M1887 The Gain in Quality-Adjusted Life Years By Switching to Esomeprazole in Those with Persistent GERD Symptoms in Primary Care: EncomPASS - a Cluster-Randomized Trial

Abstract

INTRODUCTION: An increasing number of case reports have identified acute kidney injury (AKI) secondary to acute interstitial nephritis (AIN) provoked by Proton Pump Inhibitor (PPI) therapy. The present collaborative study identifies experience from a major UK renal unit. AIMS & METHODS: All cases of biopsy-proven AIN between Jan 1st 2007 and October 1st 2008 presenting to the regional renal centre (serving a population of 1.1 million), were identified. The notes of all patients (pts) with a diagnosis of AIN and a history of PPI were analysed. Pre-PPI treatment, diagnosis and most recent plasma creatinine and estimated glomerular filtration rate (eGFR) were obtained. Pts were deemed likely to have PPI-associated AKI if a deterioration in kidney function was identified after starting PPI therapy in the absence of a history of any other medications associated with AIN and other renal or systemic causes. RESULTS: 210 kidney biopsy reports were analysed of which 27 reported AIN due to a multitude of causes. Of these, 6 cases of AIN were found to be strongly associated with PPI therapy. PPI's were the most common drug class associated with AIN. Male : Female 1 : 5. The median age at diagnosis was 66 yrs (range 60-86). All pts presented with nonspecific malaise and tiredness. 5 cases were due to omeprazole & 1 pt esomeprazole. Mean ± SD duration of PPI therapy was 7.7 ± 5.6 months, (range 5-18). Mean ± SD pre-PPI creatinine was 73 ± 30 μmol/L (range 45-103); eGFR 69 ± 23 ml/min/1.73m2 (range 4590). At diagnosis, mean ± SD creatinine was 269 ± 217 μmol/L (range 141-697) and eGFR 24 ± 16 ml/min/1.73m2 (range 5-52), representing a mean decline in eGFR of 65%. The PPI was immediately stopped in all pts. 1 pt required temporary renal replacement therapy. 5 pts were treated with steroids. The mean ± SD most recent creatinine post diagnosis was 129.5 ± 36.5 μmol/L (range 94-196) and eGFR 41 ± 11 ml/min/1.73m2 (range=23-52). Although kidney function improved following cessation of PPI and/or treatment with steroids, there was a net decline in kidney function from pre-PPI exposure levels. CONCLUSION: PPI related AIN is an important iatrogenic cause of potentially reversible AKI and is likely to be significantly underestimated. Kidney function should be assessed in patients receiving PPI therapy presenting with non specific malaise or tiredness. AIN should be considered in patients with deteriorating kidney function when receiving PPI therapy. Prompt identification of PPI induced AIN is important as our study suggests (in line with the established literature) that cessation of therapy can at least partially reverse decline in renal function inmost patients.