These metabolic abnormalities may lead to the several clinical alterations often observed in these patients, such as muscle weakness and myopathy, loss of body protein and cachexia, insulin resistance and glucose intolerance, plasma lipid abnormalities, anemia refractory to erythropoietin treatment, cardiomyopathy, and intradialytic symptoms [44,45], thus may explain the higher risk these patients are found for contrast-induced AKI, as was evident by enhanced urinary NGAL excretion. The gene discussed is LCN2; the disease is anemia (phenotype).