Given that increased circulating aldosterone in cats with concurrent CKD and hypertension does not appear to be secondary to increased renin or hyperkalaemia, alternative explanatory mechanisms include primary adrenal‐dependent pathology, local MR activation, altered sensitivity to stimuli which dictate aldosterone release or reduced aldosterone degradation (Buranakarl et al., 2004). This evidence concerns the gene NR3C2 and Hyperkalemia.