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Background Abnormal circadian blood pressure ( BP ) variations during sleep, specifically the non‐dipping (<10% fall in nocturnal BP ) and reverse‐dipping patterns (rise in nocturnal BP ), have been associated with an increased risk of cardiovascular events and target organ damage. However, the relationship between abnormal sleep BP variations and cerebral small vessel disease markers is poorly established. This study aims to assess the association between non‐dipping and reverse‐dipping BP patterns with markers of silent cerebral small vessel disease. Methods and Results MEDLINE , Embase, and Cochrane Databases were searched from inception through November 2019. Studies that reported the odds ratios (ORs) for cerebral small vessel disease markers in patients with non‐dipping or reverse‐dipping BP patterns were included. Effect estimates from the individual studies were extracted and combined using the random‐effect, generic inverse variance method of DerSimonian and Laird. Twelve observational studies composed of 3497 patients were included in this analysis. The reverse‐dipping compared with normal dipping BP pattern was associated with a higher prevalence of white matter hyperintensity with a pooled adjusted OR of 2.00 (95% CI , 1.13–2.37; I 2 =36%). Non‐dipping BP pattern compared with normal dipping BP pattern was associated with higher prevalence of white matter hyperintensity and asymptomatic lacunar infarction, with pooled OR s of 1.38 (95% CI , 0.95–2.02; I 2 =52%) and 2.33 (95% CI , 1.30–4.18; I 2 =73%), respectively. Limiting to only studies with confounder‐adjusted analysis resulted in a pooled OR of 1.38 (95% CI , 0.95–2.02; I 2 =52%) for white matter hyperintensity and 1.44 (95% CI , 0.97–2.13; I 2 =0%) for asymptomatic lacunar infarction. Conclusions The non‐dipping and reverse‐dipping BP patterns are associated with neuroimaging cerebral small vessel disease markers.

Abstract Objective The objective of this meta‐analysis of observational studies was to evaluate the association between simple renal cysts (SRC) and presence of aortic pathology such as aortic aneurysms and dissection. Methods We conducted searches in Ovid MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials from January 1960 to August 2019 to identify observational studies that examined the association between SRCs and any aortic diseases, including aortic aneurysms and dissection. Two reviewers independently extracted the data and assessed the risk of bias. The meta‐analysis was performed by STATA 14.1. Results In total, 11 observational studies with 19 719 participants were included in this meta‐analysis. Compared to individuals without SRCs, patients with SRCs had higher odds of abdominal aortic aneurysm (AAA) (adjusted OR = 2.61, 95% CI 2.34‐2.91, P < 0.001, I 2 = 0%), ascending thoracic aortic aneurysm (TAA) (adjusted OR = 1.98, 95% CI 1.09‐3.63, P = 0.03, I 2 = 90.1%), descending TAA (adjusted OR = 3.44, 95% CI, 2.67‐4.43, P < 0.001, I 2 = 0%), type A aortic dissection (AD) (adjusted OR = 1.98, 95% CI 1.32‐2.96, P = 0.001, I 2 = 12.9%), and type B AD (adjusted OR = 2.55, 95% CI, 1.31‐4.96, P = 0.006, I 2 = 76.2%). There was a higher average in the sum of diameter of SRCs among AAA compared to patients without AAA (WMD = 19.80 mm, 95% CI 13.92‐25.67, P < 0.001, I 2 = 63.8%). Conclusion SRC is associated with higher odds of aortic diseases including AAA, ascending and descending TAA, type A and type B dissection even after adjusting for confounders.

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.

Background: This study aimed to assess the association between the percentage of glomerulosclerosis (GS) in procurement allograft biopsies from high-risk deceased donor and graft outcomes in kidney transplant recipients. Methods: The UNOS database was used to identify deceased-donor kidneys with a kidney donor profile index (KDPI) score > 85% from 2005 to 2014. Deceased donor kidneys were categorized based on the percentage of GS: 0–10%, 11–20%, >20% and no biopsy performed. The outcome included death-censored graft survival, patient survival, rate of delayed graft function, and 1-year acute rejection. Results: Of 22,006 kidneys, 91.2% were biopsied showing 0–10% GS (58.0%), 11–20% GS (13.5%), >20% GS (19.7%); 8.8% were not biopsied. The rate of kidney discard was 48.5%; 33.6% in 0–10% GS, 68.9% in 11–20% GS, and 77.4% in >20% GS. 49.8% of kidneys were discarded in those that were not biopsied. Death-censored graft survival at 5 years was 75.8% for 0–10% GS, 70.9% for >10% GS, and 74.8% for the no biopsy group. Among kidneys with >10% GS, there was no significant difference in death-censored graft survival between 11–20% GS and >20% GS. Recipients with >10% GS had an increased risk of graft failure (HR = 1.27, p < 0.001), compared with 0–10% GS. There was no significant difference in patient survival, acute rejection at 1-year, and delayed graft function between 0% and 10% GS and >10% GS. Conclusion: In >85% KDPI kidneys, our study suggested that discard rates increased with higher percentages of GS, and GS >10% is an independent prognostic factor for graft failure. Due to organ shortage, future studies are needed to identify strategies to use these marginal kidneys safely and improve outcomes.

AbstractObjectiveVitamin D status plays an important role in immunoregulation, and a deficiency is believed to be related to Graft Versus Host Disease (GVHD) in patients after hematopoietic stem cell transplantation (HSCT). We aim to study the association between vitamin D deficiency and GVHD after HSCT.MethodsA literature search was conducted utilizing MEDLINE, EMBASE, and The Cochrane Library Database from inception to July 2019. Eligible studies were required to1 be clinical trials or observational studies (cohort, case‐control, or cross‐sectional studies);2 provide data to calculate the odds ratios (OR) of GVHD in HSCT patients with vitamin D deficiency. Two reviewers independently extracted the data and assessed the risk of bias. Pooled odds ratios (OR) with 95% confidence interval (CI) were estimated using random‐effects meta‐analysis through the Comprehensive Meta‐Analysis 3.3 software.ResultsIn total, 8 observational studies consisting of 1335 HSCT patients were enrolled in this systematic review. Overall, there was no significant association between vitamin D deficiency and acute GVHD (OR = 1.06, 95% CI 0.74‐1.53, P > 0.05). There was no significant association between vitamin D deficiency and chronic GVHD (OR = 1.75, 95% CI 0.72‐4.26, P > 0.05). Funnel plots and Egger regression asymmetry test were performed and showed no publication bias.ConclusionThere is not a statistically significant association between vitamin D deficiency and neither acute nor chronic GVHD.

Background and objectives This study aimed to investigate the association between in-hospital trajectories of serum sodium and risk of in-hospital and 1-year mortality in patients in hospital. Design, setting, participants, & measurements This is a single-center cohort study. All adult patients who were hospitalized from years 2011 through 2013 who had available admission serum sodium and at least three serum sodium measurements during hospitalization were included. The trend of serum sodium during hospitalization was analyzed using group-based trajectory modeling; the five main trajectories were grouped as follows: ( 1 ) stable normonatremia, ( 2 ) uncorrected hyponatremia, ( 3 ) borderline high serum sodium, ( 4 ) corrected hyponatremia, and ( 5 ) fluctuating serum sodium. The outcome of interest was in-hospital mortality and 1-year mortality. Stable normonatremia was used as the reference group for outcome comparison. Results A total of 43,539 patients were analyzed. Of these, 47% had stable normonatremia, 15% had uncorrected hyponatremia, 31% had borderline high serum sodium, 3% had corrected hyponatremia, and 5% had fluctuating serum sodium trajectory. In adjusted analysis, there was a higher in-hospital mortality among those with uncorrected hyponatremia (odds ratio [OR], 1.33; 95% CI, 1.06 to 1.67), borderline high serum sodium (OR, 1.66; 95% CI, 1.38 to 2.00), corrected hyponatremia (OR, 1.50; 95% CI, 1.02 to 2.20), and fluctuating serum sodium (OR, 4.61; 95% CI, 3.61 to 5.88), compared with those with the normonatremia trajectory. One-year mortality was higher among those with uncorrected hyponatremia (hazard ratio [HR], 1.28; 95% CI, 1.19 to 1.38), borderline high serum sodium (HR, 1.18; 95% CI, 1.11 to 1.26), corrected hyponatremia (HR, 1.24; 95% CI, 1.08 to 1.42), and fluctuating serum sodium (HR, 2.10; 95% CI, 1.89 to 2.33) compared with those with the normonatremia trajectory. Conclusions More than half of patients who had been hospitalized had an abnormal serum sodium trajectory during hospitalization. This study demonstrated that not only the absolute serum sodium levels but also their in-hospital trajectories were significantly associated with in-hospital and 1-year mortality. The highest in-hospital and 1-year mortality risk was associated with the fluctuating serum sodium trajectory. Podcast This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2020_03_25_CJN.12281019.mp3

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.

AbstractBackgroundThe 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.AimsFebuxostat 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.MethodsWe 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.ResultsNine 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).ConclusionTreating 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.

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.