The chapter contains a critical review of the current literature pertaining to the consequences of childhood and adolescent obesity/metabolic syndrome on the urogenital system, with a particular focus on microalbuminuria, renal disease, urolithiasis and lower urinary tract symptoms. The clinical implications of the current evidence with regard to the relationship between early obesity/ metabolic syndrome and the above-mentioned conditions are discussed.
© 2015 S. Karger AG, Basel
Renal DiseaseObesity and metabolic syndrome (MS) have been associated with renal damage in adults [1]. Obesity directly favors renal damage through several mechanisms [1] ( fig. 1). The obesity-related activation of the renin-angiotensin-aldosterone system is one of the most extensively studied mechanisms explaining renal injury driven by obesity [1]. Adipocytes possess a renin-angiotensin system and produce angiotensin II, thus stimulating the production of aldosterone [1]. Moreover, adipose tissue also secretes angiotensin-independent mineralocorticoid-releasing factors [1]. Thus, obesity is associated with a state of hyperaldosteronism leading to plasma expansion, glomerular hyperfiltration and damage and proteinuria, which often occurs in parallel with a state of pre-hypertension [1]. Aldosterone has also been shown to have direct negative glomerular effects in animal models, independent of blood pressure and plasma expansion [1].An obesity-associated decrease in adiponectin levels is another mechanism of renal damage because of the resultant reduced AMP-activated protein kinase in glomerular