Considering that increased urinary L-FABP is induced by decreased renal microvascular blood flow [20] and that renal hypoxia was observed in the SDT fatty rats with DKD (unpublished data), urinary L-FABP might be useful for the detection of abnormalities in renal hemodynamics aggravated by sarcopenia in addition to glomerular sclerosis leading to renal hypoxia derived from reduction of postglomerular blood flow. The gene discussed is FABP1; the disease is Glomerular sclerosis.