Chronic use of proton pump inhibitors (PPIs) in patients with chronic kidney disease (CKD) stages G3a to G4 may hasten the progression of kidney function decline, according to a new study presented at the American Society of Nephrology’s Kidney Week 2019 conference in Washington, DC.

PPIs inhibit ATPase in the stomach, which is present in other organs as well, including the kidneys. It has been thought that PPIs may have damaging effects on the course of CKD, potentially leading to metabolic acidosis (MA), which can accelerate kidney disease.

For the study, the researchers examined data of patients from the VA Informatics and Computing Infrastructure national database system. They included patients with stage 3 to 4 CKD, defined as eGFR <60 ml/min 1.73 m2 who had been receiving care for at least 5 years. Patients on dialysis, who transitioned to renal transplant, or who died were excluded from the study. 

Overall, 1406 patients were eligible in the PPI cohort with a median of 4.7 years follow-up and 573 patients were included in the no-PPI cohort with a median 4.2 years follow-up.

Compared with the no-PPI cohort, patients using PPIs chronically had a significantly increased risk of CKD progression and dialysis (aHR, 1.43; 95% CI, 1.17 to 1.74; and aHR, 1.69; 95% CI, 1.03 to 2.77, respectively), according to the study. Additionally, patients on PPIs also had a higher risk of MA (aHR, 1.83; 95% CI, 0.88 to 3.82) and all-cause mortality (aHR, 1.25; 95% CI, 0.96 to 1.64); however, these differences were not statistically significant.

The researchers concluded that the findings indicate that chronic PPI use can accelerate the progression of kidney disease in patients with CKD and that chronic PPI use should be discouraged in this population.


REFERENCE 

Giusti SG, Lin Y, Liu S, et al. The effect of proton pump inhibitor use on the development of metabolic acidosis and decline in kidney function in patients with CKD stage G3a to G4. Presented at the American Society of Nephrology Kidney Week 2019 conference held November 5-10 in Washington DC. Abstract TH-PO452.