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Abstract Background Olfactory and gustatory changes may contribute to poor appetite and food aversion in chronic kidney disease (CKD), though the prevalence of olfactory and gustatory dysfunction is not known in the CKD population. Methods We conducted a cross-sectional study among 3527 US adults aged ≥40 years old in the National Health and Nutrition Examination Survey (NHANES) between 2013 and 2014. We measured the prevalence of olfactory and gustatory dysfunction among patients with CKD defined as eGFR

Objective: To compare the mortality associated with percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) in patients with non–ST elevation acute coronary syndrome (NSTE-ACS). Methods: We searched publications from PubMed, Embase, Web of Science, and the Cochrane Library from inception until December 23, 2020. All randomized clinical trials (RCTs) and observational studies comparing all-cause mortality after treatment with CABG versus PCI for patients with NSTE-ACS with minimum follow-up of 6 months were included. Restricted mean survival time (RMST) differences from RCTs and adjusted RMST differences from observational studies were computed by reconstructing time-to-event data from published Kaplan–Meier curves. Extracted hazard ratios (HRs) were also assessed as a secondary analysis. Results: Our systematic review included an individual participant data analysis of 3 RCTs and 8 observational studies. A meta-regression showed a significant association between log-transformed HRs and duration of follow-up (−0.009 [95% confidence interval (CI), −0.002 to −0.016] log-HR per 1-year longer follow-up; P = .037), suggesting a violation of the proportional hazard assumption. Analysis of 6 studies with available RMST data showed a significant inverse association between adjusted RMST differences and cutoff years (slope, −0.028 [95% CI, −0.042 to −0.013] year difference per 1-year longer cutoff; P

BackgroundDialysis patients have been shown to have low serum carnitine due to poor nutrition, deprivation of endogenous synthesis from kidneys, and removal by hemodialysis. Carnitine deficiency leads to impaired cardiac function and dialysis-related hypotension which are associated with increased mortality. Supplementing with levocarnitine among hemodialysis patients may diminish incidence of intradialytic hypotension. Data on this topic, however, lacks consensus.MethodsWe conducted electronic searches in PubMed, Embase and Cochrane Central Register of Controlled Trials from January 1960 to 19th November 2021 to identify randomized controlled studies (RCTs), which examined the effects of oral or intravenous levocarnitine (L-carnitine) on dialysis-related hypotension among hemodialysis patients. The secondary outcome was muscle cramps. Study results were pooled and analyzed utilizing the random-effects model. Trial sequential analysis (TSA) was performed to assess the strength of current evidence.ResultsEight trials with 224 participants were included in our meta-analysis. Compared to control group, L-carnitine reduced the incidence of dialysis-related hypotension among hemodialysis patients (pooled OR = 0.26, 95% CI [0.10-0.72], p = 0.01, I2 = 76.0%). TSA demonstrated that the evidence was sufficient to conclude the finding. Five studies with 147 participants showed a reduction in the incidence of muscle cramps with L-carnitine group (pooled OR = 0.22, 95% CI [0.06-0.81], p = 0.02, I2 = 74.7%). However, TSA suggested that further high-quality studies were required. Subgroup analysis on the route of supplementation revealed that only oral but not intravenous L-carnitine significantly reduced dialysis-related hypotension. Regarding dose and duration of L-carnitine supplementation, the dose > 4,200 mg/week and duration of at least 12 weeks appeared to prevent dialysis-related hypotension.ConclusionSupplementing oral L-carnitine for at least three months above 4,200 mg/week helps prevent dialysis-related hypotension. L-carnitine supplementation may ameliorate muscle cramps. Further well-powered studies are required to conclude this benefit.

Abstract Background Fluctuations in serum phosphate levels increased mortality in end-stage renal disease patients. However, the impacts of serum phosphate changes in hospitalized patients remain unclear. This study aimed to test the hypothesis that serum phosphate changes during hospitalization were associated with in-hospital mortality. Methods We included all adult hospitalized patients from January 2009 to December 2013 that had at least two serum phosphate measurements during their hospitalization. We categorized in-hospital serum phosphate changes, defined as the absolute difference between the maximum and minimum serum phosphate, into 5 groups: 0–0.6, 0.7–1.3, 1.4–2.0, 2.1–2.7, ≥2.8 mg/dL. Using serum phosphate change group of 0–0.6 mg/dL as the reference group, the adjusted odds ratio of in-hospital mortality for various serum phosphate change groups was obtained by multivariable logistic regression analysis. Results A total of 28,149 patients were studied. The in-hospital mortality in patients with serum phosphate changes of 0–0.6, 0.7–1.3, 1.4–2.0, 2.1–2.7, ≥2.8 mg/dL was 1.5, 2.0, 3.1, 4.4, and 10.7%, respectively (p

OBJECTIVE:To evaluate the effects of omega-3 long-chain polyunsaturated fatty acids on proteinuria, estimated glomerular filtration rate (eGFR) and metabolic biomarkers among patients with diabetes. STUDY DESIGN:Meta-analysis of randomized controlled clinical trials (RCTs). SETTING & SUBJECTS:Patients with diabetes. SELECTION CRITERIA FOR STUDIES:We conducted electronic searches in PubMed, Embase and Cochrane Central Register of Controlled Trials from January 1960 to April 2019 to identify RCTs, which examined the effects of omega-3 fatty acids on proteinuria, eGFR and metabolic biomarkers among diabetic patients. RESULTS:Ten RCTs with 344 participants were included in our meta-analysis. Omega-3 fatty acids reduced the amount of proteinuria among type 2 diabetes mellitus (type 2 DM) and type 1 diabetes mellitus (type 1 DM). This association was only significant among type 2 DM (SMD = -0.29 (95% CI: -0.54, -0.03; p = 0.03). Only studies with duration of intervention of 24 weeks or longer demonstrated a significant lower proteinuria among omega-3 fatty acids compared to control group (SMD = -0.30 (95% CI: -0.58, -0.02; p = 0.04). There was a higher eGFR for both type 1 and type 2 DM groups among omega-3 fatty acids compared to control group, however, the effect was not statistically significant. Regarding serum total cholesterol, LDL-cholesterol and HbA1C, there was no significant difference comparing omega-3 fatty acids to control group. There was a non-significant systolic blood pressure reduction in the omega-3 fatty acids supplementation group compared to control. CONCLUSION:Omega-3 fatty acids could help ameliorate proteinuria among type 2 DM who received omega-3 supplementation for at least 24 weeks without adverse effects on HbA1C, total serum cholesterol and LDL-cholesterol.

Background: The healthcare systems in Asia vary greatly due to the socio‐economic and cultural diversities which impact haemophilia management. Methods: An advisory board meeting was conducted with experts in haemophilia care from Asia to understand the heterogeneity in clinical practices and care provision in the region. Findings: The overall prevalence of haemophilia in Asia ranges between 3 and 8.58/100,000 patients. Haemophilia A was more prevalent as compared to haemophilia B with a ratio of around 5:1. There is under‐diagnosis in the region due to lack of diagnosis, registries and/or lack of appropriate facilities in suburban areas. Most patients are referred to the haematologists by their families or primary care physicians, while some are identified during bleeding episodes. Genetic testing faces obstacles like resource constraints, services available at limited centres and unwillingness of patients to participate. Prophylaxis is offered for people with haemophilia (PWH) with a severe bleeding phenotype. Recombinant factors are approved in most countries across the region and are the preferred therapy. The challenges highlighted for not receiving a high standard of care include patients' reluctance to use an intravenous treatment, poor patient compliance due to frequency of infusions, budget constraints and lack of funding, insurance, availability and accessibility of factor concentrates. Prevalence of neutralizing antibodies ranged from 5% to 20% in the region. Use of immune tolerance induction and bypassing agents to treat inhibitors depends on their cost and availability. Conclusion: Haemophilia care in Asia has evolved to a great extent. However, some challenges remain for which a strategic approach along with multi‐stakeholder involvement are needed. [ABSTRACT FROM AUTHOR]

Objectives The objective of this study was to evaluate the risk of acute respiratory failure in all hospitalised patients based on admission serum ionised calcium.Design A retrospective cohort study.Setting A tertiary referral hospital in Rochester, Minnesota, USA.Participants All hospitalised patients who had serum ionised calcium measurement within 24 hours of hospital admission from January 2009 to December 2013. Patients who were mechanically ventilated at admission were excluded.Predictors Admission serum ionised calcium levels was stratified into six groups: ≤4.39, 4.40–4.59, 4.60–4.79, 4.80–4.99, 5.00–5.19 and ≥5.20 mg/dL.Primary outcome measure The primary outcome was the development of acute respiratory failure requiring mechanical ventilation during hospitalisation. Logistic regression analysis was fit to assess the independent risk of acute respiratory failure based on various admission serum ionised calcium, using serum ionised calcium of 5.00–5.19 mg/dL as the reference group.Results Of 25 709 eligible patients, with the mean serum ionised calcium of 4.8±0.4 mg/dL, acute respiratory failure requiring mechanical ventilation occurred in 2563 patients (10%). The incidence of acute respiratory failure was lowest when admission serum ionised calcium was 5.00–5.19 mg/dL, with the progressively increased risk of acute respiratory failure with decreased serum ionised calcium. In multivariate analysis with adjustment for potential confounders, the increased risk of acute respiratory failure requiring mechanical ventilation was significantly associated with admission serum ionised calcium of ≤4.39 (OR 2.52; 95% CI 2.12 to 3.00), 4.40–4.59 (OR 1.76; 95% CI 1.49 to 2.07) and 4.60–4.79 mg/dL (OR 1.48; 95% CI 1.27 to 1.72), compared with serum ionised calcium of 5.00–5.19 mg/dL. The risk of acute respiratory failure was not significantly increased when serum ionised calcium was at least 4.80 mg/dL.Conclusion The increased risk of acute respiratory failure requiring mechanical ventilation was observed when admission serum ionised calcium was lower than 4.80 mg/dL in hospitalised patients.

Background: The objective of this systematic review was to evaluate the efficacy and safety profiles of sodium-glucose co-transporter 2 (SGLT-2) inhibitors for treatment of diabetes mellitus (DM) among kidney transplant patients. Methods: We conducted electronic searches in Medline, Embase, Scopus, and Cochrane databases from inception through April 2020 to identify studies that investigated the efficacy and safety of SGLT-2 inhibitors in kidney transplant patients with DM. Study results were pooled and analyzed utilizing random-effects model. Results: Eight studies with 132 patients (baseline estimated glomerular filtration rate (eGFR) of 64.5 ± 19.9 mL/min/1.73 m2) treated with SGLT-2 inhibitors were included in our meta-analysis. SGLT-2 inhibitors demonstrated significantly lower hemoglobin A1c (HbA1c) (WMD = −0.56% [95%CI: −0.97, −0.16]; p = 0.007) and body weight (WMD = −2.16 kg [95%CI: −3.08, −1.24]; p < 0.001) at end of study compared to baseline level. There were no significant changes in eGFR, serum creatinine, urine protein creatinine ratio, and blood pressure. By subgroup analysis, empagliflozin demonstrated a significant reduction in body mass index (BMI) and body weight. Canagliflozin revealed a significant decrease in HbA1C and systolic blood pressure. In terms of safety profiles, fourteen patients had urinary tract infection. Only one had genital mycosis, one had acute kidney injury, and one had cellulitis. There were no reported cases of euglycemic ketoacidosis or acute rejection during the treatment. Conclusion: Among kidney transplant patients with excellent kidney function, SGLT-2 inhibitors for treatment of DM are effective in lowering HbA1C, reducing body weight, and preserving kidney function without reporting of serious adverse events, including euglycemic ketoacidosis and acute rejection.

Background: C3 glomerulopathy (C3G), a rare glomerular disease mediated by alternative complement pathway dysregulation, is associated with a high rate of recurrence and graft loss after kidney transplantation (KTx). We aimed to assess the efficacy of different treatments for C3G recurrence after KTx. Methods: Databases (MEDLINE, EMBASE, and Cochrane Database) were searched from inception through 3 May, 2019. Studies were included that reported outcomes of adult KTx recipients with C3G. Effect estimates from individual studies were combined using the random-effects, generic inverse variance method of DerSimonian and Laird., The protocol for this meta-analysis is registered with PROSPERO (no. CRD42019125718). Results: Twelve studies (7 cohort studies and 5 case series) consisting of 122 KTx patients with C3G (73 C3 glomerulonephritis (C3GN) and 49 dense deposit disease (DDD)) were included. The pooled estimated rates of allograft loss among KTx patients with C3G were 33% (95% CI: 12–57%) after eculizumab, 42% (95% CI: 2–89%) after therapeutic plasma exchange (TPE), and 81% (95% CI: 50–100%) after rituximab. Subgroup analysis based on type of C3G was performed. Pooled estimated rates of allograft loss in C3GN KTx patients were 22% (95% CI: 5–46%) after eculizumab, 56% (95% CI: 6–100%) after TPE, and 70% (95% CI: 24–100%) after rituximab. Pooled estimated rates of allograft loss in DDD KTx patients were 53% (95% CI: 0–100%) after eculizumab. Data on allograft loss in DDD after TPE (1 case series, 0/2 (0%) allograft loss at 6 months) and rituximab (1 cohort, 3/3 (100%) allograft loss) were limited. Among 66 patients (38 C3GN, 28 DDD) who received no treatment (due to stable allograft function at presentation and/or clinical judgment of physicians), pooled estimated rates of allograft loss were 32% (95% CI: 7–64%) and 53% (95% CI: 28–77%) for C3GN and DDD, respectively. Among treated C3G patients, data on soluble membrane attack complex of complement (sMAC) were limited to patients treated with eculizumab (N = 7). 80% of patients with elevated sMAC before eculizumab responded to treatment. In addition, all patients who responded to eculizumab had normal sMAC levels after post-eculizumab. Conclusions: Our study suggests that the lowest incidence of allograft loss (33%) among KTX patients with C3G are those treated with eculizumab. Among those who received no treatment for C3G due to stable allograft function, there is a high incidence of allograft loss of 32% in C3GN and 53% in DDD. sMAC level may help to select good responders to eculizumab.

Background and Objectives: This study aimed to report the incidence of hospital-acquired dysmagnesemia and its association with in-hospital mortality in adult general hospitalized patients. Materials and Methods: We studied 26,020 adult hospitalized patients from 2009 to 2013 who had normal admission serum magnesium levels and at least two serum magnesium measurements during hospitalization. The normal range of serum magnesium was 1.7–2.3 mg/dL. We categorized in-hospital serum magnesium levels based on the occurrence of hospital-acquired hypomagnesemia and/or hypermagnesemia. We assessed the association between hospital-acquired dysmagnesemia and in-hospital mortality using multivariable logistic regression. Results: 28% of patients developed hospital-acquired dysmagnesemia. Fifteen per cent had hospital-acquired hypomagnesemia only, 10% had hospital-acquired hypermagnesemia only, and 3% had both hospital-acquired hypomagnesemia and hypermagnesemia. Compared with patients with persistently normal serum magnesium levels in hospital, those with hospital-acquired hypomagnesemia only (OR 1.77; p < 0.001), hospital-acquired hypermagnesemia only (OR 2.31; p < 0.001), and both hospital-acquired hypomagnesemia and hypermagnesemia (OR 2.14; p < 0.001) were significantly associated with higher in-hospital mortality. Conclusions: Hospital-acquired dysmagnesemia affected approximately one-fourth of hospitalized patients. Hospital-acquired hypomagnesemia and hypermagnesemia were significantly associated with increased in-hospital mortality.

This study aims to evaluate the risk factors and the association of acute kidney injury with treatments, complications, outcomes, and resource utilization in patients hospitalized for heat stroke in the United States. Hospitalized patients from years 2003 to 2014 with a primary diagnosis of heat stroke were identified in the National Inpatient Sample dataset. End stage kidney disease patients were excluded. The occurrence of acute kidney injury during hospitalization was identified using the hospital diagnosis code. The associations between acute kidney injury and clinical characteristics, in-hospital treatments, outcomes, and resource utilization were assessed using multivariable analyses. A total of 3346 hospital admissions were included in the analysis. Acute kidney injury occurred in 1206 (36%) admissions, of which 49 (1.5%) required dialysis. The risk factors for acute kidney injury included age 20–39 years, African American race, obesity, chronic kidney disease, congestive heart failure, and rhabdomyolysis, whereas age

Background: This study aimed to assess the risk factors and the association of circulatory failure with treatments, complications, outcomes, and resource utilization in hospitalized patients for heatstroke in the United States. Methods: Hospitalized patients with a principal diagnosis of heatstroke were identified in the National Inpatient Sample dataset from the years 2003 to 2014. Circulatory failure, defined as any type of shock or hypotension, was identified using hospital diagnosis codes. Clinical characteristics, in-hospital treatment, complications, outcomes, and resource utilization between patients with and without circulatory failure were compared. Results: A total of 3372 hospital admissions primarily for heatstroke were included in the study. Of these, circulatory failure occurred in 393 (12%) admissions. Circulatory failure was more commonly found in obese patients, but less common in older patients aged ≥60 years. The need for mechanical ventilation, blood transfusion, and renal replacement therapy were higher in patients with circulatory failure. Hyperkalemia, hypocalcemia, metabolic acidosis, metabolic alkalosis, sepsis, ventricular arrhythmia or cardiac arrest, renal failure, respiratory failure, liver failure, neurological failure, and hematologic failure were associated with circulatory failure. The in-hospital mortality was 7.1-times higher in patients with circulatory failure. The length of hospital stay and hospitalization costs were higher when circulatory failure occurred while in the hospital. Conclusions: Approximately one out of nine heatstroke patients developed circulatory failure during hospitalization. Circulatory failure was associated with various complications, higher mortality, and increased resource utilizations.

Background: We aimed to describe the incidence of hospital-acquired dyschloremia and its association with in-hospital mortality in general hospitalized patients. Methods: All hospitalized patients from 2009 to 2013 who had normal admission serum chloride and at least two serum chloride measurements in the hospital were studied. The normal range of serum chloride was defined as 100–108 mmol/L. Hospital serum chloride levels were grouped based on the occurrence of hospital-acquired hypochloremia and hyperchloremia. The association of hospital-acquired hypochloremia and hyperchloremia with in-hospital mortality was analyzed using logistic regression. Results: Among the total of 39,298 hospitalized patients, 59% had persistently normal hospital serum chloride levels, 21% had hospital-acquired hypochloremia only, 15% had hospital-acquired hyperchloremia only, and 5% had both hypochloremia and hyperchloremia. Compared with patients with persistently normal hospital serum chloride levels, hospital-acquired hyperchloremia only (odds ratio or OR 2.84; p < 0.001) and both hospital-acquired hypochloremia and hyperchloremia (OR 1.72; p = 0.004) were associated with increased in-hospital mortality, whereas hospital-acquired hypochloremia only was not (OR 0.91; p = 0.54). Conclusions: Approximately 40% of hospitalized patients developed serum chloride derangements. Hospital-acquired hyperchloremia, but not hypochloremia, was associated with increased in-hospital mortality.

Background and Objectives: The optimal range of serum potassium at hospital discharge is unclear. The aim of this study was to assess the relationship between discharge serum potassium levels and one-year mortality in hospitalized patients. Materials and Methods: All adult hospital survivors between 2011 and 2013 at a tertiary referral hospital, who had available admission and discharge serum potassium data, were enrolled. End-stage kidney disease patients were excluded. Discharge serum potassium was defined as the last serum potassium level measured within 48 h prior to hospital discharge and categorized into ≤2.9, 3.0–3.4, 3.5–3.9, 4.0–4.4, 4.5–4.9, 5.0–5.4 and ≥5.5 mEq/L. A Cox proportional hazards analysis was performed to assess the independent association between discharge serum potassium and one-year mortality after hospital discharge, using the discharge potassium range of 4.0–4.4 mEq/L as the reference group. Results: Of 57,874 eligible patients, with a mean discharge serum potassium of 4.1 ± 0.4 mEq/L, the estimated one-year mortality rate after discharge was 13.2%. A U-shaped association was observed between discharge serum potassium and one-year mortality, with the nadir mortality in the discharge serum potassium range of 4.0–4.4 mEq/L. After adjusting for clinical characteristics, including admission serum potassium, both discharge serum potassium ≤3.9 mEq/L and ≥4.5 mEq/L were significantly associated with increased one-year mortality, compared with the discharge serum potassium of 4.0–4.4 mEq/L. Stratified analysis based on admission serum potassium showed similar results, except that there was no increased risk of one-year mortality when discharge serum potassium was ≤3.9 mEq/L in patients with an admission serum potassium of ≥5.0 mEq/L. Conclusion: The association between discharge serum potassium and one-year mortality after hospital discharge had a U-shaped distribution and was independent of admission serum potassium. Favorable survival outcomes occurred when discharge serum potassium was strictly within the range of 4.0–4.4 mEq/L.

This study aimed to assess the one-year mortality risk based on discharge serum chloride among the hospital survivors. We analyzed a cohort of adult hospital survivors at a tertiary referral hospital from 2011 through 2013. We categorized discharge serum chloride; ≤96, 97–99, 100–102, 103–105, 106–108, and ≥109 mmoL/L. We performed Cox proportional hazard analysis to assess the association of discharge serum chloride with one-year mortality after hospital discharge, using discharge serum chloride of 103–105 mmoL/L as the reference group. Of 56,907 eligible patients, 9%, 14%, 26%, 28%, 16%, and 7% of patients had discharge serum chloride of ≤96, 97–99, 100–102, 103–105, 106–108, and ≥109 mmoL/L, respectively. We observed a U-shaped association of discharge serum chloride with one-year mortality, with nadir mortality associated with discharge serum chloride of 103–105 mmoL/L. When adjusting for potential confounders, including discharge serum sodium, discharge serum bicarbonate, and admission serum chloride, one-year mortality was significantly higher in both discharge serum chloride ≤99 hazard ratio (HR): 1.45 and 1.94 for discharge serum chloride of 97–99 and ≤96 mmoL/L, respectively; p < 0.001) and ≥109 mmoL/L (HR: 1.41; p < 0.001), compared with discharge serum chloride of 103–105 mmoL/L. The mortality risk did not differ when discharge serum chloride ranged from 100 to 108 mmoL/L. Of note, there was a significant interaction between admission and discharge serum chloride on one-year mortality. Serum chloride at hospital discharge in the optimal range of 100–108 mmoL/L predicted the favorable survival outcome. Both hypochloremia and hyperchloremia at discharge were associated with increased risk of one-year mortality, independent of admission serum chloride, discharge serum sodium, and serum bicarbonate.

Background and objectives: Calcium concentration is strictly regulated at both the cellular and systemic level, and changes in serum calcium levels can alter various physiological functions in various organs. This study aimed to assess the association between changes in calcium levels during hospitalization and mortality. Materials and Methods: We searched our patient database to identify all adult patients admitted to our hospital from January 1st, 2009 to December 31st, 2013. Patients with ≥2 serum calcium measurements during the hospitalization were included. The serum calcium changes during the hospitalization, defined as the absolute difference between the maximum and the minimum calcium levels, were categorized into five groups: 0−0.4, 0.5−0.9, 1.0−1.4, 1.5−1.9, and ≥2.0 mg/dL. Multivariable logistic regression was performed to assess the independent association between calcium changes and in-hospital mortality, using the change in calcium category of 0−0.4 mg/dL as the reference group. Results: Of 9868 patients included in analysis, 540 (5.4%) died during hospitalization. The in-hospital mortality progressively increased with higher calcium changes, from 3.4% in the group of 0−0.4 mg/dL to 14.5% in the group of ≥2.0 mg/dL (p < 0.001). When adjusted for age, sex, race, principal diagnosis, comorbidity, kidney function, acute kidney injury, number of measurements of serum calcium, and hospital length of stay, the serum calcium changes of 1.0−1.4, 1.5−1.9, and ≥2.0 mg/dL were significantly associated with increased in-hospital mortality with odds ratio (OR) of 1.55 (95% confidence interval (CI) 1.15−2.10), 1.90 (95% CI 1.32−2.74), and 3.23 (95% CI 2.39−4.38), respectively. The association remained statistically significant when further adjusted for either the lowest or highest serum calcium. Conclusion: Larger serum calcium changes in hospitalized patients were progressively associated with increased in-hospital mortality.

Background: Calcium-phosphate product is associated with mortality among patients with end-stage kidney disease on dialysis. However, clinical evidence among hospitalized patients is limited. The objective of this study was to investigate the relationship between admission calcium-phosphate product and 1-year mortality in hospitalized patients. Materials and Methods: All adult patients admitted to a tertiary referral hospital in 2009–2013 were studied. Patients who had both available serum calcium and phosphate measurement within 24 h of hospital admission were included. Admission calcium-phosphate product (calcium × phosphate) was stratified based on its distribution into six groups:

Background: The aim of this study was to assess the relationship between admission serum potassium and one-year mortality in all adult hospitalized patients. Methods: All adult hospitalized patients who had an admission serum potassium level between the years 2011 and 2013 at a tertiary referral hospital were enrolled. End-stage kidney disease patients were excluded. Admission serum potassium was categorized into levels of ≤2.9, 3.0−3.4, 3.5−3.9, 4.0−4.4, 4.5−4.9, 5.0−5.4, and ≥5.5 mEq/L. Cox proportional hazard analysis was performed to assess the independent association between admission serum potassium and one-year mortality after hospital admission, using an admission potassium level of 4.0−4.4 mEq/L as the reference group. Results: A total of 73,983 patients with mean admission potassium of 4.2 ± 0.5 mEq/L were studied. Of these, 12.6% died within a year after hospital admission, with the lowest one-year mortality associated with an admission serum potassium of 4.0−4.4 mEq/L. After adjustment for age, sex, race, estimated glomerular filtration rate (eGFR), principal diagnosis, comorbidities, medications, acute kidney injury, mechanical ventilation, and other electrolytes at hospital admission, both a low admission serum potassium ≤3.9 mEq/L and elevated admission potassium ≥5.0 mEq/L were significantly associated with an increased risk of one-year mortality, when compared with an admission serum potassium of 4.0−4.4 mEq/L. Subgroup analysis of chronic kidney disease and cardiovascular disease patients showed similar results. Conclusion: This study demonstrated that hypokalemia ≤3.9 mEq/L and hyperkalemia ≥5.0 mEq/L at the time of hospital admission were associated with higher one-year mortality.

Background: Acute kidney injury (AKI) is a well-established complication of extra-corporal membrane oxygenation (ECMO) in the adult population. The data in the pediatric and neonatal population is still limited. Moreover, the mortality risk of AKI among pediatric patients requiring ECMO remains unclear. Thus, this meta-analysis aims to assess the incidence of AKI, AKI requiring renal replacement therapy and AKI associated mortality in pediatric/neonatal patients requiring ECMO. Methods: A literature search was performed utilizing MEDLINE, EMBASE, and the Cochrane Database from inception through June 2019. We included studies that evaluated the incidence of AKI, severe AKI requiring renal replacement therapy (RRT) and the risk of mortality among pediatric patients on ECMO with AKI. Random-effects meta-analysis was used to calculate the pooled incidence of AKI and the odds ratios (OR) for mortality. Results: 13 studies with 3523 pediatric patients on ECMO were identified. Pooled incidence of AKI and AKI requiring RRT were 61.9% (95% confidence interval (CI): 39.0−80.4%) and 40.9% (95%CI: 31.2−51.4%), respectively. A meta-analysis limited to studies with standard AKI definitions showed a pooled estimated AKI incidence of 69.2% (95%CI: 59.7−77.3%). Compared with patients without AKI, those with AKI and AKI requiring RRT while on ECMO were associated with increased hospital mortality ORs of 1.70 (95% CI, 1.38−2.10) and 3.64 (95% CI: 2.02−6.55), respectively. Conclusions: The estimated incidence of AKI and severe AKI requiring RRT in pediatric patients receiving ECMO are high at 61.9% and 40.9%, respectively. AKI among pediatric patients on ECMO is significantly associated with reduced patient survival.