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Biomedical subjects

T Deckert

Publications and source records attributed to T Deckert.

At least 55 records · Page 3Linked to original sources
PubMed1991

Kidney volume in type 1 (insulin-dependent) diabetic patients with normal or increased urinary albumin excretion: effect of long-term improved metabolic control.

Forty-seven patients with type 1 (insulin-dependent) diabetes mellitus and 14 normal subjects had renal volume determined by an ultrasonic technique. Renal volume of 299 +/- 49 ml/1.73 m2 (mean +/- SD) in type 1 diabetic patients with normal urinary albumin excretion exceeded that in the normal subjects (245 +/- 53 ml/1.73 m2, p less than 0.05). Compared with diabetic patients with normal urinary albumin excretion, renal volume was significantly higher in patients with microalbuminuria (372 +/- 24 ml/1.73 m2, p less than 0.05) and patients with clinical nephropathy (352 +/- 48 ml/1.73 m2, p less than 0.05). In a multiple linear regression with HbA1c, urinary albumin excretion, age, diabetes duration and mean blood pressure as independent variables, variations in HbA1c could account for 33% of the variations in kidney volume (n = 47, r = 0.57, p less than 0.01). The other variables played no role. When only patients without clinical nephropathy were included, HbA1c and kidney volume remained significantly correlated (n = 34, r = 0.60, p less than 0.01). In those patients a strong correlation between kidney volume and function, i.e. the glomerular filtration rate was found (n = 34, r = 0.70, p less than 0.01); metabolic control and function were also correlated (n = 34, r = 0.62, p less than 0.01). The urinary albumin excretion accounted for only 6% of the variation of the kidney volume (NS). In nine patients with microalbuminuria the kidney volume could be reduced during 2 years of improved metabolic control by means of insulin infusion pumps.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Increased blood pressure and erythrocyte sodium/lithium countertransport activity are not inherited in diabetic nephropathy.

Genetic predisposition to essential hypertension, represented by maximal erythrocyte sodium/lithium countertransport activity, has been suggested as a marker for the risk of developing clinical nephropathy in Type 1 (insulin-dependent) diabetes mellitus. To evaluate this hypothesis we measured arterial blood pressure and maximal sodium/lithium countertransport activity of erythrocytes in 80 parents of 49 Type 1 diabetic patients with clinical nephropathy, 78 parents of 49 normoalbuminuric patients and 17 age-matched non-diabetic individuals. The two diabetic groups were carefully matched. In the two groups of parents blood pressure and cell sodium/lithium countertransport activity showed no significant differences (137/83 vs 133/81 mm Hg and 0.33 vs 0.32 mmol/(1 cells x h) respectively). The proportion of parents who had died or received antihypertensive drugs was similar in the two groups. The patients with Type 1 diabetes had significantly higher sodium/lithium countertransport compared to the 39 non-diabetic control subjects independently of the presence or absence of nephropathy (p less than 0.002). However, patients with nephropathy tended to have higher sodium/lithium countertransport activity than normoalbuminuric patients (0.48 vs 0.41 mmol/(1 cells x h), p = 0.06). We conclude that genetic predispositions to essential hypertension and increased maximal erythrocyte sodium/lithium countertransport activity do not appear to be risk markers for the development of clinical nephropathy in Type 1 diabetic patients.

Antiporters↗
PubMed1990

Prevalence of hypertension in type 1 (insulin-dependent) diabetes mellitus.

The prevalence of hypertension in a representative sample (n = 10202) of the Danish general population aged 16-59 years was assessed to 4.4% based on three blood pressure readings. In Type 1 (insulin-dependent) diabetic patients of similar age (n = 1703) the prevalence was determined in a similar way to 14.7% (p less than 0.00001). The excess prevalence in Type 1 diabetic patients was due to hypertension in patients with incipient and clinical nephropathy as the prevalence of hypertension among diabetic patients with normal urinary albumin excretion (essential hypertension) was 3.9%, similar to that observed in the general population. The patients with Type 1 diabetes and essential hypertension had higher systolic (146 +/- 19 vs 133 +/- 18 mm Hg, p less than 0.00001) and diastolic blood pressure (87 +/- 12 vs 79 +/- 7 mm Hg, p less than 0.00001), but less changes in the eye background than patients with incipient nephropathy (urinary albumin excretion 30-300 mg/24 h) (p less than 0.03), indicating that the two groups were also different with respect to other microangiopathic lesions. Patients with essential hypertension were defined as having a normal urinary albumin excretion before and during antihypertensive treatment (if any). They were followed-up for a 58 (6-234) month period. We confirmed that hypertension is more common among Type 1 diabetic patients than in the general population and found the prevalence of essential hypertension similar in Type 1 diabetic patients to the non-diabetic population. This supports our hypothesis that hypertension is very unlikely to be the cause of diabetic nephropathy.

Adolescent↗
PubMed1990

Relationship between blood pressure and urinary albumin excretion in development of microalbuminuria.

Two hundred nine consecutive normotensive insulin-dependent diabetic (IDDM) patients were followed prospectively from November 1982 to January 1988. Patient urinary albumin excretion rate (UAE) had to be normal (less than 30 mg/24 h) on at least two occasions before inclusion in the study. Patients were aged 18-50 yr with a duration of diabetes of 10-30 yr. UAE was measured every 4 mo, and supine blood pressure was measured annually. Two hundred five patients completed the study. Five years later, 15 patients had developed persistent microalbuminuria with median UAE greater than 30 mg/24 h for at least 2 yr (group 2), and 190 patients stayed normoalbuminuric (group 1). Although within normal range, initial UAE was significantly elevated in group 2 compared with group 1 (mean 19 mg/24 h [range 15-23 mg/24 h] vs. 11 mg/24 h [10-12], 95% confidence interval [CI], P less than 0.001). Initially, there was no difference in blood pressure between group 2 (mean systolic 122 mmHg [117-127], diastolic 80 mmHg [76-84]) and group 1 (mean 126 mmHg [124-128], 79 mmHg [78-80], 95% CI), and a significant increase in diastolic blood pressure could first be detected during the 3rd yr of persistent microalbuminuria (mean systolic 132 mmHg [124-140], diastolic 85 mmHg [81-89] vs. 128 mmHg [126-130], 79 mmHg [78-80], P less than 0.05). Initial hemoglobin A1c was significantly elevated in group 2 compared with group 1 (9.6% [8.8-10.4] vs. 8.5% [8.3-8.7], P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Partial normalization by dietary cod-liver oil of increased microvascular albumin leakage in patients with insulin-dependent diabetes and albuminuria.

In a double-blind crossover study, we compared the effects of eight weeks of dietary supplementation with cod-liver oil with the effects of supplementation with olive oil on endothelial permeability, blood pressure, and plasma lipid levels in 18 patients with insulin-dependent diabetes mellitus and albuminuria. When the patients received the cod-liver-oil supplement, the mean (+/- SEM) transcapillary escape rate of albumin (as compared with the base-line rate) decreased from 8.7 +/- 0.5 to 6.9 +/- 0.6 percent per hour (P less than 0.01), and the blood pressure decreased from 146 +/- 4/90 +/- 2 mm Hg to 139 +/- 4/85 +/- 2 mm Hg (P less than 0.05). There was no correlation, however, between cod-liver oil's effect on the transcapillary escape rate of albumin and its effect on blood pressure. There was no change from base line after the patients received the olive-oil supplement. During dietary supplementation with cod-liver oil, the plasma concentration of high-density lipoprotein cholesterol increased and the concentrations of very-low-density lipoprotein cholesterol and triglycerides decreased (P less than 0.05 for all comparisons), but the level of low-density lipoprotein cholesterol did not change. In contrast, during supplementation with olive oil, the concentration of low-density lipoprotein cholesterol decreased and the levels of very-low-density lipoprotein cholesterol and triglyceride increased (P less than 0.05 for all comparisons), but there was no change in the level of high-density lipoprotein. No changes were observed in the glomerular filtration rate, degree of albuminuria, insulin requirement, glycosylated hemoglobin level, or blood glucose level during supplementation with either oil. We conclude that dietary supplementation with cod-liver oil lowers the elevated transcapillary escape rate of albumin characteristic of patients with insulin-dependent diabetes and albuminuria, independently of its effect on blood pressure--perhaps by decreasing vascular permeability. We did not find any effect of cod-liver oil on urinary albumin excretion.

Adult↗
PubMed1989

High-performance liquid chromatofocusing and column affinity chromatography of in vitro 14C-glycated human serum albumin. Demonstration of a glycation-induced anionic heterogeneity.

High-performance liquid chromatofocusing of human serum albumin (HSA) after in vitro glycation with purified [14C]glucose has shown that with increasing glycation time a progressive increase in two major anionic fractions (pI 4.8 and 4.65) occurs, while the pI 4.9 fraction decreases in parallel. As early as after 5 days of glycation time, the [14C]glucose content in the anionic fractions was markedly higher than in the pI 4.9 fraction. After 10 and 15 days of glycation, a considerable heterogeneity of 10-15 components could be demonstrated. In addition, phenyl-boronic acid (PBA) affinity chromatography was applied and an enrichment of the more glycated species could be obtained using this method. We conclude that, in contrast to previous reports, glycation of HSA induces anionic heterogeneity (in accordance with the theoretically expected loss of positively charged amino groups) and, although the efficiency in separating non-glycated from monoglycated HSA was found to be very low, an enrichment of these anionic species can be achieved using PBA affinity chromatography.

Chromatography, Affinity↗
PubMed1989

Features of endothelial dysfunction in early diabetic nephropathy.

The release of tissue plasminogen activator (tPA) by vascular endothelial cells during exercise was studied in forty men with insulin-dependent diabetes. Three groups, matched for age and diabetes duration, were defined as: group I (n = 19), normal urinary albumin excretion (less than 30 mg/24 h); group II (n = 11), incipient diabetic nephropathy (30-300 mg albumin excreted per 24 h); and group III (n = 10), clinical diabetic nephropathy (more than 300 mg albumin excreted per 24 h). Nine non-diabetic men served as controls. The rise in tPA antigen with exercise was similar in the controls and group I but significantly smaller in groups II and III (p less than 0.01). The albumin transcapillary escape rate was significantly higher in groups II and III than in group I and normal controls (p less than 0.01). The basal plasma level of von Willebrand factor was higher in groups III (p less than 0.01) and II (difference not significant, p = 0.06) than in group I and normal controls. These findings suggest that insulin-dependent diabetic patients with only slightly raised urinary albumin excretion have general endothelial cell dysfunction or damage. It is not yet clear whether these changes are important in the pathogenesis of thrombosis and atherosclerosis in these patients.

Adolescent↗
PubMed1989

Albuminuria reflects widespread vascular damage. The Steno hypothesis.

Albuminuria in Type 1 (insulin-dependent) diabetes is not only an indication of renal disease, but a new, independent risk-marker of proliferative retinopathy and macroangiopathy. The coincidence of generalised vascular dysfunction and albuminuria, advanced mesangial expansion, proliferative retinopathy, and severe macroangiopathy suggests a common cause of albuminuria and the severe renal and extrarenal complications associated with it. Enzymes involved in the metabolism of anionic components of the extracellular matrix (e.g. heparan sulphate proteoglycan) vulnerable to hyperglycaemia, seem to constitute the primary cause of albuminuria and the associated complications. Genetic polymorphism of such enzymes is possibly the main reason for variation in susceptibility.

Albuminuria↗
PubMed1989

Improved survival in patients with diabetic nephropathy.

The effect of early antihypertensive treatment on survival of patients with diabetic nephropathy was evaluated by studying two cohorts of Type 1 (insulin-dependent) diabetic patients developing persistent proteinuria in I: 1957-1973 (late treatment group n = 49) and II: 1979-1983 (early treatment group n = 71). At onset of nephropathy, the two cohorts were comparable with regard to age (29(8) vs 30(8) years, mean (SD], duration of diabetes (16(6) vs 18(7) years), blood pressure (132(16)/85(11) vs 134(16)/86(8) mm Hg), proteinuria (0.8(0.5-1.2) vs 0.8(0.6-1.2) g x 24 h-1, median (quartiles] and serum creatinine (87(14) vs (85(16) mumol x 1(-1]. The patients were followed frequently at the outpatients' clinic until death or for a median duration of 8 years. In the first cohort antihypertensive treatment was seldom used, whereas, in the second cohort antihypertensive treatment was started when blood pressure reached 144(18)/93(7) mm Hg. The probability of survival with a functioning kidney for more than 8 years was 48% in the first cohort and 87% in the second cohort, p less than 0.001. The improvement of survival was due mainly to a decreased mortality from uraemia. Early antihypertensive treatment is the most likely explanation for this improvement.

Adult↗
PubMed1989

Normal urinary albumin excretion in recently diagnosed type 1 diabetic patients.

The urinary excretion of albumin and retinol binding protein were measured in 51 recently diagnosed Type 1 diabetic patients and 48 control subjects, matched for age and sex. The diabetic patients, admitted consecutively to the Steno Memorial Hospital, were all studied 3 to 6 months after the onset of diabetes. Urinary albumin excretion (median and 95% confidence interval) was similar in the diabetic patients and normal control subjects (8 (6-11) vs 8 (6-11) mg 24-h-1, NS). Four diabetic patients had urinary albumin excretion in the microalbuminuric range of 30-300 mg 24-h-1. There was no significant difference between the two groups in urinary excretion of retinol binding protein. The distribution among the individuals of both urinary proteins was positively skewed and similar in the two groups. In conclusion, no significant differences in the urinary excretion of albumin and retinol binding protein were found between recently diagnosed Type 1 diabetic patients and normal subjects.

Adult↗
PubMed1989

Limb salvage in diabetics with foot ulcers.

The healing results in 491 ulcers in 272 diabetic patients are reported. Soft moulded insoles and shoe corrections were the main part of the therapy. There were 329 (67%) neuropathic, 87 (17%) traumatic, 44 (9%) ischaemic and 31 (6%) ulcers of other various pathogenesis. Thirty seven per cent of the ulcers were complicated with invasive infection. Within the period of observation of 18 months (3-39 months) healing was obtained in 79% of the patients (88% of the ulcers) and major amputation was carried out in 8% (4% of the ulcers). There were 21 major amputations, which in 18 cases was due to ischaemia. Thus in only 3 cases (1% of the patients) neuropathy as complicated by invasive infection caused major amputation. Fifty nine ulcers (12%) were classified as relapsing ulcers or ulcers with new localizations and were caused by severe deformity of the foot (58 cases) often in combination with neglect of prophylaxis (7 cases). Only one recurrent ulcer was caused by ischaemia. The series shows that shoe corrections and insoles are effective in treating diabetic neuropathic ulcers. Recurrent ulcerations are caused by severe foot deformity and neglect of therapy. Loss of limbs is caused by ischaemia and invasive infection.

Adult↗
PubMed1988

Impaired aerobic work capacity in insulin dependent diabetics with increased urinary albumin excretion.

To assess whether decreased aerobic work capacity was associated with albuminuria in insulin dependent diabetics aerobic capacity was measured in three groups of 10 patients matched for age, sex, duration of diabetes, and degree of physical activity. Group 1 comprised 10 patients with normal urinary albumin excretion (less than 30 mg/24 h), group 2 comprised 10 with incipient diabetic nephropathy (urinary albumin excretion 30-300 mg/24 h, and group 3 comprised 10 with clinical diabetic nephropathy (urinary albumin excretion greater than 300 mg/24 h). Ten non-diabetic subjects matched for sex, age, and physical activity served as controls. Oxygen uptake was similar in the four groups at rest and during a 75 W workload. Maximal oxygen uptake was also similar in the control subjects and group 1 (median 41.7, (range 29.1-53.0) ml/kg/min v 38.5 (26.6-59.2) ml/kg/min, respectively), but was significantly lower in group 2 (27.7 (13.9-44.3) ml/kg/min) and group 3 (22.6-36.7) ml/kg/min). The difference in maximal oxygen uptake between groups 1 and 2 was 10.8 ml/kg/min (95% confidence interval 3.6 to 23.4 ml/kg/min) and between groups 1 and 3, 11.7 ml/kg/min (4.9 to 22.5 ml/kg/min). These differences were not explained by differences in metabolic control or the degree of autonomic neuropathy. Thus the insulin dependent diabetics with only slightly increased urinary albumin excretion had an appreciably impaired aerobic work capacity which could not be explained by autonomic neuropathy or the duration of diabetes. Whether the reduced capacity is due to widespread microangiopathy or another pathological process affecting the myocardium remains to be established.

Adolescent↗
PubMed1988

Abnormalities in plasmas concentrations of lipoproteins and fibrinogen in type 1 (insulin-dependent) diabetic patients with increased urinary albumin excretion.

Type 1 (insulin-dependent) diabetic patients with clinical nephropathy have a more than ten-fold increase in mortality of cardiovascular diseases compared with diabetic patients without nephropathy. The risk factors for cardiovascular disease, plasma concentrations of lipoproteins and fibrinogen, were investigated in 74 long-term diabetic patients: 37 with normal urinary albumin excretion, 20 with incipient nephropathy and 17 with overt clinical nephropathy based on urinary albumin excretion. The groups were matched according to sex, age and diabetes duration. The concentration of plasma cholesterol, very low density lipoprotein cholesterol, low density lipoprotein cholesterol, triglyceride and fibrinogen rose with increasing urinary albumin excretion. The plasma concentrations of these lipoproteins and fibrinogen were 11-14% higher in the patients with incipient nephropathy and 26-87% higher in the patients with overt clinical nephropathy compared with the patients without nephropathy. The plasma concentration of high density lipoprotein cholesterol was unaffected by albuminuria. Patients with normal urinary albumin excretion and HbA1c greater than 8.0% had significantly higher very low density lipoprotein- and lower high density lipoprotein cholesterol concentrations compared with patients with HbA1c less than 8.0%. Simple addition of the described risk factors can only account for a minor part of the greatly increased cardiovascular mortality in patients with diabetic nephropathy. An additional and possibly more decisive factor might be a change in the arterial wall, a change which promotes lipid accumulation and/or facilitates thrombus formation.

Adult↗
PubMed1988

Improved metabolic control does not alter the charge-dependent glomerular filtration of albumin in uncomplicated type 1 (insulin-dependent) diabetes.

The selectivity index, i.e. clearance of non glycated albumin/clearance of glycated albumin was studied in fourteen patients with Type 1 (insulin-dependent) diabetes and normal urinary albumin excretion. The index was increased above one in all patients, and correlated significantly to HbA1c. It was, however, unaffected by 12 weeks of improved metabolic control with a mean decline in HbA1c of 1.9% in seven patients. We conclude that the increased electronegative charge of the glomerular filtration barrier observed in uncomplicated diabetes is related to long term metabolic control but not reversible during twelve weeks of strict metabolic control. This indicates a slow turnover of the components responsible for the increased charge selectivity in uncomplicated diabetes.

Adult↗