Relationship between exercise and urinary liver-type fatty acid-binding protein in middle-aged and older individuals

A decline in exercise capacity, including aerobic fitness and muscular strength, has been associated with various poor health-related outcomes, including cardiovascular disease and all-cause mortality [۱, ۲]. Exercise capacity is also an independent predictor of the development and progression of chronic kidney disease (CKD) [۳, ۴]. Exercise capacity of patients with CKD is generally lower than that of healthy population norms or that of healthy control groups [۵]. Thus, it is apparent that a decline in the exercise capacity can induce various renal outcomes; however, the pathophysiological mechanism that links the decline in exercise capacity to the development of renal dysfunction remains unclear. Age-related renal changes are initially characterized by a loss of peritubular capillaries due to intrarenal arterial changes, such as arteriolosclerosis and intimal and medial hypertrophy [۶, ۷]. A reduction in peritubular capillary blood flow leads to tubular hypoperfusion and hypoxia and eventually to tubular atrophy and tubulointerstitial fibrosis, which is the main cause of renal dysfunction induced with aging [۸, ۹]. A traditional viewpoint is that the progression of renal dysfunction is associated with the degree of tubulointerstitial, rather than glomerular damage [۱۰]. Therefore, renal tubular evaluations may be more important than glomerular evaluations, such as estimated glomerular filtration rate (eGFR) and albuminuria, for identifying the development of renal dysfunction with aging.