Metabolic syndrome and chronic kidney disease.

TLDR: Despite the strong association of MetS with CKD, a causal relationship has not been proven and more studies are needed to precisely elucidate the mechanisms that might lead upstream factors such as insulin resistance, hypertension, dyslipidemia and inflammation to cause renal fibrosis.

Abstract: Purpose of review The association of the metabolic syndrome (MetS) with cardiovascular risk, mortality, type 2 diabetes mellitus, stroke, nonfatty liver disease and gout is well known. However, the association of the MetS with chronic kidney disease (CKD) is now emerging. This review discusses the epidemiology, pathology and potential mechanisms for the relationship of MetS with CKD. Recent findings Studies show that patients with MetS have a 2.5-fold higher risk of developing CKD. The risk of microalbuminuria is also increased two-fold in the MetS. Renal dysfunction becomes apparent long before the appearance of hypertension or diabetes in MetS. Compared with healthy controls, patients with MetS have increased microvascular disease-tubular atrophy, interstitial fibrosis, arterial sclerosis and global and segmental sclerosis. Studies suggest that the renal fibrosis seen in MetS might be caused by a constellation of insulin resistance, hypertension, dyslipidemias and inflammation, and result in a heightened expression of adipocytokines, angiotensin and inflammatory cytokines such as interleukin-6 and tumour necrosis factor-alpha. Summary Despite the strong association of MetS with CKD, a causal relationship has not been proven. More studies are needed to precisely elucidate the mechanisms that might lead upstream factors such as insulin resistance, hypertension, dyslipidemia and inflammation to cause renal fibrosis.