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Poor Metabolic Control, Hypertension and Microangiopathy Independently Increase the Transcapillary Escape Rate of Albumin in Diabetes

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Poor Metabolic Control, Hypertension and Microangiopathy Independently Increase the Transcapillary Escape Rate of Albumin in Diabetes Diabetologia (1983) 25:260-263 Diabetologia Springer-Verlag1983 Poor Metabolic Control, Hypertension and Microangiopathy Independently Increase the Transcapillary Escape Rate of Albumin in Diabetes J. A. O'Hare 1, J. B. Ferriss 1, B. Twomey2 and D. J. O'Sullivan 1 Departments of 1Medicine and 2Medical Physics, Regional Hospital and University College, Cork, Ireland Summary. Available evidence indicates that poor metabolic was similar in non-diabetic control subjects (5.5 +0.7%/h) control and raised blood pressure each accelerate the develop- and in both Type 1 (5.3 + 1.2%/h) and Type 2 (5.1 + 0.6%/h) ment of diabetic microangiopathy. Microangiopathy is asso- normotensive diabetic patients without long-term complica- ciated with excess albumin deposition in capillary basement tions. During poor metabolic control the transcapillary escape membranes and it has been suggested that increased extrava- rate of albumin was significantly higher than in non-diabetic sation of plasma constituents may lead to basement mem- subjects (8.8_+0.8%/h and 5.5_+0.7%/h respectively, p< brane thickening. We measured the transcapillary escape rate 0.01). With improved control values fell significantly to 6.3 + of albumin, an indicator of the rate of extravasation of intra- 0.9%/h (p < 0.02), not significantly different from control sub- vascular albumin from the circulation per unit time, following jects. When compared with normotensive diabetic patients intravenous injection of mSI-human serum albumin. We ex- free of complications (5.2 _+ 0.6%/h), the transcapillary escape amined the independent effects on the transcapillary escape rate of albumin was elevated in hypertensive diabetic patients rate of albumin of non-ketotic poor metabolic control, hyper- without microangiopathy (8.6+ 1.3%/h, p<0.01), in hyper- tension and microangiopathy. We studied non-diabetic con- tensive diabetic patients with microangiopathy (9.2 + 1.2%/h, trol subjects and diabetic patients, initially when in non-ketot- p< 0.005), and in normotensive diabetic patients with micro- ic poor metabolic control and again when control had been angiopathy (8.1+0.9%/h, p<0.02). We conclude that the improved. We also studied normotensive well-controlled dia- transcapillary escape rate of albumin is independently elevat- betic patients without microangiopathy, normotensive well- ed by poor metabolic control, by hypertension and by micro- controlled diabetic patients with microangiopathy, hyperten- angiopathy. sive well-controlled diabetic patients without microangiopa- thy and hypertensive well-controlled diabetic patients with Key words: Diabetes mellitus, capillary permeability, plasma microangiopathy. The transcapillary escape rate of albumin volume, hypertension, microangiopathy, metabolic control. There is increasing evidence that poor metabolic con- space per unit time [13]. We investigated whether poor trol plays an important role in the development of dia- metabolic control, raised blood pressure and the pres- betic microangiopathy [1]. Hypertension may also ence of microangiopathy independently affect TER- accelerate the development of retinopathy [2] and albumin in diabetic patients. nephropathy [3, 4]. Capillary basement membrane thickening is an early sign of diabetic microangiopathy Subjects and Methods [5] and is associated with excess albumin deposition [6, 7]. Increased permeability to small molecules [8] and to albumin [9, 10] has been reported in the microcircula- Subjects tion of diabetic patients. It has been hypothesised that Control subjects and diabetic patients without complications: We com- excess extravasation of plasma constituents could inter- pared TER-albumin in non-diabetic control subjects and in normo- fere with normal basement membrane degradation and tensive diabetic patients (blood pressure consistently< 140/ lead to progressive thickening [11, 12]. 90mmHg), who were free of long-term diabetic complications. Diabetic patients were classified according to the proposals of the The transcapillary escape rate of albumin (TER-al- National Diabetes Data Group [14]. Patients were considered free of bumin) is a measure of the fraction of the intravascular clinically apparent complications if they had no retinopathy (assessed mass of albumin that passes into the extravascular by direct ophthalmoscopy through dilated pupils), no symptoms and J. A. O'Hare et al.: Transcapillary Escape in Diabetes 261 signs of peripheral neuropathy, no autonomic neuropathy (assessed was discarded to avoid contamination with blood from the previous by the pulse rate response to a maximum deep breathing and by the sample. Plasma (3ml) was used for radioactivity counting to postural change in blood pressure), and no significant proteinuria 10,000counts in triplicate using a 'well' type scintillation counter (urinary protein < 0.18 g/24 h: normal range < 0.2 g/24 h, n = 38). Pat- (Nuclear Enterprises, Reading, UK). Background correction was ients were asymptomatic, had minimal glycosuria and no ketonuria. made for subjects who had previous TER-albumin measurements. Further patient details are given in Table 1. Using a Hewlett Packard desk computer (HP 9815 A, Palo Alto, Cali- Controls were normotensive non-diabetic subjects with a negative fornia, USA), a linear regression equation was derived from log ra- past and family history of diabetes. They were ambulatory in-patients dioactivity against time. From the slope of this equation the TER-al- either admitted for minor surgical procedures or recovered from bumin was derived and expressed as percentage per hour [13]. short-term illness not involving the cardiovascular, renal or hepatic Intra-assay coefficient of variation for TER-albumin was 8.6%. Fre- systems. All had normal plasma urea, creatinine, proteins, sodium, quently repeated measurements of TER-albumin on the same subject potassium and calcium and normal liver function tests. were not ethically justifiable because of the radiation exposure in- volved. However three measurements in the same subject over an Diabetic patients duringpoor and improved metabolic control: We ex- eight-month period gave a coefficient of variation of 11.2%. Plasma amined eight non-ketotic normotensive diabetic patients (six males), volume was calculated by extrapolation to zero time for radioactivity whose mean age was 41 years (range 27-64 years) and whose mean from the regression equation, and the exact volume of 125I-HSA in- duration of diabetes was 5 years (range 1 month-19 years). Six had jected was calculated by weighing the syringe before and after injec- Type 2 (non-insulin-dependent)and two had Type 1 (insulin-depen- tion. Plasma volume was calculated by a standard method and ex- dent) diabetes. Six were free of clinical evidence of long-term diabetic pressed in relation to body surface area [15]. complications, while two had background retinopathy. None had Plasma albumin, urea, creatinine and bicarbonate were measured proteinuria, cardiac failure or peripheral vascular disease and none by an autoanalyser (SMAC, Technicon, Tarrytown, NY, USA), blood was receiving medication other than for the control of diabetes. Pat- glucose by the glucose oxidase method and HbA1 by ion exchange ients were studied on two occasions; firstly when each had polydip- chromatography (Bio-Rad Laboratories, Richmond, California; nor- sia, polyuria and heavy glycosuria but was free of ketonuria. Follow- mal range 4.9%-8%). Urinary albumin was measured by a colorimet- ing the initial study, control was improved by dietary reinforcement in ric method [16] using HSA as standard. all, by the introduction of glibenclamide (three subjects), by the intro- Results are expressed as mean+ SEM. Statistical analysis is by duction of insulin (two subjects) and by an increase of insulin dosage paired and unpaired Student's t-tests as appropriate, and by Pearson's (three subjects). Patients were then discharged from hospital and ad- correlation coefficient. mitted for re-study an average of 3 weeks later (range 2-6 weeks). On the second occasion patients were asymptomatic and had minimal or no glycosuria. Results Diabetic patients with complications and/or hypertension: Three ad- Comparison of Non-diabetic Subjects ditional groups of diabetic patients were studied: (1) normotensive and Diabetic Patients Without Complications diabetic patients with retinopathy and other long-term complica- tions (n=12); (2) hypertensive diabetic patients (blood pressure Control subjects and diabetic patients without compli- > 150/90mmHg as outpatients on two or more occasions) free of cations were of similar age, body weight and had similar clinically apparent specific complications (n= 11), and (3) hyperten- blood pressure levels. In the diabetic patients, 24-h uri- sive patients with specific long-term diabetic complications (n=9) (Table 1). Hypertension was untreated in all. None had thirst, poly- nary albumin excretion was similar to that of an ex- uria or ketonuria. None was in cardiac failure or had symptomatic panded control group of 38 normal subjects. TER-albu- peripheral vascular disease. Some Type 2 diabetic patients (Table 1) rain, plasma volume and plasma albumin concentration were treated with insulin after the failure of dietary reinforcement and were similar in control and diabetic subjects (Table 1). oral hypoglycaemic drugs to control hyperglycaemia [14]. TER-albumin was similar in five Type 1 and seven Type 2 diabetic patients (5.3 _+ 1.2 and 5.1 + 0.6%/h, Protocol respectively). All subjects were studied as hospital in-patients.
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