Our data showing that IGF1R activation is reduced in peripheral nerves from mice overexpressing IGFBP5, and that mice lacking IGF1R signaling in motoneurons show similar signs of motor neuropathy as IGFBP5-overexpressing mice strongly suggest that the up-regulation of IGFBP5 is also responsible for microangiopathy, heart failure, kidney failure, reduced bone mass and other pathological findings associated with diabetes. This evidence concerns the gene IGFBP5 and kidney failure.