#1786 Correlation of electrolyte disturbances in community-acquired acute kidney injury

Abstract

Abstract Background and Aims Acute renal injury can cause electrolyte disorders that increase patient morbidity and mortality. There are few data in the literature describing these alterations and the possible correlation between them in patients with community-acquired AKI (CA-AKI). The purpose of this study is to analyze the correlation between electrolyte disorders 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 incidence of changes in sodium, potassium, chloride, bicarbonate, calcium, and phosphorus in these patients and their correlations. 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 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 most frequent ionic alterations at a global level were low bicarbonate (78.3%), hyperkalemia (53.05%), hypocalcemia (49.6%) and hyponatremia (41.5%). When analyzing whether electrolyte alterations occurred simultaneously: 2.2% of cases did not present any, 6.3% only one, 18.2% two, 26.4% three, 26.1% four, 14.9% five and 5.9% six simultaneous alterations. There were no statistically significant differences between groups on mortality during admission. Higher mortality at discharge has been found in patients with a greater number of ionic alterations (p = 0.046). In our sample, positive correlations were found between sodium-bicarbonate (r = 0.184; p < 0.001), peak creatinine-potassium (r = 0.182; p < 0.001), potassium-chloride (r = 0.167 p < 0.001), sodium-chloride (r = 0.614; p < 0.001), phosphorus-peak creatinine (r = 0.394; p < 0.001), pH-bicarbonate (r = 0.747, p < 0.001) and phosphorus–PTH (r = 0.330; p < 0.001). Negative correlations were found between sodium–potassium (r = −0,123; p = 0.002), bicarbonate-potassium (r = −0.354; p < 0.001), potassium-pH (r = −0.390; p < 0.001), peak creatinine–chlorine (r = −0.013; p = 0.004), bicarbonate–chlorine (r = −0.236; p < 0.001), calcium–phosphorus (r = −0.174; p < 0.001), calcium–peak creatinine (r = −0.138; p = 0.001) and bicarbonate–peak creatinine (r = −0.274; p < 0.001). Conclusion In our series of patients with CA-AKI, many statistically significant correlations were found between altered electrolytes in acute renal failure. Most of these associations can be explained by the pathophysiology of acute kidney injury. However, it should be noted that not all cases have such a clear explanation. It is important to consider that all patients in our study had already developed acute renal failure upon admission. Therefore, these results should be interpreted with caution and confirmed through further evaluations. We suggest that additional research in this area is necessary to improve the management and prognosis of this condition.