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T Deckert

Publications and source records attributed to T Deckert.

At least 19 recordsLinked to original sources
PubMed1995

Effect of low-dose heparin on urinary albumin excretion in insulin-dependent diabetes mellitus.

We investigated the effect of heparin on urinary albumin excretion in patients with insulin-dependent diabetes mellitus. 39 patients with persistent urinary albumin excretion of 30-300 mg/24 h were randomly treated for 3 months with subcutaneous injections twice daily of isotonic saline, 5000 IU unfractionated heparin, or 2000 anti-Xa IU low-molecular-weight heparin. Unfractionated and low-molecular-weight heparin induced a significant reduction in urinary albumin excretion (p = 0.04 and p = 0.004). The mechanism and clinical relevance is unknown but deserve further attention.

Adult↗
PubMed1995

Diurnal variation in glomerular charge selectivity, urinary albumin excretion and blood pressure in insulin-dependent diabetic patients.

The urinary albumin excretion rate (AER) in a subgroup of patients with insulin-dependent diabetes mellitus (IDDM) steadily increases. In these patients a concomitant reduction of the glomerular charge selectivity index (SI) has been demonstrated. The aim of the present study was to evaluate whether diurnal variation in AER could be related to a diurnal variation in SI and/or a diurnal blood pressure variation. Thirty-three patients with IDDM, 27 with normal albumin excretion (AER < 20 micrograms/min; group D(o)) and six with incipient nephropathy (AER from 20 to 200 micrograms/min; group DA), were studied. AER and SI (renal clearance ratio of total-IgG/IgG4) were measured in three different urine collecting periods: period A (8:00 a.m. to 12:00 a.m.), period B (12:00 a.m. to bedtime) and period C (bedtime to 8:00 a.m.). A significant increase in SI was seen during the nighttime: period A, 1.6 (0.2 to 3.8; mean, range); period B, 1.7 (0.3 to 3.0); and period C, 2.0 (0.2 to 4.0); P = 0.01. Corresponding to this observation, an overall significant decrease in AER was found: period A, 10 (3 to 137) micrograms/min (median, range); period B, 8 (3 to 84) micrograms/min; and period C, 5 (0 to 78) micrograms/min; P < 0.001. In all three sampling periods a negative correlation was found between AER and SI. When group D(o) was analyzed alone, the results were similar. Diurnal variation in blood pressure was significantly positively correlated with AER in group DA, but was not correlated to variation in AER in D(o). We suggest that in normoalbuminuric IDDM patients diurnal variation in AER is related to diurnal variation in SI.

Adolescent↗
PubMed1995

Reduced glomerular size- and charge-selectivity in clinically healthy individuals with microalbuminuria.

The pathophysiologic mechanism behind microalbuminuria, a potential atherosclerotic risk factor, was explored by measuring fractional clearances of four endogenous plasma proteins of different size and electric charge (albumin, beta 2-microglobulin, immunoglobulin G, and immunoglobulin G4). Twenty-eight clinically healthy individuals with microalbuminuria, defined as a urinary albumin excretion of 6.6-150 micrograms min-1, and 60 matched control subjects were studied. Fractional immunoglobulin G clearance was higher (geometric means (95% confidence intervals)) 3.0 (2.3-3.9) x 10(-6), n = 28, vs. 2.1 (1.8-2.4) x 10(-6), n = 60; P = 0.02), whereas the ratio immunoglobulin G clearance/immunoglobulin G4 clearance was lower (geometric means (95% confidence intervals)) 1.8 (1.4-2.2), n = 28, vs. 2.3 (2.0-2.5), n = 60; P = 0.03) in microalbuminuric than in normoalbuminuric individuals. Fractional beta 2-microglobulin clearance was similar in the two groups. Since total IgG and the IgG4 subclass are of similar size and configuration but electrically neutral and negative, respectively; these findings indicate that microalbuminuria is associated with decreased size- and charge-selectivity of the glomerular vessel wall. Hypothetically, such alterations may reflect generalized vascular abnormalities linking microalbuminuria to atherogenesis.

Adult↗
PubMed1995

Serum sialic acid concentration is elevated in IDDM especially in early diabetic nephropathy.

OBJECTIVES: Elevated serum sialic acid concentration is a strong predictor of cardiovascular mortality in non-diabetic subjects. Because patients with insulin-dependent diabetes mellitus (IDDM) and albuminuria have a highly increased cardiovascular morbidity and mortality, we hypothesized that IDDM patients with albuminuria would have an increased concentration of serum sialic acid. DESIGN: Cross-sectional study. SETTING: Outpatient clinic at Steno Diabetes Centre, Gentofte, Denmark. SUBJECTS: Twenty-six non-diabetic controls and 74 IDDM patients with normoalbuminuria (urinary albumin excretion [UAE] < 30 mg 24 h-1; n = 37), incipient nephropathy (UAE 30-300 mg 24 h-1; n = 20) and clinical nephropathy (UAE > 300 mg 24 h-1; n = 17), matched for sex, age and body mass index (BMI). MAIN OUTCOME MEASURES: Serum sialic acid concentration, concurrent fasting blood glucose, glycated haemoglobin (HbA1c), serum creatinine, plasma fibrinogen and erythrocyte sedimentation rate. RESULTS: Normoalbuminuric patients had a higher serum sialic acid concentration (mmol L-1) than non-diabetic controls (1.83 +/- 0.24 vs. 1.67 +/- 0.26; P < 0.02). Serum sialic acid concentration was further increased in patients with incipient nephropathy (2.02 +/- 0.37; P < 0.03) and in patients with clinical nephropathy (2.13 +/- 0.33; P < 0.002) compared with normoalbuminuric IDDM patients. Serum sialic acid correlated strongly with plasma fibrinogen (r = 0.78; P < 0.0001) and erythrocyte sedimentation rate (r = 0.62; P < 0.0001). In a multiple regression analysis including UAE, retinopathy status, fasting blood glucose, HbA1c, mean blood pressure, serum creatinine, age, BMI, duration and smoking. UAE and fasting blood glucose were the independent variables which correlated significantly with serum sialic acid concentration (P < 0.0001 and P < 0.05, respectively). CONCLUSION: Serum sialic acid is elevated in IDDM especially in albuminuric patients. Whether elevated serum sialic acid is predictive for early diabetic nephropathy and cardiovascular disease in IDDM has to be shown in the future.

Adult↗
PubMed1995

The natural course of microalbuminuria in insulin-dependent diabetes: a 10-year prospective study.

The purpose of this study was to describe the clinical course in patients followed right from the onset of microalbuminuria to the development of diabetic nephropathy. A 10-year prospective follow-up of 209 consecutive normotensive insulin-dependent diabetic patients with normal urinary albumin excretion (UAE < 30 mg 24 h-1), age 34 (18-50) years and duration of diabetes 17 (10-30) years was performed. Twenty-four-hour urinary albumin excretion was measured every 4 months, glycated haemoglobin and supine blood pressure was measured annually. Two-hundred (96%) patients completed 10 (range 5-10) years follow-up. Twenty-nine (15%) patients developed persistent microalbuminuria (UAE 30-300 mg 24 h-1). Eight of these have progressed to nephropathy and one had died of diabetic nephropathy. Multiple stepwise logistic regression analysis demonstrated baseline urinary albumin excretion (p = 0.0016) and glycated haemoglobin (p = 0.0014) but not blood pressure as predictors of development of microalbuminuria within the following 10 years. The median annual increase in urinary albumin excretion was 27 (range 17-65) % in the 29 patients developing microalbuminuria. The median duration from onset of microalbuminuria to development of nephropathy was 7 years. The prevalence of patients receiving antihypertensive treatment (BP > 140/90 mmHg) increased from 10% at onset of microalbuminuria to 45% 4 years after onset of microalbuminuria. The prevalence of patients with proliferative retinopathy increased from 7% at onset of microalbuminuria to 28% 4 years after onset of microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Nephropathy and coronary death--the fatal twins in diabetes mellitus.

In summary, the decreased concentration of heparan sulphate within the extracellular matrix of patients with insulin-dependent diabetes mellitus is caused by a combination of genetic factors and poor metabolic control. Decreased concentrations of heparan sulphate are seen in patients with diabetes mellitus and proteinuria and this might be the explanation for the proteinuria as well as the expansion of the mesangium and the intimal dysfunction, including increased permeability of the vessel wall to macromolecules, which is present in such patients. Thus, the effective remodelling of extracellular matrix might explain coincidence of proteinuria, decline in renal function and premature atherosclerosis in patients with diabetes mellitus.

Albuminuria↗
PubMed1994

The predictive value of microalbuminuria in IDDM. A five-year follow-up study.

OBJECTIVE: To investigate the predictive value of microalbuminuria and the annual increase of albumin excretion as risk factors for diabetic nephropathy. RESEARCH DESIGN AND METHODS: A 5-year follow-up of patients with microalbuminuria (urinary albumin excretion [UAE] = 30-299 mg/24 h) and matched patients with normoalbuminuria (UAE < 30 mg/24 h). The initial classification was based on one single 24-h urine collection. The annual increase in UAE was calculated by linear regression analysis of log-transformed UAE on time. This study was conducted at the outpatient clinic of the Steno Diabetes Center. The study subjects included 118 insulin-dependent diabetes mellitus (IDDM) patients between 18 and 50 years of age with microalbuminuria and 112 matched control patients with normal UAE with an age at diabetes onset of < 31 years. The main outcome measures were UAE, annual change in UAE rate (percentage per year), and the prevalence of retinopathy. RESULTS: After 5 years, 39 (33%, 24-42 CI [95% confidence interval]) patients with microalbuminuria had normoalbuminuria, 57 (48%, 38-57 CI) still had microalbuminuria, and 22 (19%, 12-27 CI) had developed diabetic nephropathy. Among the 112 patients with normoalbuminuria in 1985, 9 (8%, 4-15 CI) had developed microalbuminuria, and 2 (2%, 0-6 CI) had developed diabetic nephropathy. Of the 79 patients with persistent albuminuria, only 36 (46%, 34-57 CI) were progressors with a rate of progression of > 5%/year. Progressors had significantly higher HbAlc, higher mean blood pressure, and a higher incidence of proliferative retinopathy compared with nonprogressors. Multiple regression analysis only identified mean HbAlc as an independent predictor of the rate of progression. Smoking was significantly more prevalent in patients with persistent albuminuria. CONCLUSIONS: Microalbuminuria is a predictor of progression to diabetic nephropathy; however, not as strong as suggested previously. Calculation of the annual increase in UAE seems to be a more specific method of identifying patients who will develop diabetic nephropathy.

Adult↗
PubMed1994

Endothelial function and serum lipids in the course of developing microalbuminuria in insulin-dependent diabetes mellitus.

Changed endothelial function and dyslipidemia are features of insulin-dependent diabetes mellitus complicated with clinical nephropathy. The time relationship between the appearance of these abnormalities is however not well known. We have therefore studied the coincidence of microalbuminuria, endothelial dysfunction and dyslipidemia during a 10 year prospective study of 209 insulin-dependent diabetic patients with normal urinary albumin excretion. Twenty-three patients developed progressing microalbuminuria defined as a median urinary albumin excretion > 30 mg/24-h in two consecutive years and a progression rate in albuminuria higher than 5% per year. Thirty patients who remained normoalbuminuric throughout the observation period were randomly selected to obtain a control group with comparable degree of glycaemic control. The mean level of von Willebrand factor before onset of microalbuminuria tended to be higher in patients developing microalbuminuria than in the control group (NS), but there was no increase in von Willebrand factor in the patients who developed microalbuminuria. Total cholesterol did not change, but a significant decrease in high density lipoprotein cholesterol was observed in patients who developed microalbuminuria. In conclusion, the study demonstrated coincidence of microalbuminuria and decreasing high density lipoprotein cholesterol, but no coincidence between onset of microalbuminuria and endothelial dysfunction assessed by von Willebrand factor.

Adolescent↗
PubMed1993

[Microalbuminuria--a valuable diagnostic parameter].

The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria, frequent examinations are warranted for early detection of retinopathy, hypertension and for optimizing the glycaemic control. In patients with non-insulin dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk-factors (hypertension, dyslipidemia, tobacco and obesity). In the non-diabetic population there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to further clarify the role of microalbuminuria as an independent risk factor in the background population.

Albuminuria↗
PubMed1993

Size- and charge selectivity of glomerular filtration in Type 1 (insulin-dependent) diabetic patients with and without albuminuria.

Albuminuria is the first clinical event in the development of diabetic nephropathy. We assessed glomerular charge- and size selectivity in 51 patients with Type 1 (insulin-dependent) diabetes mellitus of juvenile onset and 11 healthy individuals. Patients were allocated to five groups. The urinary albumin excretion rate was normal in group D1; 30-100 mg/24 h in group D2; 101-300 mg/24 h in group D3 and greater than 300 mg/24 h in groups D4 and D5. Group D5 had elevated serum creatinine (above 110 mumol/l). Glomerular filtration rate and renal plasma flow were determined by constant infusion techniques and tubular protein reabsorption by excretion of beta 2-microglobulin. Charge selectivity was estimated from the IgG/IgG4 selectivity index. Size selectivity was measured by dextran clearance. Dextran was measured by refractive index detection after fractionation (2 A fractions in the range 26-64 A) by size exclusion chromatography. IgG/IgG4 selectivity index was significantly decreased in patients with albuminuria (p < 0.001). The drop in IgG/IgG4 selectivity index was found in patients with minimal albuminuria (D2) and was not accompanied by any changes in tubular function or glomerular haemodynamics. Size selectivity was significantly altered only in patients with the most advanced nephropathy (D5) as reflected by an increase in the clearance of 62 A dextran (p < 0.04). We conclude that loss of glomerular charge selectivity precedes or accompanies the formation of new glomerular macromolecular pathways in the development of diabetic nephropathy.

Adult↗
PubMed1993

Diabetes mellitus induced inhibition of glucosaminyl N-deacetylase: effect of short-term blood glucose control in diabetic rats.

Inhibition of glucosaminyl N-deacetylase activity, a key enzyme in heparan sulphate sulphation, may be involved in the development of late diabetic vascular complications. We examined the effect of short- and long-term metabolic control on N-deacetylase activity in streptozotocin diabetic H and U rats. Spontaneously diabetic BB rats were included in parts of the study. Over a 3-week period blood glucose was maintained at predetermined levels (6-10 mmol/l or 10-20 mmol/l) by insulin treatment and then during the final 2 days rapidly reversed in half of each group. In the U rats, the hepatic N-deacetylase activity significantly decreased by 10-15% following short- and long-term poor metabolic control and the inhibition was entirely reversed by short-term good control. In the H rats a similar, not significant, effect was seen. BB rats in long-term poor control showed a 10% reduction in hepatic N-deacetylase activity (p = 0.003). Glomerular N-deacetylase activity was reduced in U rats after long-term poor control (p = 0.004) but not in H and BB rats. There was an overall correlation between urinary albumin excretion and glomerular N-deacetylase activity (r = -0.60, p < 0.0001). We conclude that diabetes-induced inhibition of hepatic N-deacetylase is not restricted to the streptozotocin diabetic model, and that short-term blood glucose control is of major importance. Genetic factors and tissue specificity influence the vulnerability of the enzyme. Finally, the study suggests an association between N-deacetylase activity and urinary albumin excretion.

Albuminuria↗
PubMed1993

Plasma disappearance of glycated and non-glycated albumin in type 1 (insulin-dependent) diabetes mellitus: evidence for charge dependent alterations of the plasma to lymph pathway.

The fractional plasma escape rates of glycated and non-glycated albumin have earlier been measured in groups of Type 1 (insulin-dependent) diabetic patients and control subjects. The escape of non-glycated albumin was similar in control subjects and normoalbuminuric patients, but elevated in patients with micro or macroalbuminuria. In all groups the escape rate of glycated albumin was lower than that of non-glycated albumin. Glycation increases the anionic charge of albumin. To assay for charge-dependent alterations of transport a selectivity index (non-glycated albumin/glycated albumin transport ratio) was determined from the disappearance data. The index was high in control subjects (1.021 +/- 0.0057 (SEM)). This reflects a mean difference between the two escape rates of 2.1% per hour (for comparison the mean of the fractional escape rate of non-glycated albumin of the normal control subjects was 4.7% per hour). The index was numerically even higher in normoalbuminuric patients (1.031 +/- 0.0047 (SEM)), but reached significantly lower levels in patients with microalbuminuria (1.013 +/- 0.0030 (SEM), p < 0.02). Patients with clinical nephropathy had very low levels indicating loss of selectivity (1.002 +/- 0.0068 (SEM), p < 0.001). This pattern accords well with measurements of renal clearance selectivity indices, suggesting a general, progressive deterioration of anionic perivascular barrier components in diabetic microangiopathy. The structural target for these changes is likely to be the glycosaminoglycans of the glomerular basal membrane and the interstitial matrix.

Albuminuria↗
PubMed1993

Glucosaminyl N-deacetylase in cultured fibroblasts; comparison of patients with and without diabetic nephropathy, and identification of a possible mechanism for diabetes-induced N-deacetylase inhibition.

Impaired heparan sulphate biosynthesis through diabetes-induced inhibition of glucosaminyl N-deacetylase may have a central role in the development of diabetic nephropathy, and genetic differences in the vulnerability of the N-deacetylase could influence the risk of developing nephropathy. We studied N-deacetylase activity in fibroblast cultures from Type 1 (insulin-dependent) diabetic patients with (n = 14) or without (n = 13) diabetic nephropathy, together with non-diabetic control subjects (n = 7). No difference in N-deacetylase activity was found (p = 0.13), and no inhibition of N-deacetylase was found in cultures grown at 25 mmol/l glucose. N-deacetylase activity was inversely correlated to growth rate (r = -0.59, p = 0.0008), and in patients with nephropathy a negative correlation between HbA1C and fibroblast N-deacetylase activity (r = -0.72, p = 0.012) was found. Cell-cycle analysis revealed an increased fraction of S-phase cells in patients with nephropathy (28%(21-52%)) compared to healthy control subjects (17% (9-24%)), p = 0.0008, but not between patients with and without nephropathy (latter group 26%(11-43%)), p = 0.43. Forskolin, an activator of protein kinase A, specifically decreased N-deacetylase activity, whereas activation of protein kinase C produced a combined reduction in N-deacetylase activity and total protein synthesis. In conclusion, no constitutive defects in N-deacetylase activity were found in fibroblasts from these patients. Further studies should consider possible associations between fibroblast characteristics and pre-biopsy environmental parameters related to cellular memory phenomena. Finally, activation of protein kinase A provides a potential general pathway for regulating N-deacetylase activity.

Adult↗
PubMed1992

Urinary excretion of retinol-binding protein in type 1 (insulin-dependent) diabetic patients with microalbuminuria and clinical diabetic nephropathy.

The urinary excretion of retinol-binding protein (RBP) was studied in 101 insulin-dependent diabetic patients allocated to three groups according to 24-h urinary albumin excretion rate (UAE) (median of three urine collections): group 1 (n = 45), normal UAE less than 30 mg/24 h; group 2 (n = 27), microalbuminuria (UAE 30-300 mg/24 h); and group 3 (n = 29), clinical diabetic nephropathy (UAE greater than 300 mg/24 h). We used 23 healthy subjects as controls. Fractional clearance of RBP (FC-RBP) and its 24-h urinary excretion rate (URBP) were higher in each diabetic group than in healthy subjects, the highest values being found in group 3. Groups 1 and 2 did not differ in URBP and FC-RBP. There was a correlation between FC-RBP and haemoglobin A1c in both the total diabetic cohort (P less than 0.001) and in diabetic patients in groups 1 and 2 with a glomerular filtration rate of more than 90 ml/min (P less than 0.05). No correlation was found between FC-RBP and UAE and/or duration of diabetes in any of the diabetic groups. We conclude that the increased urinary excretion of RBP, indicating proximal tubular dysfunction, is already present in normoalbuminuric insulin-dependent diabetic patients and correlates with metabolic control. Further deterioration in proximal tubular function was not observed in microalbuminuric patients, but is a late event in clinical diabetic nephropathy.

Adult↗
PubMed1992

Is diabetic nephropathy an inherited complication?

For yet unidentified reasons less than 50% of patients with insulin-dependent mellitus develop diabetic nephropathy. Genetic factors have been suggested as risk markers for development of nephropathy in diabetes. To further evaluate this hypothesis we studied the prevalence of nephropathy in diabetic siblings of diabetic patients with and without nephropathy. From a representative sample of 619 patients with insulin-dependent diabetes, we identified 20 patients with and 29 patients without nephropathy having diabetic siblings. Diabetic nephropathy (defined as urinary albumin excretion greater than 300 mg/24 hr) was found in 7 out of 21 siblings to patients with nephropathy and 3 out of 30 siblings to normoalbuminuric patients (P less than 0.04). No significant differences between the two groups of siblings with respect to age, diabetes duration, sex distribution, blood pressure or glycosylated hemoglobin A1c-levels were found. A significant correlation within sib-pair of glycosylated hemoglobin A1c was found (r = 0.47; P less than 0.001). We conclude that familial clustering of diabetic nephropathy does occur. This clustering may either be due to genetic inheritance or to sib-similarities due to shared environment, as indicated by the correlation of glycosylated hemoglobin A1c within sib-pairs.

Albuminuria↗
PubMed1992

Microalbuminuria. Implications for micro- and macrovascular disease.

Microalbuminuria is diagnosed when the UAER is greater than 20 but less than 200 micrograms/min. The prevalence of microalbuminuria among diabetic patients is 15-20%. Persistent microalbuminuria in diabetic patients is a risk marker not only of renal disease, but also of proliferative retinopathy and cardiovascular morbidity and mortality. Even among nondiabetic individuals, those with microalbuminuria tend to have an increased cardiovascular morbidity. The established cardiovascular risk factors, such as smoking, elevated plasma cholesterol, fibrinogen, and hypertension, are seen more frequently in diabetic patients with persistent microalbuminuria than in normoalbuminuric diabetic patients of similar age, sex, and diabetes duration. However, these risk factors cannot by themselves explain the cardiovascular overmortality in these patients. In addition, insulin resistance or genetic disposition to hypertension or cardiovascular disease fails to be the missing link. Accumulating evidence suggests a common pathogenetic mechanism for microalbuminuria and premature atherosclerosis (i.e., qualitative alterations of the extracellular matrix, including decreased density and sulfation of HS-PG). Decreased density of HS in the glomeruli may lead to albuminuria and mesangial proliferation. In the intima of large vessel walls, decreased density and/or sulfation of HS may enhance several of the processes involved in premature atherosclerosis. Diabetes affects the composition and structure of the extracellular matrix in many ways and leads to decreased density and sulfation of HS-PG by several mechanisms. Genetic differences in the sulfation of HS and/or genetic defects in the coordinated biosynthesis of HS-PG might contribute to decreased concentration and sulfation of HS-PG in susceptible individuals. It is hoped that susceptibility genes can be identified soon, thereby making prevention of severe late diabetic complications more successful.

Albuminuria↗
PubMed1992

Transcapillary filtration of plasma protein in long-term type 1 (insulin dependent) diabetic patients.

To study the pathophysiologic mechanism leading to increased transcapillar sieving of albumin in patients with diabetic nephropathy, subcutaneous interstitial concentrations of albumin, transferrin, total IgG and IgG-4 was measured in 30 long-term type 1 diabetic patients using the skin suction blister method. Eight normal subjects served as controls. The patients were divided in groups according to their urinary albumin excretion: normal (n = 11), micro-albuminuria (n = 9), and clinical nephropathy (n = 10). Results were expressed as the blister to serum concentration ratio (Cb:Cs) of each macromolecule. Normoalbuminuric patients had lower Cb:CsIgG ratio than healthy controls (0.28 +/- 0.04 vs. 0.35 +/- 0.09, p = 0.03). The lowest Cb:CsIgG ratio (0.23 +/- 0.07) was found in patients with clinical nephropathy. The same trend could be demonstrated in the other Cb:Cs ratios, but differences there were not significant. No differences related to capillary charge- or size-selectivity could be demonstrated between the groups. The results might reflect an increase of intracapillary hydrostatic pressure or increased capillary hydraulic permeability in the diabetic state per se, augmented during the development of microvascular complications.

Adult↗