The RAAS is upregulated early in CKD1 and plasma renin, aldosterone and angiotensin I and II have been demonstrated to be increased in the circulation of cats with experimentally induced CKD.2 The RAAS is responsible for progressive renal injury not only by increasing glomerular pressure, but also by direct fibroproliferative effects via the induction of a variety of pro-inflammatory and profibrotic mediators.3 Chronic RAAS activation contributes to further loss of nephrons via mechanisms such as vasoconstriction, glomerular hypertension, proteinuria and fibrosis.4 Here, REN is linked to chronic kidney disease.