The association between olfactory and gustatory dysfunction and chronic kidney disease.

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 < 60 ml/min/1.73m2 using the "scratch and sniff" NHANES Pocket Smell Test and quinine whole-mouth test. We also examined the association between CKD and olfactory/gustatory dysfunction, and nutritional markers. RESULTS: The prevalence of olfactory dysfunction was 30% among CKD and 15% among non-CKD (p < 0.001). The prevalence of gustatory dysfunction was 13% among CKD and 17% among non-CKD (p = 0.10). After adjusting for confounders, CKD was significantly associated with olfactory dysfunction (OR = 1.47, 95% CI [1.07, 2.01]; p = 0.02) but not gustatory dysfunction (OR = 1.76, 95%CI [0.99, 3.11]; p = 0.05). Among the CKD population, the odds of olfactory dysfunction was 72% higher for every 10 kg decrease in grip strength (OR = 1.72, 95% CI [1.39, 2.13]; adjusted p = 0.005). CONCLUSION: CKD was associated with higher odds of olfactory but not gustatory dysfunction. Olfactory dysfunction was associated with lower grip strength among those with CKD. Screening and early intervening on olfactory dysfunction among CKD may preserve muscle strength and improve nutritional status in this vulnerable population.

Hospital-acquired serum phosphate derangements and their associated in-hospital mortality.

BACKGROUND: We aimed to report the incidence of hospital-acquired hypophosphataemia and hyperphosphataemia along with their associated in-hospital mortality. METHODS: We included 15 869 adult patients hospitalised at a tertiary medical referral centre from January 2009 to December 2013, who had normal serum phosphate levels at admission and at least two serum phosphate measurements during their hospitalisation. The normal range of serum phosphate was defined as 2.5-4.2 mg/dL. In-hospital serum phosphate levels were categorised based on the occurrence of hospital-acquired hypophosphataemia and hyperphosphataemia. We analysed the association of hospital-acquired hypophosphataemia and hyperphosphataemia with in-hospital mortality using multivariable logistic regression. RESULTS: Fifty-three per cent (n=8464) of the patients developed new serum phosphate derangements during their hospitalisation. The incidence of hospital-acquired hypophosphataemia and hyperphosphataemia was 35% and 27%, respectively. Hospital-acquired hypophosphataemia and hyperphosphataemia were associated with odds ratio (OR) of 1.56 and 2.60 for in-hospital mortality, respectively (p value<0.001 for both). Compared with patients with persistently normal in-hospital phosphate levels, patients with hospital-acquired hypophosphataemia only (OR 1.64), hospital-acquired hyperphosphataemia only (OR 2.74) and both hospital-acquired hypophosphataemia and hyperphosphataemia (ie, phosphate fluctuations; OR 4.00) were significantly associated with increased in-hospital mortality (all p values <0.001). CONCLUSION: Hospital-acquired serum phosphate derangements affect approximately half of the hospitalised patients and are associated with increased in-hospital mortality rate.

Outcomes of kidney retransplantation in recipients with prior posttransplant lymphoproliferative disorders: An analysis of the 2000-2019 UNOS/OPTN database.

This study utilized the UNOS database to assess clinical outcomes after kidney retransplantation in patients with a history of posttransplant lymphoproliferative disease (PTLD). Among second kidney transplant patients from 2000 to 2019, 254 had history of PTLD in their first kidney transplant, whereas 28,113 did not. After a second kidney transplant, PTLD occurred in 2.8% and 0.8% of patients with and without history of PTLD, respectively (p = .001). Over a median follow-up time of 4.5 years after a second kidney transplant, 5-year death-censored graft failure was 9.5% vs. 12.6% (p = .21), all-cause mortality was 8.3% vs. 11.8% (p = .51), and 1-year acute rejection was 11.0% vs. 9.3% (p = .36) in the PTLD vs. non-PTLD groups, respectively. There was no significant difference in death-censored graft failure, mortality, and acute rejection between PTLD and non-PTLD groups in adjusted analysis and after propensity score matching. We conclude that graft survival, patient survival, and acute rejection after kidney retransplantation are comparable between patients with and without history of PTLD, but PTLD occurrence after kidney retransplantation remains higher in patients with history of PTLD.

Risk of Symptomatic Kidney Stones During and After Pregnancy.

RATIONALE & OBJECTIVE: There are several well-known anatomical and physiological changes during pregnancy that could contribute to kidney stone formation, but evidence that they increase the risk of kidney stones during pregnancy is lacking. We determined whether there was an increased risk of a first-time symptomatic kidney stone during and after pregnancy. STUDY DESIGN: A population-based matched case-control study. SETTING & PARTICIPANTS: 945 female first-time symptomatic kidney stone formers aged 15-45 years and 1,890 age-matched female controls in Olmsted County, MN, from 1984-2012. The index date was the date of onset of a symptomatic kidney stone for both the case and her matched controls. EXPOSURE: The primary exposure was pregnancy with assessment for variation in risk across different time intervals before, during, and after pregnancy. Medical records were manually reviewed to determine the conception and delivery dates for pregnancies. OUTCOME: Medical record-validated first-time symptomatic kidney stone. ANALYTICAL APPROACH: Conditional and unconditional multivariable logistic regression analysis. RESULTS: Compared with nonpregnant women, the odds of a symptomatic kidney stone forming in women was similar in the first trimester (OR, 0.92; P=0.8), began to increase during the second trimester (OR, 2.00; P=0.007), further increased during the third trimester (OR, 2.69; P=0.001), peaked at 0 to 3 months after delivery (OR, 3.53; P<0.001), and returned to baseline by 1year after delivery. These associations persisted after adjustment for age and race or for diabetes mellitus, hypertension, and obesity. These results did not significantly differ by age, race, time period, or number of prior pregnancies. Having a prior pregnancy (delivery date>1year ago) was also associated with a first-time symptomatic kidney stone (OR, 1.27; P=0.01). LIMITATIONS: Observational study design in a predominantly White population. The exact timing of stone formation cannot be determined. CONCLUSIONS: Pregnancy increases the risk of a first-time symptomatic kidney stone. This risk peaks close to delivery and then improves by 1 year after delivery, though a modest risk of a kidney stone still exists beyond 1 year after delivery.

Febuxostat as a renoprotective agent for treatment of hyperuricaemia: a meta-analysis of randomised controlled trials.

BACKGROUND: The objective of this meta-analysis of randomised controlled clinical trials (RCT) was to evaluate the effects of febuxostat on kidney function in patients with hyperuricaemia. AIMS: Febuxostat is a xanthine oxidase inhibitor that decreases uric acid production. Recent studies suggested the renoprotective effect of febuxostat among hyperuricaemia patients. The aim of this study was to evaluate the effects of febuxostat on kidney function in patients with hyperuricaemia. METHODS: We conducted electronic searches in PubMed, Embase and Cochrane Central Register of Controlled Trials from January 1960 to July 2019 to identify RCT that examined the effects of febuxostat in adult patients with hyperuricaemia on serum creatinine, estimated glomerular filtration rate (eGFR), albuminuria, blood pressure parameters, major cardiovascular events, diarrhoea, joint pain, stroke and arrhythmia. RESULTS: Nine RCT with 2141 participants were included in this meta-analysis. Compared to placebo, the febuxostat group showed a higher eGFR at 6 months with a weighted mean difference (WMD) of 2.86 mL/min/1.73 m2 (P < 0.001), as well as the end of studies (eGFR WMD 2.69 mL/min/1.73 m2 , P < 0.001). There was also lower serum creatinine (SrCr WMD = -0.04 mg/dL, P < 0.001), reduction in systolic blood pressure (SBP WMD = -1.18 mmHg, P < 0.001) and diastolic blood pressure (DBP WMD = -1.14 mmHg, P = 0.04). There was no statistical difference between febuxostat and placebo in major cardiovascular events, diarrhoea, joint symptoms, stroke events and arrhythmia. Subgroup analysis among chronic kidney disease showed the febuxostat group had higher eGFR than the placebo group (eGFR WMD = 2.69 mL/min/1.73 m2 , P < 0.001). CONCLUSION: Treating hyperuricaemia with febuxostat may slow the progression of chronic kidney disease irrespective of baseline renal function without significantly associated increased risks of major cardiovascular events, diarrhoea, joint symptoms, arrhythmia and stroke, compared to placebo.

Comparison of hospitalization outcomes for delivery and resource utilization between pregnant women with kidney transplants and chronic kidney disease in the United States.

BACKGROUND: This study aimed to assess outcomes of delivery hospitalizations, including acute kidney injury (AKI), obstetric and foetal events and resource utilization among pregnant women with kidney transplants compared with pregnant women with no known kidney disease and those with chronic kidney disease (CKD) Stages 3-5. METHOD: Hospitalizations for delivery in the US were identified using the enhanced delivery identification method in the National Inpatient Sample dataset from the years 2009 to 2014. Diagnoses of CKD Stages 3-5, kidney transplantation, along with obstetric events, delivery methods and foetal events were identified using ICD-9-CM diagnosis and procedure codes. Patients with no known kidney disease group were identified by excluding any diagnoses of CKD, end stage kidney disease, and kidney transplant. Multivariable logistic regression accounting for the survey weights and matched regression was conducted to investigate the risk of maternal and foetal complications in women with kidney transplants, compared with women with no kidney transplants and no known kidney disease, and to women with CKD Stages 3-5. RESULT: A total of 5, 408, 215 hospitalizations resulting in deliveries were identified from 2009 to 2014, including 405 women with CKD Stages 3-5, 295 women with functioning kidney transplants, and 5, 405, 499 women with no known kidney disease. Compared with pregnant women with no known kidney disease, pregnant kidney transplant recipients were at higher odds of hypertensive disorders of pregnancy (OR = 3.11, 95% CI [2.26, 4.28]), preeclampsia/eclampsia/HELLP syndrome (OR = 3.42, 95% CI [2.54, 4.60]), preterm delivery (OR = 2.46, 95% CI [1.75, 3.45]), foetal growth restriction (OR = 1.74, 95% CI [1.01, 3.00]) and AKI (OR = 10.46, 95% CI [5.33, 20.56]). There were no significant differences in rates of gestational diabetes or caesarean section. Pregnant women with kidney transplants had 1.30-times longer lengths of stay and 1.28-times higher costs of hospitalization. However, pregnant women with CKD Stages 3-5 were at higher odds of AKI (OR = 5.29, 95% CI [2.41, 11.59]), preeclampsia/eclampsia/HELLP syndrome (OR = 1.72, 95% CI [1.07, 2.76]) and foetal deaths (OR = 3.20, 95% CI [1.06, 10.24]), and had 1.28-times longer hospital stays and 1.37-times higher costs of hospitalization compared with pregnant women with kidney transplant. CONCLUSION: Pregnant women with kidney transplant were more likely to experience adverse events during delivery and had longer lengths of stay and higher total charges when compared with women with no known kidney disease. However, pregnant women with moderate to severe CKD were more likely to experience serious complications than kidney transplant recipients.

Inpatient burden and mortality of heatstroke in the United States.

BACKGROUND: This study aimed to assess inpatient prevalence, characteristics, outcomes, and resource utilisation of hospitalisation for heatstroke in the United States. Additionally, this study aimed to explore factors associated with in-hospital mortalities of heatstroke. METHODS: The 2003-2014 National Inpatient Sample database was used to identify hospitalised patients with a principal diagnosis of heatstroke. The inpatient prevalence, clinical characteristics, in-hospital treatments, outcomes, length of hospital stay, and hospitalisation cost were studied. Multivariable logistic regression was performed to identify independent factors associated with in-hospital mortality. RESULTS: A total of 3372 patients were primarily admitted for heatstroke, accounting for an overall inpatient prevalence of heatstroke amongst hospitalised patients of 36.3 cases per 1 000 000 admissions in the United States with an increasing trend during the study period (P < .001). Age 40-59 was the most prevalent age group. During the hospital stay, 20% required mechanical ventilation, and 2% received renal replacement therapy. Rhabdomyolysis was the most common complication. Renal failure was the most common end-organ failure, followed by neurological, respiratory, metabolic, hematologic, circulatory, and liver systems. The in-hospital mortality rate of heatstroke hospitalisation was 5% with a decreasing trend during the study period (P < .001). The presence of end-organ failure was associated with increased in-hospital mortality, whereas more recent years of hospitalisation was associated with decreased in-hospital mortality. The median length of hospital stay was 2 days. The median hospitalisation cost was $17 372. CONCLUSION: The inpatient prevalence of heatstroke in the United States increased, while the in-hospital mortality of heatstroke decreased.

Efficacy and safety of febuxostat for treatment of asymptomatic hyperuricemia among kidney transplant patients: A meta-analysis of observational studies.

BACKGROUND: The objective of this meta-analysis of observational studies was to evaluate the efficacy and safety profiles of febuxostat in treating hyperuricemia among kidney transplant patients. METHODS: We conducted electronic searches in PubMed, Embase, and Cochrane Central Register of Controlled Trials from January 1960 to July 2019 to identify studies that investigated the effects of febuxostat in kidney transplant patients on uric acid as well as safety profiles including estimated glomerular filtration rate (eGFR), hemoglobin level (Hb), white blood cell counts (WBC), liver enzymes, and trough level of tacrolimus. RESULTS: Seven observational studies with 367 participants were included in this meta-analysis. Compared with allopurinol, the febuxostat group demonstrated a higher odds of achieving target uric acid levels lower than 6 mg/dL within 12 months (OR = 2.9, P = .004). However, there was no statistical difference in change of uric acid (WMD = -1.0 mg/dL/y, P = .32) and change in allograft eGFR within a year (WMD = 0.01 mL/min/1.73 m2 /y, P = .98) between febuxostat and allopurinol. Regarding safety profiles, there were no statistical differences in eGFR, Hb, WBC, liver enzymes (AST, ALT), and trough level of tacrolimus between baseline and at the study end. Only one study reported suspected graft loss among febuxostat group. CONCLUSION: Among kidney transplant patients, treating hyperuricemia with febuxostat showed a higher odds of reaching the target of serum uric acid < 6 mg/dL compared with allopurinol without causing significant side effects including change in tacrolimus level, liver function, decline in renal graft function, and bone marrow function.

Impact of serum phosphate changes on in-hospital mortality.

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 < 0.001). When adjusted for confounding factors, larger serum phosphate changes were associated with progressively increased in-hospital mortality with odds ratios of 1.35 (95% 1.04-1.74) in 0.7-1.3 mg/dL, 1.98 (95% CI 1.53-2.55) in 1.4-2.0 mg/dL, 2.68 (95% CI 2.07-3.48) in 2.1-2.7 mg/dL, and 5.04 (95% CI 3.94-6.45) in ≥2.8 mg/dL compared to serum phosphate change group of 0-0.6 mg/dL. A similar result was noted when we further adjusted for either the admission or mean serum phosphate during hospitalization. CONCLUSION: Greater serum phosphate changes were progressively associated with increased in-hospital mortality.

Admission serum phosphate levels and the risk of respiratory failure.

BACKGROUND: The objective of this study was to evaluate the relationship between admission serum phosphate and in-hospital respiratory failure requiring mechanical ventilation in hospitalised patients. METHODS: We analysed a cohort of all adult patients admitted at a tertiary referral hospital between the year 2009 and 2013. We included patients who had available serum phosphate and were not on mechanical ventilation within 24 hours of hospital admission. We stratified admission serum phosphate based on its distribution into 6 groups: ≤2.4, 2.5-3.0, 3.1-3.6, 3.7-4.2, 4.3-4.8 and ≥4.9 mg/dL. We performed multivariable logistic regression analysis to assess the odds ratio of in-hospital respiratory failure requiring mechanical ventilation based on admission serum phosphate, using phosphate level of 3.1-3.6 as the reference group. RESULTS: This study enrolled a total of 37 728 hospitalised patients, with a mean admission serum phosphate of 3.8 ± 1.1 mg/dL. Of these patients, 2792 (7.4%) developed respiratory failure requiring mechanical ventilation during hospitalisation. Increased incidence of respiratory failure requiring mechanical ventilation was observed in both decreased and increased admission serum phosphate, assuming the J-shaped curve. In adjusted analysis, admission serum phosphate of ≤2.4 and 2.5-3.0 mg/dL was significantly associated with increased risk of respiratory failure requiring mechanical ventilation with odds ratio (OR) of 1.18 (95% confidence interval [CI] 1.01-1.40) and 1.19 (95% CI 1.04-1.35), respectively. Similarly, admission serum phosphate of 4.3 to 4.8 and ≥4.9 mg/dL was significantly associated with increased risk of respiratory failure requiring mechanical ventilation with OR of 1.19 (95% CI 1.05-1.36) and 1.58 (95% CI 1.37-1.82), respectively. CONCLUSION: Our study revealed the J-shaped association between serum phosphate level at admission and risk of respiratory failure requiring mechanical ventilation in unselected hospitalised patients.

The prognostic importance of serum sodium levels at hospital discharge and one-year mortality among hospitalized patients.

BACKGROUND: The optimal range of serum sodium at hospital discharge is unclear. Our objective was to assess the one-year mortality based on discharge serum sodium in hospitalized patients. METHODS: We analyzed a cohort of hospitalized adult patients between 2011 and 2013 who survived hospital admission at a tertiary referral hospital. We categorized discharge serum sodium into five groups; ≤132, 133-137, 138-142, 143-147, and ≥148 mEq/L. We assessed one-year mortality risk after hospital discharge based on discharge serum sodium, using discharge sodium of 138-142 mEq/L as the reference group. RESULTS: Of 55 901 eligible patients, 4.9%, 29.8%, 56.1%, 8.9%, 0.3% had serum sodium of ≤132, 133-137, 138-142, 143-147, and ≥148 mEq/L, respectively. We observed a U-shaped association between discharge serum sodium and one-year mortality, with nadir mortality in discharge serum sodium of 138-142 mEq/L. When adjusting for potential confounders, including admission serum sodium, one-year mortality was significantly higher in both discharge serum sodium ≤137 and ≥143 mEq/L, compared with discharge serum sodium of 138-142 mEq/L. The mortality risk was the most prominent in elevated discharge serum sodium of ≥148 mEq/L (HR 3.86; 95% CI 3.05-4.88), exceeding the risk associated with low discharge serum sodium of ≤132 mEq/L (HR 1.43; 95% CI 1.30-1.57). CONCLUSION: The optimal range of serum sodium at discharge was 138-142 mEq/L. Both hypernatremia and hyponatremia at discharge were associated with higher one-year mortality. The impact on higher one-year mortality was more prominent in hypernatremia than hyponatremia.

Association of serum chloride level alterations with in-hospital mortality.

BACKGROUND: We aimed to assess the association between alterations in serum chloride levels during hospitalisation and mortality. METHODS: We reviewed all adult patients admitted to our hospital from the year 2009 to 2013, who had at least two serum chloride measurements during hospitalisation. The serum chloride change during hospitalisation, defined as the absolute difference between the highest and lowest serum chloride levels, was categorised into seven groups; 0-2, 3-4, 5-6, 7-8, 9-10, 11-12 and ≥13 mEq/L. Multivariable logistic regression was performed to assess the independent association between serum chloride change and in-hospital mortality, using the serum chloride change of 0-2 mEq/L as the reference group. RESULTS: A total of 57 880 patients, with median serum chloride change of 5 (IQR 3-9) mEq/L, were studied. The in-hospital mortality was progressively increased with larger chloride change, from 0.6% in group of 0-2 mEq/L to 5.9% in group of ≥13 mEq/L (p<0.001). In adjusted analysis, serum chloride change of ≥7 mEq/L was significantly associated with increased in-hospital mortality. For upward trend, serum chloride change of ≥3 mEq/L was significantly associated with increased in-hospital mortality, whereas, for downward trend, serum chloride change was not consistently associated with in-hospital mortality. CONCLUSION: Alterations in serum chloride during hospitalisation were associated with increased hospital mortality. The association was more prominent with upward than downward trend of serum chloride.

The Effects of Restricted Protein Diet Supplemented With Ketoanalogue on Renal Function, Blood Pressure, Nutritional Status, and Chronic Kidney Disease-Mineral and Bone Disorder in Chronic Kidney Disease Patients: A Systematic Review and Meta-Analysis.

OBJECTIVE: To systemically review the meta-analysis exploring the effectiveness and safety of restricted protein diet supplemented with ketoanalogues (KAs) when compared with regular diet or low protein diet (LPD) without KAs in chronic kidney disease (CKD) patients. STUDY DESIGN AND METHODS: We conducted electronic searches in PubMed, Scopus, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov from January 1960 to May 2018 to identify randomized controlled clinical trials that explored the effects of restricted protein diet including vegetarian and mixed type of protein with KAs on kidney endpoints including the changes in estimated glomerular filtration rate (eGFR) and proteinuria, nutritional status, and CKD-mineral bone disorder. RESULTS: Seventeen RCTs with 1,459 participants were included in our meta-analysis. Restricted protein diet with KAs significantly preserved eGFR and reduced proteinuria, serum phosphate, parathyroid hormone (PTH) level, systolic blood pressure, diastolic blood pressure, and serum cholesterol. By subgroup analysis, very low protein diet (VLPD) with KAs was plausibly superior to LPD with KAs in slowing the decline in eGFR. Only VLPD with KAs significantly improved serum PTH, systolic blood pressure, and diastolic blood pressure while both regimens significantly decreased serum phosphate. Only LPD with KAs significantly raised serum albumin and serum calcium. CONCLUSION: Restricted protein diet supplemented with KAs could effectively improve kidney endpoints including preserving eGFR and diminishing proteinuria, blood pressure levels, and CKD-mineral bone disorder parameters without causing malnutrition. VLPD with KAs appears to provide more effectiveness in slowing the decline in eGFR, lowering blood pressure, reducing serum PTH, and less increasing serum calcium level.

Serum Potassium Levels at Hospital Discharge and One-Year Mortality among Hospitalized Patients.

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 hours 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.

Impact of Changes in Serum Calcium Levels on In-Hospital Mortality.

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.

The Effect of Randomized Beta-Carotene Supplementation on CKD in Men.

Introduction: Beta-carotene (BC) protects the body against free radicals that may damage the kidney and lead to the development of acute kidney injury and chronic kidney disease (CKD). Previous studies in animal models have demonstrated a potential protective effect of 30 mg/kg BC supplementation on renal ischemia or reperfusion injury and subsequently improved kidney function. The extension of these findings to humans, however, remains unclear. Methods: Our study leverages previously collected data from the Physicians' Health Study I (PHS I), a large-scale, long-term, randomized trial of middle-aged and older US male physicians testing 50 mg BC every other day for primary prevention of cardiovascular disease and cancer. We examined the impact of randomized BC supplementation on self-reported incident CKD identified by self-reports stating "yes" to kidney disease from annual follow-up questionnaires from randomization in 1982 through the end of the randomized BC intervention at the end of 1995, and on CKD defined as an estimated glomerular filtration rate (eGFR) < 60 ml/min per 1.73 m2 at the end of 1995. Analyses compared incident CKD between BC supplementation and placebo using Cox proportional hazards regression models and logistic regression. We also examined whether smoking status (current vs. former or never smoker) or other factors modified the effect of randomized BC supplementation on CKD. Results: A total of 10,966 participants were randomized to BC, and 10,952 participants were randomized to a placebo group. Baseline characteristics between randomized BC groups were similar. There was no significant benefit between BC supplementation and self-reported incident CKD after adjusting for age and randomized aspirin treatment (hazard ratio [HR] = 0.97, 95% confidence interval [CI]: 0.86-1.08, P-value = 0.56). Stratified by smoking status, there was no significant benefit of BC supplementation and self-reported incident CKD either among former or never smokers (HR = 0.95, 95% CI: 0.84-1.07, P-value = 0.41) or current smokers (HR = 1.08, 95% CI: 0.78-1.50, P-value = 0.64). Smoking status did not modify the association between BC supplementation and incident CKD (P-interaction = 0.47). In subgroup analysis among those with available serum creatinine at the study end (5480 with BC and 5496 with placebo), there was no significant benefit between BC supplementation and CKD based on eGFR < 60 ml/min per 1.73 m2 (odds ratio [OR] = 0.96, 95% CI: 0.85-1.08, P-value = 0.49). Conclusion: Long-term randomized BC supplementation did not affect the risk of incident CKD in middle-aged and older male physicians.

Association of hypochloremia with mortality among patients requiring continuous renal replacement therapy.

BACKGROUND: Serum chloride derangement is common in critically ill patients requiring continuous renal replacement therapy (CRRT). We aimed to assess the association between serum chloride levels before and during CRRT with mortality. METHODS: This is a retrospective cohort study of critically ill patients receiving CRRT for acute kidney injury from December 2006 through November 2015 in a tertiary referral hospital in the United States. We used logistic regression to assess serum chloride before and mean serum chloride during CRRT as predictors for 90 days mortality after CRRT initiation. The normal reference range for serum chloride was 99-108 mmol/L. RESULTS: Of 1282 eligible patients, 25%, 50%, and 25% had hypochloremia, normochloremia, and hyperchloremia, respectively. The adjusted odds ratio for 90 days mortality in patients with hypochloremia before CRRT was 1.82 (95% CI 1.29-2.55). During CRRT, 4%, 70%, 26% of patients had mean serum chloride in the hypochloremia, normochloremia, and hyperchloremia range, respectively. The adjusted odds ratio for 90 days mortality in patients with mean serum chloride during CRRT in the hypochloremia range was 2.96 (95% CI 1.43-6.12). Hyperchloremia before and during CRRT was not associated with mortality. The greater serum chloride range during CRRT was associated with increased mortality (OR 1.29; 95% CI 1.13-1.47 per 5 mmol/L increase). CONCLUSION: Hypochloremia before and during CRRT is associated with higher mortality.

The effect of levocarnitine supplementation on dialysis-related hypotension: A systematic review, meta-analysis, and trial sequential analysis.

BACKGROUND: Dialysis 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. METHODS: We 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. RESULTS: Eight 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. CONCLUSION: Supplementing 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.

Dietary Risk Factors for Incident and Recurrent Symptomatic Kidney Stones.

OBJECTIVE: To compare dietary factors between incident symptomatic stone formers and controls, and among the incident stone formers, to determine whether dietary factors were predictive of symptomatic recurrence. PATIENTS AND METHODS: We prospectively recruited 411 local incident symptomatic kidney stone formers (medical record validated) and 384 controls who were seen at Mayo Clinic in Minnesota or Florida between January 1, 2009, and August 31, 2018. Dietary factors were based on a Viocare, Inc, food frequency questionnaire administered during a baseline in-person study visit. Logistic regression compared dietary risk factors between incident symptomatic stone formers and controls. Incident stone formers were followed up for validated symptomatic recurrence in the medical record. Cox proportional hazards models estimated risk of symptomatic recurrence with dietary factors. Analyses adjusted for fluid intake, energy intake, and nondietary risk factors. RESULTS: In fully adjusted analyses, lower dietary calcium, potassium, caffeine, phytate, and fluid intake were all associated with a higher odds of an incident symptomatic kidney stone. Among incident stone formers, 73 experienced symptomatic recurrence during a median 4.1 years of follow-up. Adjusting for body mass index, fluid intake, and energy intake, lower dietary calcium and lower potassium intake were predictive of symptomatic kidney stone recurrence. With further adjustment for nondietary risk factors, lower dietary calcium intake remained a predictor of recurrence, but lower potassium intake only remained a predictor of recurrence among those not taking thiazide diuretics or calcium supplements. CONCLUSION: Enriching diets in stone formers with foods high in calcium and potassium may help prevent recurrent symptomatic kidney stones.

Trends in the prevalence of kidney stones in the United States from 2007 to 2016.

The overall prevalence of kidney stones (KS) in the US rose from 3.2% in 1980 to 10.1% in 2016, but the trends in important subgroups have not been reported. We examined the prevalence trends of KS in subgroups of age, sex and race in the US and identified relevant laboratory factors associated with a history of KS using National Health and Nutrition Examination Survey (NHANES) data. We conducted a cross-sectional study among 28,209 US adults aged ≥ 20 years old in the NHANES from 2007 to 2016. We calculated the prevalence of a self-reported history of KS by using weights and standardized to the 2010 US Census population. We also compared relevant laboratory values according to the history of KS. The prevalence of KS decreased from 8.7% in 2007-2008 to 7.2% in 2011-2012 but then increased to 9.0% in 2013-2014 and 10.1% in 2015-2016. However, the overall prevalence of KS increased over 2007-2016 (p-trend = 0.02). Prevalence of KS among men was higher than women. Among men aged 20-79, there were significant quadratic trends in the prevalence of KS. Whereas, the prevalence of KS increased as a linear trend among women aged 20-59 years over 2007-2016. There were no consistent trends in the prevalence of KS by race. The prevalence trend of KS among non-Hispanic whites was 9.8% from 2007 to 2010 then dropped to 7.9% in 2011-2012 and increased to 10.6% in 2013-2014 and 12.1% in 2015-2016. A similar trend was also observed among non-Hispanic blacks. Among Hispanic, the prevalence of KS was 7.6% in 2007-2008 and 7.4% in 2009-2010 and then fluctuated over the next several time periods. For non-Hispanic Asians, the range was 4.4-4.6%. Regarding relevant laboratory factors, after adjusting for sex, race, age, BMI, smoking status, alcohol drinking, history of diabetes and gout, urine albumin-creatinine ratio and serum osmolality were independently associated with the history of KS in women and men. In conclusion, there was substantial variability in KS prevalence across individual 2-year time periods. This variation of period-specific prevalence values emphasizes the importance of looking at long-term trends and using more than a single 2-year cycle in analyses to increase the precision of the estimate. However, there was an overall increase in the prevalence of KS over 2007-2016.