These mechanisms include volume expansion, drop in glomerular filtration rate, sympathetic activation, renin-angiotensin-aldosterone system activation, vasoconstriction, electrolyte imbalance, and inflammatory and humoral factors.[13] Thus, the relationship between hydronephrosis and cardiac function in our study may be a “subclinical” form of type 3 or type 4 CRS because none of the patients had clinical symptoms of heart failure and all had normal renal function. This evidence concerns the gene REN and congenital rubella syndrome.