Abstract

Abstract Background and Aims Medications are a relatively common cause of acute kidney injury (AKI) in hospitalized patients and those in the intensive care unit (ICU). However, we know less about the influence of outpatient medication in patients admitted from the emergency room who already have a community-acquired AKI (CA-AKI) The purpose of this study is to analyze the impact of outpatient medication in a cohort of patients with CA-AKI admitted to the nephrology service of a tertiary level hospital. Method This is a single-center, observational, longitudinal, and retrospective study based on a cohort of patients with CA-AKI admitted to the Nephology Service of a third level hospital from January 2010 to December 2018. We analyzed the characteristics of outpatient medication in these patients and their clinical consequences during admission and follow-up after hospital discharge. Results A total of 639 patients were included in the final analyses. The mean age was 72.93 ± 13.38 years. 61.7% were men. Charlson comorbidity index (CCI) was 5.87 ± 2.4 points. The length of stay was 11.63 ± 10.14 days. In view of the Etiology of AKI, 72.1% had prerenal AKI and 27.9% non-prerenal. 436 patients had a history of previous chronic kidney disease (CKD) (68.23%). AKI KDIGO stages were: stage I, 105 cases (16.4%); stage II, 67 cases (10.5%); stage III 467 cases (63.1%). Hemodialysis (HD) was required in 114 patients (17.8%). 62 patients (9.7%) died during hospital stay. The average number of drugs ingested prior to admission was 8.45 ± 4.11 with no differences by sex. Percentage of patients taking drug groups: diuretics 62.8%; Angiotensin-converting enzyme inhibitors (ACEI) or Angiotensin receptor Blockers (ARB) 68.4%; combination of diuretics with ACEI/ARB 50.9%; Proton-pump inhibitors (PPI) 64.1%; Statins 43.5%; Beta blockers 30.7%; allopurinol 25.8%; Anticoagulants 20.2%; Metformin 13.8%; Spironolactone 13.5%. There was a significant positive correlation between age (r=0.189; p<0.001), baseline creatinine (r=0.258; p<0.001), and CCI (r=0.43; p<0.001), with the number of drugs. There was a significant inverse correlation between peak creatinine during admission (r=−0.170; p<0.001), length of stay (r=−0.109; p 0 0.006), and number of drugs. Patients with prerenal etiology consumed significantly more drugs than those with parenchymal or obstructive etiology (9.09 ± 3.9 vs 6.77 ± 4.1 and 6.92 ± 4.3 respectively) The number of drugs did not influence the AKI stage, mortality during admission, nor the need for dialysis or ICU admission. Patients taking non-potassium sparing diuretics had significantly lower sodium (137.1 ± 5.73 vs 135.75 ± 5.9 mmol/L; p=0.005) and chloride levels (99.94 ± 9 vs 98.42 ± 8.1 mmol/L; p=0.029) compared to those who did not take them. Patients taking potassium-sparing diuretics (6.49 ± 1.55 vs 5.14 ± 1.32 mmol/L; p<0.001), ACEI/ARBs (5.42 ± 1.44 vs 5.12 ± 1.4 mmol/L; p=0.014) or beta-blockers (5.51 ± 1.38 vs 5.24 ± 1.44 mmol/L; p=0.030) presented significantly hyperkalemia compared to those who did not take them. After performing a multivariate linear regression analysis, the only drugs that was associated with hyperkalemia were potassium-sparing diuretics (B 1.35; 95% CI 1.05-1.66; p<0.001). In the follow-up after discharge, patients taking 6 or fewer drugs had better survival than those taking 7 to 12, and the latter better than those taking more than 12 drugs (log rank test: Chi square 24.47; p<0.0001) In the univariate cox regression, the number of drugs significantly influenced survival (Exp(B) 1.069; 95% CI 1.043-1.096; p<0.0001). Conclusion The patients in our series with CA-AKI were polymedicated, mainly those of prerenal etiology, with a clear correlation with age, baseline creatinine and previous comorbidity and with a prominence of ACEIs/ARBs, diuretics, and PPIs. Certain drugs had a significant impact on ionic alterations, adding morbidity to the condition. The number of drugs ingested is a marker of survival after hospital discharge. It is necessary to optimize outpatient drug management to prevent the development of CA-AKI and their consequences.

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