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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Combined renal and pancreatic transplantation in patients with juvenile diabetes mellitus, diabetic nephropathy and renal insufficiency is designed to improve the poor prognosis observed with hemodialysis or renal transplantation alone. Interest has recently shifted from pancreatic organ to islet transplantation, in view of the absence of complications with the latter. However, no permanent success with islet transplants in diabetic patients has so far been reported. In the series presented, one patient with juvenile diabetes and subsequent renal failure was successfully treated with simultaneous kidney and intrasplenic pancreatic islet allotransplants. One year after the operation the patient has normal blood glucose levels without exogenous insulin, despite treatment with prednisone.
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PMID:[Successful allotransplantation of an island of Langerhans]. 11 44

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
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PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

The influence of pregnancy on the progression of diabetic nephropathy in diabetic women with pre-existing moderate renal insufficiency is a subject of considerable controversy in the literature. In four of five female patients with type I diabetes mellitus with pre-existing impaired renal function (creatinine clearance less than 80 ml/min), significant proteinuria (greater than 2 g/24 h urine) and hypertension we have found a further decline in renal function during pregnancy, with an increased deterioration rate of creatinine clearance in comparison to the time before and after pregnancy. The mean decline of the glomerular filtration rate was 1.8 ml/min per month during pregnancy and 1.4 ml/min per month postpartum until the start of dialysis treatment. The difference in the progression of diabetic nephropathy during and after pregnancy can be explained by increased hypertension during pregnancy, especially in the third trimester, despite an intensified antihypertensive therapy. The long-term effect of pregnancy on renal function in our patients was therefore an earlier requirement for renal replacement therapy than would have been expected without pregnancy.
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PMID:Influence of pregnancy on progression of diabetic nephropathy and subsequent requirement of renal replacement therapy in female type I diabetic patients with impaired renal function. 131 67

This is a case report of a 35-year-old woman with a 15-year history of type I diabetes mellitus, who developed extensive macrovascular calcifications of the abdominal aorta and all its tributaries within 7 months of developing renal insufficiency. The patient was maintained on hemodialysis and peritoneal dialysis for a total of 3 months, then underwent combined cadaveric renal and pancreatic islet transplantation. Although some vascular calcifications are known to occur in elderly patients and in patients with long-standing uremia, it was the rapidity and extent of development of these lesions in this young woman that is astonishing.
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PMID:Rapid development of extensive macrovascular calcifications in a type I diabetic patient. 177 22

The objective of the work was to evaluate the basic parameters of zinc metabolism, i.e. serum levels and urinary excretion of zinc (Zn) in insulin dependent diabetes. The authors investigated a group of diabetics with normal renal function (DM) and with chronic renal insufficiency as a result of diabetic nephropathy (RIDM). Two control groups were formed by healthy volunteers (C) and non-diabetic subjects with chronic renal insufficiency (RI). In diabetics without impaired renal functions (DM) the Zn serum levels did not differ significantly from controls, urinary excretion was significantly raised. The authors did not reveal a correlation of serum Zn levels with parameters of compensation of diabetes nor with the insulin dose. Urinary Zn output correlated positively with proteinuria and the average blood sugar level during the collection of urine. The authors did not find a correlation with diuresis, fractional water excretion, glycosuria or urea excretion. The fractional Zn clearance in diabetic subjects was significantly raised and correlated with the mean blood sugar level. This finding suggests a decline of the tubular Zn absorption in hyperglycaemia. In diabetics with renal failure (RIDM) the results did not differ from non-diabetics with the same degree of renal insufficiency: serum Zn levels were, as compared with healthy controls, in both groups significantly reduced, the urinary excretion being normal. Thus insulin dependent diabetes nor its metabolic compensation do not influence in a marked way serum Zn levels but lead to higher urinary Zn losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum levels and urinary excretion of zinc in patients with insulin-dependent diabetes]. 220 24

Little is known of the natural history of nephropathy in type 2 (non-insulin-dependent) diabetes, yet type 2 diabetes is a major cause of end-stage renal disease in the United States. The incidence rate of heavy proteinuria was determined in Pima Indians participating in a longitudinal population study of diabetes and its complications. Heavy proteinuria was defined by a urine protein (g/liter) to urine creatinine (g/liter) ratio greater than or equal to 1.0 (greater than or equal to 113 mg protein/nmol creatinine), a level which corresponds to a urine protein excretion rate of about 1 g/day. The incidence rates of proteinuria in diabetic Pimas were 4, 12, 37, and 106 cases/1,000 person-years at risk in the periods 0 to 5, 5 to 10, 10 to 15, and 15 to 20 years after the diagnosis of diabetes. The cumulative incidence rates were 2%, 8%, 23%, and 50% at 5, 10, 15, and 20 years, respectively. The duration of diabetes, severity of diabetes as determined by the degree of hyperglycemia and type of treatment, and blood pressure were risk factors for proteinuria. The presence of heavy proteinuria was strongly associated with the development of renal insufficiency, defined by serum creatinine greater than or equal to 2.0 mg/dl (greater than or equal to 177 mumol/liter). The incidence of proteinuria in type 2 diabetes in Pima Indians was as high as that reported in type 1 diabetes in other populations and represents a frequent, serious complication of the disease.
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PMID:Incidence of proteinuria in type 2 diabetes mellitus in the Pima Indians. 278 25

Recent recommendations in textbooks suggest the use of the combination of insulin treatment with oral antidiabetic agents in NIDDM, especially in secondary failures and insulin resistance with exogenous insulin. This new view in treatment policy is based on literature data in C-peptide positive IDDM patients. Better metabolic control with lower exogenous insulin dosages could also be obtained in NIDDM. If no medical contraindication for drug treatment exists (liver or renal insufficiency, drug interactions, etc.), a combination therapy trial can be considered as an intermediate step between oral antidiabetic agents alone and insulin as monotherapy. Long-term maintenance of endogenous secretion and limited peripheral hyperinsulinism can be considered as potential benefits of this combination therapy.
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PMID:Facts about combination therapy in NIDDM: insulin + oral antidiabetic agents. 304 38

In 97 patients with type I diabetes mellitus, 155 patients with type II diabetes mellitus, and two matched control groups, serum concentrations of laminin P1, a non-collagenous component of basement membranes, were determined by radioimmunoassay to see whether laminin P1 might be a valuable indicator of microangiopathic complications in diabetics. Independent of the type of diabetes, serum laminin concentrations in patients without nephropathy or with early renal damage as assessed by microalbuminuria were comparable with those of the control subjects. Patients with macroproteinuria or with renal insufficiency had significantly increased serum laminin P1 concentrations. Diabetic retinopathy was not found to influence serum laminin P1 concentrations. These data indicate that serum laminin P1 concentrations are increased in advanced diabetic nephropathy.
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PMID:Serum concentrations of laminin P1 in diabetics with advanced nephropathy. 319 51

Already at the time of diagnosis of juvenile onset diabetes mellitus, there are morphological and functional changes in the kidney. The kidneys and the individual glomeruli are considerably enlarged, and the glomerular filtration increased. In experimental diabetes mellitus the metabolism of the glomerular basement membrane is increased. These abnormalities are reversible by meticulous metabolic control. Their relationship to the diabetic glomerulosclerosis that causes uremia twenty to thirty years later is not clear. Carefully analyzed extensive clinical experience confirms that good metabolic control delays the onset of symptomatic diabetic renal disease, as expected from experimental studies. Normalization of even a slightly elevated blood pressure may be important to slow the progression of the renal insufficiency. Better methods for the management of the diabetic state and better education of the patients may be important to postpone the heroic endeavours of renal or pancreatic transplantation or dialysis.
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PMID:Diabetic nephropathy. Pathogenesis and prevention. 693 19

Lp(a) has atherogenic and thrombotic properties and is considered to be a major risk factor for the development of atherosclerotic disease. The risk of cardiovascular disease is increased in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), and Lp(a) has attracted attention as a potential risk factor in diabetic patients. Lp(a) levels are "probably" elevated in IDDM patients and related to altered metabolic control and increased urinary albumin excretion rate or renal insufficiency, although results are controversial. There appears to be a real difference between the Lp(a) of patients with proliferative diabetic retinopathy and those with or without background retinopathy. The plasma Lp(a) level may therefore be associated with microangiopathy in some IDDM patients. However, data relating Lp(a) to complications of diabetes are limited, and the literature is conflicting. The few available data suggest that Lp(a) is not elevated in NIDDM patients and that there is no strong link between blood glucose control and plasma Lp(a). There is no clear evidence as to whether Lp(a) is related to microalbuminuria in NIDDM patients. There is little evidence for a correlation between increased risk of cardiovascular disease and plasma Lp(a) among diabetic patients. However, some diabetic patients with coronary heart disease have elevated plasma Lp(a), which seems to be correlated with genetic factors (especially the isoforms of apolipoprotein a) rather than to diabetes per se. Lp(a) synthesis and catabolism could be influenced by insulin or by diabetes and its metabolic concomitants. The atherogenic and thrombogenic potential of Lp(a) could also be increased in diabetic patients. Plasma Lp(a) should be measured for both IDDM and NIDDM patients. If the Lp(a) level is elevated, it seems reasonable to check the other major vascular risk factors.
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PMID:[Lipoprotein (a) and diabetes mellitus]. 762 73


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