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

Necropsy of a patient who died of uremia complicating juvenile diabetes revealed selective calcification of the perineurial sheaths in the sciatic nerves. The calcium phosphate deposits were limited to the outer layers of the perineurium while the innermost lamellae were free. Structural analysis, including electron diffraction and X-ray microanalysis, showed electron-dense, spicular deposits, which were composed mainly of finely crystallized hydroxyapatite. The end-stage diabetic nephropathy of the patient was associated with an extremely high calcium phosphorus ion product known to favour metastatic calcification. The mechanism of the selective localization of the calcium phosphate deposits to the outer layers of the perineurial sheaths is discussed with reference to the structure and suggested barrier function of the perineurium in regard to phosphate ions.
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PMID:Calcification of the perineurium. A case report. 18 98

To clarify whether glomerular hyperfiltration or disturbances in renal tubular function may be early markers of the later development of nephropathy a follow-up study was performed in 34 young Type 1 diabetic patients, who had originally been investigated 12 years previously. The initial median age was 14 (range 7-18) years and median diabetes duration 7 (2-14) years. At initial examination only one of the 34 diabetic patients exhibited increased urinary albumin excretion rate. The median glomerular filtration rate was increased (136 vs 107 ml min-1 1.73 m-2; p less than 0.0001) and median threshold concentration of phosphate per litre of glomerular filtrate was decreased (1.27 vs 1.76 mmol l-1; p less than 0.0001) in the diabetic group as compared to that of 28 healthy children. At follow-up 17 patients showed increased urinary albumin excretion rate and the median glomerular filtration rate in this group was significantly lower than that of 17 patients with normal urinary albumin excretion rate (108 vs 125 ml min-1 1.73 m-2; p less than 0.05). However, no relationships were found between the increased urinary albumin excretion (incipient and/or overt diabetic nephropathy) at follow-up to either the initial glomerular filtration rate (134 vs 137 ml min-1 1.73 m-2; p greater than 0.05) or to renal tubular function assessed from urinary excretion rate of beta 2-microglobulin (0.059 vs 0.069 microgram min-1; p greater than 0.05) and the renal threshold concentration of phosphate per litre of glomerular filtrate (1.29 vs 1.22 mmol l-1; p greater than 0.05).
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PMID:Does increased glomerular filtration rate or disturbed tubular function early in the course of childhood type 1 diabetes predict the development of nephropathy? 151 70

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

We studied the effect of pyridoxal-5'-phosphate (PAL-P) on protein glycosylation and diabetic nephropathy in NSY mice. In experiment 1, an in vitro model of the browning phenomenon involving the incubation of lysine and glucose was inhibited by PAL-P. In experiment 2, administration of PAL-P to congenitally diabetic NSY mice markedly reduced the thickening of the glomerular basement membrane. These results suggest that PAL-P has the potential to be used for reducing the nephrotic complications of diabetes mellitus.
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PMID:The in vitro and in vivo inhibition of protein glycosylation and diabetic vascular basement membrane thickening by pyridoxal-5'-phosphate. 191 2

The progression of diabetic nephropathy can be arrested by an improvement in diabetic control. High glucose concentrations increase the flux through the aldose reductase pathway, and it has been proposed that this may contribute to renal damage. Aldose reductase is present in both the glomerulus and the renal tubule. Biochemical changes associated with increased sorbitol production have been demonstrated in animal models, including myo-inositol depletion, reduced Na+-K+ ATPase activity, and activation of the pentose phosphate and glucuronate-xylose pathways. Selective inhibition of aldose reductase reverses these biochemical changes and prevents some of the structural and functional abnormalities in diabetic rats. The potential beneficial effects of aldose reductase inhibitors on diabetic kidney disease in man are at present being investigated.
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PMID:Aldose reductase in the etiology of diabetic complications: 2. Nephropathy. 252 43

In a study of the effect of a low-protein diet on the progression of renal disease 19 insulin-dependent diabetic patients with persistent clinical proteinuria were observed for 12-39 (mean 29) months while they were on a normal-protein diet (1.13 [0.06] g/kg per day), then for 12-49 (mean 33) months on a low-protein diet (0.67 [0.03] g/kg per day). The low-protein diet had no adverse effect on nutrition or glycosylated haemoglobin concentration. Mean supine blood pressure (BP) fell slightly on the low-protein diet and was probably due to the start or modification of antihypertensive medication in 9 patients. The mean rate of decline in glomerular filtration rate fell from 0.61 (SEM 0.14) ml/min per month with the normal-protein diet to 0.14 (0.08) with the low-protein diet, and this effect remained highly significant after adjustment for blood pressure, energy intake, and glycosylated haemoglobin. The rise in the fractional clearance of albumin during a normal-protein diet stopped with the low-protein diet, and there was a significant fall in albumin excretion from 467 (95% CI 234-895) micrograms/24 h on the normal-protein to 340 (138-719) on the low-protein diet. Thus, a low-protein diet, with its reduction in protein and possibly other dietary components such as phosphate or fat, seems to retard the rate of decline of glomerular filtration rate in diabetic nephropathy independently of blood pressure changes and glycaemic control.
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PMID:Restriction of dietary protein and progression of renal failure in diabetic nephropathy. 196 36

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

In order to evaluate the differences in morbidity and mortality of diabetics on haemodialysis (HD), data on 12 patients with diabetic nephropathy and 14 non-diabetic patients have been analyzed retrospectively since 1982. The groups were matched for sex, age and duration of HD. We analyzed the differences in survival rate, the number of hospitalization days and the causes of death. Values of BUN, creatinine, calcium, phosphate, cholesterol and triglycerides, alkaline phosphatase, erythrocyte count and haemoglobin were compared throughout the dialysis period. No significant differences occurred between the two groups as regards blood chemistry values (except for creatinine) throughout the observation period. The number of hospitalization days per month of dialysis was significantly different: 1.8 days in diabetic versus 0.9 days in non-diabetic patients (p less than 0.005). This difference is due to a higher rate of vascular access complications and infections. The 3-year survival rate on HD was 73% in type I diabetics (controls 93%), while none of the type II diabetics survived for more than 24 months on HD. The most common causes of death in the diabetic patients were cardiovascular (44%) and septic (44%) complications, followed by cerebrovascular problems (12%). We conclude from our study that the reason for the poor prognosis of diabetic patients on HD is not lack of efficiency of the procedure, but progression of the multisystemic diabetic condition.
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PMID:[Results of chronic hemodialysis treatment in patients with diabetic nephropathy]. 335 18

Proteinuria is the clinical hallmark of diabetic nephropathy and the harbinger of progressive renal disease. Therefore, the present study was designed to examine the effect of phosphate restriction on the proteinuria of streptozotocin-induced diabetes mellitus in the rat. Uninephrectomy was performed in experimental and control groups to worsen the degree of diabetic nephropathy. Proteinuria was prevented in Sprague-Dawley rats treated with the intestinal phosphate binder, dihydroxyaluminum aminoacetate (DHAAA) (24.75 +/- 20.35 mg/d at 3 months v control, 77.45 +/- 44.72 mg/d, P less than 0.001); an effect that was independent of protein and caloric intake, plasma albumin and lipids, severity of diabetes, mean arterial pressures, cardiac output, and renal calcium accumulation. The effect of DHAAA on protein excretion and glomerular hemodynamics was examined in similarly prepared Munich-Wistar rats; these rats did not tolerate long-term studies. Three weeks of DHAAA again caused a consistent fall in proteinuria (5.98 +/- 7.28 v 34.94 +/- 24.28 mg/d) and in transmembrane hydraulic pressure difference (41.1 +/- 1.2 v 46.4 +/- 2.8 mm Hg, P less than 0.005). In conclusion, phosphate restriction significantly decreases the proteinuria of Sprague-Dawley and Munich-Wistar uninephrectomized rats with streptozotocin-induced diabetes mellitus. Micropuncture of Munich-Wistar rats suggests that a reduction of intraglomerular pressure may be at least partially responsible for such an effect.
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PMID:Phosphate restriction reduces proteinuria of the uninephrectomized, diabetic rat. 337 33

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.
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PMID:Effects of low-protein diet on experimental diabetic nephropathy in the rat. 390 11


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