Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

European Resuscitation Council Guidelines for Resuscitation.

http://academic.oup.com/milmed/article-pdf/146/7/506/24126715/milmed-146-7-506.pdf

Goodman and Gilman's The Pharmacological Basis of Therapeutics

EVOLUTION: Of Mice . . .

S1018 The Effect of Laparoscopy and/or Fast Track Multimodal Management on Postoperative Gastrointestinal Motility After Colonic Surgery

Background: The number of patients waiting for heart transplantation (HTX) is increasing. Optimizing the use of all available donor hearts is crucial. While mortality seems not to be affected by donor cardiopulmonary resuscitation (CPR), the impact of donor CPR on days alive and out of hospital (DAOH) is unclear. Methods: This retrospective study included adults who underwent HTX at the University Hospital Duesseldorf, Germany from 2010–2020. Main exposure was donor-CPR. Secondary exposure was the length of CPR. The primary endpoint was DAOH at one year. Results: A total of 187 patients were screened and 171 patients remained for statistical analysis. One-year mortality was 18.7%. The median DAOH at one year was 295 days (interquartile range 206–322 days). Forty-two patients (24.6%) received donor-CPR hearts. The median length of CPR was 15 (9–21) minutes. There was no significant difference in DAOH between patients with donor-CPR hearts versus patients with no-CPR hearts (CPR: 291 days (211–318 days) vs. no-CPR: 295 days (215–324 days); p = 0.619). Multivariate linear regression revealed that there was no association between length of CPR and DAOH (unstandardized coefficients B: −0.06, standard error: 0.81, 95% CI −1.65–1.53, p = 0.943). Conclusions: Donor CPR status and length of CPR are not associated with reduced DAOH at one year after HTX.

/pdf/impact-of-cardiopulmonary-resuscitation-of-donors-on-days-2tq3991x.pdf

Impact of Cardiopulmonary Resuscitation of Donors on Days Alive and Out of Hospital after Orthotopic Heart Transplantation

Magnesium spielt eine Schlusselrolle in vielen verschiedenen enzymatischen und zellularen Prozessen und ist daher von wachsendem Interesse fur die perioperative Medizin. Wahrend experimentelle Studien vielversprechende Ansatze fur verschiedene Krankheitsbilder liefern, sind die Ergebnisse groser klinischer Studien widerspruchlich. Potentielle Indikationen und Therapieempfehlungen werden ebenso wie die zugrundeliegende Physiologie in vorliegendem Ubersichtsartikel vorgestellt.

Adjuvanzien in der modernen Anästhesie – Magnesium

Obesity is a growing medical problem in Europe and the USA. Plastic surgery is increasing in popularity as a treatment option for correcting skin surplus after dieting. This is often done in private clinics, and is not without risk. In this case, the early symptoms of disproportionate pain and swelling were not followed by immediate inspection in a hospital. The patient died within 48 hours due to clostridium infection. We advocate a 24/7 postoperative care facility, and recommend a sequence of diagnostic and therapeutic measures.

Lethal complication after abdominal wall reduction

Introduction: Hexokinase II (HKII) is a glycolytic enzyme which can be bound to mitochondria (mtHKII) or free in the cytosol. Previous studies showed that increased amounts of mtHKII protect the heart against ischemia/reperfusion (I/R) injury.

Hypothesis: Reduced mtHKII binding increases I/R damage by increased respiration and ROS production.

Methods: Langendorff perfused rat hearts were exposed to 20 min saline, 1 μM TAT-only or 200 nM or 1 μM TAT-HKII treatment, followed by 15 min ischemia and 30 min reperfusion. TAT-HKII contains the binding motif of HKII and translocates HKII from the mitochondria. During the complete protocol cardiac oxygen consumption, and cardiac function (rate pressure product) were measured and reactive oxygen species (ROS) were determined by DHE fluorescence. Mitochondrial oxygen tension was measured using protoporphyrin IX delayed fluorescence before and after 20 min peptide treatment. During reperfusion necrosis was measured by LDH activity in effluent.

In addition, in Langendorff perfused mice hearts the effect of 15 min peptide treatment was studied on ischemia (NADH epifluorescence) and cell death (LDH activity).

Results: In the 1 μM TAT-HKII hearts MVO2, corrected for cardiac function, increased, and mitochondrial oxygen tension was reduced during peptide treatment. However, this was not observed after treatment with 200 nM TAT-HKII, nor in the control groups. During reperfusion MVO2/RPP was increased in both treatment groups. ROS production increased in both TAT-HKII exposed groups during ischemia (normalized values (mean±SEM) 1.14±0.05 (200 nM) and 1.17±0.08 (1 μM) versus 1.09±0.06 (control)) and reperfusion (1.58±0.24 (200 nM) and 1.84±0.15 (1 μM) versus 1.30±0.17 (control)). The altered oxygen consumption and increased ROS production were accompanied by increased LDH activity during reperfusion in both TAT-HKII treated groups. LDH activity increased to (mean±SEM) 27.1±4.1 and 42.9±4.2 μmol/30min/g heart for the 200 nM and 1 μM TAT-HK treated hearts, respectively. No LDH activity was observed in control groups.

Exposure to TAT-HKII did cause borderline ischemia (increased NADH epifluorescence) during 1 μM TAT-HKII treatment, which was not associated with cell death. No ischemia was detected during 200 nM TAT-HKII treatment.

Conclusion: Reduction of mtHKII by TAT-HKII treatment turns reversible ischemia in irreversible ischemia. This might be caused by increased ROS production during ischemia and reperfusion, and increased oxygen consumption.

/pdf/tat-hkii-induced-reduction-in-mitochondrial-bound-hexokinase-24avk4nk0v.pdf

TAT-HKII induced reduction in mitochondrial bound hexokinase II increases ischemia reperfusion injury by increased respiration and increased ROS levels

Markus W. Hollmann

Papers

S1018 The Effect of Laparoscopy and/or Fast Track Multimodal Management on Postoperative Gastrointestinal Motility After Colonic Surgery

Impact of Cardiopulmonary Resuscitation of Donors on Days Alive and Out of Hospital after Orthotopic Heart Transplantation

Adjuvanzien in der modernen Anästhesie – Magnesium

Lethal complication after abdominal wall reduction

TAT-HKII induced reduction in mitochondrial bound hexokinase II increases ischemia reperfusion injury by increased respiration and increased ROS levels