Serum Phosphorus Management with Sucroferric Oxyhydroxide as a First-Line Phosphate Binder within the First Year of Hemodialysis.

INTRODUCTION: Sucroferric oxyhydroxide (SO), a non-calcium, chewable, iron-based phosphate binder (PB), effectively lowers serum phosphorus (sP) concentrations while reducing pill burden relative to other PBs. To date, SO studies have largely examined treatment-experienced, prevalent hemodialysis populations. We aimed to explore the role of first-line SO initiated during the first year of dialysis. METHODS: We retrospectively analyzed deidentified data from adults receiving in-center hemodialysis who were prescribed SO monotherapy within the first year of hemodialysis as part of routine clinical care. All patients continuing SO monotherapy for 12 months were included. Changes from baseline in sP, achievement of sP ≤5.5 and ≤4.5 mg/dL, and other laboratory parameters were analyzed quarterly for 1 year. RESULTS: The overall cohort included 596 patients, 286 of whom had a dialysis vintage ≤3 months. In the 3 months preceding SO initiation, sP rapidly increased (mean increases of 1.02 and 1.65 mg/dL in the overall cohort and incident cohort, respectively). SO treatment was associated with significant decreases in quarterly sP (mean decreases of 0.26-0.36; p < 0.0001 for each quarter and overall). While receiving SO, 55-60% of patients achieved sP ≤5.5 mg/dL and 21-24% achieved sP ≤4.5 mg/dL (p < 0.0001 for each quarter and overall vs. baseline). Daily PB pill burden was approximately 4 pills. Serum calcium concentrations increased and intact parathyroid hormone concentrations decreased during SO treatment (p < 0.0001 vs. baseline). CONCLUSIONS: Among patients on hemodialysis, initiating SO as a first-line PB resulted in significant reductions in sP while maintaining a relatively low PB pill burden.

Acute kidney injury among salicylate intoxication hospitalisations in the United States.

BACKGROUND: This study aimed to evaluate the risk factors and the association of acute kidney injury (AKI) with outcomes, and resource utilisation in patients hospitalised because of salicylate intoxication in the United States. METHODS: Hospitalised patients with a primary diagnosis of salicylate intoxication from 2003 to 2014 were identified in the National Inpatient Sample (NIS) database. End-stage kidney disease patients were excluded. The occurrence of AKI was identified using hospital diagnosis code. Clinical characteristics, in-hospital treatment, outcomes and resource utilisation were compared between patients with and without AKI. RESULTS: A total of 13 787 eligible hospital admissions were included in the analysis. AKI occurred in 1279 (9.3%) admissions. Older age, male sex, more recent year of hospitalisation, anaemia, hypertension, congestive heart failure, chronic kidney disease, volume depletion, sepsis and ventricular arrhythmia/cardiac arrest were significantly associated with increased risk of AKI, whereas Hispanic race was associated with decreased risk. AKI was significantly associated with increased risk of organ failure, and in-hospital mortality. In addition, the need for ventilation support, blood component transfusion, renal replacement therapy, length of hospital stay and hospitalisation cost were higher in AKI patients. CONCLUSION: Approximately one tenth of salicylate intoxication patients developed AKI during hospitalisation. AKI was associated with higher morbidity, mortality and resource utilisations.

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.

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.

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.

Impact of ANCA-Associated Vasculitis on Outcomes of Hospitalizations for Goodpasture's Syndrome in the United States: Nationwide Inpatient Sample 2003-2014.

Background and objectives: Goodpasture's syndrome (GS) is a rare, life-threatening autoimmune disease. Although the coexistence of anti-neutrophil cytoplasmic antibody (ANCA) with Goodpasture's syndrome has been recognized, the impacts of ANCA vasculitis on mortality and resource utilization among patients with GS are unclear. Materials and Methods: We used the National Inpatient Sample to identify hospitalized patients with a principal diagnosis of GS from 2003 to 2014 in the database. The predictor of interest was the presence of ANCA-associated vasculitis. We tested the differences concerning in-hospital treatment and outcomes between GS patients with and without ANCA-associated vasculitis using logistic regression analysis with adjustment for other clinical characteristics. Results: A total of 964 patients were primarily admitted to hospital for GS. Of these, 84 (8.7%) had a concurrent diagnosis of ANCA-associated vasculitis. Hemoptysis was more prevalent in GS patients with ANCA-associated vasculitis. During hospitalization, GS patients with ANCA-associated required non-significantly more mechanical ventilation and non-invasive ventilation support, but non-significantly less renal replacement therapy and plasmapheresis than those with GS alone. There was no significant difference in in-hospital outcomes, including organ failure and mortality, between GS patients with and without ANCA-associated vasculitis. Conclusions: Our study demonstrated no significant differences between resource utilization and in-hospital mortality among hospitalized patients with coexistence of ANCA vasculitis and GS, compared to those with GS alone.

Outcomes of patients with autosomal-dominant polycystic kidney disease on peritoneal dialysis: A meta-analysis.

BACKGROUND: Complications related to peritoneal dialysis (PD) in patients with autosomal-dominant polycystic kidney disease (ADPKD), including intraperitoneal rupture of renal cyst, hernia, membrane failure and peritonitis, have been reported. However, long-term clinical outcomes of ADPKD patients on PD remain unclear. We performed this meta-analysis to assess the risks of death, technique failure and peritonitis in ADPKD patients on PD. METHODS: A systematic review was conducted using MEDLINE, EMBASE and Cochrane databases from inception to October 2017 to identify studies that evaluated the outcomes of ADPKD patients on PD, including the risks of death, technique failure and peritonitis. Non-ADPKD patients on PD were used as controls. Effect estimates from the individual study were extracted and combined using the random-effect, generic inverse variance method of DerSimonian and Laird. RESULTS: Twelve cohort studies with a total of 14 673 patients on PD (931 ADPKD and 13 742 non-ADPKD patients) were enrolled. Compared with non-ADPKD status, ADPKD was associated with significantly decreased mortality risk with pooled odds ratio (OR) of 0.68 (95% confidence interval (CI), 0.53-0.86; I2 = 0). There were no associations of ADPKD with the risks of technique failure of PD and peritonitis with pooled OR of 0.93 (95% CI, 0.79-1.10; I2 = 0) and 0.88 (95% CI, 0.75-1.05; I2 = 0), respectively. We found no publication bias as assessed by Egger's regression asymmetry test, with P = 0.90, 0.28 and 0.60 for the risks of mortality, technique failure and peritonitis in ADPKD patients on PD, respectively. CONCLUSION: Compared with non-ADPKD patients on PD, our study demonstrates that ADPKD patients on PD have 0.68-fold decreased mortality risk. There are no associations of ADPKD status with the risks of technique failure or peritonitis.

Kidney Recovery From Acute Kidney Injury After Hematopoietic Stem Cell Transplant: A Systematic Review and Meta-Analysis.

Patients with the recovery of kidney function after an episode of acute kidney injury (AKI) have better outcomes compared to those without recovery. The current systematic review is conducted to assess the rates of kidney function recovery among patients with AKI or severe AKI requiring kidney replacement therapy (KRT) within 100 days after hematopoietic stem cell transplant (HSCT). Methods The Ovid MEDLINE, EMBASE, and Cochrane databases were systemically searched from database inceptions through August 2019 to identify studies reporting the rates of recovery from AKI after HSCT. The random-effects and generic inverse variance methods of DerSimonian-Laird were used to combine the effect estimates obtained from individual studies. Results A total of 458 patients from eight cohort studies with AKI after HSCT were identified. Overall, the pooled estimated rates of AKI recovery among patients with AKI and severe AKI requiring KRT within 100 days were 58% (95%CI: 37%-78%) and 10% (95%CI: 2%-4%), respectively. Among patients with AKI recovery, the pooled estimated rates of complete and partial AKI recovery were 60% (95%CI: 39%-78%) and 29% (95%CI: 10%-61%), respectively. There was no clear correlation between study year and the rate of AKI recovery (p=0.26). Conclusion The rate of recovery from AKI after HSCT depends on the severity of AKI. While recovery is common, complete recovery is reported in about two-thirds of all AKI patients. The rate of recovery among those with AKI requiring renal replacement therapy (RRT) is substantially lower.

Incidence and Characteristics of Kidney Stones in Patients on Ketogenic Diet: A Systematic Review and Meta-Analysis.

Very-low-carbohydrate diets or ketogenic diets are frequently used for weight loss in adults and as a therapy for epilepsy in children. The incidence and characteristics of kidney stones in patients on ketogenic diets are not well studied. Methods: A systematic literature search was performed, using MEDLINE, EMBASE, and Cochrane Database of Systematic Reviews from the databases' inception through April 2020. Observational studies or clinical trials that provide data on the incidence and/or types of kidney stones in patients on ketogenic diets were included. We applied a random-effects model to estimate the incidence of kidney stones. Results: A total of 36 studies with 2795 patients on ketogenic diets were enrolled. The estimated pooled incidence of kidney stones was 5.9% (95% CI, 4.6-7.6%, I2 = 47%) in patients on ketogenic diets at a mean follow-up time of 3.7 +/- 2.9 years. Subgroup analyses demonstrated the estimated pooled incidence of kidney stones of 5.8% (95% CI, 4.4-7.5%, I2 = 49%) in children and 7.9% (95% CI, 2.8-20.1%, I2 = 29%) in adults, respectively. Within reported studies, 48.7% (95% CI, 33.2-64.6%) of kidney stones were uric stones, 36.5% (95% CI, 10.6-73.6%) were calcium-based (CaOx/CaP) stones, and 27.8% (95% CI, 12.1-51.9%) were mixed uric acid and calcium-based stones, respectively. Conclusions: The estimated incidence of kidney stones in patients on ketogenic diets is 5.9%. Its incidence is approximately 5.8% in children and 7.9% in adults. Uric acid stones are the most prevalent kidney stones in patients on ketogenic diets followed by calcium-based stones. These findings may impact the prevention and clinical management of kidney stones in patients on ketogenic diets.

The impact of race on hospitalization outcomes for goodpasture's syndrome in the United States: nationwide inpatient sample 2003-2014.

BACKGROUND: Goodpasture's syndrome is a rare and life-threatening autoimmune disease. While Goodpasture's syndrome is well described in Caucasian and Asian populations, its prevalence and outcomes among African American and Hispanic populations are unclear. We conducted this study to assess the impacts of race on hospital outcomes among patients with Goodpasture's syndrome. METHODS: The National Inpatient Sample database was used to identify hospitalized patients with a principal diagnosis of Goodpasture's syndrome from 2003 to 2014. Goodpasture's syndrome patients were grouped based on their race. The differences in-hospital supportive care for organ failure and outcomes between Caucasian, African American, and Hispanic Goodpasture's syndrome patients were assessed using logistic regression analysis. RESULTS: Nine hundred and sixty-four patients were hospitalized with a primary diagnosis of Goodpasture's syndrome. Of these, 786 were included in the analysis: 622 (79%) were Caucasian, 73 (9%) were African American, and 91 (12%) were Hispanic. Hispanics had significantly lower use of plasmapheresis. The use for mechanical ventilation, noninvasive ventilation support, and renal replacement therapy in African Americans and Hispanics were comparable to Caucasians. There was no significant difference in organ failure, sepsis, and in-hospital mortality between African Americans and Caucasians. In contrast, Hispanics had higher in-hospital mortality than Caucasians but similar risk of organ failure and sepsis. CONCLUSION: African American and Hispanic populations account for 9% and 12% of hospitalizations for Goodpasture's syndrome, respectively. While there is no significant difference in in-hospital mortality between African Americans and Caucasians, Hispanics with Goodpasture's syndrome carry a higher in-hospital mortality compared to Caucasians.

Efficacy and Safety of SGLT-2 Inhibitors for Treatment of Diabetes Mellitus among Kidney Transplant Patients: A Systematic Review and Meta-Analysis.

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/1.73m2) 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.

Impact of Admission Calcium-phosphate Product on 1-year Mortality among Hospitalized Patients.

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: <21, 21-<27, 27-<33, 33-<39, 39-<45, and ≥45 mg2/dL2. Multivariate cox proportional hazard analysis was performed to evaluate the association between admission calcium-phosphate product and 1-year mortality, using the calcium-phosphate product of 33-<39 mg2/dL2 as the reference group. RESULTS: A total of 14,772 patients were included in this study. The mean admission calcium-phosphate product was 34.4 ± 11.3 mg2/dL2. Of these patients, 3194 (22%) died within 1 year of hospital admission. In adjusted analysis, admission calcium-phosphate product of ≥45 mg2/dL2 was significantly associated with increased 1-year mortality with hazard ratio of 1.41 (95% 95% confidence interval 1.25-1.67), whereas lower admission calcium-phosphate product was not significantly associated with 1-year mortality. CONCLUSION: Elevated calcium-phosphate product was significantly associated with increased 1-year mortality in hospitalized patients.

Association of serum magnesium level change with in-hospital mortality.

The objective of this study was to assess the association of in-hospital mortality risk based on change in serum magnesium levels in hospitalised patients. All adult patients admitted to our hospital from years 2009 to 2013 with at least two serum magnesium measurements during hospitalisation were included. Serum magnesium change, defined as the absolute difference between the highest and lowest serum magnesium, was categorised into six groups: 0-0.2, 0.3-0.4, 0.5-0.6, 0.7-0.8, 0.9-1.0, ≥1.1 mg/dL. In-hospital mortality was the outcome of interest. Logistic regression was used to assess the association between serum magnesium change and in-hospital mortality, using serum magnesium change of 0.0-0.2 mg/dL as the reference group. A total of 42 141 patients, with the median serum magnesium change during hospital stay of 0.3 (IQR 0.2-0.6) mg/dL, were studied. In-hospital mortality based on serum magnesium change of 0-0.2, 0.3-0.4, 0.5-0.6, 0.7-0.8, 0.9-1.0, ≥1.1 mg/dL was 1.3%, 2.3%, 3.1%, 5.0%, 6.5%, and 8.8%, respectively (p<0.001). After adjustment for potential confounders, increased serum magnesium change was significantly associated with higher in-hospital mortality with adjusted OR of 1.39 (95% 1.14-1.69) in serum magnesium change of 0.3-0.4, 1.48 (95% CI 1.21 to 1.81) in 0.5-0.6, 1.89 (95% CI 1.53 to 2.34) in 0.7-0.8, 1.85 (95% CI 1.45 to 2.37) in 0.9-1.0 and 1.89 (95% CI 1.48 to 2.41) in ≥1.1 mg/dL when compared with serum magnesium change group of 0-0.2 mg/dL. Increased in-hospital mortality was associated with both downward and upward trends of serum magnesium change during hospitalisation. The greater extent of change in serum magnesium levels was progressively associated with increased in-hospital mortality.

Hospitalizations for Acute Salicylate Intoxication in the United States.

BACKGROUND: The objective of this study was to describe inpatient prevalence, characteristics, outcomes, and resource use for acute salicylate intoxication hospitalizations in the United States. METHODS: A total of 13,805 admissions with a primary diagnosis of salicylate intoxication from 2003 to 2014 in the National Inpatient Sample database were analyzed. Prognostic factors for in-hospital mortality were determined using multivariable logistic regression. RESULTS: The overall inpatient prevalence of salicylate intoxication among hospitalized patients was 147.8 cases per 1,000,000 admissions in the United States. The average age was 34 ± 19 years. Of these, 35.0% were male and 65.4% used salicylate for suicidal attempts. Overall, 6% required renal replacement therapy. The most common complications of salicylate intoxication were electrolyte and acid-base disorders, including hypokalemia (25.4%), acidosis (19.1%), and alkalosis (11.1%). Kidney failure (9.3%) was the most common observed organ dysfunction. In-hospital mortality was 1.0%. Increased in-hospital mortality was associated with age ≥30, Asian/Pacific Islander race, diabetes mellitus, hyponatremia, ventricular arrhythmia, kidney failure, respiratory failure, and neurological failure, while decreased in-hospital mortality was associated with African American and Hispanic race. CONCLUSION: hospitalization for salicylate intoxication occurred in 148 per 1,000,000 admissions in the United States. Several factors were associated with in-hospital mortality.

SGLT2 Inhibitors and Kidney Outcomes in Patients with Chronic Kidney Disease.

Globally, diabetes mellitus is a leading cause of kidney disease, with a critical percent of patients approaching end-stage kidney disease. In the current era, sodium-glucose co-transporter 2 inhibitors (SGLT2i) have emerged as phenomenal agents in halting the progression of kidney disease. Positive effects of SGLT2i are centered on multiple mechanisms, including glycosuric effects, tubule-glomerular feedback, antioxidant, anti-fibrotic, natriuretic, and reduction in cortical hypoxia, alteration in energy metabolism. Concurrently, multiple kidney and cardiovascular outcome studies have reported remarkable advantages of SGLT2i including mortality benefits. Additionally, the superiority of combination therapies (SGLT2I along with metformin/DDP-4 Inhibitors) in treatment-naïve diabetic patients is further looked into with potential signal towards glycemic and blood pressure control. Reported promising results initiate a gateway for future research targeting kidney outcomes with combination therapies as an initial approach. In the current paper, we summarize leading cardiovascular and kidney outcome trials in patients with type 2 diabetes, the role of SGLT2i in non-diabetic proteinuric kidney disease, and the potential mechanisms of action of SGLT2i with special focus on combination therapy as an initial therapeutic approach in treatment-naïve diabetic patients.

Outcomes of Kidney Transplantation in Fabry Disease: A Meta-Analysis.

BACKGROUND: Fabry disease (FD) is a rare X-linked lysosomal storage disorder with progressive systemic deposition of globotriaosylceramide, leading to life-threatening cardiac, central nervous system, and kidney disease. Current therapy involves symptomatic medical management, enzyme replacement therapy (ERT), dialysis, kidney transplantation, and, more recently, gene therapy. The aim of this systematic review was to assess outcomes of kidney transplantation among patients with FD. METHODS: A comprehensive literature review was conducted utilizing MEDLINE, EMBASE, and Cochrane Database, from inception through to 28 February 2020, to identify studies that evaluate outcomes of kidney transplantation including patient and allograft survival among kidney transplant patients with FD. Effect estimates from each study were extracted and combined using the random-effects generic inverse variance method of DerSimonian and Laird. RESULTS: In total, 11 studies, including 424 kidney transplant recipients with FD, were enrolled. The post-transplant median follow-up time ranged from 3 to 11.5 years. Overall, the pooled estimated rates of all-cause graft failure, graft failure before death, and allograft rejection were 32.5% (95%CI: 23.9%-42.5%), 14.5% (95%CI: 8.4%-23.7%), and 20.2% (95%CI: 15.4%-25.9%), respectively. In the sensitivity analysis, limited only to the recent studies (year 2001 or newer when ERT became available), the pooled estimated rates of all-cause graft failure, graft failure before death, and allograft rejection were 28.1% (95%CI: 20.5%-37.3%), 11.7% (95%CI: 8.4%-16.0%), and 20.2% (95%CI: 15.5%-26.0%), respectively. The pooled estimated rate of biopsy proven FD recurrence was 11.1% (95%CI: 3.6%-29.4%), respectively. There are no significant differences in the risks of all-cause graft failure (p = 0.10) or mortality (0.48) among recipients with vs. without FD. CONCLUSIONS: Despite possible FD recurrence after transplantation of 11.1%, allograft and patient survival are comparable among kidney transplant recipients with vs. without FD.

Serum Klotho in Living Kidney Donors and Kidney Transplant Recipients: A Meta-Analysis.

α-Klotho is a known anti-aging protein that exerts diverse physiological effects, including phosphate homeostasis. Klotho expression occurs predominantly in the kidney and is significantly decreased in patients with chronic kidney disease. However, changes in serum klotho levels and impacts of klotho on outcomes among kidney transplant (KTx) recipients and kidney donors remain unclear. A literature search was conducted using MEDLINE, EMBASE, and Cochrane Database from inception through October 2019 to identify studies evaluating serum klotho levels and impacts of klotho on outcomes among KTx recipients and kidney donors. Study results were pooled and analyzed utilizing a random-effects model. Ten cohort studies with a total of 431 KTx recipients and 5 cohort studies with a total of 108 living kidney donors and were identified. After KTx, recipients had a significant increase in serum klotho levels (at 4 to 13 months post-KTx) with a mean difference (MD) of 243.11 pg/mL (three studies; 95% CI 67.41 to 418.81 pg/mL). Although KTx recipients had a lower serum klotho level with a MD of = -234.50 pg/mL (five studies; 95% CI -444.84 to -24.16 pg/mL) compared to healthy unmatched volunteers, one study demonstrated comparable klotho levels between KTx recipients and eGFR-matched controls. Among kidney donors, there was a significant decrease in serum klotho levels post-nephrectomy (day 3 to day 5) with a mean difference (MD) of -232.24 pg/mL (three studies; 95% CI -299.41 to -165.07 pg/mL). At one year following kidney donation, serum klotho levels remained lower than baseline before nephrectomy with a MD of = -110.80 pg/mL (two studies; 95% CI 166.35 to 55.24 pg/mL). Compared to healthy volunteers, living kidney donors had lower serum klotho levels with a MD of = -92.41 pg/mL (two studies; 95% CI -180.53 to -4.29 pg/mL). There is a significant reduction in serum klotho levels after living kidney donation and an increase in serum klotho levels after KTx. Future prospective studies are needed to assess the impact of changes in klotho on clinical outcomes in KTx recipients and living kidney donors.

Hospital-Acquired Serum Chloride Derangements and Associated In-Hospital Mortality.

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.

Impact of admission serum magnesium levels on long-term mortality in hospitalized patients.

BACKGROUND: The impact of admission serum magnesium on long-term mortality in hospitalized patients was unclear. This study aimed to assess the long-term mortality risk based on admission of serum magnesium in hospitalized patients. METHODS: This was a retrospective cohort study conducted at a tertiary referral hospital. We included all adult patients admitted to Mayo Clinic Hospital, Minnesota, between 1 January 2009 and 31 December 2013, who had available admission serum magnesium. We categorized serum magnesium into ≤1.4, 1.5-1.6, 1.7-1.8, 1.9-2.0, 2.1-2.2, ≥2.3 mg/dL. We estimated the 1-year mortality risk based on various admission serum magnesium levels using Kaplan-Meier plot and assessed the association of admission serum magnesium with 1-year mortality using Cox proportional hazard analysis. We selected serum magnesium of 1.7-1.8 mg/dL as the reference group for mortality comparison. RESULTS: We included a total of 65,974 patients, with a mean admission serum magnesium of 1.9 ± 0.3 mg/dL in this study. The 1-year mortality was 15.7%, 15.8%, 15.5%, 16.7%, 19.0%, and 25.6% in admission serum magnesium of ≤1.4, 1.5-1.6, 1.7-1.8, 1.9-2.0, 2.1-2.2, ≥2.3 mg/dL, respectively (p < 0.001). After adjustment for confounders, admission serum magnesium of 1.9-2.0, 2.1-2.2, and ≥2.3 mg/dL were significantly associated with increased 1-year mortality compared with magnesium of 1.7-1.8 mg/dL with adjusted HR of 1.09 (95% CI 1.02-1.15), 1.22 (95% CI 1.14-1.30), and 1.55 (95% CI 1.45-1.55), respectively. There was no significant difference in 1-year mortality risk between low serum magnesium ≤1.6 mg/dL and magnesium of 1.7-1.8 mg/dL. CONCLUSION: Hypermagnesemia, but not hypomagnesemia, at the time of hospital admission was associated with increased 1-year mortality among hospitalized patients.

Impact of rhabdomyolysis on outcomes of hospitalizations for heat stroke in the United States.

BACKGROUND: The objective of this study was to evaluate the predictors and associated outcomes of rhabdomyolysis in admitted patients for heat stroke in the United States. METHODS: The National Inpatient Sample was utilized to identify hospitalized patients with a primary diagnosis of heat stroke from the years 2003-2014. Rhabdomyolysis was identified using hospital diagnosis code. We compared the clinical characteristics, in-hospital treatment, complications, outcomes, and resource utilization between patients with and without rhabdomyolysis. RESULTS: A total of 3,372 hospital admissions for heat stroke were studied. Of these, rhabdomyolysis occurred in 1049 (31%) admissions. The risk factors for rhabdomyolysis were age 20-39 years, male sex, African American race, history of alcohol drinking, whereas age ≥60 years, smoking, history of diabetes mellitus, and hypertension were associated with lower risk of rhabdomyolysis. Patients with rhabdomyolysis had greater requirements for mechanical ventilation, blood component transfusion, and renal replacement therapy. Rhabdomyolysis was significantly associated with increased risk of hyponatremia, hypernatremia, hyperkalemia, hypocalcemia, serum phosphorus and magnesium derangement, metabolic acidosis, sepsis, ventricular arrhythmia or cardiac arrest, renal failure, respiratory failure, liver failure, neurological failure, hematologic failure, and in-hospital mortality. Length of hospital stay and hospitalization cost were higher when rhabdomyolysis occurred during hospital stay. CONCLUSION: Rhabdomyolysis occurred in about one-third of hospitalized patients for heat stroke and was associated with increased morbidity, mortality, and resource utilization.