IR contributes to normal nephron function by preventing loss of albumin during glomerular filtration, proximal tubular maintenance of glucose homeostasis, sodium reabsorption, and defense against urinary tract infection (52–55); these effects of insulin on the kidney are achieved by selective recruitment of IR substrate 1 (IRS-1) versus IRS-2 (56). The gene discussed is IRS2; the disease is urinary tract infection.