Complications After Hand-Assisted Laparoscopic Living Donor Nephrectomy.

OBJECTIVE: To study the complications of hand-assisted laparoscopic living donor nephrectomy (HALLDN) with an emphasis on complications occurring early after hospital discharge up to 120 days after surgery. PATIENTS AND METHODS: We retrospectively categorized complications using the Clavien-Dindo classification in 3002 HALLDNs performed at 1 center from January 1, 2000, through December 31, 2019. In addition to overall summaries, modeling was used to identify correlates of complications before and after living donation. RESULTS: Of these donors, 87% were White, 59% were female, the mean age was 45 years (range, 18-77 years), 30.3% had a body mass index of at least 30, and 36.3% had previous abdominopelvic surgery. There were no deaths related to the surgery. The incidence of major complications (intraoperative complications plus Clavien-Dindo grade ≥III postoperatively) was 2.5% (n=74). The overall complication rate was 12.4% (n=371), including 15 intraoperative, 76 postoperative before discharge, and 280 after discharge to 120 days. Reoperation was required in 1.8% of patients (n=54), and all but 1 of these were incision-related problems. Seventy-six percent of all complications occurred after discharge, including 85% of the reoperations. For major complications, no risk factor was found. Risk factors for any complication included paramedian incision (hazard ratio [HR], 2.54; 95% CI, 1.49 to 4.34; P<.001); a history of abdominopelvic surgery (HR, 1.37; 95% CI, 1.07 to 1.76; P=.01), male sex (HR, 1.37; 95% CI, 1.07 to 1.76; P=.01), non-White race (HR, 1.40; 95% CI, 1.05 to 1.88; P=.02), and early era of the experience. CONCLUSION: Most major complications of HALLDN occur after discharge, suggesting that close follow-up is warranted and that the current literature may underestimate the true incidence.

Chronic graft-versus-host disease in pancreas after kidney transplant recipients - An unrecognized entity.

Graft-versus-host disease (GVHD), a common complication after peripheral blood stem cell or bone marrow transplantation, rarely occurs in kidney and pancreas transplant recipients. The true incidence may be confounded by the rarity of the disorder, with a resultant lack of appreciation of the diagnosis as a potential cause of common clinical manifestations such as cytopenias and immune dysfunction. Reports of GVHD in kidney and pancreas transplant recipients almost uniformly describe patients in the early posttransplant period (days to months) with the typical manifestations of acute GVHD involving the skin, liver, and intestines. In contrast, reports of solid organ transplant recipients with clinical features more consistent with chronic GVHD (cGVHD) are lacking, raising concern of underrecognition of this severe complication. Occurrence later after transplant may be even more likely to result in lack of recognition. We report 2 cases of possible cGVHD occurring in recipients of pancreas after kidney transplantation, which were diagnosed at 5.5 and 42 months after pancreas transplant. Both patients presented with severe pancytopenia, multiple opportunistic infections, and features suggestive of cGVHD. Transplant professionals should be aware of the possibility of acute and cGVHD in pancreas after kidney transplant recipients and be able to recognize the clinical manifestations.

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.

Impact of admission serum ionized calcium levels on risk of acute kidney injury in hospitalized patients.

This study aimed to investigate the risk of acute kidney injury (AKI) in hospitalized patients based on admission serum ionized calcium levels. This is a cohort study of all hospitalized adult patients, from January 2009 to December 2013 at a tertiary referral hospital, who had available serum ionized calcium at the time of admission. We excluded patients who had end-stage kidney disease or AKI at admission. We stratified admission serum ionized calcium into 6 groups; ≤ 4.39, 4.40-4.59, 4.60-4.79, 4.80-4.99, 5.00-5.19, and ≥ 5.20 mg/dL. We used serum creatinine criterion of KDIGO definition for diagnosis of AKI. We performed logistic regression analysis to assess the risk of in-hospital AKI occurrence based on admission serum ionized calcium, using serum ionized calcium of 5.00-5.19 mg/dL as the reference group. We studied a total of 25,844 hospitalized patients. Of these, 3,294 (12.7%) developed AKI in hospital, and 622 (2.4%) had AKI stage 2 or 3. We observed a U-shaped association between admission serum ionized calcium and in-hospital AKI, with nadir in-hospital AKI was in serum ionized calcium of 5.00-5.19 mg/dL. After adjustment for confounders, low serum ionized calcium of 4.40-4.59, ≤ 4.39 mg/dL and elevated serum ionized calcium ≥ 5.20 mg/dL were associated with increased risk of AKI with odds ratio of 1.33 (95% CI 1.14-1.56), 1.45 (95% CI 1.21-1.74), and 1.26 (95% CI 1.04-1.54), respectively. Both hypocalcemia, and hypercalcemia at the time of admission were associated with an increased risk of hospital-acquired AKI.

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.

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.

Trajectories of Serum Sodium on In-Hospital and 1-Year Survival among Hospitalized Patients.

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.

Risk of acute respiratory failure among hospitalized patients with various admission serum albumin levels: A cohort study.

Serum albumin is a marker of nutritional and frailty status. This study aimed to assess the association between serum albumin at the time of admission and the risk of acute respiratory failure (ARF) in hospitalized patientsThis cohort study, performed at a tertiary referral hospital, included all hospitalized adult patients from January 2009 to December 2013 who had serum albumin measurement and were not on mechanical ventilation within 24 hours of hospital admission. Serum albumin was stratified into 2.4, 2.5 to 2.9, 3.0 to 3.4, 3.5 to 3.9, 4.0 to 4.4, and ≥4.5 g/dL. Multivariate logistic regression analysis was performed to obtain adjusted odds ratio (OR) of risk of ARF requiring mechanical ventilation based on various admission serum albumin levels.Of 12,719 patients, ARF requiring mechanical ventilation occurred in 1128 (8.9%) during hospitalization. Hypoalbuminemia was associated with increased risk of ARF, in particular when serum albumin was ≤2.4 g/dL. Compared with serum albumin of 4.0-4.4 g/dL, serum albumin ≤2.4 g/dL at admission was associated with 2.38-time higher odds of ARF during hospitalization (OR 2.38, 95% confidence interval [CI] 1.84-3.07). In contrast, elevated serum albumin ≥4.5 g/dL was associated with lower odds of ARF (OR 0.68, 95% CI 0.48-0.97).Admission serum albumin level lower than 3.5 g/dL was associated with a higher risk of ARF requiring mechanical ventilation, whereas elevated serum albumin level at least 4.5 g/dL was associated with a lower risk of ARF. Therefore, admission albumin level at admission might be useful in the prediction of ARF during hospitalization.

Risk of respiratory failure among hospitalized patients with various admission serum potassium levels.

BACKGROUND: The objective of this study was to assess the relationship between admission serum potassium and the risk of respiratory failure requiring mechanical ventilation in all hospitalized patients. METHODS: All non-dialysis and non-mechanically ventilated patients who had serum potassium measurement at admission from 2011 to 2013 were studied. Serum potassium levels were stratified into five groups; ≤3.4, 3.5 to 3.9, 4.0 to 4.4, 4.5 to 4.9, 5.0 to 5.4, and ≥5.5 mEq/L. The outcome of interest was the respiratory failure requiring mechanical ventilation during hospitalization. Logistic regression analysis was performed to assess the independent risk of in-hospital respiratory failure requiring mechanical ventilation based on various admission serum potassium, using serum potassium of 4.0 to 4.4 mEq/L as the reference group. RESULTS: Of 67,034 eligible patients, with the mean admission serum potassium of 4.2 ± 0.5 mEq/L, 2,886 (4.3%) patients developed respiratory failure requiring mechanical ventilation during hospitalization. As demonstrated by U-shaped association, increased risk of in-hospital respiratory failure was significantly associated with low admission serum potassium ≤ 3.4 mEq/L (odds ratio 1.36, p-value <0.001) and high admission serum potassium ≥5.5 mEq/L (odds ratio 1.37, p-value = 0.01). CONCLUSION: Increased risk of in-hospital respiratory failure requiring mechanical ventilation was noted when serum potassium was below 3.5 mEq/L or above 5.4 mEq/L at the time of hospital admission. Patients with either hypokalemia or hyperkalemia are at risk of respiratory failure requiring mechanical ventilation.

Hospital mortality and long-term mortality among hospitalized patients with various admission serum ionized calcium levels.

BACKGROUND: We conducted a single-center historical cohort study to evaluate the association between admission serum ionized calcium and mortality in hospitalized patients. METHODS: We included hospitalized patients from January 2009 to December 2013 who had available serum ionized calcium at the time of admission. We assessed the in-hospital and 1-year mortality risk based on admission serum ionized calcium using multivariate logistic and Cox proportional hazard analysis, respectively. To test non-linear association, we categorized serum ionized calcium into six groups; ≤4.39, 4.40-4.59, 4.60-4.79, 4.80-4.99, 5.00-5.19, ≥5.20 mg/dL and selected serum ionized calcium of 4.80-4.99 mg/dL as a reference group. RESULTS: We studied a total of 33,255 hospitalized patients. The mean admission serum ionized calcium at 4.8 ± 0.4 mg/dL. Hospital and 1-year mortality observed in 1,099 (3%) and 5,239 (15.8%), respectively. We observed a U-shaped association between admission serum ionized calcium and in-hospital and 1-year mortality. Ionized calcium lower threshold for increased in-hospital and 1-year mortality rates was ≤4.59 and ≤4.39 mg/dL, respectively. Ionized calcium upper threshold for increased in-hospital and 1-year mortality rates was ≥5.20 mg/dL. CONCLUSION: Both hypocalcemia and hypercalcemia were associated with increased short- and long-term mortality with a U-shape relationship.

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.

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.

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 Association of Low Admission Serum Creatinine with the Risk of Respiratory Failure Requiring Mechanical Ventilation: A Retrospective Cohort Study.

To assess the association between low serum creatinine (SCr) value at admission and the risk of respiratory failure requiring mechanical ventilation in hospitalized patients. A retrospective cohort study was conducted at a tertiary referral hospital. All hospitalized adult patients from 2011 through 2013 who had an admission SCr value were included in this study. Patients who were mechanically ventilated at the time of admission were excluded. Admission creatinine was stratified into 7 groups: ≤0.4, 0.5-0.6, 0.7-0.8, 0.9-1.0, 1.1-1.2, 1.3-1.4, and ≥1.5 mg/dL. The primary outcome was the occurrence of respiratory failure requiring mechanical ventilation during hospitalization. Logistic regression analysis was used to assess the independent risk of respiratory failure based on various admission SCr, using SCr of 0.7-0.8 mg/dL as the reference group in the analysis of all patients and female subgroup and of 0.9-1.0 mg/dL in analysis of male subgroup. A total of 67,045 eligible patients, with the mean admission SCr of 1.0 ± 0.4 mg/dL, were studied. Of these patients, 799 (1.1%) had admission SCr of ≤0.4 mg/dL, and 2886 (4.3%) developed respiratory failure requiring mechanical ventilation during hospitalization. The U-curve relationship between admission SCr and respiratory failure during hospitalization was observed, with the nadir incidence of in-hospital respiratory failure in SCr of 0.7-0.8 mg/dL and increased in-hospital respiratory failure associated with both reduced and elevated admission SCr. After adjustment for confounders, very low admission SCr of ≤0.4 mg/dL was significantly associated with increased in-hospital respiratory failure (OR 3.11; 95% CI 2.33-4.17), exceeding the risk related to markedly elevated admission SCr of ≥1.5 mg/dL (OR 1.61; 95% CI 1.39-1.85). The association remained significant in the subgroup analysis of male and female patients. Low SCr value at admission is independently associated with increased in-hospital respiratory failure requiring mechanical ventilation in hospitalized patients.

The Propensity for Inducing Atrial Fibrillation: A Comparative Study on Old versus Young Rabbits.

It is well established that atrial fibrillation (AF) is far more common in elderly humans. Autonomic activation is thought to be an operative mechanism for AF propensity. The aim of the study was to investigate the impact of age on atrial tachyarrhythmia induction in a rabbit model. Six old (aged 4-6 years) and 9 young (aged 3-4 months) New Zealand white rabbits were subjected to a catheter-based electrophysiological study. Atrial tachyarrhythmia susceptibility was tested by burst pacing before and after infusion of increasing concentrations of acetylcholine. Both young and old rabbits were in normal sinus rhythm at the beginning of the infusion/burst pacing protocol. The old rabbits had faster heart rates and a marked increase in atrial tachyarrhythmias compared to the young rabbits. Nonsustained and sustained AF events were more frequent in the old rabbits. No significant fibrosis was observed in the atria of either young or old rabbits. In conclusion, the old rabbits have a greater propensity for induction of AF. The significantly faster heart rates in the old rabbits suggest that dominant sympathetic activity may play an important role in the propensity for AF in this group.

Atrial tachycardia provoked in the presence of activating autoantibodies to ß2-adrenergic receptor in the rabbit.

BACKGROUND: A recent clinical study of patients with inappropriate sinus tachycardia reported that autoantibodies to ß-adrenergic receptors (ß2ARs) could act as agonists to induce atrial arrhythmias. OBJECTIVE: To test the hypothesis that activating autoantibodies to the ß2AR in the rabbit atrium are arrhythmogenic. METHODS: Five New Zealand white rabbits were immunized with a ß2AR second extracellular loop peptide to raise ß2AR antibody titers. A catheter-based electrophysiologic study was performed on anesthetized rabbits before and after immunization. Arrhythmia occurrence was determined in response to burst pacing before and after the infusion of acetylcholine in incremental concentrations of 10 µM, 100 µM, and 1 mM at 1 mL/min. RESULTS: In the preimmune studies when ß2AR antibody titers were undetectable, of a total of 20 events, only 3 episodes of nonsustained (<10 seconds) atrial arrhythmias were induced. In the postimmune studies when ß2AR antibody titers ranged from 1:160,000 to 1:1.28 million, burst pacing induced 10 episodes of nonsustained or sustained (≥10 seconds) arrhythmias in 20 events (P = .04 vs preimmune; χ(2) and Fisher exact test). Taking into account only the sustained arrhythmias, there were 6 episodes in 20 events in the postimmune studies compared with 0 episodes in 20 events in the preimmune studies (P = .02). Immunized rabbits demonstrated immunoglobulin G deposition in the atria, and their sera induced significant activation of ß2AR in transfected cells in vitro compared to the preimmune sera. CONCLUSIONS: Enhanced autoantibody activation of ß2AR in the rabbit atrium leads to atrial arrhythmias mainly in the form of sustained atrial tachycardia.