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)

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

The onset of diabetic nephropathy is characterized by subclinical elevation of urinary albumin excretion, so-called 'microalbuminuria' (M). Dietary assessments were carried out in 15 insulin-dependent diabetic patients with persistent M and an equal number with persistently normal albumin excretion. The groups were matched for sex, age, duration of diabetes, body mass index, insulin dose and glycosylated haemoglobin; there were no significant differences in systemic blood pressure, glomerular filtration rate, blood glucose and serum albumin concentrations between the groups; retinopathy was significantly more frequent in patients with M. Diabetics with persistent M were found to consume a significantly larger amount of fat (expressed as grams and percentage of total energy) and a significantly smaller percentage of total energy as carbohydrate than patients with normal albumin excretion; total dietary energy was larger in those with persistent M, but the difference was not significant. No significant differences were found in protein and fibre intakes between the groups. Our findings suggest that an excess in the dietary consumption of fat relative to carbohydrate might play an important role in the pathogenesis of early nephropathy in insulin-dependent diabetes mellitus. We emphasize the importance of careful attention to nutrient intake in the prevention and treatment of diabetic complications.
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PMID:Nutrient intake in insulin-dependent diabetic patients with incipient nephropathy. 318 Nov 4

Proteinuria in diabetes is associated with progressive glomerular damage. We studied the effects of 3-wk dietary protein restriction on proteinuria and renal function in 10 insulin-dependent diabetic men with diabetic nephropathy. Patients were randomly assigned by a crossover design to 40-g low-protein diet (LPD) or usual-protein diet (UPD). Glomerular filtration rate and renal plasma flow were measured by inulin and p-aminohippurate clearance at the end of each period under conditions of sustained euglycemia. Total calorie intake, body weight, serum albumin and total protein concentrations, hematocrit, blood pressure, and glucose control were similar during the two diets. Achieved protein intake was 46 +/- 3 g/day during LPD and 81 +/- 4 g/day during UPD (P less than .001). Urinary urea appearance and plasma urea were significantly lower on LPD. Median total urinary protein was reduced from 3.9 g/day (range 0.5-12.3) on UPD to 2.4 (range 0.2-9.0) on LPD (P less than .006), and there was a significant fall in the median fractional clearance of albumin from 2.0 x 10(-4) (range 0.1-90.9) on UPD to 1.0 x 10(-4) (range 0.1-51.4) on LPD and IgG from 2.1 x 10(-5) (range 0.2-238) to 1.5 x 10(-5) (range 0.1-77) (P less than .006 and P less than .02, respectively). The reabsorption rate of beta 2-microglobulin was similar on the two diets and glomerular filtration rate, renal plasma flow, and filtration fraction remained unchanged. Thus, short-term dietary protein restriction reduces diabetic proteinuria independently of blood glucose or systemic blood pressure changes by improving glomerular permselectivity.
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PMID:Renal response to restricted protein intake in diabetic nephropathy. 319 38

In this solid-phase competitive enzymoimmunoassay for albumin in human urine, antiserum to human serum albumin labeled with horseradish peroxidase (EC 1.11.1.7) is incubated with solid-phase-bound human serum albumin in the presence of sample or standard. Results obtained correlate well (r = 0.96) with those of an established fluoroimmunoassay. The present assay covers the range 0.9 to 200 mg/L and can be performed within 1 h. These characteristics, together with the simplicity of the assay protocol, make it very useful for monitoring low concentrations of albumin in urine. Detection of such minimal albuminuria allows initiation of therapy that may prevent development of clinical proteinuria and associated diabetic nephropathy.
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PMID:Rapid, competitive enzymoimmunoassay for albumin in urine. 351 93

During a four-year period, 17 massively obese patients without clinically apparent systemic disease underwent renal biopsy for marked proteinuria. Clinical information and biopsy results were compared with those in 34 normal-body-weight controls matched for age, sex, and similar presentation. Histopathologic changes characteristic of focal glomerulosclerosis were found in nine (53%) of the obese patients and two (6%) of the controls. In addition, five (29%) of the obese patients had occult diabetic nephropathy, while no diabetic changes were seen in controls. Clinically, obese patients resembled controls in most respects. Serum albumin level, however, was higher than in controls (3.5 +/- 0.2 vs 2.5 +/- 0.1 g/dL). Indeed, obese patients with focal glomerulosclerosis had normal serum albumin levels (4.0 +/- 0.1 g/dL). Thus, primary renal disease in massively obese patients with marked proteinuria differed in several important respects from that seen in normal-body-weight patients with a similar degree of proteinuria.
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PMID:Renal disease in patients with massive obesity. 371 96

In an attempt to define the nature of renal selectivity in diabetes mellitus, we have determined the free sulfhydryl (SH) groups of serum and urinary albumin in 9 normal subjects and 24 diabetic patients with various grades of renal involvement, as defined by their urinary excretion rates of albumin (alb. UER): 8 with alb. UER less than 10 micrograms/min (Group A), 6 with alb. UER between 10 and 30 micrograms/min (Group B), 5 with alb. UER between 30 and 200 micrograms/min (Group C) and 5 with alb. UER greater than 200 micrograms/min (Group D). The free SH group content of urinary albumin was three to four fold increased in comparison with its serum homologue in normal subjects and in diabetics with normal or slightly increased alb. UERs (Groups A and B). Diabetics in Group C showed a two-fold increase in free SH groups of urinary albumin compared to serum albumin and diabetics with clinical nephropathy (Group D) showed no increase at all. The SH group content of urinary albumin correlated in all diabetics with the concentration of glycosyl albumin and the of urinary/serum albumin SH groups ratio was inversely correlated with alb. UER. From these observations concerning the selectivity properties of the renal filter in normal and diabetic subjects, it is concluded that the mechanism for progression of diabetic nephropathy may be the hyperfiltration of albumin with an altered conformational state.
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PMID:Conformational mediated renal selectivity towards albumin in diabetes mellitus. 372 Oct 35

Eight patients with insulin-dependent diabetes mellitus and progressive renal dysfunction as determined by serial serum creatinine values were placed on a diet containing 40 g of high-biologic-value protein. Selected factors of renal function were determined over a 12-month interval. After the first 12 months of the protein-limited diet, creatinine clearance was not significantly changed. The rate of decline in renal function during the dietary protein restriction slowed from the rate over the prior 12 months in seven patients. Five of these seven demonstrated improvement in renal function. Daily urinary protein excretion decreased significantly, from 2105 +/- 1355 to 142 +/- 164 mg/d (2.11 +/- 1.36 to 0.14 +/- 0.16 g/d). Body weight did not change significantly, whereas serum albumin level increased significantly from a mean of 3.5 +/- 0.6 to 4.3 +/- 0.3 g/dL (35 +/- 6 to 43 +/- 3 g/L). These findings suggest that dietary protein restriction has a beneficial role in treating patients with diabetic nephropathy.
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PMID:The effect of dietary protein restriction on the progression of diabetic nephropathy. A 12-month follow-up. 382 26

The isoelectric points of albumin purified by pseudo-ligand chromatography on Affi-Gel Blue were determined simultaneously in serum and urine of 11 normal subjects and 25 diabetic patients, subdivided in groups according to their urinary excretion rates of albumin. Serum albumin was constituted by a single homogeneous peak at 4.7 (pI) in normal subjects, whereas the levels for diabetic patients covered this band and some other microheterogeneous levels, ranging from 3.5 to 7 pI. By affinity chromatography with Concanavalin A-Sepharose and immunoelectrophoretic techniques, all these micro-heterogeneous bands were characterized as glycosyl albumin. In normal subjects and diabetic patients whose urinary excretion rate of albumin was normal or increased only slightly (10 to 100 micrograms/min), the pattern of urinary albumin included a main band with normal pI (4.7) and some remarkable amounts of more anionic bands (pI between 4.0 and 4.7) if compared to the native protein, which was characterized as glycosyl albumin. Such a difference was not detected in urines of diabetic patients with clinical nephropathy. These results indicate that the non-enzymatic glycosylation of albumin is a main determinant of the excretion of this protein into urine, in spite of the anionic electrical charge. We describe also the renal selectivity properties in humans that may be viewed as a model for the study of renal disease, but the role of such a mechanism in early diabetic nephropathy remains unknown.
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PMID:Electrical charge of serum and urinary albumin in normal and diabetic humans. 383 28

Subclinical elevation of urinary albumin excretion early in the course of insulin-dependent diabetes has been shown to predict later clinical proteinuria. An agglutination test (Three-drop Albutest) to detect these lesser degrees of albuminuria has been developed. Rabbit anti-human albumin antiserum is immobilized on latex beads. In the presence of human albumin and additional antiserum in solution, a visible precipitate appears. Concentration of solid and liquid phase antiserum have been adjusted to detect urinary albumin concentrations ranging between 2.5 and 17 mg/dl, undetectable by a standard clinical method (Albustix, Ames Company, Miles Laboratories Ltd, Stoke Poges, Slough, Bucks, England). The test is specific for albumin, failing to cross-react with other plasma proteins present in urine or with bovine serum albumin. It is simple to perform and is read within 5 min. This test should find a place in the early detection of diabetics with subclinical albuminuria and in monitoring the success of attempts to reverse this risk factor for clinical diabetic nephropathy.
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PMID:Detection of potentially reversible diabetic albuminuria. A three-drop agglutination test for urinary albumin at low concentration. 717 93

Protectin (CD59) is a low molecular weight glycophosphoinositol-anchored inhibitor of the membrane attack complex of complement (MAC) that is present, for example, on the membranes of endothelial cells and on epithelial cells of glomeruli and distal tubuli. To examine for the possibility that CD59 becomes detached from cell surfaces following cell injury, this study evaluated renal excretion of CD59 in patients with idiopathic membranous glomerulonephritis (MGN; N = 21), diabetic nephropathy (DNP; N = 15) and in healthy control subjects (N = 13). CD59 in human urine was quantitated by a competitive solid-phase radioimmunoassay having approximately 13 kDa soluble urinary CD59 as a standard. Immunofluorescence microscopy demonstrated a decreased expression of CD59 in the glomeruli of MGN patients. Using a Triton X-114 phase separation method 91 to 97% of urinary CD59 was found to be in a soluble form without anchor-associated phospholipid. The mean (+/- SEM) level of urinary CD59 was 5.6 +/- 0.2 micrograms/ml in MGN patients, 3.7 +/- 0.4 micrograms/ml in healthy controls (P < 0.001) and 2.6 +/- 0.1 in DNP patients (P < 0.001). When related to urinary creatinine (UCr) the corresponding values were 11.9 +/- 5.6, 4.8 +/- 0.3 (P = 0.021) and 4.4 +/- 0.2 (P < 0.002), respectively. The amount of CD59 in urine correlated with the urinary excretion of soluble terminal complement complexes, SC5b-9 (r = 0.594, P < 0.006) in MGN patients. The excretion of CD59 also correlated with the excretion of the inflammatory mediator IL-1 beta (r = 0.671, P = 0.001) but not with TNF-alpha (r = 0.314, P = 0.178). No correlation of CD59 excretion was observed with duration of the disease level of proteinuria, serum albumin concentration or serum creatinine level. Based on these findings we speculate that the increased excretion of CD59 into urine in MGN patients is due to complement activation and inflammation induced shedding of CD59 from glomerular cells.
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PMID:Urinary excretion of protectin (CD59), complement SC5b-9 and cytokines in membranous glomerulonephritis. 754 24


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