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)

Pentoxifylline is a drug with hemorheological actions used in the management of microcirculatory abnormalities, such as those usually seen in diabetic patients. The drug has been successfully used in improving peripheral and central circulation, as well as proteinuria of long-term diabetes. With the hypothesis that pentoxifylline reduces proteinuria in patients with IDDM and NIDDM, with a wide range of urinary protein excretion, 86 diabetic patients were studied. Forty-one patients with IDDM were stratified in 2 subgroups: one of 18 patients with microalbuminuria, and the other of 23 patients with overt proteinuria. In the same way, 45 patients with NIDDM were divided in 2 subgroups: one of 23 patients with microalbuminuria, and the other of 22 patients with proteinuria. Patients in each subgroup were randomized to receive either placebo or pentoxifylline 1,200 mg/d, during 4 months, using a double blind design. At the beginning of the study and after treatment, 24-hour urinary albumin excretion was measured by nephelometry in each patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pentoxifylline reduces proteinuria in insulin-dependent and non insulin-dependent diabetic patients. 773 73

Diabetic nephropathy is the only increasing cause of renal failure in the Western world. It affects a large proportion of both insulin-dependent (IDDM) and non-insulin-dependent diabetic (NIDDM) patients. A critical stage in the development of diabetic renal disease is the onset of microalbuminuria, defined as an albumin excretion rate of 30 to 300 mg/day. Microalbuminuria predicts progression to renal failure and early cardiovascular mortality in both IDDM and NIDDM patients. Microalbuminuria is associated with a constellation of other risk factors for small and large vessel damage which include raised blood pressure, poor glycemic control, plasma lipid and clotting factor abnormalities, left ventricular hypertrophy, and insulin resistance. Treatment with angiotensin-converting enzyme inhibitors corrects microalbuminuria and prevents progression to persistent proteinuria. Good blood glucose control significantly reduces the risk of progression from normoalbuminuria to microalbuminuria. The treatment of microalbuminuria appears highly cost-beneficial and substantially increases life expectancy. The development of microalbuminuria, for which all diabetic patients aged 12 to 70 years should be screened, should alert the physician to set in motion a program of assessment, monitoring, and correction of all risk factors for renal and cardiovascular disease.
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PMID:Prognostic significance of microalbuminuria. 781 38

To clarify the clinical and pathological significance of thin glomerular basement membranes (Thin-GBM) appearing in evident diabetics, we examined the renal biopsies from 179 diabetes mellitus (DM) patients with urinary abnormalities in which the number of non insulin dependent diabetes mellitus cases was 140 cases while the remaining 39 cases had insulin dependent diabetes mellitus. In addition, 17 of these cases were found to have either segmental or diffuse Thin-GBM by electron microscopy. The clinical and morphological parameters between the diabetics with Thin-GBM (DM-Thin-GBM) and the diabetics without Thin-GBM (the controls) were significantly different regarding DM duration (DM-Thin-GBM vs control: 5.3 +/- 5.5 vs 9.8 +/- 6.5 years, p < 0.01), Ccr (67.0 +/- 25.5 ml/min vs 45.6 +/- 24.4 ml/min, p < 0.01), the incidence of hematuria (52.9% vs 24.5%, p < 0.05) and hypertension (13.3% vs 51.3%, p < 0.05). The severity of glomerular damage was mild in the DM-Thin-GBM group as compared to the control. The renal survival rate from the onset of urinary abnormalities was higher in the DM-Thin-GBM group than in the control (p < 0.01). In the case of DM-Thin-GBM, the grade of proteinuria correlated with the mean width of the thickened GBM (p < 0.01) and the spread of the thickened GBM which was more than 500 nm in width (p < 0.001). The severity of microscopic hematuria correlated with the spread of the Thin-GBM (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thin glomerular basement membrane in diabetic patients with urinary abnormalities. 852 10

In November 1990, we carried out a survey of chronic complications of diabetes in more than 2000 diabetic patients who were seen on one day in 35 medical institutions including university hospitals, other hospitals and small clinics. More than 60% were aged 55-74 years. About 7% of patients had IDDM. Hypertension was present in 38.5%. Proteinuria was positive in 20% and 1% of patients were on dialysis therapy. 28% had visual disturbance and 2.9% had blindness in one or both eyes. Retinopathy was observed in 38% and proliferative retinopathy in 10%. The prevalences of myocardial infarction, angina pectoris, cerebral infarction and foot ulcer and gangrene were 2.1%, 4.7%, 5.7% and 2%, respectively, including the histories of these complications. Amputation of lower extremities was seen in only 0.6%. Microangiopathies were generally more frequent and more severe in IDDM than NIDDM. The prevalence of microangiopathy was as common as, but macroangiopathy seems less frequent than, the figures given in 'Diabetes in America'.
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PMID:Prevalence of chronic complications in Japanese diabetic patients. 785

Tubular damage is a recognized feature of both overt diabetic nephropathy and glomerulonephritis. However, the pattern and mechanism of tubular damage in the two clinical settings remain unclear. Two groups of patients with macroalbuminuria (albuminuria > 300 mg/day) were studied. Group 1 comprised 41 patients with biopsy proven primary glomerulonephritis and group 2 comprised 28 patients with clinical diabetic nephropathy due to insulin dependent diabetes mellitus. Serum creatinine, creatinine clearance, glomerular proteinuria (albuminuria and transferrinuria), markers of tubular damage such as urinary excretion of lysosomal enzyme (N-acetyl glucosaminidase), brush border enzymes (leucine aminopeptidase and gamma-glutamyl transferase) and retinol binding protein (tubular protein) were measured. Both groups were comparable in serum creatinine, creatinine clearance, glomerular proteinuria and excretion of N-acetyl-glucosaminidase. However, a significantly higher degree of tubular brush border enzymuria and a lower level of tubular proteinuria were seen in group 1 than in group 2. In group 1, albuminuria correlated to tubular enzymuria and tubular proteinuria. However, there was no correlation in diabetic patients between parameters of glomerular and tubular damage or dysfunction. The data presented suggested that the pattern of tubulopathy is different in patients with comparable degree of macroalbuminuria due to diabetic nephropathy and glomerulonephritis. Moreover, in diabetic nephropathy contrary to glomerulonephritis, markers of tubular damage are unrelated to glomerular proteinuria. This may suggest different mechanisms of tubular damage in the two clinical settings. We recommended that in all patients with proteinuria, particularly those with diabetic nephropathy, markers of renal tubular damage may be useful in monitoring the course of their disease.
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PMID:Tubulopathy with macroalbuminuria due to diabetic nephropathy and primary glomerulonephritis. 786 56

The progression of diabetic nephropathy can be positively influenced by maintaining a low blood pressure level. This has been shown in studies with conventional antihypertensive treatment as well as with ACE inhibitors. Whether the latter group of drugs is more effective remains to be proven and was the aim of our study. In a prospective randomized study we compared the effects of ACE inhibition and beta-blockade on retarding progression of renal function in IDDM patients with an early stage of overt diabetic nephropathy. Twenty-nine patients were studied for 2 years, 15 were randomized for treatment with captopril and 14 for atenolol. Every 6 weeks blood pressure and urinary albumin and total protein excretion were measured. GFR was measured every 6 months as 51Cr-EDTA clearance. Baseline values for blood pressure, renal function and albuminuria were identical in the two groups. The effect of both drugs on blood pressure was not significantly different. In the captopril-treated patients MAP before and after 2 years was 110 +/- 3 (SEM) and 100 +/- 2 mm Hg, respectively and in the atenolol-treated patients 105 +/- 2 vs 101 +/- 2 mm Hg. Both drugs reduced albuminuria and total proteinuria to the same extent. With captopril albuminuria decreased from 1549 (989-2399) to 851 (537-1380) mg/24 h and proteinuria from 2.5 (1.6-3.8) to 1.2 (0.8-1.8) g/24 h. With atenolol albuminuria decreased from 933 (603-1445) to 676 (437-1047) mg/24 h and proteinuria from 1.5 (1.0-2.4) to 0.9 (0.6-1.5) g/24 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril and atenolol are equally effective in retarding progression of diabetic nephropathy. Results of a 2-year prospective, randomized study. 774 19

The development of kidney disease in diabetes mellitus can be viewed as a two-stage process: (1) the development of proteinuria, and (2) its progression to chronic renal failure. Determinants of the latter were examined in 439 IDDM patients who had nephropathy and participated in the Diabetic Retinopathy Study. Using serum creatinine levels obtained during the follow-up period to assess the rate of loss of renal function, we found that only one-third of these patients experienced a rapid loss of function, while the others had slowly declining or unchanging renal function despite the presence of proteinuria and severe diabetic retinopathy. Among the many baseline variables examined, only elevated cholesterol and elevated systemic blood pressure were predictors of a rapid loss of renal function. Patients with this rapid loss of renal function also had the highest risk of death due to cardiovascular causes, as well as all causes. Once again, hypercholesterolemia was the major predictor of these deaths. In conclusion, efforts should be undertaken early to identify patients who are rapidly losing renal function so that interventions to modify systemic blood pressure and hypercholesterolemia may prevent or postpone the development of renal failure and death in patients with IDDM.
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PMID:Hypercholesterolemia--a determinant of renal function loss and deaths in IDDM patients with nephropathy. 815 81

Diabetic nephropathy is an uncommon finding in the pediatric age group. Previous reports have demonstrated that persistent proteinuria does not occur during the first five years following the diagnosis of insulin dependent diabetes mellitus. We report a prepubertal female child with less than five years duration of diabetes who developed persistent proteinuria and histologic changes diagnostic of diabetic nephropathy. The earlier than expected diabetic nephropathy noted in our patient raises the question regarding the need for earlier surveillance for diabetic nephropathy in children with a family history of chronic diabetic complications.
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PMID:Diabetic nephropathy in a prepubertal diabetic female. 818 23

Although 30% to 40% of patients with type I diabetes mellitus develop diabetic nephropathy, the usual signs of clinical nephropathy are often thought to be delayed until adulthood. We studied 13 adolescents with type I diabetes mellitus for 5 to 14 years who had renal biopsies completed because of clinical problems, including proteinuria, hematuria, or hematuria plus proteinuria. Changes typical of diabetes were seen by light and immunofluorescence microscopy; evidence of other renal diseases was not noted. On electron microscopy evaluation, glomerular basement membrane width was increased in 11 patients. In seven patients, mesangial volume was elevated above the normal range. Peripheral capillary filtration surface density was diminished below the normal range in five patients. Thus, several of these adolescents had severe glomerular lesions that were indicative of overt diabetic nephropathy. Within 2 to 3 years after biopsy, at least two patients were dialysis dependent. Thus, the adolescent diabetic patient with a relatively short duration of diabetes may be developing progressive diabetic renal lesions, and the clinical signs and symptoms at presentation may not be those typically seen in diabetic nephropathy.
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PMID:Renal disease in adolescents with type I diabetes mellitus: a report of the Southwest Pediatric Nephrology Study Group. 825 23

In IDDM or NIDDM, the total plasma cholesterol and triglycerides are usually within normal limits when the blood glucose is controlled. Marked hypertriglyceridemia can develop with loss of glycemic control and is often due to superimposed genetic abnormalities in lipoprotein metabolism. Tight control in IDDM usually reduces LDL and VLDL to normal levels and may raise HDL above the normal range. Low HDL cholesterol and mild to moderate elevations of VLDL triglyceride are common in NIDDM if obesity or proteinuria is also present. Both HDL and LDL may be smaller and more dense and may be enriched with triglyceride as compared with cholesterol. These abnormalities may require weight loss for control. The increased incidence of cardiovascular disease in diabetes is unexplained but is amplified by the well-defined cardiovascular risk factors. The new American Diabetes Association guidelines call for treatment of high triglycerides and LDL cholesterol to be aggressively reduced. Triglycerides should be under 200 mg/dL, are considered borderline high between 200 and 400 mg/dL, and high when above 400 mg/dL. Low HDL is defined as less than 35 mg/dL. Control of obesity with diet and exercise and reduced intake of saturated fat and cholesterol are important first steps. If needed, drug therapy is appropriate to reduce LDL to levels below 130 mg/dL in all adult diabetics and below 100 mg/dL in those with cardiovascular disease.
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PMID:Lipoprotein disorders in diabetes mellitus. 828 28


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