Whether the powerful high-blood pressure medicine rostafuroxin will be effective for a particular patient can be predicted from a set of gene variants.

Giuseppe Bianchi at the Prassis sigma-tau Research Institute in Milan, Italy, and his colleagues show how the drug works. It normalizes sodium transport in the kidneys that is disrupted by two specific mechanisms: a mutated version of a protein called adducin and a boost in levels of a hormone called ouabain. The researchers identify several gene variants heralding the faulty mechanisms and, in a second paper, show that patients with certain combinations of variants in five specific genes respond well to rostafuroxin, but not necessarily to two other blood-pressure medicines.

The key combination of variants is present in about 25% of patients.

Science Transl. Med. 2, 59ra86 (2010); Science Transl. Med. 2, 59ra87 (2010)