In other words, it is not fully understood whether it is caused by excessive sensitivity to drugs at therapeutic serum concentrations or by elevated serum concentrations secondary to renal failure [1]. Data on serial measurement of serum concentrations of AV nodal blocking agents and additional agents such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers during the development of BRASH syndrome are limited. This evidence concerns the gene ACE and kidney failure.