ABSTRACT
Hyperglycemia has been causally linked to vascular and glomerular dysfunction by a variety of biochemical mechanisms, including a glucose-dependent abnormality in nitric oxide [NO] production and action. Nitric oxide is a candidate for mediating hyper filtration and the increased vascular permeability induced by diabetes. Serum nitric oxide concentrations were assessed in 30 children and young adolescent with type 1 diabetes, 15 with and 15 without microalbuminuria compared with a well-balanced group of healthy control subjects. In all subjects, glomerular filtration rate [GFR] was determined using Cockcroft formula. Our study showed that serum nitric oxide values were significantly higher in microalbuminuria diabetic patients than in the other 2 groups [group I versus group II; 46.7 + 7.9 versus. 32.2 +/- 6.1 [micro]mol/l, P < 0.05; while group I versus group III, 46.7 +/- 7.9 versus 25.4 +/- 4.2 [micro]mol/11 P < 0.02]. GFR was significantly and positively related to albumin excretion rate [AER] levels [r[2] = 0.75, P < 0.0001], whereas Serum nitric oxide was independently associated with both AER and GFR values [B = 2.086, P < 0.05, B = 1.273, P < 0.0085, respectively]. These findings suggest a strong link between circulating nitric oxide, glomerular hyper filtration, and microalbuminuria in type 1 diabetic patients with early nephropathy. Mean HbA[1c] serum concentration was significantly higher in microalbuminuric than in normoalbuminuric diabetic subjects [P < 0.05] and was independently associated with AER values, suggesting a role for chronic hyperglycemia in the genesis of diabetic nephropathy. HbA[1c] serum concentration was significantly and positively related to serum nitric oxide [r[2] = 0.45, P = 0.0063] and GFR values [r[2] = 0.57, P = 0.0011], suggesting that chronic hyperglycemia may act through a mechanism that involves increased nitric oxide generation and/or action
Conclusion: we suggest that in type 1 diabetic patients with early nephropathy, chronic hyperglycemia is associated with an increased nitric oxide biosynthesis and action that contributes to generating glomerubr hyper filtration and persistent microalbuminuria
ABSTRACT
In order to evaluate the role of vascular endothelial growth factor [VEGF] in the pathology of CHF, this study was conducted on 96 subjects [57 males and 39 females]. Sixty-eight of them had congestive heart failure of various etiologies [40 males and 28 females with an age ranged from 18 to 76 years with a mean +/- SD of 47.83 +/- 16.2] together with 28 apparently healthy individuals [17 males and 11 females with ages ranged from 18 to 65 years with a mean +/- SD of 33.2 +/- 11] as the control group. The patients were classified into five groups according to the etiology of congestive heart failure. All groups were subjected to history taking and clinical examination with a special emphasis on the symptoms and signs suggestive of CHF and manifestations of underlying, cause laboratory investigations [CBC, lipid profile, fasting and two-hour postprandial blood sugar, renal function tests, serum transaminases, ESR, antistreptolysin O titer, C-reactive protein and thyroid function tests], ECG, chest X-ray, echocardiography and abdominal sonography. Vascular endothelial growth factor [VEGF] serum level was determined by a commercially available ELISA test