In patients with generalized vasculitis, the withdrawal of cyclophosphamide and the substitution of azathioprine after remission did not increase the rate of relapse. Thus, the duration of exposure to cyclophosphamide may be safely reduced.
To identify early metabolic abnormalities in non-insulin-dependent diabetes mellitus (NIDDM), we measured sensitivity to insulin and insulin secretion in 26 first-degree relatives of patients with NIDDM and compared these subjects both with 14 healthy control subjects with no family history of NIDDM and with 19 patients with NIDDM. The euglycemic insulin-clamp technique, indirect calorimetry, and infusion of [3-3H]glucose were used to assess insulin sensitivity. Total-body glucose metabolism was impaired in the first-degree relatives as compared with the controls (P less than 0.01). The defect in glucose metabolism was almost completely accounted for by a defect in nonoxidative glucose metabolism (primarily the storage of glucose as glycogen). The relatives with normal rates of metabolism (mean +/- SEM, 1.81 +/- 0.27 mg per kilogram of body weight per minute) and impaired rates (1.40 +/- 0.22 mg per kilogram per minute) in oral glucose-tolerance tests had the same degree of impairment in glucose storage as compared with healthy control subjects (3.76 +/- 0.55 mg per kilogram per minute; P less than 0.01 for both comparisons). During hyperglycemic clamping, first-phase insulin secretion was lacking in patients with NIDDM (P less than 0.01) and severely impaired in their relatives with impaired glucose tolerance (P less than 0.05) as compared with control subjects; insulin secretion was normal in the relatives with normal glucose tolerance. We conclude that impaired glucose metabolism is common in the first-degree relatives of patients with NIDDM, despite their normal results on oral glucose-tolerance tests. Both insulin resistance and impaired insulin secretion are necessary for the development of impaired glucose tolerance in these subjects.
Summary.We examined the impact of hypertension and microalbuminuria on insulin sensitivity in patients with Type 2 (non-insttlin-dependent) diabetes mellitus using the euglycaemic insulin clamp technique in 52 Type 2 diabetic patients and in 19 healthy control subjects. Twenty-five diabetic patients had hypertension and 19 had microalbuminuria. Hypertension per se was associated with a 27 % reduction in the rate of total glucose metabolism and a 40 % reduction in the rate of non-oxidative glucose metabolism compared with normotensive Type 2 diabetic patients (both p < 0.001). Glucose metabolism was also impaired in normotensive microalbuminuric patients compared with normotensive normoalbuminuric patients (29.4 + 2.2 vs 40.5 + 2.8 gmol. kg lean body mass -1. min-t; p = 0.012), primarily due to a reduction in non-oxidative glucose metabolism (12.7+2.9 vs 21.1+2.6btmol.kg lean body mass 1. min-1;p = 0.06). In a factorial ANOVA design, however, only hypertension (p = 0.008) and the combination of hypertension and microalbuminuria (p = 0.030) were significantly associated with the rate of glucose metabolism. The highest triglyceride and lowest HDL cholesterol concentrations were observed in Type 2 diabetic patients with both hypertension and microalbuminuria. Of note, glucose metabolism was indistinguishable from that in control subjects in Type 2 diabetic patients without hypertension and microalbuminuria (40.5 + 2.8 vs 44.4_+ 2.8 gmol. kg lean body mass -1. rain 1). We conclude that insulin resistance in Type 2 diabetes is predominantly associated with either hypertension or microalbuminuria or with both.
Anuric automated peritoneal dialysis (APD) patients experience significant detrimental changes in membrane function over a relatively short time period. Glucose appears to enhance these changes independent of residual renal function. Icodextrin use in these circumstances is associated with less deterioration in membrane function.
Abstractgression to end stage renal failure occurs shortly after,Objective-To investigate the predictive value of indicating that macroalbuminuria (albumin excretion microalbuminuria (albumin excretion rate 30-300 rate > 300 mg/24 h reflects an advanced stage of mg/24 h) as a risk factor for overt diabetic nephro-diabetic kidney disease. The finding that micropathy in patients with longstanding insulin depen-albuminuria (albumin excretion rate 30-300 mg/24 h) dent diabetes.indicates early diabetic nephropathy and predicts Design-10 year follow up of patients with normo-progression to overt nephropathy has allowed early albuminuria (albumin excretion rate <30 mg/24 h), diagnosis and preventive interventions at an early microalbuminuria (30-300 mg/24 h), and macro-stage."4 But most studies of microalbuminuria in albuminuria (>300 mg/24 h) based on two out of diabetic nephropathy have included patients with a three timed overnight urine samples. information is urgently needed in order to define Main outcome measures-Urinary albumin appropriate screening and follow up programmes for excretion rate, mortality, and prevalence of diabetic diabetic patients. complications after 10 years.Results-56 patients were re-examined at 10 year Patients and methods follow up, 10 had died, five were lost to follow up, and one was excluded because of non-diabetic In 1980 we recruited from our outpatient clinic 72 kidney disease. At initial screening 22 patients had consecutive patients with longstanding (over 15 years), macroalbuminuria, 18hadmicroalbuminuria, and 26 insulin dependent diabetes who were negative for C had normal albumin excretion. Only five (28%, 950/o peptide. All had urinary albumin excretion rates confidence interval 10% to 54%) of the micro-measured (table I). Patients were considered negative albuminuric patients developed macroalbuminuria for C peptide if peptide concentration six minutes after during the 10 year follow up and none developed end an intravenous injection of 1 mg glucagon was less than stage renal failure. Two (8%, 1% to 25%) normo-02 nmol/l. One patient was later excluded from the Fourth Department of albuminuric patients developed macroalbuminuria follow up study because of coexisting renal disease Medicine, Helsinki and four (15%, 4% to 35%) became micro-(proteinuria and haematuria were present at onset of University Hospital, albuminuric. Seven (32%, 14% to 5/5%) of the macro-diabetes). Ten patients died during the 10 year follow Glycatedhaemoglobin (%/) 9 9 (0 3; 5 8-13 3) 10 4 (0 3; 7 6-13 1)1129 (0 5; 7 3-16 6) aenswrdfidashvghyrtsonfter Insulindose (IU/kg) 064(003;036-103)
The Xbal polymorphism of the glycogen synthase gene identifies a subgroup of patients with NIDDM characterized by a strong family history of NIDDM, a high prevalence of hypertension, and marked insulin resistance.
This study reemphasizes the importance of poor glycemic control and smoking as independent risk factors for progression of AER. Furthermore, development of micro- or macroalbuminuria in NIDDM was associated with neuropathy and male sex.
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