Incidental chronic kidney disease in metabolic syndrome

The prevalence of metabolic syndrome (MetS) and chronic kidney disease (CKD) are increasing worldwide. Patients with these conditions are strongly prone to the development of and death from cardiovascular disease. Emerging data suggest that the process of development of incident CKD in patients with MetS is independent of that for diabetes and hypertension. However, the mechanism for the emergence of CKD remains elusive. Renal histopathologic changes have been recognized in MetS, including tubular atrophy, interstitial fibrosis, and arterial sclerosis, suggesting microvascular disease. Moreover, glomerular lesions in patients with MetS often have greater global and segmental glomerulosclerosis. Studies have shown several pathways linking insulin resistance and/or hyperinsulinemia with incidental CKD. First, insulin resistance with compensatory hyperinsulinemia promotes inappropriate activation of the renin- angiotensin system which induces aldosterone excess and glomerular hypertension. Second, insulin resistance increases oxidative stress which has also been implicated in the renal progression of glycoxidation and lipid peroxidation Third, insulin resistance enhances mesangial cell proliferation and extracellular matrix protein expansion via the stimulation of endothelin-1 and growth factors including transforming growth factor-b1 and insulin-like growth factor-1. Finally, insulin resistance downregulates the renal action of peroxisome proliferator activated receptors which elicit foam cell formation, renal lipotoxicity and endothelial dysfunction. Identification of MetS may help clinicians to be aware of its components so that therapeutic intervention on components of MetS can be initiated to avoid incident CKD and further cardiovascular disease.