Abstract Background and Aims Hyperkalemia (HK) (serum K>5.0 mEq/L) is a chronic condition in patients with chronic kidney disease (CKD) associated with high morbidity and mortality, and it is a frequent reasons for renin angiotensin aldosterone inhibition (RAASi) discontinuation. Patiromer is a non-absorbed, sodium-free, K+ binder that has been shown to reduce serum K+ in patients with HK, and thereby enable RAASi therapy, which is supported by randomized trial evidence. The description of patiromer utilization in patients with moderate to advanced CKD in the real-world setting in Europe is lacking. The objective of this analysis was to describe predictors of patiromer initiation and time to discontinuation among CKD patients using contemporary (April 2018-October 2020) data from German participants in CKD Outcomes and Practice Patterns Study (CKDopps). Method We identified 136 patiromer users (116 with matching K measurement) during the observation period. Patients with eGFR <60ml/min/1.73m2 and a serum potassium ≥4mEq/L who never initiated patiromer during the follow up were used as a comparison. We used the most recent lab and drug use information available within the 6-month period prior to baseline, which was defined as either first use of patiromer, April 1, 2018, or entry into the PDOPPS study. The median time between the most recent K+ measurement and baseline was 45 days for non-patiromer users and 4 days for patiromer users. Logistic regression models were used to test associations between patient factors and whether the patient was in the patiromer initiation group or the comparison group. Time on patiromer was estimated using a Kaplan-Meier curve, censoring for death, dialysis, transplantation, or loss of follow-up. Results Patiromer was prescribed to ≥2 patients in 11 clinics, one patient in 19 clinics, and zero patients in 57 clinics. Patients prescribed patiromer had lower eGFR (23.2 [15.8, 28.6] vs 36.9 [27.7, 46.3]ml/min) and higher serum K levels (5.6 [5.4, 6.1] vs 4.6 [4.3, 5.0]ml/min). There were no major differences according to patiromer use in other demographic, clinical, and biochemical characteristics. Despite the differences in serum K, use of RAAS inhibitors was similar in patiromer users (83%) versus non-users (80%). Thirty three percent of patiromer users were prescribed polystyrene sulfonate (SPS) before patiromer initiation. In a multiple logistic regression models (including serum K, CKD stage, gender, age, prescription of RAASi, diabetes, coronary artery disease, heart failure), patiromer use was strongly associated more advanced CKD stage (independently of high serum K), with odds ratios of initiation >3 for CKD stage 4 or 5 versus CKD stage 3. Among new users, 90% of patients had active prescription at 30 days and about one-half had active prescription at one year (Figure). Conclusion The main predictors of Patiromer initiation were advanced CKD stage and hyperkalemia. Treatment decisions did not appear to be based on other patient or clinical characteristics. Patiromer was often prescribed to patients already receiving alternative HK treatment (SPS), suggesting use for chronic hyperkalemia rather than response to acute event. Further analysis with a larger population and measurements of K+ before and after patiromer initiation may improve the understanding of its pharmacoutilization in moderate to advanced CKD.