Nonalcoholic fatty liver disease (NAFLD), which is strongly and bidirectionally asso
ciated with metabolic syndrome and its individual features, encompasses a spectrum of
 liver diseases ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis

 (NASH) and carries the risk of developing cirrhosis and hepatocellular carcinoma in a pro
portion of cases [1].The latter entity exhibits glomerular hypertrophy, focal dilatation of
 the afferent arteriole and glomerular perihilar capillaries, and perihilar segmental sclerosis;
 mildly increased mesangial matrix and the thickening of glomerular basement membranes
 (i.e., diabetes-like features), interstitial fibrosis, foot process effacement, and hypertrophy
 of podocyte cell bodies may also occur [20].The pathogenesis of NAFLD involves
 a profound perturbation of metabolic homeostasis; a reprogramming of the interplay be
tween hepatocytes, sinusoidal endothelial cells, and hepatic stellate cells; a rearrangement  of the liver immune landscape; and a remodeling of the hepatic microvasculature and
 stromal microenvironment [7].Interestingly, the metabolic pathways, cellular phenomena, and molecular
 mediators involved in NAFLD and CKD are similar to each other and include insulin
 resistance, ectopic fat deposition, and the activation of the insulin/PI3K/Akt/mTOR and
 transforming growth factor-pathways [20,23].To date, however, there are no systematic studies evaluating kidney
 histology among patients with NAFLD and, usually, in such cases a reference is rather
 made to the functional classification of CKD stages based on the estimated glomerular
 f
 iltration rate (eGFR) and proteinuria, both in clinical practice and in the research arena [11].New insights into liver cell-cell interactions
 will define the molecular pathways that culminate in hepatic fibrogenesis and identify

 novel targets to interrupt disease progression to adverse clinical outcomes [10].These severe liver-related outcomes usually result from the progression
 of NAFLD diagnosed as NASH, although a subgroup of NAFLD patients diagnosed as
 NAFLmayalsodevelop liver fibrosis, indicating a propensity for progression [1].