Introduction and Aims The neutrophil-to-lymphocyte (NLR) and platelet-to-lymphocyte (PLR) ratios have been identified as markers of inflammation and endothelial dysfunction in recent literature. Both are easily measured, reproducible and inexpensive, therefore cost-effective. To date, its usefulness as prognostic markers in community-acquired acute kidney injury (CA-AKI) has not been evaluated. The aim of this study was to analyze the usefulness of the NLR and PLR in terms of morbidity and mortality in community-acquired acute kidney injury. Method We established a cohort of 308 patients with community-acquired acute kidney injury (CA-AKI) admitted to the Nephrology service of a third level hospital from January 2010 to February 2015. NLR and PLR ratios were obtained with the levels of the first analysis performed at admission. Results We studied 308 patients with CA-AKI, 180 were men (58,4 %), mean age was 73.22 (±13,95). The mean length of stay was 12,25 days (±11,69). The etiology of CA-AKI was divided in prerenal 214 cases (69.5%); renal 71 cases (23.1%); obstructive 23 cases (7,5%). AKI KDIGO stages were stage I, 45 cases (14.6%); stage II, 34 cases (11%); stage III 229 cases (74.4%). Previous chronic kidney disease (CKD) was detected in 212 cases (68.8%). A total of 54 patients (17,15%) required hemodialysis and 38 patients died during admission (12.3%). Mean NLR was 9.14 ± 8,47 (95% IC 8,2-10,1). Mean PLR was 236,99 ± 228,41 (95% IC 211,38-262,6). NLR according to etiology was: prerenal 8,55±6,8; renal 9,37±9,8; obstructive 13,99±14,82 (significant differences of the latter group compared to the prerenal group). PLR according to etiology: prerenal 228,31±216,34; renal 236,15±233,77; obstructive 320,37±304,89 (non-significant differences). Within the group of prerenal origin, 79 cases were complicated by the development of acute tubular necrosis (ATN). These cases presented a higher NLR (NLR of ATN 10,7±10,28 vs NLR of pure prerenal 7,8±5,6; p=0,026). There were no significant differences between the PLR of the pure prerenal group and the group with ATN (225,95±262,54 vs 285,78±278,61). The NLR showed a significant correlation with the peak creatinine (r= 0,186; p = 0,001) and with the serum albumin (r= -0,237; p < 0,001). The PLR also showed correlation with the peak creatinine (r= 0,134, p = 0,018) and the serum albumin (r = 0,165, p= 0,07).The NLR, but not the PLR, was associated with the length of hospital stay (multiple linear regression analysis). Through a multivariate binary logistic regression analysis, the variables that were independently associated with mortality during admission were the Liaño individual severity index and the NLR (OR 1,060; IC 95 % 1.014 – 1,108). The variables that were ruled out by the model were sex, age, Charlson comorbidity index, peak creatinine, serum albumin, chronic kidney disease, etiology of AKI (prerenal vs. non prenal), potassium, KDIGO stage of AKI, need of hemodialysis and PLR. The best cut-off point of the NLR to predict mortality was 6,68 (AUC 0,584; sensitivity 0.60; specificity 0.58; Youden index 0.178) Conclusion In our cohort of patients affected by CA-AKI, the NLR was associated with the morbidity and the mortality during admission. More studies are need to confirm this finding, but the easiness of obtaining it and its economic cost make it cost-effective, giving the NLR a leading role in assessing the risk of CA-AKI.
Introduction and Aims Hyperkalemia (hyperK) is an analytical alteration that frequently occurs in the context of acute kidney injury (AKI) adding morbidity to the patient. We know little about the associated factors and the clinical consequences of this complication in patients with community-acquired acute kidney injury (CA-AKI). The aim of present study was to analyze the predisposing factors and the clinical consequences of the hiperK in patients with CA-AKI. Method The present study is based on a cohort of patients with CA-AKI admitted to the Nephology Service of a third level hospital from January 2010 to February 2015. Hyperkalemia was defined by the laboratory of our hospital as potassium levels above 5.1 meq / L Results A total of 308 patients were included in the final analyses. The mean age was 73,22±13,95 years. 58,4% were men. Charlson comorbidity index (CCI) was 7,16 ±2,7 points. The mean of drugs ingested daily was 7,81±3,66 and the length of stay 12,25±11,69 days. In view of the Etiology of AKI, 69,5% prerenal AKI and 30,5% non-prerenal ones. 212 patients had a history of previous chronic kidney disease (CKD) (68.8%). Hemodialysis (HD) was required in 54 patients (17.15%). 38 patients (12.3%) died during hospital stay. HyperK occurred in 173 cases (56,2 %). Mean potassium was 5,45±1,41 meq/L (95% IC 5,29-5,61) (range 2.65-9.70). There was a significant correlation between potassium and pH (r = - 0.328; p <0,001) as well as between K and CCI (r= 0,284; p <0,001). There was an association between hyperK and intake of potassium-sparing diuretics (p<0,001); ACEI/ARB (p=0,003) and beta blocker (p<0,001). There was no association with CKD nor NSAID intake. Using a multiple linear regression model the equation that predicted serum potassium level was: K = 36,44 – (4,4 x pH) + 0,98 (if intake of potassium-sparing diuretics) + (0.10 x CCI). Potassium level did not influence the length stay. Patients with HyperK required HD in a higher proportion (23.7 vs. 9.6%; p 0.01) and also had higher mortality during hospital stay (15.6 vs. 8.1%; p 0.048). After a follow-up of 971±702 days after hospital discharge, Kaplan-Meier survival curves showed a significant difference (Log Rank (Mantel-Cox): Chi-square 20,1; p< 0,001) between patients with hyperK and patients that did not present it. Conclusion HyperK occurred in just over half of our patients. The potassium level was significantly determined by the previous comorbidity, pH and the intake of potassium-sparing diuretics. HyperK patients required HD and died in a greater proportion during hospital stay than the others. Mortality after discharge was higher in patients who presented hyperK during hospital stay. Appropriate measures must be taken to correct hyperK early in patients with CA-AKI.
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