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

All IDDM patients without late complications have blood pressures similar to the nondiabetic background population, and those who develop clinical nephropathy in Denmark have no familial predisposition to hypertension. Blood pressure remains normal until after development of microalbuminuria, indicating no primary role for hypertension in the pathogenesis of nephropathy. When microalbuminuria is present it does, however, play a crucial role in the progression of nephropathy. Sodium retention, possibly induced by hyperinsulinemia, and perhaps glucose-coupled sodium reabsorption in insulin treated patients, seem to play a central role in elevating the blood pressure, but this needs further clarification.
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PMID:Hypertension in the course of insulin dependent diabetes mellitus and its pathogenetic mechanisms. 214 1

Eight patients with type I diabetes mellitus have been operated on to form a distal splenorenal anastomosis (DSRA). A critical period (the 6th and the 7th days) postoperation has been observed when severe metabolic acidosis develops; to prevent its development, transfusions of 4% sodium bicarbonate solution (1.5-2.01) have been administered before the critical period for 24 hrs, with the metabolic condition monitored by biochemical analyses. Studies of metabolism in these patients after surgery have revealed a complete normalization of the acid-base balance and of potassium level, as well as a reduction of the blood glucose concentration. The doses of exogenic insulin have been reduced by 30%, this being associated with a tendency to an increase of the levels of endogenic insulin, C-peptide and glucagon of the blood. This helps a better stabilization of the diabetic process after the formation of a DSRA.
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PMID:[Characteristics of the postoperative period in diabetes mellitus type 1 in patients with distal splenorenal anastomosis]. 219 74

The role of the renin angiotensin system for the regulation of kidney function in diabetes mellitus is uncertain. Results from studies in diabetic animals suggest that a reduced activity in this system contributes to the renal hyperperfusion and hyperfiltration in diabetes. The renal sensitivity to angiotensin II in diabetic patients is also unknown. Changes in renal hemodynamics were measured after infusion of two low doses of angiotensin II in ten young type 1 diabetic patients without complications and in ten healthy controls. The renin and angiotensin II levels were found to be the same in both groups. The baseline glomerular filtration rate was higher in the diabetics. During the highest angiotensin II dose, the 51Cr-EDTA and PAH clearance decreased 14 +/- 15 and 157 +/- 118 ml/min in the diabetics and 14 +/- 15 and 146 +/- 109 in the controls respectively. The changes in blood pressure and renal vascular resistance or sodium excretion did not differ between the groups. A malfunction of the renin angiotensin system is thus unlikely as a cause of the glomerular hyperfiltration in type 1 diabetes.
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PMID:Renal sensitivity to angiotensin II in type 1 diabetes. 227 50

We examined renal responses to a pharmacological dosage of human atrial natriuretic peptide (hANP) and the potential interference of nifedipine administration with the effects of hANP on kidney function in healthy subjects and normoglycemic patients with type 1 diabetes mellitus. Ten healthy volunteers (age, 28 +/- 1 years) and ten patients (age, 33 +/- 2 years; diabetes duration; 14 +/- 3 years; HbAI 7.2% +/- 0.2%) were studied. According to a double-blind, randomized, placebo-controlled trial design, three experiments were performed in each subject using the double-dummy technique: placebo only, hANP only, and nifedipine + hANP. As i.v. bolus injection 100 micrograms hANP was given; nifedipine was applied buccally, at a dose of 10 mg 90 min before and at a dose of 5 mg together with hANP injection. At base-line and in the placebo only experiment, patients did not differ from controls. In the hANP only experiment, in both groups hANP resulted in increased urinary volume and both sodium and chloride excretion (P less than 0.05 vs placebo only experiment). In patients, hANP-induced increase in electrolyte excretion was greater than in controls (P less than 0.05). In the nifedipine + hANP experiment, hANP-induced changes in renal indexes were enhanced in controls (P less than 0.05 vs hANP only experiment) but not in patients. Thus, diuretic response to nifedipine + hANP in patients was decreased in comparison with controls (P less than 0.05). In patients, however, nifedipine administration decreased the hANP-induced increase in urinary albumin excretion (P less than 0.05 vs hANP only experiment). Creatinine clearance was uninfluenced throughout the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nifedipine on renal responses to human atrial natriuretic peptide in healthy subjects and normoglycemic patients with type 1 diabetes mellitus. 253 91

Acute insulin administration shows an antinatriuretic effect in normal man. Thus it can be postulated that insulin therapy resulting in circulating hyperinsulinemia can lead to sodium retention and in turn to hypertension in insulin dependent diabetes. Moreover it has been proved that atrial natriuretic peptide (ANP) plays a major role in modulating natriuresis in man. The aim of the present study was to investigate the relationship between insulin and ANP in modulating sodium metabolism in seven insulin dependent diabetic patients in comparison with eight normal control subjects at baseline and during a saline infusion (2 mmol/kg/90 min) at euglycemic blood levels. Diabetics received a subcutaneous insulin infusion (0.015 U/kg/hr) resulting in a two fold higher plasma free insulin levels (16 +/- 2 microU/ml) than in control subjects (7 +/- 2 microU/ml). During saline challenge sodium excretion rate increased by 29 +/- 6% in control patients and only by 6 +/- 0.7% in diabetic patients (p less than 0.01). At baseline ANP plasma concentrations were significantly higher in diabetic patients than in control subjects (diabetics = 37 +/- 8 pg/ml and controls = 21 +/- 3 (p less than 0.01). After saline challenge ANP concentration rose to 71 +/- 9 pg/ml in control subjects, whereas no significant change above baseline values was shown by diabetic patients.
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PMID:Sodium metabolism in insulin dependent diabetic patients. Role of insulin and atrial natriuretic peptide. 253 10

An increased albumin excretion rate is recognized as an important early marker for incipient kidney disease in patients with diabetes mellitus. Many different techniques have been used, and a single void technique has been proposed as the simplest method for screening for increased albumin excretion. We evaluated a previous observation that single void samples during water diuresis yield increased albumin excretion rates. Timed day, night, and 24 hour albumin excretion rates (AER) were obtained in 35 patients with Type I diabetes mellitus. This was followed by examination of 8 consecutive half-hour specimens obtained during continued water diuresis. We compared 26 patients with low AER (less than 20 micrograms/min/24 hr sample) to 9 patients with high AER (greater than 20 and less than 200 micrograms/min/24 hr). Sampling began 60 min after the initiation of the waterload. At first, the AER in the low AER group was significantly higher than it was at night, but it decreased over 60 to 90 min of sampling to levels comparable with daytime AER. This was paralleled by a similar pattern in urine flow rate, sodium, and solute excretion. The AER in the high AER group did not increase with the water load and remained high throughout the study periods. The pattern of urine flow rate, sodium, and solute excretion was similar to that of the group with low AER. The study demonstrates that early sampling after water-induced diuresis leads to overestimation of AER in patients with low AER as compared to patients with high AER.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of water loading on albumin excretion in type I diabetes mellitus. 253 9

It has been shown that red blood cell Li/Na exchange, also called countertransport (Li/Na CTT) is increased in patients with insulin dependent diabetes mellitus (IDDM) with clinical or subclinical nephropathy and elevated blood pressure. Because recent experimental evidence confirms that red cell Li/Na CTT is a mode of functioning of the Na/H exchange (Na/H CTT), we have measured both transport modes in 23 IDDM (16 hypertensive and seven normotensive) and in eight normotensive controls with normal glucose tolerance. Na/H and Li/Na CTT were significantly increased in hypertensive compared to normotensive diabetics and controls. Na/H CTT was 78 +/- 28 mmol/L cell/h in hypertensive IDDM, 50 +/- 21 in normotensive IDDM, and 55 +/- 24 in the controls. Li/Na CTT was 0.37 +/- 0.13 mmol/L cell/h, 0.27 +/- 0.10, and 0.25 +/- 0.11, respectively. Na/H and Li/Na CTT were significantly correlated (r = .38, P less than .05). The proximal tubule sodium reabsorption, measured as the fractional Li+ reabsorption, was significantly correlated to red cell Na/H CTT (r = .38, n = 29, P less than .05), but not to the Li/Na CTT (r = .21, n = 29). In conclusion this work confirms that Na/H and Li/Na CTT are function modes of the same transporter and that an increased activity of Na/H CTT might play a role in the blood pressure increase in IDDM.
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PMID:Na/H and Li/Na exchange in red blood cells of normotensive and hypertensive patients with insulin dependent diabetes mellitus (IDDM). 253 45

The Na+-pumping activity of the erythrocyte plasma membrane in diabetic subjects was studied together with the lipid composition. Insulin-dependent diabetes mellitus (IDDM) patients (n = 25) were divided into young (28.1 +/- 7.4 yr old, mean +/- SD; n = 16) and old (7.17 +/- 9.8 yr old; n = 10) subjects; the age of non-insulin-dependent (NIDDM) patients was 70.7 +/- 11.5 yr (n = 10). The Na+-pumping activity, estimated from both Na+-K+-ATPase and ouabain binding, was significantly decreased in IDDM and NIDDM subjects, but its insulin sensitivity was retained only in young IDDM subjects. The total cholesterol and phospholipid content of the erythrocyte plasma membrane was lowered in IDDM subjects, and cholesterol-to-phospholipid molar ratio was significantly decreased. In NIDDM subjects the significant decreased of the two lipid components did not alter their ratio. The analysis of major phospholipid components of erythrocyte membranes revealed that only phosphatidylcholine is significantly increased in young diabetic subjects. The fatty acid composition of major phospholipid classes was significantly altered in all cases: the unsaturation index appeared to be increased in phosphatidylserine and sphingomyelin for both IDDM and NIDDM subjects and was also increased in phosphatidylcholine in the latter group.
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PMID:Membrane lipid alterations and Na+-pumping activity in erythrocytes from IDDM and NIDDM subjects. 254 70

The effect of cyclosporine A therapy on blood pressure and renal function was assessed in 11 young adults with type 1 diabetes of recent onset (7 +/- 1 weeks). Metabolic control and renal haemodynamics and function were evaluated at 3-month intervals before, during and after cessation of a 6-month course of cyclosporine A (initial dose 7.5 mg/kg per day, then adapted on whole-blood trough levels of 401 +/- 45 and 308 +/- 49 ng/ml at 3 and 6 months, respectively). A significant increase in blood pressure (from 117 +/- 2/65 +/- 2 to 122 +/- 2/72 +/- 3 mmHg; P less than 0.01) and a decrease in 99Tc-DTPA (diethylene triaminepentaacetic acid) clearance (124 +/- 6 to 98 +/- 5 ml/min per m2; P less than 0.01) were observed after 3 months of cyclosporine A; both alterations remained unchanged after 6 months. No variation in body weight, 24-h urinary sodium or urinary albumin excretion was observed. Blood pressure and the glomerular filtration rate returned to basal levels 3 months after the cyclosporine A therapy ceased. These results suggest that even moderate doses of cyclosporine A have a reversible deleterious effect on blood pressure and renal function in young diabetic patients.
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PMID:Effect of cyclosporine on blood pressure and renal function of recent type 1 diabetes mellitus. 263 15

End Stage Renal Disease (ESRD) is a common consequence of diabetic nephropathy (DN). DN is the major cause of death in patients with IDDM, accounting for greater than 40% of deaths with this form of diabetes. There is no clearly documented therapeutic technique that will prevent or reverse progressive renal damage in IDDM. While pancreatic transplantation and "cure" of diabetes in experimental animals may be associated with some histological reversal of renal pathology, this has not been documented in humans. Most studies agree that once diabetic renal disease is present (as documented by proteinuria), progression is inevitable, albeit the rate of progression may be altered by different therapeutic methods. There is considerable hope that "tight metabolic control" will prevent the initial damage that leads to DN and ESRD, but evidence remains inconclusive. There is some evidence that careful monitoring for microalbuminuria will allow for very early detection of damage and alterations in therapy. Our studies have documented a decrease in both morbidity and mortality in IDDM in patients who have been competitive athletes, suggesting that promotion of physical fitness may be a valuable means of delaying progression of renal disease while control of BP delays progression. Early detection and aggressive therapy is recommended. Some studies utilizing diets low in sodium and/or protein appear beneficial but more studies are needed before pediatric application.
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PMID:Can management strategies alter the course of diabetic nephropathy? 263 85


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