Glomerular hyperfiltration in obesity represents a maladaptive hemodynamic response involving increased renal blood flow, elevated filtration pressure, sodium retention, activation of the renin-angiotensin-aldosterone system, and adipose tissue-derived inflammatory and hormonal signals, such as leptin and TNF-α, which promote endothelial dysfunction and renal injury49. The gene discussed is LEP; the disease is endothelial dysfunction.