reasons for referral included hypertension (79%), proteinuria (56%), and decreased GFR (3%). When comparing patients with and without hematuria, those with hematuria had a significantly longer duration of diabetes (12.8 +/- 3.1 versus 10.8 +/- 3.7 years, p < 0.05). The groups did not differ significantly with regard to age (18.3 +/- 1.8 versus 17.1 +/- 2.9 years), height (162.2 +/- 10.4 versus 159.3 +/- 11.3 cm), weight (63.9 +/- 10.9 versus 59.4 +/- 14.8 kg), systolic blood pressure (137.2 +/- 11.9 versus 133.2 +/- 13.2 mm Hg), diastolic blood pressure (85.6 +/- 7.6 versus 83.9 +/- 13.4 mm Hg), serum creatinine (1.0 +/- 0.18 versus 1.0 +/- 0.43 mg/dL), blood urea nitrogen (15 +/- 5 versus 13 +/- 4 mg/dL), glomerular filtration rate (117 +/- 34 versus 117 +/- 46 mL/min/1.73 m2), 24-h urine protein (2311 +/- 3862 versus 570 +/- 476 mg/day), or microalbuminuria (75 +/- 41 versus 34 +/- 35 micrograms/min). We detected a significant association between retinopathy and microscopic hematuria (sensitivity 47%, specificity 82%, p < 0.05), but no association between labstix proteinuria or sex and hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematuria in children and adolescents with insulin-dependent diabetes mellitus. 754 85

Progression of diabetic nephropathy is now associated with intrarenal hemodynamic disorders (renal hyperperfusion, hyperfiltration, intraglomerular hypertension). The cause of these disorders is unclear. It is supposed that the relaxation factor which is produced by the vascular endothelium (endothelial relaxation factor-ERF) and an endogenous nitrogen oxide (NO) can cause the above intrarenal hemodynamic alterations in diabetes mellitus. The production of ERF/NO in 35 patients with insulin-dependent diabetes mellitus who had varying severities of diabetic nephropathies were examined. These included the following groups: 1) patients without diabetic nephropathy (n = 9); 2) those with incipient diabetes mellitus (n = 12), 3) those with severe diabetes mellitus (n = 14). From groups 1 and 2, 5 patients with hyperfiltration were identified, their glomerular filtration rate were more than 140 ml/ml. The ability of the cells to produce ERF/NO was indirectly estimated, by determining the levels of human platelet guanylate cyclase in the presence of L-arginine, a NO precursor, the accumulation of cGMP in the cells and plasma. When L-arginine was present, the activity of guanylate cyclase was virtually unchanged in Group 1, but it was substantially increased in Groups 2 and 3, by reaching its peak in patients with hyperfiltration (Group 4). The platelet and plasma levels of cGMP corresponded to the enhancement of guanylate cyclase activity in the presence of L-arginine and increased as diabetic nephropathy progressed. Thus, it is suggested that there is ERF/NO hyperproduction in patients at a high risk for diabetic nephropathy (those having hyperfiltration). ERF/NO is likely to promote the dilation of glomerular arterioles, which results in the development of hyperfiltration and intraglomerular hypertension, causing diabetic nephropathy progression.
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PMID:[Endothelial relaxation factor in the development of diabetic nephropathy]. 762 82

Results of the Diabetes Control and Complications Trial indicate that intensive insulin treatment of patients with type I diabetes would greatly reduce the incidence of diabetic nephropathy. Another multicenter trial indicates that modest protein restriction is of no value in children with chronic renal failure. The relationship between urea nitrogen excretion and total nitrogen excretion in children differs from that in adults. A repeated crossover study found that ketoacids slow progression of renal failure, in comparison with amino acid supplements to the same diet. Long-term protein restriction does not lead to protein deficiency at the onset of dialysis. When combined with essential amino acid supplements, a low-protein diet may gradually correct hypoalbuminemia in nephrotic subjects.
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PMID:Nutritional therapy for progressive renal failure. 792 56

To assess whether moderate dietary protein restriction can delay the progression of overt diabetic nephropathy, 22 subjects with insulin-dependent diabetes mellitus were randomly assigned to an unrestricted protein diet (> 1.6 g.kg body wt-1.d-1) or a moderately protein-restricted diet (0.8 g.kg body wt-1.d-1) and followed prospectively for six mo. Direct isotope methods were used to assess renal function. Protein intake was assessed by measurement of urinary urea nitrogen. The two groups were well-matched for age, sex, duration of diabetes, glycemic control, blood pressure, and degree of renal insufficiency. Patients consuming the unrestricted protein diet (n = 11) showed a progressive decline in glomerular filtration rate of 1.3 mL.min-1.mo-1 with no change in proteinuria. Patients consuming the moderately protein-restricted diet showed a marked decrease in the degree of proteinuria (2.15-1.13 g/d, P = 0.036) and a stabilization of glomerular filtration rate. This occurred independently of changes in blood pressure or glycemic control. Moderate dietary protein restriction can ameliorate progression of overt diabetic nephropathy.
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PMID:Effect of moderate dietary protein restriction on the progression of overt diabetic nephropathy: a 6-mo prospective study. 809 94


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