Genetic polymorphism as described with angiotensin-converting enzyme gene has been proposed as a putative mediator of diabetic nephropathy. We substantiate the hypothesis that genetic variants of the ACE have significant impacts on diabetic nephropathy. To assess the possible association between the three ACE polymorphic variants and DN in an ethnically homogeneous type 2 diabetic population from Kutch region. A 287-bp insertion/deletion polymorphism in intron 16 of the ACE gene was examined by polymerase chain reaction using a case-control approach conducted with 309 unrelated type 2 diabetic patients of Kutch origin (159 Ahir and 150 Rabari, with [10 years duration of T2DM). Of the patients, 143 had nephropathy {AER[30 mg/day (Ahir, n:73 and Rabari, n:70)} and were considered as cases; all others {n:166 (86 Ahir and 80 Rabari)} were normoalbuminuric (AER\30 mg/day) and were treated as controls. Suitable descriptive statistics was used for different variables. Genotype frequencies in all groups were all in accordance with the Hardy-Weinberg equilibrium. Genotypic distribution was significantly different between cases and controls (Ahir: x 2 :8.87, 2 d.f. p = 0.0118; Rabari: x 2 :11.01, 2 d.f. p = 0.0041). Multivariate logistic regression analysis revealed that DD genotype was a significant and strongest independent predictor of microalbuminuria (Ahir: p = 0.0362, OR = 2.65, 95 % CI 1.89-6.36; Rabari: p = 0.024, OR = 2.81, 95 % CI 1.9-6.65). However, it did not independently change the odds of having macroalbuminuria versus microalbuminuria. Analysis of the association under various genetic models revealed that ACE I/D polymorphic variant contribute to DN susceptibility under recessive mode only. Genetic variation at the ACE locus as D/D variant in intron 16, contribute to an increased risk of nephropathy in T2DM patients but not extent of DN severity, and thus this polymorphism might be considered as genetic risk factors for DN among patients with type 2 diabetes.
Introduction: Obesity has become a major health problem worldwide due to high comorbidity and an increasing prevalence. It is the greatest risk factor for obstructive sleep apnea (OSA). Owing to lack of data on the association of obesity and OSA within the country, the present study was designed to evaluate the pattern of sleep disordered breathing (SDB) among obese Indian subjects. Material and Method:The study was prospectively carried out in Sleep Laboratory of LRS Institute of Tuberculosis and Respiratory Diseases, New Delhi. 30 obese [having body mass index BMI > 27.5 kg/m 2 ] and 10 non-obese (having BMI < 27.5 kg/m 2 ) subjects were consecutively enrolled into the study (obesity) and the control (non-obese) groups respectively as per the World Health Organization (WHO) Criteria of Obesity for Asians. Detailed clinical history including that of sleep was taken, a physical examination along with anthropometric measurements like neck circumference (NC), waist circumference (WC) and hip circumference (HC) was done and laboratory investigations were performed in all subjects, who thereafter, underwent an overnight polysomnography (PSG) on Compumedics E-Series sleep software. Sleep was staged as per Rechtshaffen and Kales (R & K) rules and SDB evaluated as per standard criteria. Data was subjected to statistical analysis. Results: There were 16 obese, 8 severely obese & 6 morbidly obese subjects. Respective characteristics of the obesity and the control group subjects showed a mean age of 47.73 and 40.90 years, a male-female ratio of 19: 11 and 7:3, and a mean BMI of 33.46 and 23.73 kg/m 2 . Mean Apnoea-Hypopnoea Index (AHI) was significantly higher among the subjects of the obesity group as compared to the controls. Similarly, mean AHI was significantly higher among the obese males, those having NC between 35 to < 45 cms, symptomatics, those having 4 to 6 number of symptoms, and those having co-morbidities as compared to the respective non-obese counterparts. Mean value of sleep latency was higher, while that of Total Sleep Time (TST) & sleep efficiency lower in the obesity than the control group. Oxygen De-saturation Index (ODI) and indices of arousal, Periodic Limb Movement (PLM) in Sleep (PLMS) & PLM with arousals were significantly higher in the obesity as compared to the control group respectively. No significant differences were noticed between the groups with regard to sleep stage percentages.
Chronic kidney disease (CKD) has become a worldwide community health problem in people with type, 2 diabetes obesity and long-term hyperglycemia may cause renal vascular complications. The aim of this study was to see if there was any connection between BMI, haemoglobin and CKD in DM patients. This case study was conducted in department of Medicine, Era′s Lucknow Medical College and Hospital, ERA University, Lucknow. The analysis was performed for 18 months.When compared to CKD patients, the non-CKD group's mean BMI was marginally higher. Older age, female sex, hypertension, and diet plant were all linked to the involvement of CKD in multivariable study. There was same connection between CKD and haemoglobin in this study. The negative relationship between BMI, Hb and CKD could indicate reverse causality. While a diabetic patient's BMI does not cause them to develop CKD, it is possible that CKD causes them to have a lower BMI and Hb level.
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