Inflammation in diabetic kidney disease.

Diabetes mellitus entails significant health problems worldwide. The pathogenesis of diabetes is multifactorial, resulting from interactions of both genetic and environmental factors that trigger a complex network of pathophysiological events, with metabolic and hemodynamic alterations. In this context, inflammation has emerged as a key pathophysiology mechanism.

Diabetic kidney disease: from physiology to therapeutics.

Diabetic kidney disease (DKD) defines the functional, structural and clinical abnormalities of the kidneys that are caused by diabetes. This complication has become the single most frequent cause of end-stage renal disease. The pathophysiology of DKD comprises the interaction of both genetic and environmental determinants that trigger a complex network of pathophysiological events, which leads to the damage of the glomerular filtration barrier, a highly specialized structure formed by the fenestrated endothelium, the glomerular basement membrane and the epithelial podocytes, that permits a highly selective ultrafiltration of the blood plasma.

Beneficial effects of selective vitamin D receptor activation by paricalcitol in chronic kidney disease.

In chronic kidney disease patients, active vitamin D level progressively declines in the course of the disease. This phenomenon is accompanied by elevation of parathyroid hormone, resulting in secondary hyperparathyroidism (SHPT), increased phosphorus levels, and hypocalcemia. All these disorders are associated with high rates of cardiovascular morbidity and mortality in these patients.