ABSTRACT
INTRODUCTION: Endocan and endoglin have been shown to play a role in angiogenesis. Aberrant excessive angiogenesis is a main factor in the development of diabetic nephropathy. In this study we evaluated endocan and endoglin levels in diabetes patients with and without albuminuria and compared them with healthy subjects. Therefore we aimed at gaining a better understanding of the role of angiogenesis in diabetic nephropathy and to assess the predictive role of endocan and endoglin as markers of diabetic nephropathy progression. MATERIAL AND METHODS: Ninety-six type 2 diabetes patients were classified according to their 24-hour urinary albumin excretion rate. Forty type 2 diabetes patients with normoalbuminuria (urinary albumin excretion < 30 mg/day), 56 type 2 diabetes patients with diabetic nephropathy (with a urinary albumin excretion ≥ 30 mg/day) and 35 healthy non-diabetic control subjects were included. Their anthropometric features, arterial blood pressures, fasting glucose, glycated hemoglobin, urea, creatinine, lipids, endocan and endoglin levels were measured and compared to each other. RESULTS: Endocan and endoglin levels of diabetics patients were higher than those of the controls. In comparison of endocan and endoglin levels of diabetic nephropathy patients with controls, p-values were < 0.001 and 0.002 respectively. In comparison of normoalbuminuric diabetic patients with controls, p-values were 0.001 and 0.017 respectively. Endocan levels of diabetic nephropathy cases were higher than those of normoalbuminuric patients (p = 0.011) but there was no statistically significant difference in endoglin levels between them (p = 0.822). CONCLUSIONS: Endocan might be a more reliable marker of diabetic nephropathy development than endoglin.
ABSTRACT
BACKGROUND: Osteoprotegerin (OPG), which was recently identified as a vascular marker, is increased in patients with diabetes mellitus (DM). This study evaluated the frequency of the OPG gene single nucleotide A163G polymorphism and its association with diabetic microvascular and macrovascular complications. METHODS: The A163G polymorphism of the OPG gene was assessed in the peripheral blood of 116 patients with type 2 DM and 107 healthy subjects by polymerase chain reaction and restriction fragment length polymorphism. Microvascular and macrovascular complications were evaluated in diabetic patients. RESULTS: Statistical analysis showed no significant difference in distribution of the OPG A163G polymorphism in the diabetic and control groups. Similarly, this polymorphism was not associated with microvascular or macrovascular complications. CONCLUSIONS: This OPG polymorphism does not play a role in the development of microvascular and macrovascular complications in patients with DM.
