Mechanistically, on the one hand, excessive accumulation of RSF can elevate the intra-abdominal pressure, compress the low-pressure renal venous structures and leading to renal volume expansion, increase in renal interstitial pressure, and activation of the renin-angiotensin-aldosterone system (RAAS) (29), which activation may contribute to IR and CKD (30, 31). The gene discussed is REN; the disease is chronic kidney disease.