Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary excretion of beta2-microglobulin, albumin, kappa light chains, transferrin, and IgG as well as their concentration ratios were assessed in 27 nondiabetic patients with proteinuria and in 72 IDDM patients, 41 with proliferative retinopathy (PR) and 31 without retinopathy, matched for age, duration of diabetes, and treatment. The mean excretions of albumin, transferrin, and IgG were similar in patients with nondiabetic proteinuria and in IDDM patients with PR and were significantly higher than in IDDM patients without retinopathy. Despite similar albumin excretion, the amount of excreted kappa light chains was significantly higher in IDDM patients than in patients with nondiabetic proteinuria, resulting in an elevated kappa chain/albumin ratio. Furthermore, diabetic subjects without microalbuminuria showed increased kappa chain/albumin ratio, indicating that increased urinary excretion of kappa chains may be an early sign of diabetic nephropathy. Determination of kappa light chain excretion may have clinical implications in the differentiation between proteinuria of diabetic and nondiabetic origin. The ratio kappa chain/albumin was independent of the excretion of beta2-microglobulin in patients with PR, suggesting that the reduced ability to reabsorb immunoglobulin light chains may occur earlier than that of beta2-microglobulin in the development of tubular dysfunction in insulin-dependent diabetes mellitus.
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PMID:Urinary excretion of plasma proteins in diabetic subjects. Increased excretion of kappa light chains in diabetic patients with and without proliferative retinopathy. 392 92

To evaluate the role of renal haemodynamic factors in the pathophysiology of diabetic nephropathy, we determined by radionuclear techniques glomerular filtration rate (GFR) and renal plasma flow (RPF) in 18 patients affected by insulin dependent diabetes mellitus (IDDM) in good metabolic control, with normal blood pressure and plasma creatinine. GFR and RPF measured in the same patients after ten months correlated with proteinuria and duration of diabetes. Our finding of a significant correlation between the decline of RPF and duration of diabetes may support the haemodynamic hypothesis of progression of diabetic nephropathy.
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PMID:Radionuclear determination of glomerular filtration rate and renal plasma flow to detect early decrease of renal function in insulin dependent diabetes. 399 57

Eighteen individuals with IDDM (type I) and diabetic nephropathy in whom the initial glomerular filtration rate (GFR) was reduced but not below 60 ml/min per 1.73 m2 were observed for an average of 3 yr. The rate of further decline of GFR was found to range between -2 and 21 ml/min/yr. The duration of diabetes until the GFR was first found to be reduced varied between 14 and 33 yr and was not correlated to the ensuing rate of decline in GFR (r = -0.13). In 10 individuals who developed uremia 40 yr or more after onset of IDDM, the development of persistent proteinuria was followed by hypertension and increased serum creatinine 2 yr later and by terminal uremia after an average of 8 yr. This is also the normal time span for individuals who develop terminal uremia after shorter duration of diabetes. We conclude that the course of clinical diabetic nephropathy is not more favorable in individuals with late onset of this complication and that there is no point at which a person with diabetes can be considered to be spared from developing diabetic nephropathy.
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PMID:Time as a risk factor in diabetic nephropathy. 407 45

Two kidneys were removed from a cadaveric donor with 17-year history of type 1 diabetes. At the time of death the donor had proteinuria but normal serum creatinine, and on histological examination the kidneys showed features of established diabetic nephropathy including diffuse glomerulosclerosis and thickening of mesangial matrix and capillary basement membranes. After transplantation into non-diabetic recipients (cold ischaemia times 46 h and 52 h) the kidneys functioned well with standard immunosuppression. Renal biopsy specimens taken 7 months after transplantation showed almost complete resolution of the nephropathy and both patients remain free from proteinuria after a further 7 months. As well as indicating that longstanding type 1 diabetes need not always contraindicate kidney donation, these observations are relevant to the pathogenesis and management of diabetic nephropathy.
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PMID:Reversal of diabetic nephropathy in human cadaveric kidneys after transplantation into non-diabetic recipients. 613 20

A randomized double blind trial was performed to investigate the effect of the platelet aggregation inhibitor ticlopidine on the rate of decline in renal function in diabetic nephropathy. Twenty-two patients with insulin dependent diabetes complicated by nephropathy completed the trial--11 on ticlopidine, and 11 on placebo for one year. Ticlopidine effectively reduced platelet aggregation in vitro. Renal clearance of 51Cr-EDTA declined from 39 +/- 10 to 30 +/- 13 ml/min per 1.73 m2 body surface in the ticlopidine group and from 42 +/- 9 to 39 +/- 13 in the placebo group. The difference in decline between the two groups was not significant. In the ticlopidine group renal function expressed as the slope coefficient for 1/S-creatinine per month remained the same as before the trial. It is concluded that although there is much evidence to suggest a role of platelets in the development or progression of diabetic nephropathy treatment with ticlopidine could not prevent this process.
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PMID:A platelet aggregation inhibitor--ticlopidine--in diabetic nephropathy: a randomized double blind study. 670 80

This is the first part of a study dealing with the predicted effect of early renal function changes on later development of diabetic nephropathy. Renal function was studied by the clearance method in 128 children with insulin dependent diabetes mellitus after 0, 2, 5 and 10 years duration of the disease. The glomerular filtration rate (GFR) and filtration fraction were significantly increased after 0-5 years, but after 10 years the GFR did not differ from that of controls, which finding might indicate an earlier onset of diabetic nephropathy in children. Renal plasma flow did not differ significantly from that of controls. Increased fractional sodium excretion in cases of recent onset might indicate inadequate adaptation of the proximal tubules to the increased filtered load or to inadequate insulin therapy. An inverse correlation was found between GFR and metabolic control as evaluated clinically and by glucosylated haemoglobin concentration, i.e., poor metabolic control corresponded with high glomerular filtration rates.
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PMID:Early renal functional changes in children with insulin-dependent diabetes mellitus--their relation to metabolic control. 671 11

Forty-seven patients with insulin-dependent diabetes (IDDM) and diabetic nephropathy and 47 controls with IDDM without diabetic nephropathy were interviewed about their previous and current smoking habits. The patients in the two groups were matched according to sex, age, age at onset, and duration of diabetes. All patients in the nephropathy group had proteinuria and decreased glomerular filtration. None in the control group had ever had proteinuria as tested by dip stick. The total amount of smoking until date of interview was estimated for each individual and presented as an index. The patients with nephropathy had a significantly higher smoking index than the controls. In the nephropathy group there were also more numerous current smokers, more heavy smokers and fewer individuals who had never smoked than in the control group. The link between diabetic renal microangiopathy and smoking may be through mechanisms such as increased platelet aggregation, accentuated tissue hypoxia and hemodynamic or metabolic effects of repeated noradrenaline release.
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PMID:Smoking and diabetic nephropathy. 673 Oct 38

Factors possibly influencing the development of diabetic retinopathy were studied in 112 randomly selected type 1 diabetics having no or minimal retinopathy (group A) and in 82 type 1 diabetics with known severe diabetic retinopathy. The latter comprised those with severe background retinopathy (group B, n = 17) and those having proliferative retinopathy without (group C, n = 38) and with group D, n = 27) diabetic nephropathy. Nonretinopaths (group A) were of similar sex ratio, body weight, and age at diagnosis of diabetes but had been diabetic longer (p less than 0.001) and were thus older (p less than 0.001) than retinopaths (groups B-D). The distribution of HLA antigens of the A, B, and C loci was similar in nonretinopaths and retinopaths with the exception that HLA B7 showed a reduced (p less than 0.05) prevalence in the retinopaths (6% versus 17%) and was singularly underrepresented in group D, where no patients had this antigen. Mean postprandial plasma glucose and HbA1 concentrations were higher (p less than 0.01 and p less than 0.001) and cigarette smoking was more prevalent (p less than 0.01) in the retinopathy groups B-D than in group A. Systolic and diastolic blood pressures were similar in groups A-C, with higher (p less than 0.001) values only in group D. There was no association between insulin antibody binding in the serum or measurable plasma C-peptide immunoreactivity and retinopathy status. The risk of development of diabetic retinopathy in type 1 diabetes may be related to HLA-associated genetic factors and to cigarette smoking.
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PMID:HLA antigens and other risk factors in the development of retinopathy in type 1 diabetes. 707 2

It has been recently reported that in type 1 diabetes the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme gene is associated with the presence of diabetic nephropathy. Tissue angiotensin I-converting enzyme is determined by I/D polymorphism, and it has been speculated that in diabetes differences of local angiotensin II availability determine the risk of renal disease. Since angiotensin II is thought to play an important role in the evolution of renal disease in general, we tested whether genotype distribution of the I/D polymorphism is also different in patients with immunoglobulin A-glomerulonephritis (IgA-GN). Furthermore we compared IgA-GN patients with (1) stable renal function or (2) terminal renal failure to investigate a potential role of the I/D polymorphism in the renal prognosis. We examined 122 patients with biopsy-confirmed IgA-GN who had stable renal function and 82 dialysis-dependent or transplanted patients with biopsy-confirmed IgA-GN. Furthermore, in 134 healthy individuals used as controls we analyzed the DNA for normal distribution of genotypes and allele frequencies. The polymorphic region was amplified using polymerase chain reaction with specific primers. Alleles were detected on 2% agarose gels. Genotype distributions and allele frequencies were not significantly different between controls and patients with IgA-GN and stable renal function. Furthermore, no significant difference in genotype distribution was detected between patients with IgA-GN and stable renal function compared with patients with IgA-GN and end-stage renal failure, although a trend for a higher frequency of DD-homozygotes was noted in the latter group (P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No association of converting enzyme insertion/deletion polymorphism with immunoglobulin A glomerulonephritis. 748 24

Diabetic nephropathy is a progressive renal disease and represents a serious late complication of diabetes. There are familial clustering and huge ethnic differences in the occurrence of diabetic nephropathy, which point to a genetic predisposition. Diabetic nephropathy is defined by persistent albuminuria (albumin excretion rate [AER] > 300 mg/day), declining glomerular filtration rate and rising blood pressure. Several years of incipient nephropathy, characterized by worsening microalbuminuria (AER 30 to 300 mg/day or 20 to 200 micrograms/min), which is Albustix-negative and detectable by special assays only, are followed by established nephropathy. The natural history of nephropathy differs between insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In IDDM, nephropathy develops in 30 to 40% of cases. The incidence peaks after 15 to 16 years of diabetes. In NIDDM, estimates of prevalence range from 15 to 20%, and nephropathy often supervenes after a shorter known duration of diabetes than in IDDM. GFR is often increased above normal (hyperfiltration) from the onset of IDDM due to increased renal blood flow, glomerular capillary hypertension and increased filtration surface. The glomeruli are hypertrophied and the kidneys enlarged. In both IDDM and NIDDM, GFR begins to decline irreversibly, when AER has risen to 100 to 300 mg/day at an average rate of 10 ml/min. per year. This is due to progressive reduction of the filtration surface area through mesangial expansion. Serum creatinine levels begin to rise when GFR falls below 50 ml/min, and then end-stage renal failure follows after an average of five years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic nephropathy: significance of microalbuminuria and proteinuria in Type I and Type II diabetes mellitus]. 749 50


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