NaHCO₃ loading causes increased arterial pressure and kidney damage in rats with chronic kidney disease

Sodium bicarbonate (NaHCO₃) is commonly utilized as a therapeutic to treat metabolic acidosis in people with chronic kidney disease (CKD). While increased dietary sodium chloride (NaCl) is known to promote volume retention and increase blood pressure, the effects of NaHCO₃ loading on blood pressure and volume retention in CKD remain unclear. In the present study, we compared the effects of NaCl and NaHCO₃ loading on volume retention, blood pressure, and kidney injury in both 2/3 and 5/6 nephrectomy remnant kidney rats, a well-established rodent model of CKD. We tested the hypothesis that NaCl loading promotes greater volume retention and increases in blood pressure than equimolar NaHCO₃. Blood pressure was measured 24 h daily using radio telemetry. NaCl and NaHCO₃ were administered in drinking water ad libitum or infused via indwelling catheters. Rats were housed in metabolic cages to determine volume retention. Our data indicate that both NaHCO₃ and NaCl promote hypertension and volume retention in remnant kidney rats, with salt-sensitivity increasing with greater renal mass reduction. Importantly, while NaHCO₃ intake was less pro-hypertensive than equimolar NaCl intake, NaHCO₃ was not benign. NaHCO₃ loading significantly elevated blood pressure and promoted volume retention in rats with CKD when compared with control rats receiving tap water. Our findings provide important insight into the effects of sodium loading with NaHCO₃ in CKD and indicate that NaHCO₃ loading in patients with CKD is unlikely to be benign.