Citations

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

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.

Abstract Background Studies comparing all treatment options for frequently-relapsing/steroid-dependent (FR/SD) minimal change disease (MCD) in adults are lacking. Methods Medical records of 76 adults with FR/SD MCD who were treated with corticosteroids as the first-line therapy were reviewed. Treatment options were compared for the time to relapse, change of therapy and progression (relapse on full-dose treatment). Results Second-line treatments included rituximab (RTX; n = 13), mycophenolate mofetil (MMF; n = 12), calcineurin inhibitors (CNI; n = 26) and cyclophosphamide (CTX; n = 16). During the second-line treatments, 48 (71.6%) patients relapsed at median 17 (range 2–100) months. The majority of relapses occurred during dose tapering or off drug. Twenty of 65 (30.8%) changed therapy after the first relapse. The median time to relapse after the second line was 66 versus 28 months in RTX versus non-RTX groups (P = 0.170). The median time to change of treatment was 66 and 44 months, respectively (P = 0.060). Last-line treatment options included RTX (n = 8), MMF (n = 4), CNI (n = 3) and CTX (n = 2). Seven (41.2%) patients had a relapse during the last-line treatment at median 39 (range 5–112) months. The median time to relapse was 48 versus 34 months in the RTX versus non-RTX groups (P = 0.727). One patient in the RTX group died presumably of heart failure. No major adverse event was observed. During the median follow-up of 81 (range 9–355) months, no patients developed end-stage renal disease. Conclusions Relapse is frequent in MCD in adults. Patients treated with RTX may be less likely to require a change of therapy and more likely to come off immunosuppressive drugs.

Abstract Background Fibrillary glomerulonephritis (FGN) is a rare type of glomerulonephritis with poor prognosis, with no known effective therapies available for treatment. The objective of the study was to evaluate the efficacy and safety of rituximab in treatment of patients with FGN and to investigate the effect of rituximab on DNAJB9 levels. Methods This was a pilot prospective clinical trial in which patients with idiopathic FGN were treated with two courses of rituximab (1 g each) 2 weeks apart at the beginning and then again at 6 months. Primary outcome was defined as preservation of kidney function at 12 months with stable or increased creatinine clearance. Secondary outcome was defined as achieving complete remission (CR) defined as proteinuria &lt;300 mg/24 h or partial remission (PR) with proteinuria &lt;3 g/24 h and at least 50% reduction in the proteinuria. DNAJB9 levels were also measured in the serum at baseline, 6 and 12 months. Results The creatinine clearance did not change significantly during this time, from 47.7 mL/min/1.73 m2 at baseline to 43.7 mL/min/1.73 m2 during follow-up (P = 0.15). Proteinuria declined from 4.43 (1.6–5.53) g/24 h at baseline to 1.9 (0.46–5.26) g/24 h at 12 months but did not reach significance (P = 0.06). None of the patients reached CR, and 3 of the 11 achieved PR. There was no change in the DNAJB9 levels following treatment with rituximab. The most common adverse event was nasal congestion, fatigue and muscle cramps. Conclusions Treatment of patients with two courses of rituximab over a span of 6 months was associated with stabilization of renal function but did not result in a significant change in proteinuria and with no change in the DNAJB9 levels.

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

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

ABSTRACTAimThis study aimed to assess the relationship between admission Calcium‐phosphate (CaP) and in‐hospital mortality in hospitalized patients.MethodsAll adult hospitalized patients who had both admission serum calcium and phosphate levels available between years 2009 and 2013 were enrolled. Admission CaP was categorized based on its distribution into six groups (<21, 21–<27, 27–<33, 33 39, 39–<45 and ≥45 mg2/dL2). Multivariate logistic regression was used to assess the association between admission CaP and in‐hospital mortality, using the CaP of 27–<33 mg2/dL2 as the reference group.ResultsAbut 14 772 patients were included in the analysis. The association between CaP and in‐hospital mortality was U‐shaped with the lowest in‐hospital mortality in CaP of 27–<33 mg2/dL2. After adjusting for potential confounders, both CaP <21 and ≥39 mg2/dL2 were associated with higher in‐hospital mortality. Subgroup analysis demonstrated that the highest in‐hospital mortality risk in both chronic kidney disease (CKD) and non‐CKD patients occurred when CaP ≥ 45 mg2/dL2.ConclusionCaP levels on admission were associated with in‐hospital mortality. Highest mortality risk was observed in hospitalized patients with admission CaP of ≥45 mg2/dL2 in both CKD and non‐CKD patients.