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)

In an investigation into the effect of prostaglandin E1 on proteinuria in nephrotic diabetic nephropathy, five patients were treated with 40 micrograms prostaglandin E1 administered intravenously over 2 h twice daily for 4 weeks. The following parameters were compared before and after treatment: protein excretion in urine; total serum protein concentration; serum albumin concentration; creatinine clearance; blood urea nitrogen; and serum creatinine content. A further five patients with nephropathy resulting from non-insulin-dependent diabetes mellitus were selected as controls. Analysis of the results using Student's t-test showed no significant change in any of the parameters before and after treatment.
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PMID:Influence of prostaglandin E1 on slight proteinuria in non-azotaemic diabetics. 156 24

A study was carried out in four patients with nephrotic diabetic nephropathy in order to determine if decreased creatinine clearance observed during prostaglandin E1 therapy was reversible on discontinuation of therapy. The patients received 40 micrograms prostaglandin E1 intravenously twice daily for 4 weeks and creatinine clearance and daily excretion of urinary protein were measured immediately before, during and 2 weeks after therapy. Total serum protein and serum albumin were also determined. There was a significant decrease in creatinine clearance during therapy and after therapy clearance increased but not significantly. It is concluded that decreased creatinine clearance during prostaglandin E1 therapy has a partial reversibility on discontinuation of the treatment.
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PMID:Decreased creatinine clearance which may be observed during prostaglandin E1 therapy: is it reversible with discontinuation of therapy? 177 10

Treatment of non-insulin-dependent diabetes mellitus patients with nephropathy of the nephrotic type using 40 micrograms prostaglandin E1 given intravenously twice daily for 4 weeks reduced the urinary protein concentration. Prostaglandin E1 also increased the total serum protein and serum albumin concentrations, and reduced creatinine clearance and plasma renin activity following frusemide loading. Treatment with the prostaglandin did not, however, significantly affect the blood urea nitrogen and the serum creatinine concentration. It is concluded that prostaglandin E1 has overt effects on diabetic nephropathy.
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PMID:Influence of prostaglandin E1 on heavy proteinuria in slightly azotaemic diabetics. 186 54

This study was carried out on 55 diabetic patients, 20 of whom had diabetic nephropathy, and 10 controls. Glycosylated haemoglobin, glycosylated serum protein, glucoprotein, serum protein electrophoresis, blood urea, serum creatinine and beta 2-microglobulin were measured. A significant increase of glucoprotein was observed in patients with diabetic nephropathy. No correlation was found between glycosylated serum protein and glycosylated haemoglobin and duration of diabetes. Glycosylated serum protein showed a positive correlation with beta 2-microglobulin, indicating a link between renal involvement and the rise in glycosylated serum protein. Whether there is a pathogenic relation between glycosylated serum protein and the development of nephropathy awaits further evidence.
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PMID:Glycosylated proteins in diabetic nephropathy. 258 Dec 43

In this paper we studied the effects of a low-protein, low-phosphorus supplemented diet in 8 type I diabetics with 'overt' diabetic nephropathy and mild or severe renal insufficiency. We examined the following parameters: the rate of decline of creatinine clearance, the urinary protein loss, the total serum protein, the daily insulin requirement, the serum fasting glucose, the pattern of serum lipids (serum total cholesterol, HDL cholesterol and serum triglycerides), the mean blood pressure and body weight. The rate of decline of creatinine clearance decreased monthly from 1.48 +/- 0.20 ml/min during a previous 15.6-month period of unrestricted protein diet (UPD), to 0.13 +/- 0.3 ml/min during the 11.4 months on the supplemented diet (SD). The mean blood pressure did not differ during UPD (130.9 +/- 7.0 mmHg) and during SD (128.1 +/- 1.6 mmHg). Urinary protein loss significantly decreased on SD, and total serum protein increased. The daily insulin requirement and the serum fasting glucose levels significantly decreased on SD. Serum cholesterol was lower during SD than during UPD, while serum HDL cholesterol and serum triglycerides were not significantly modified. In some patients the body weight decreased on SD as a consequence of the disappearance of edema. In conclusion, on the basis of these preliminary observations, the SD slows the progression of renal failure and seems to exert several beneficial and no unwanted side-effects in renal failure of type I diabetics.
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PMID:Effects of a low-phosphorus, low-protein diet supplemented with essential amino acids and keto analogues on 'overt' diabetic nephropathy. 343 63

Nephropathy continues to be the most serious complication in type I-diabetics. When we started chronic hemodialysis in these patients 15 years ago survival figures were poor. Later on the survival rate for diabetics undergoing hemodialysis has improved progressively. The aim of this report was to present our own experience in hemodialysis treatment of insulin-dependent diabetics. The cumulative survival rate of 46 insulin-dependent diabetics undergoing hemodialysis has increased progressively and now amounts to 70% after one year, and 50% after two years of treatment. At the same time we could attain a certain improvement of metabolic control. Nutrition has also been improved, as indicated by increased transferrin (p less than 0.05) and stable serum protein levels. Systolic blood pressure control became better (p less than 0.05) but, a fluid overload was still present. Here, further improvements are necessary to increase the survival rate. Therefore, the survival of diabetic patients with hemodialysis may be approaching that of non-diabetics. In some patients retinopathy was improved after one year of treatment. Despite a better prognosis for survival in diabetics treated by chronic hemodialysis we suggest that the successful renal transplantation should be the treatment of choice in patients suffering from diabetic nephropathy. In general, hemodialysis and renal transplantation should be started earlier than hitherto, i.e. already at creatinine levels of about 600 mumol/l, and at urea levels of 30 mmol/l. Strict metabolic and blood pressure control, as well as early laser coagulation therapy of retinopathy should be instituted for patients with creatine levels above 200 mumol/l, in close cooperation of a diabetologist, nephrologist, and ophthalmologist. This will be our future therapeutic strategy for these patients.
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PMID:Clinical course in insulin-dependent diabetics undergoing hemodialysis. 398 29

In order to clarify the mechanism of proteinuria in diabetic nephropathy, ultrastructural changes of the glomerular basement membrane (GBM) in patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method". The normal human GBM showed a fine meshwork structure consisting of fibrils forming the small pores. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, hitherto unknown cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. In some portions, these cavities presented a honeycomb-like appearance. The diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules. These enlarged structures are believed to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. These results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.
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PMID:Ultrastructural changes of the glomerular basement membrane in diabetic nephropathy revealed by newly devised tissue negative staining method. 769 3

To clarify the ultrastructural changes of the glomerular basement membrane (GBM) in diabetic nephropathy, the renal tissues of the patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method." A fine meshwork structure consisting of fibrils forming the small pores are observed in the normal human GBM. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. As the diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules, these enlarged structures are considered to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. The present results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.
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PMID:The ultrastructural disruption of the glomerular basement membrane in diabetic nephropathy revealed by "tissue negative staining method". 857 48

The present study was conducted to determine whether iridoid total glycoside from Cornus officinalis was effective in regulating expression of transforming growth factor beta 1 (TGF-beta1) and preventing overdeposition of extracellular matrix (ECM) in a diabetes state. An experimental rat model of diabetic nephropathy (DN) was successfully induced by one intraperitoneal injection of streptozotocin at a dose of 60 mg x kg(-1) and maintained for 12 weeks. All rats had free access to standard chow and water. Four groups: normal control, diabetic control, diabetic rats with aminoguanidine treatment and diabetic rats with iridoid total glycoside treatment were used in this experiment. All treatments were administered by intragastric gavage (ig). At the end of the experiment, serum was collected for ELISA determination of TGF-beta1 protein level; renal cortex was dissected for reverse transcription polymerase chain reaction (RT-PCR) analysis of its mRNA expression; and immunohistochemistry was introduced to observe ECM deposition. A significantly higher level of protein and mRNA expression of TGF-beta1, and also overdeposition of fibronectin and laminin was found in diabetic rats. Both iridoid total glycoside and aminoguanidine were effective in decreasing serum protein level and glomerular mRNA expression of TGF-beta1, and in preventing renal overdeposition of fibronectin and laminin. This study suggests that iridoid total glycoside is a beneficial agent for prevention and therapy of DN.
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PMID:Effects of iridoid total glycoside from Cornus officinalis on prevention of glomerular overexpression of transforming growth factor beta 1 and matrixes in an experimental diabetes model. 1525 32

Diabetic nephropathy (DN) is a renal disease which develops as a consequence of diabetes mellitus. Microalbuminuria is the earliest clinical sign of DN. There are no specific diagnostic biomarkers for type 2 diabetics with nephropathy other than microalbuminuria and macroalbuminuria. However, microalbuminuria does not constitute a sole independent indicator for type 2 diabetics with nephropathy, and thus, another screening method, such as a biomarker assay, is required in order to diagnose it more correctly. Therefore, we have utilized two-dimensional electrophoresis (2-DE) to identify human serum protein markers for the more specific and accurate prediction of progressive nephropathy in type 2 diabetes patients, via comparisons of the serum proteome in three experimental groups: type 2 diabetes patients without microalbuminuria (DM, n = 30), with microalbuminuria (MA, n = 29), and with chronic renal failure (CRF, n = 31). As a result, proteins which were differentially expressed with statistical significance (p < 0.05) in MA and CRF groups as compared to those in DM group were selected and identified by ESI-Q-TOF MS/MS. Among these identified proteins, two proteins which might be useful as diagnostic biomarkers of type 2 diabetics with nephropathy were verified by Western blotting: extracellular glutathione peroxidase (eGPx) and apolipoprotein (ApoE) were found to exhibit a progressive reduction in MA and CRF groups. Notably, eGPx was further verified by ELISA using DM (n = 100) and MA (n = 96) patient samples. Collectively, our results show that the two proteins identified in this study may constitute potential biomarkers for the diagnosis of type 2 diabetics with nephropathy.
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PMID:Proteome analysis of serum from type 2 diabetics with nephropathy. 1726 29


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