Congenital obstructive nephropathy is the primary cause of chronic renal failure in children. Disorders of mitochondrial energy metabolism may be a primary factor underlying tubular cell apoptosis in hydronephrosis. The beta-F1-ATPase (ATP5B) and electron transfer flavoprotein beta subunit (ETFB) metabolic markers are involved in mitochondrial energy metabolism in other diseases. ATP5B and ETFB were associated with worsening renal injury. ATP5B and ETFB may be novel markers in hydronephrosis.