The liver-kidney axis: Is serum leptin a potential link in non-alcoholic fatty liver disease-associated chronic kidney disease?

The prevalence of non-alcoholic fatty liver disease (NAFLD) is ∼25–30 % [1], [2] and chronic kidney disease (CKD) ∼10–15 % in the general adult population [3], [4]. NAFLD occurs either as non-alcoholic fatty liver (NAFL, simple steatosis) or non-alcoholic steatohepatitis (NASH). NASH may cause severe conditions such as liver cirrhosis or hepatocellular carcinoma [1], [2], [3]. The rate of progression to cirrhosis is not clear, but some studies showed rates of up to 15 % of the patients.

Patients with NAFLD exhibit multiple risk factors for CKD. Both CKD and NAFLD include features of the metabolic syndrome (MetS) [4], [5], [6]. The combination of hyperglycemia, systemic/hepatic insulin resistance (IR), arterial hypertension, obesity and atherogenic dyslipidemia is regarded as metabolic syndrome [7], [8]. Obesity is closely associated with diabetes and hypertension. Therefore, it is a risk factor also for CKD [9]. Leptin is secreted by adipocytes and suppresses food consumption. Leptin triggers increased energy usage. It is one of the key cytokines controlling energy metabolism [10], [11]. During the end stage of renal dysfunction, the removal of leptin from the circulation decreases due to functional changes in the renal tubules and structural changes in the glomerular basement membrane, and therefore hyperleptinemia is frequently observed in patients with CKD [12], [13], [14]. Hepatic stellate cells (HCS’s) produce proteins which induce fibrotic changes in the composition of the extracellular matrix. Activated HCS’s also produce leptin. Some authors have postulated that leptin may have a relevance in liver fibrogenesis [15]. But there are conflicting results in some studies about the role of leptin in the NAFLD progression. It has been shown that there is not any statistically significant correlation between high serum leptin levels and NASH [16]. In recent studies, NAFLD is reported to be a risk factor for CKD [2], [7]. Increased incidence of CKD in NAFLD patients has been shown in both retrospective and prospective cohort studies [17], [18]. However, the association of leptin with CKD in NAFLD patients has not yet been elucidated.

In the literature, our study is the first study in which the association and causal link between leptin and CKD in NAFLD patients has been investigated.

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