Increased intrarenal post‐glomerular blood flow is a key condition for the development of calcineurin inhibitor‐induced renal tubular acidosis in kidney transplant recipients

Background: Hyperchloremic metabolic acidosis (HCMA) from renal tubular acidosis (RTA) is common in kidney transplant (KT) recipients. Calcineurin inhibitors (CNIs) are a potential cause of RTA, and whether HCMA is a determinant of poor graft prognosis is controversial. Methods: The subjects were living‐donor KT recipients (LDKTRs, n = 47) and matched donors (n = 43). All cases of rejection, extrarenal causes, and respiratory disorders were excluded. HCMA was defined as having a [Na+]–[Cl−] value of ≤34 or starting alkalization. We determined the potential causes of HCMA in LDKTRs at 3 months (m) and 1 year (y) post‐KT. We examined renal hemodynamic parameters in 26 LDKTRs at 1 y post‐KT: namely, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF; GFR/RPF) and pre‐/post‐glomerular vascular resistance (pre‐/postVR). Results: The HCMA incidence in the 3‐m post‐KT LDKTR group was higher than that of the donors (51.0% vs. 6.9%, p