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  • 1
    Electronic Resource
    Electronic Resource
    Insulin and glucagon secretion in diabetic and non-diabetic patients with circulating islet cell antibodies (1977)
    Springer
    Diabetologia 13 (1977), S. 451-458 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes ; autoimmunity and diabetes ; islet cell antibodies ; insulin and glucagon secretion ; glucose and arginine infusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty-nine patients (14 non-diabetics, 8 chemical diabetics, and 17 overt diabetics) with circulating islet cell antibodies (ICA) were studied. Insulin and glucagon secretion after oral (100 g) and intravenous glucose loading (200 mg/kg bolus injection followed by an infusion of 20 mg/min over 60 min) and arginine infusion (25 g over 30 minutes) were evaluated in these patients and in non diabetic and diabetic ICA-negative controls. In the non-diabetic groups with or without ICA, insulin and glucagon responses to glucose were similar. Moreover, in ICA positive patients the response of these hormones to arginine infusion was reduced. Similar alterations in insulin and glucagon secretion were observed in the ICA positive and negative patients with chemical or overt diabetes. In particular, fasting hyperglucagonaemia and glucagon hyperresponse to arginine are associated with a lack of insulin secretion in the patients with overt diabetes. Hormonal differences between diabetics with and without ICA could not be detected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01234495
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  • 2
    Electronic Resource
    Electronic Resource
    The metabolic response to hyperglycaemic clamping in insulin-dependent diabetes (1981)
    Springer
    Diabetologia 20 (1981), S. 113-117 
    Details
    ISSN: 1432-0428
    Keywords: Artificial endocrine pancreas ; glucose clamping ; hyperglycaemia ; insulin-dependent diabetes ; blood glucose ; ketone bodies ; alanine ; lactate ; pyruvate ; ketogenesis ; insulin ; glucagon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The metabolic and hormonal effects of stable hyperglycaemia (10–12 mmol/l) have been examined in five insulin-dependent diabetics and compared with the results of 8 h (1200 to 2000 h) normoglycaemic (5–6 mmol/l) clamping. Glucose levels were maintained using a glucose controlled insulin infusion system. Mean blood lactate, pyruvate, total ketone bodies, glycerol and plasma nonesterified fatty acids were similar during the period of stable glycaemia at the two glucose levels. In contrast mean blood alanine was markedly elevated during hyperglycaemic clamping (0.384 ± 0.008 vs 0.298 ± 0.021 mmol/l) and 3-hydroxybutyrate was slightly decreased (0.068 ± 0.007 vs 0.084 ± 0.008 mmol/l). Plasma glucagon levels were raised during hyperglycaemic clamping and growth hormone slightly decreased. There was a close positive correlation between mean blood alanine and mean blood glucose (r = 0.79, p 〈 0.01), and a negative correlation of alanine with the amount of insulin infused (r =-0.72, p 〈 0.01). It is suggested that the raised alanine results from increased peripheral glucose utilisation. In general a short period of stable hyperglycaemia is not associated with a worsening of metabolic abnormalities in insulin-dependent diabetic subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00262012
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  • 3
    Electronic Resource
    Electronic Resource
    The metabolic and hormonal response to acute normoglycaemia in type 1 (insulin-dependent) diabetes: Studies with a glucose controlled insulin infusion system (artificial endocrine pancreas) (1982)
    Springer
    Diabetologia 23 (1982), S. 220-228 
    Details
    ISSN: 1432-0428
    Keywords: Metabolic control ; artificial pancreas ; lactate ; pyruvate ; glycerol ; non-esterified fatty acids ; total ketone bodies ; glucose turnover ; glucose recycling ; glucagon ; growth hormone ; Type 1 diabetes ; subcutaneous insulin therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twelve insulin deficient Type 1 (insulin-dependent) diabetic subjects were studied over an 11 1/2 h period during both subcutaneous insulin therapy and closed loop insulin delivery, using a glucose controlled insulin infusion system (Biostator) programmed to maintain normoglycaemia. Results were compared with those from 21 age and weight-matched normal subjects. Using the Biostator, normoglycaemia was achieved in all diabetic subjects within 3.5 h and normal profiles maintained thereafter. Blood metabolite and hormone values were evaluated during the subsequent 8 h normoglycaemic period. Subcutaneous therapy resulted in abnormal glucose levels throughout the study period (mean 8 h value 8.3±0.7 compared with 5.6±0.3 mmol/l on feedback control and 5.5.±0.1 mmol/l in normal subjects). The mean value of lactate and pyruvate over the final 8 h period was 25% higher in diabetic patients than in normal subjects with no difference between the two insulin treatments (blood lactate: 0.94±0.04 on subcutaneous insulin, 0.91±0.04 on feedback control and 0.74±0.03 mmol/l in control subjects). The pre-prandial peaks of blood glycerol and plasma non-esterified fatty acids were significantly decreased or absent during both feedback control and subcutaneous therapy in comparison with the normal subjects, whereas after the midday and evening meals, total ketone body levels were significantly higher in the diabetic patients. Peripheral serum free insulin levels were two-to fourfold greater in the diabetic than in the normal subjects. There were no significant differences between levels in diabetic patients receiving subcutaneous insulin or on the Biostator. Glucose turnover (1600–1800 h) was normal on feedback control (1.41±0.20 versus 1.55±0.18 mg · kg-1 · min-1 in the normal subjects) but was significantly decreased during subcutaneous insulin (1.04±0.09 mg · kg-1 · min-1). There was, in addition, a decrease in glucose recycling during both subcutaneous insulin therapy and feedback control in the diabetic subjects. These data suggest that although fine control of glucose metabolism both in terms of circulating concentrations and rates of production can be achieved by feedback-control, insulin infusion by the peripheral route is associated with significant metabolic abnormalities, at least in the short term. Longer term studies and examination of portal insulin delivery seem warranted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00252845
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  • 4
    Electronic Resource
    Electronic Resource
    The effects of different plasma insulin concentrations on lipolytic and ketogenic responses to epinephrine in normal and Type 1 (insulin-dependent) diabetic humans (1992)
    Springer
    Diabetologia 35 (1992), S. 129-138 
    Details
    ISSN: 1432-0428
    Keywords: Ketone bodies ; non-esterified fatty acids ; epinephrine ; insulin ; stable isotopes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was performed to verify: (1) the ability of different insulin concentrations to restrict the lipolytic and ketogenic responses to exogenous epinephrine administration; (2) whether the ability of insulin to suppress the lipolytic and ketogenic responses during epinephrine administration is impaired in Type 1 (insulin-dependent) diabetic patients. Each subject was infused on separate occasions with insulin at rates of 0.2, 0.4, and 0.8 mU·kg−1·min−1 while normoglycaemic. To avoid indirect adrenergic effects on endocrine pancreas secretions, the so-called “islet clamp” technique was used. Rates of appearance of palmitic acid, acetoacetate, and 3-hydroxybutyrate were simultaneously measured with an infusion of 13C-labelled homologous tracers. After a baseline observation period epinephrine was exogenously administered at a rate of 16 ng·kg−1·min−1. At low insulin levels (20 μU/ml) the lipolytic response of comparable magnitude was detected in normal and Type 1 diabetic patients. However, the ketogenic response was significantly higher in Type 1 diabetic patients. During epinephrine administration, similar plasma glucose increments were observed in the two groups (from 4.74±0.53 to 7.16±0.77 mmol/l (p〈0.05) in Type 1 diabetic patients and from 4.94±0.20 to 7.11±0.38 mmol/l (p〈0.05) in normal subjects, respectively). At intermediate insulin levels (35 μU/ml) no significant differences were found between Type 1 diabetic patients and normal subjects, whereas plasma glucose levels rose from 4.98±0.30 to 6.27±0.66 mmol/l (p〈0.05) in Type 1 diabetic patients, and from 5.05±0.13 to 6.61±0.22 mmol/l (p〈0.05) in normal subjects. At high insulin levels (70 μU/ml) the lipolytic response was detectable only in Type 1 diabetic patients; the ketogenic response was reduced in both groups. During the third clamp, a significant rise in plasma glucose concentration during epinephrine infusion was observed in both groups. In conclusion this study shows that at low insulin levels Type 1 diabetic patients show an increased ketogenic response to epinephrine, despite their normal nonesterified fatty acid response. Instead, high insulin levels are able to restrict the ketogenic response to epinephrine in both normal and Type 1 diabetic subjects, although there is a still detectable lipolytic response in the latter. In the presence of plasma free insulin levels that completely restrict the ketogenic response in the same group, there is still a distinct glycaemic response. Plasma insulin levels in Type 1 diabetic patients are a major determinant of the metabolic response to epinephrine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402544
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  • 5
    Electronic Resource
    Electronic Resource
    Impaired response to angiotensin II in Type 1 (insulin-dependent) diabetes mellitus. Role of prostaglandins and sodium-lithium countertransport activity (1991)
    Springer
    Diabetologia 34 (1991), S. 595-603 
    Details
    ISSN: 1432-0428
    Keywords: Prostaglandins ; angiotensin ; sodium-lithium countertransport ; hypertension ; diabetic nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pathogenesis of diabetic nephropathy remains elusive. A role for renal prostaglandins in antagonizing the hormonal effects of renin-angiotensin II has been postulated as a putative factor leading to hyperfiltration in patients with Type 1 (insulin-dependent) diabetes mellitus. Our aim was to elucidate the effects of angiotensin II on kidney haemodynamics and on blood pressure in eight normal subjects, in nine normotensive, in nine hypertensive with normal sodium-lithium countertransport activity in erythrocytes, in seven hypertensive without and in eight hypertensive Type 1 diabetic patients with microalbuminuria and with high sodium-lithium countertransport activity in erythrocytes. Angiotensin II infusion 4ng·kg−1·min−1 for 60 min) decreased the glomerular filtration rate to a greater extent in normal subjects (−20%), than in normotensive patients (−5% p〈0.01), in hypertensive patients with normal sodium-lithium countertransport activity in erythrocytes (−8% p〈0.01) in hypertensive patients with high sodium-lithium countertransport (−6% p〈0.01) and in hypertensive microalbuminuric patients (−5% p〈0.01) with Type 1 diabetes. The urinary excretion rate of vasodilatory prostaglandins was two-three fold higher in all patients than in normal subjects. Acute indomethacin treatment restored a normal response to angiotensin II infusion in normotensive patients, but did not change the renal haemodynamic response in normal subjects. With regard to hypertensive patients with and without microalbuminuria indomethacin treatment restored a normal response to angiotensin II in some but not all patients. An inverse relation was found between angiotensin II-induced decrease in the glomerular filtration rate and the sodium-lithium countertransport activity in erythrocytes during indomethacin treatment. Hypertensive and microalbuminuric patients with a sodium-lithium countertransport activity higher than 0.41 mmol·l erythrocyte−1·h−1 (the upper limit in normal subjects) also had a greater intimal plus medial thickness of the carotid artery using an ultrasonic imaging technique. Chronic indomethacin administration (30 days) significantly decreased the baseline overnight fasting glomerular filtration rate in normotensive and in hypertensive patients with normal but not in hypertensive and microalbuminuric patients with high sodium-lithium countertransport activity. In conclusion these results demonstrate that: (1) excessive synthesis of vasodilatory prostaglandins antagonizes the regulation of renal haemodynamics by angiotensin II, at least partially accounting for hyperfiltration in Type 1 diabetes, (2) elevated sodium-lithium countertransport activity in erythrocytes identifies a subgroup of patients with Type 1 diabetes and hypertension, with and without microalbuminuria, in whom the normalization of urinary excretion rate of prostaglandins does not restore a normal response to angiotensin II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400280
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  • 6
    Electronic Resource
    Electronic Resource
    Arterial hypertension and microalbuminuria in IDDM: The Italian Microalbuminuria Study (1994)
    Springer
    Diabetologia 37 (1994), S. 1015-1024 
    Details
    ISSN: 1432-0428
    Keywords: Key words Insulin-dependent diabetes mellitus ; arterial hypertension ; borderline hypertension ; microalbuminuria ; diabetic nephropathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Arterial hypertension and poor glycaemic control are central to the development of microalbuminuria in insulin-dependent diabetes mellitus (IDDM). Recent consensus has established sensitive criteria for their detection and treatment, although the proportion of patients who may benefit is unclear. Between 1988 and 1990, we measured urinary albumin to creatinine concentration ratio (A/C) in 3,636 adult out-patients with IDDM of more than 3 years duration, serum creatinine under 133 μmol/l and who were not undergoing antihypertensive treatment. A/C indicating microalbuminuria (≥ 2.38/2.96 mg/mmol, male/female) was found in 620 of 3,451 patients without proteinuria, and associated with hypertension (blood pressure ≥ 140 and/or 90 mm Hg; p = 0.0016; rate: 39.6 %), independent of diabetes duration (p = 0.0082) and male gender (p = 0.0350; relative risk = 1.16; 95 % confidence interval: 1.01–1.32). Hypertension was less common among those with normal A/C (27.5 %, p 〈 0.0001) but was positively related with diabetes duration. Of the 1,015 patients with A/C ≥ 2.0 mg/mmol 529 were reexamined. Glycated haemoglobin levels exceeded 3 SD above the mean of normal in 84.3 % of the 198 microalbuminuric patients (AER = 20–200 μg/min), but were comparably poor (79.2 %) in normoalbuminuria. Duration of diabetes was inversely related to glycated haemoglobin only in microalbuminuria (0.05 〈 p 〈 0.1). Intervention to lower blood pressure remains mainly restricted to those patients with long-term diabetes and slower development of kidney disease. Near-normalisation of glycaemia remains the priority for the majority of patients with microalbuminuria. [Diabetologia (1994) 37: 1015–1024]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400465
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  • 7
    Electronic Resource
    Electronic Resource
    Patterns of renal injury in NIDDM patients with microalbuminuria (1996)
    Springer
    Diabetologia 39 (1996), S. 1569-1576 
    Details
    ISSN: 1432-0428
    Keywords: Keywords NIDDM ; renal structure ; microalbuminuria ; glomerular filtration rate.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microalbuminuria predicts overt nephropathy in non-insulin-dependent diabetic (NIDDM) patients; however, the structural basis for this functional abnormality is unknown. In this study we evaluated renal structure and function in a cohort of 34 unselected microalbuminuric NIDDM patients (26 male/8 female, age: 58 ± 7 years, known diabetes duration: 11 ± 6 years, HbA1 c: 8.5 ± 1.6 %). Systemic hypertension was present in all but 3. Glomerular filtration rate (GFR) was 101 ± 27 ml · min–1· 1.73 m–2 and albumin excretion rate (AER) 44 (20–199) μg/min. Light microscopic slides were categorized as: C I) normal or near normal renal structure; C II) changes “typical” of diabetic nephropathology in insulin-dependent diabetes (IDDM) (glomerular, tubulo-interstitial and arteriolar changes occurring in parallel); C III) “atypical” patterns of injury, with absent or only mild diabetic glomerular changes associated with disproportionately severe renal structural changes including: important tubulo-interstitial with or without arteriolar hyalinosis with or without global glomerular sclerosis. Ten patients (29.4 %) were classified as C I, 10 as C II (29.4 %) and 14 as C III (41.2 %); none of these patients had any definable non-diabetic renal disease. GFR, AER and blood pressure were similar in the three groups, while HbA1 c was higher in C II and C III than in C I patients. Diabetic retinopathy was present in all C II patients (background in 50 % and proliferative in 50 %). None of the patients in C I and C III had proliferative retinopathy, while background retinopathy was observed in 50 % of C I and 57 % of C III patients. In summary, microalbuminuric NIDDM patients are structurally heterogeneous with less than one third having “typical” diabetic nephropathology. The presence of both “typical” and “atypical” patterns of renal pathology was associated with worse metabolic control, suggesting that hyperglycaemia may cause different patterns of renal injury in older NIDDM compared to younger IDDM patients. [Diabetologia (1996) 39: 1569–1576]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050616
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  • 8
    Electronic Resource
    Electronic Resource
    Abnormal Na + /H + antiport activity in cultured fibroblasts from NIDDM patients with hypertension and microalbuminuria (1996)
    Springer
    Diabetologia 39 (1996), S. 717-724 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Non-insulin-dependent diabetes mellitus ; arterial hypertension ; microalbuminuria ; skin fibroblasts ; sodium-hydrogen exchange ; intracellular pH.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An increased activity of Na + /H + antiport has been reported in leukocytes and fibroblasts from insulin-dependent diabetic (IDDM) patients with nephropathy. To test whether a similar abnormality is present in fibroblasts from non-insulin-dependent diabetic (NIDDM) patients with microalbuminuria and hypertension, we examined intracellular pHi and Na + /H + antiport activity, using the pH sensitive dye 2 ′, 7 ′–bis (2–carboxyethyl–5(6)-carboxyfluorescein (BCECF), in cultured skin fibroblasts obtained from 34 NIDDM patients, divided into four groups based upon whether they had microalbuminuria or hypertension, or both: Group 1, nine NIDDM patients with microalbuminuria and hypertension. Group 2, nine NIDDM patients with hypertension and normal albumin excretion rate. Group 3, seven NIDDM patients with microalbuminuria and normal blood pressure. Group 4, nine NIDDM patients with normal blood pressure and normal albumin excretion rate. Nine normal subjects served as control group. Resting pHi was more alkaline in fibroblasts from Group 1 (7.22 ± 0.03; p 〈 0.05), Group 2 (7.21 ± 0.02; p 〈 0.05) and Group 3 (7.19 ± 0.02, p = 0.17) than in Group 4 and normal subjects. This was due to higher Vmax values of Na + /H + antiport activity in cultured fibroblasts from Group 1 (52.1 ± 5.3 mmol H + /min; p 〈 0.05), Group 2 (57.7 ± 8.3; p 〈 0.05) and Group 3 (60.6 ± 7.4, p 〈 0.05) than those from Group 4 (31.2 ± 3.6) or control subjects (31.3 ± 3.5). The intracellular pH for half-maximal activation, Hill coefficient and buffering power capacity was similar in all the groups. These data suggest that in vitro phenotypic abnormalities of long-term cultured fibroblasts from NIDDM patients with microalbuminuria and/or hypertension are likely to be, at least in part, independent of the degree of metabolic control in vivo and to be an intrinsic feature of these cells. [Diabetologia (1996) 39: 717–724]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418544
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  • 9
    Electronic Resource
    Electronic Resource
    Elevated sodium-lithium countertransport activity in erythrocytes is predictive of the development of microalbuminuria in IDDM (1997)
    Springer
    Diabetologia 40 (1997), S. 654-661 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; erythrocyte sodium-lithium countertransport activity ; hypertension.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pathogenetic mechanisms other than the quality of metabolic control may play a role in the development of diabetic nephropathy. Some cross-sectional studies have shown that elevated erythrocyte sodium-lithium countertransport (Na + /Li + CT) activity may be linked to incipient or overt nephropathy in insulin-dependent diabetic (IDDM) patients. The aim of the present work was to ascertain if high erythrocyte Na + /Li + CT activity anticipates the development of microalbuminuria in IDDM patients. Evaluation of this cation transport system was carried out in 159 normotensive, normoalbuminuric IDDM patients, who were divided into two groups: those with values above (Group A) and those with values below (Group B) the median level in the overall population (300 μmol/erythrocytes × h). A total of 79 patients in Group A and 80 in Group B underwent periodic examinations over a similar time period (5.2 years, range 3.3–7.4 years and 5.4 years, range 3.4–7.5 years, respectively). Median sodium-lithium countertransport activity was stable when evaluated after 2 and 4 years of follow-up. Only seven patients were excluded from the protocol because changes in their sodium-lithium countertransport activity placed them on the other side of the median value with respect to their baseline measurement. Thus, 152 patients completed the study (76 in Group A and 76 in Group B). Of the 76 patients in Group A, 17 developed persistent microalbuminuria (22.3 %). The number of patients in Group B showing persistent microalbuminuria was significantly lower (4 of 76; 5.2 %; p 〈 0.01). The sensitivity of erythrocyte Na + /Li + CT in predicting the development of microalbuminuria was 85 % and its specificity was 55 %. Seven patients of Group A and five of Group B developed arterial hypertension. Subjects in Group A had significantly higher mean HbA1 c values of twice yearly measurements than those in Group B (9.6 ± 1.7 vs 8.3 ± 1.7 %, p 〈 0.002, mean ± SD) despite similar daily insulin requirements. Systolic and diastolic blood pressure levels were also evaluated every 6 months and were significantly higher in the Group A than in the Group B patients, although on average within the normal range. The odds ratio for developing persistent microalbuminuria in IDDM with elevated baseline erythrocyte Na + /Li + CT activity after adjustment for gender and baseline albumin excretion rate, and mean 6 monthly plasma creatinine, HbA1 c and systolic and diastolic blood pressure levels was 4.2 (95 % confidence intervals 2.0–11.1). It was also found that the percentage of offspring having both parents with Na + /Li + CT activity above the median value was significantly higher in Group A than in Group B (Group A vs Group B: 35 vs 19 %; p 〈 0.01). On the contrary the percentage of offspring whose erythrocyte Na + /Li + CT was lower in both parents was lower in Group A than in Group B: 10 vs 38 %, p 〈 0.01). Parents of Group A offspring had arterial hypertension more frequently than those of Group B. These results indicate that erythrocyte Na + /Li + CT activity is a useful diagnostic tool in identifying normotensive, normoalbuminuric patients who may be predisposed to develop persistent microalbuminuria. This disorder in the cation transport system is associated with poor metabolic control, higher blood pressure, and male sex; it also appears to be, at least partly, genetically transmitted. [Diabetologia (1997) 40: 654–661]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050730
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  • 10
    Electronic Resource
    Electronic Resource
    Clustering of albumin excretion rate abnormalities in Caucasian patients with NIDDM (1997)
    Springer
    Diabetologia 40 (1997), S. 816-823 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Non-insulin-dependent diabetes mellitus ; micro-macroalbuminuria ; familial clustering ; sib pair analysis ; diabetic retinopathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Proteinuria and nephropathy have been found to cluster in families of non-insulin-dependent diabetic (NIDDM) Pima Indian, and in Caucasian insulin-dependent diabetic (IDDM) patients. No information is at present available for Caucasian NIDDM patients. The aim of the present study was to determine whether micro-macroalbuminuria (AER + ) is associated with albumin excretion rate abnormalities in diabetic and non-diabetic siblings of probands with NIDDM and AER + . We identified 169 Caucasian families with one NIDDM proband (the patient with longest known NIDDM duration) (101 families with only NIDDM siblings, 33 families with both NIDDM and non-NIDDM siblings and 35 families with only non-NIDDM siblings). Of the probands 56 had AER + [Prob-NIDDM-(AER + )], 78 had AER– [Prob-NIDDM-(AER–)], 74 siblings of Prob-NIDDM-(AER + ), and 113 siblings of Prob-NIDDM-(AER–) also had NIDDM. Data on albuminuria and retinopathy from multiple sibling pairs when the size of the sibship was more than two was adjusted according to a weighting factor. The odds ratio for AER + , in siblings of Prob-NIDDM-(AER + ) adjusted for age, hypertension, glycated haemoglobin A1 c and other confounding variables was 3.94 (95 % confidence intervals: 1.93–9.01) as compared to siblings of Prob-NIDDM-(AER–). The 74 siblings of Prob-NIDDM-(AER + ) had higher prevalence of proliferative retinopathy than siblings of Prob-NIDDM-(AER–) (14 vs 2 %; p 〈 0.01). We also identified 66 non-diabetic siblings of 41 NIDDM probands with AER + and 36 non-diabetic siblings of 27 NIDDM probands with AER–. Albumin excretion was two times higher, although still within the normal range, in the non-diabetic siblings of Prob-NIDDM-(AER + ) than in siblings of Prob-NIDDM-(AER–) [median = 13.5 (range 0.5–148) vs 6.6 (range 1–17) μg/min (p 〈 0.05)]. In conclusion higher rates of albumin excretion aggregate in Caucasian families with NIDDM. Proliferative retinopathy is more frequently observed in families showing a clustering of AER + and NIDDM. These findings suggest that familial factors play a role in the pathogenesis of renal and retinal complications in NIDDM. [Diabetologia (1997) 40: 816–823]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050754
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