Background and objectivesSepsis-associated AKI is a heterogeneous clinical entity. We aimed to agnostically identify sepsis-associated AKI subphenotypes using deep learning on routinely collected data in electronic health records.Design, setting, participants, & measurementsWe used the Medical Information Mart for Intensive Care III database, which consists of electronic health record data from intensive care units in a tertiary care hospital in the United States. We included patients ≥18 years with sepsis who developed AKI within 48 hours of intensive care unit admission. We then used deep learning to utilize all available vital signs, laboratory measurements, and comorbidities to identify subphenotypes. Outcomes were mortality 28 days after AKI and dialysis requirement.ResultsWe identified 4001 patients with sepsis-associated AKI. We utilized 2546 combined features for K-means clustering, identifying three subphenotypes. Subphenotype 1 had 1443 patients, and subphenotype 2 had 1898 patients, whereas subphenotype 3 had 660 patients. Subphenotype 1 had the lowest proportion of liver disease and lowest Simplified Acute Physiology Score II scores compared with subphenotypes 2 and 3. The proportions of patients with CKD were similar between subphenotypes 1 and 3 (15%) but highest in subphenotype 2 (21%). Subphenotype 1 had lower median bilirubin levels, aspartate aminotransferase, and alanine aminotransferase compared with subphenotypes 2 and 3. Patients in subphenotype 1 also had lower median lactate, lactate dehydrogenase, and white blood cell count than patients in subphenotypes 2 and 3. Subphenotype 1 also had lower creatinine and BUN than subphenotypes 2 and 3. Dialysis requirement was lowest in subphenotype 1 (4% versus 7% [subphenotype 2] versus 26% [subphenotype 3]). The mortality 28 days after AKI was lowest in subphenotype 1 (23% versus 35% [subphenotype 2] versus 49% [subphenotype 3]). After adjustment, the adjusted odds ratio for mortality for subphenotype 3, with subphenotype 1 as a reference, was 1.9 (95% confidence interval, 1.5 to 2.4).ConclusionsUtilizing routinely collected laboratory variables, vital signs, and comorbidities, we were able to identify three distinct subphenotypes of sepsis-associated AKI with differing outcomes.

Background: Women comprise approximately one-third of the advanced heart failure population but may receive fewer advanced heart failure therapies including left ventricular assist devices (LVADs). During the early pulsatile-flow device era, women had higher post-LVAD mortality and increased complications. However, knowledge about these differences in the continuous-flow device era is limited. Therefore, we sought to explore temporal trends in LVAD utilization and post-LVAD mortality by sex. Methods and Results: Patients with LVAD implantation from 2004 to 2016 were identified using the Nationwide Inpatient Sample. Trends in LVAD utilization and post-LVAD inpatient mortality were compared by sex and device era. Although LVADs are being increasingly utilized for patients with advanced systolic heart failure, women continue to represent a smaller proportion of LVAD recipients—25.8% in 2004 to 21.9% in 2016 ( P for trend, 0.91). Women had increased inpatient mortality after LVAD implantation compared with men in the pulsatile-flow era (46.9% versus 31.1%, P <0.0001) but not in the continuous-flow era (13.3% versus 12.1%, P =0.27; P for interaction=0.0002). Inpatient mortality decreased for both sexes over time after LVAD, with a sharp fall in 2008 to 2009. Female sex was independently associated with increased post-LVAD inpatient mortality beyond adjustment for demographics and risk factors during the pulsatile-flow era (odds ratio, 2.13; 95% CI, 1.45–3.10; P <0.0001) but not during the continuous-flow era (1.18; 0.93–1.48; P =0.16). Conclusions: Although utilization of LVAD therapy increased over time for both sexes, LVAD implantation remains stably lower in women, which may suggest a potential underutilization of this potentially life-saving therapy. Prospective studies are needed to confirm these findings.

Pulmonary embolism (PE) is a major cause of cardiovascular morbidity and mortality. Obstructive sleep apnea (OSA) is increasingly recognized in the ageing population, especially with the rising obesity epidemic. The impact of OSA on inpatient mortality in PE is not well understood. We used the Nationwide Inpatient Sample databases from 2005 to 2016 to identify 755,532 acute PE patients (age18 years). Among these 61,050 (8.1%) were OSA+. Temporal trends in length of stay (LOS), inpatient mortality and its association with OSA in PE patients were analyzed. The proportion of PE patients who were OSA+ increased from 2005 to 2016. OSA+ PE patients were younger and predominantly men. Despite a higher prevalence of traditional risk factors for inpatient mortality in OSA+ patients, OSA was associated with a lower risk of mortality in PE patients (OR, 95% CI; p: unadjusted 0.56, 0.53-0.58; p<0.0001 and adjusted 0.55, 0.52-0.58; p<0.0001). Overall mortality and LOS in PE patients decreased over time. Relative to OSA- patients, there was a slight increase in mortality among OSA+ PE patients over time, although the LOS remained unchanged between the 2 groups. In conclusion, OSA+ PE patients had a lower inpatient mortality compared to OSA- patients despite a higher prevalence of traditional mortality risk factors. Secondary pulmonary hypertension related to OSA with pre-conditioning of the right ventricle to elevated afterload may potentially explain the protective effect of OSA on mortality in PE. However, mechanistic studies need to further elucidate the links behind this association.

AIM:To measure C-reactive protein (CRP) levels in patients of acute pancreatitis and evaluate if CRP levels predict the severity of pancreatitis by correlating these levels with-1. C T Severity Index (CTSI). 2. Presence of complications. 3. Time taken for recovery. METHOD: Between the years 2007 and 2009 fifty patients diagnosed to have acute pancreatitis were included in this study. Their CRP levels were sent on second day of admission and CT scan done after 72 hours of admission. RESULTS: CRP levels of 63mg/dl and above are significantly associated with increased time to recovery (R>7D), (p-0.004). A significant association was seen between the presence of complications and a CTSI >7, (p-0.0002). There was no significant correlation or association between the CRP levels and CTSI as indicated by a value of 0.040528 (test of correlation) and p-<0.05. CONCLUSION: High serum CRP levels have predicted prognosis as well as mortality in this study. CTSI can be a very accurate predictor of development of complications in a case of acute pancreatitis. INTRODUCTION:Acute pancreatitis is major cause of acute abdominal pain. The clinical presentation of the acute pancreatitis is variable. Most of these patients recover without specific complications. Some patients however display severe complications such as pancreatic as cites and pancreatic necrosis; these patients show high morbidity and mortality.The role of diagnostic markers (pancreatic enzymes such as amylase and lipase) as prognostic indicators has been a failure. Other biochemical markers like CRP, pro-calcitonin and the like are under evaluation as prognostic indicators. CRP estimation is cheap and easily available. In this study we have attempted to see if a single and early estimation of CRP levels is an effective predictor of morbidity and mortality in acute pancreatitis.We have attempted association between CRP, radiological imaging, and the clinical features and outcome of acute pancreatitis.

There have been recent significant advances in short‐term outcomes in renal transplantation, however, long‐term allograft survival remains a challenge. With reported incidences as high of 74.5% of chronic graft loss in patients with biopsies showing transplant glomerulopathy (TG), this syndrome represents an important factor for chronic allograft complications. In this review we show an overview of the novel mechanistic insights into pathogenesis of TG, as well as a brief description of the pathology, diagnosis and newer prognostic indices within TG diagnosis. These data raise intriguing roles for cell‐mediated immunity and podocyte stress in TG as well as reinforce previous associations of TG with ABMR. We also delve into management strategies for TG and report the paucity of existing clinical trial data for this prevalent condition in renal transplants.