Crit Care

International audienc

Covichem: A biochemical severity risk score of COVID-19 upon hospital admission

Clinical and laboratory predictors of COVID-19 severity are now well described and combined to propose mortality or severity scores. However, they all necessitate saturable equipment such as scanners, or procedures difficult to implement such as blood gas measures. To provide an easy and fast COVID-19 severity risk score upon hospital admission, and keeping in mind the above limits, we sought for a scoring system needing limited invasive data such as a simple blood test and co-morbidity assessment by anamnesis. A retrospective study of 303 patients (203 from Bordeaux University hospital and an external independent cohort of 100 patients from Paris Pitié-Salpêtrière hospital) collected clinical and biochemical parameters at admission. Using stepwise model selection by Akaike Information Criterion (AIC), we built the severity score Covichem. Among 26 tested variables, 7: obesity, cardiovascular conditions, plasma sodium, albumin, ferritin, LDH and CK were the independent predictors of severity used in Covichem (accuracy 0.87, AUROC 0.91). Accuracy was 0.92 in the external validation cohort (89% sensitivity and 95% specificity). Covichem score could be useful as a rapid, costless and easy to implement severity assessment tool during acute COVID-19 pandemic waves

Characterization of acute kidney injury in critically ill patients with severe coronavirus disease 2019

Abstract Background Coronavirus disease 2019 (COVID-19)-associated acute kidney injury (AKI) frequency, severity and characterization in critically ill patients has not been reported. Methods Single-centre cohort performed from 3 March 2020 to 14 April 2020 in four intensive care units in Bordeaux University Hospital, France. All patients with COVID-19 and pulmonary severity criteria were included. AKI was defined using Kidney Disease: Improving Global Outcomes (KDIGO) criteria. A systematic urinary analysis was performed. The incidence, severity, clinical presentation, biological characterization (transient versus persistent AKI; proteinuria, haematuria and glycosuria) and short-term outcomes were evaluated. Results Seventy-one patients were included, with basal serum creatinine (SCr) of 69 ± 21 µmol/L. At admission, AKI was present in 8/71 (11%) patients. Median [interquartile range (IQR)] follow-up was 17 (12–23) days. AKI developed in a total of 57/71 (80%) patients, with 35% Stage 1, 35% Stage 2 and 30% Stage 3 AKI; 10/57 (18%) required renal replacement therapy (RRT). Transient AKI was present in only 4/55 (7%) patients and persistent AKI was observed in 51/55 (93%). Patients with persistent AKI developed a median (IQR) urine protein/creatinine of 82 (54–140) (mg/mmol) with an albuminuria/proteinuria ratio of 0.23 ± 20, indicating predominant tubulointerstitial injury. Only two (4%) patients had glycosuria. At Day 7 after onset of AKI, six (11%) patients remained dependent on RRT, nine (16%) had SCr >200 µmol/L and four (7%) had died. Day 7 and Day 14 renal recovery occurred in 28% and 52%, respectively. Conclusion Severe COVID-19-associated AKI is frequent, persistent, severe and characterized by an almost exclusive tubulointerstitial injury without glycosuria

Nephrol Ther

L’insuffisance rénale aiguë est une complication fréquente en réanimation. Elle survient chez plus de 50 % des patients. L’insuffisance rénale aiguë est responsable d’une augmentation de la morbidité (durée d’hospitalisation, dépendance à la dialyse) et de la mortalité. La définition de l’insuffisance rénale aiguë communément admise est issue du travail collaboratif Kidney Disease: Improving Global Outcomes (KDIGO). Elle a permis d’uniformiser les pratiques et de sensibiliser les praticiens à la surveillance de la créatinine plasmatique et de la diurèse. L’insuffisance rénale aiguë de réanimation est une maladie systémique comprenant une atteinte circulatoire, endothéliale, épithéliale et fonctionnelle cellulaire. Elle ne s’accompagne pas d’une réparation ad integrum. Après une agression prolongée, une réparation inadéquate débute avec l’installation de processus fibrotiques. De multiples mécanismes sont impliqués (arrêt du cycle cellulaire, transition épithélio-mésenchymateuse, dysfonction mitochondriale). Un continuum existe donc entre insuffisance rénale aiguë et insuffisance rénale chronique, reliées par différents phénotypes de récupération rénale. Ainsi, les mesures de prévention afin d’éviter la survenue d’agression rénale prennent une place majeure à tous les stades de la prise en charge en réanimation. Le néphrologue doit être impliqué dans toutes les étapes, de la prévention du premier épisode d’insuffisance rénale aiguë (à l’arrivée en réanimation) jusqu’au suivi au long cours et la prise en charge d’une éventuelle maladie rénale chronique.Acute kidney injury is a common complication in intensive care unit. Its incidence is variable according to the studies. It is considered to occur in more than 50 % of patients. Acute kidney injury is responsible for an increase in morbidity (length of hospitalization, renal replacement therapy) but also for excess mortality. The commonly accepted definition of acute kidney injury comes from the collaborative workgroup named Kidney Disease: Improving Global Outcomes (KDIGO). It made it possible to standardize practices and raise awareness among practitioners about monitoring plasma creatinine and also diuresis. Acute kidney injury in intensive care unit is a systemic disease including circulatory, endothelial, epithelial and cellular function involvement and an acute kidney injury is not accompanied by ad integrum repair. After prolonged injury, inadequate repair begins with a fibrotic process. Several mechanisms are involved (cell cycle arrest, epithelial-mesenchymal transition, mitochondrial dysfunction) and result in improper repair. A continuum exists between acute kidney disease and chronic kidney disease, characterized by different renal recovery phenotypes. Thus, preventive measures to prevent the occurrence of kidney damage play a major role in management. The nephrologist must be involved at every stage, from the prevention of the first acute kidney injury (upon arrival in intensive care unit) to long-term follow-up and the care of a chronic kidney disease

Clin Chim Acta

Acute kidney injury (AKI) is an infrequent complication of inflammatory bowel disease and can be exceptionally linked to interstitial nephritis secondary to anti-inflammatory drugs, such as Pentasa® (5-ASA). We present an case of an 80-year-old man who presented chronic diarrheas treated by Pentasa®. He developed AKI, evidenced by high plasma creatinine dosed in his local laboratory. At the hospital admission, plasma creatinine was exceptionally undetectable by the enzymatic method while Jaffe's method successfully determined it. Creatinine measurement by the enzymatic method was gradually restored during hospital stay, concomitant with the discontinuation of 5-ASA administration, suggesting that this drug could interfere with creatinine enzymatic assay. Creatinine enzymatic assays combine serial reactions. The last one called Trinder reaction, catalyzed by a peroxidase, uses HO to convert uncolored dye in a colored compound, proportionally to creatinine concentration. We showed that AKI related-plasma accumulation of 5-ASA, could participate in the negative interference observed on creatinine measurement, by scavenging HO. Interestingly, all Trinder reaction-based measurements (uric acid, lipase, lactate, triglycerides and cholesterol) were affected. Negative interference of 5-ASA was confirmed by interferogram experiments on all Trinder reaction-dependent assays. All Trinder-dependent parameters should be interpreted with the patient's treatment knowledge, in particular salicylate derivatives

The Incidence of Chronic Kidney Disease Three Years after Non-Severe Acute Kidney Injury in Critically Ill Patients: A Single-Center Cohort Study

The risk of chronic kidney disease (CKD) following severe acute kidney injury (AKI) in critically ill patients is well documented, but not after less severe AKI. The main objective of this study was to evaluate the long-term incidence of CKD after non-severe AKI in critically ill patients. This prospective single-center observational three-years follow-up study was conducted in the medical intensive care unit in Bordeaux’s hospital (France). From 2013 to 2015, all patients with severe (kidney disease improving global outcomes (KDIGO) stage 3) and non-severe AKI (KDIGO stages 1, 2) were enrolled. Patients with prior eGFR < 90 mL/min/1.73 m2 were excluded. Primary outcome was the three-year incidence of CKD stages 3 to 5 in the non-severe AKI group. We enrolled 232 patients. Non-severe AKI was observed in 112 and severe AKI in 120. In the non-severe AKI group, 71 (63%) were male, age was 62 ± 16 years. The reason for admission was sepsis for 56/112 (50%). Sixty-two (55%) patients died and nine (8%) were lost to follow-up. At the end of the follow-up the incidence of CKD was 22% (9/41); Confidence Interval (CI) 95% (9.3–33.60)% in the non-severe AKI group, tending to be significantly lower than in the severe AKI group (44% (14/30); CI 95% (28.8–64.5)%; p = 0.052). The development of CKD three years after non-severe AKI, despite it being lower than after severe AKI, appears to be a frequent event highlighting the need for prolonged follow-up

Nephrol Dial Transplant

Patients suffering from acute kidney injury (AKI) in intensive care unit (ICU) could have various renal trajectories and outcomes. Aims were to assess the various clinical trajectories after AKI in ICU and to determine risk factors for developing chronic kidney disease (CKD). We conducted a prospective five-year follow-up study in a medical ICU in Bordeaux University Hospital (France). The patients who received invasive mechanical ventilation, catecholamine infusion or both and developed an AKI from September 2013 to May 2015 were included. In the Cox analysis, the violation of the proportional hazard assumption for AKD was handled using appropriate interaction terms with time, resulting in time-dependent HR. 232 patients were enrolled. Age was 62 ± 16 years and median follow-up was 52 [6-1553] days. At day 7, 109/232 (47%) patients progressed to Acute Kidney Disease (AKD) and 66/232 (28%) recovered. A linear trajectory (AKI, AKD then CKD) was followed by 44/63 (70%) of CKD patients. The cumulative incidence of CKD was 30 [24-36] % at 5-year follow-up. In a multivariable Cox model, in the six months following AKI, the HR for CKD was higher in AKD patients (HR 29.2 [8.5-100.7]; p<0.0001). After six months, HR for CKD was 2.2 [0.6-7.9]; p = 0.21 (n = 172 patients). There were several clinical trajectories of kidney disease after ICU acquired AKI. CKD risk was higher in AKD patients only in the first six months. Lack of renal recovery, rather than AKD per se, was associated with the risk of CKD

Bridging gut microbiota composition with extended-spectrum beta-lactamase Enterobacteriales faecal carriage in critically ill patients (microbe cohort study)

Abstract Background The worldwide dissemination of extended spectrum beta-lactamase producing Enterobacteriales (ESBL-E) is of major concern. Microbiota may play a role in the host resistance to colonization with ESBL-E, but the underlying mechanisms remain unknown. We aimed to compare the gut microbiota composition between ESBL-producing E. coli or K. pneumoniae carriers and ESBL-E non-carriers according to the bacterial species. Results Among 255 patients included, 11 (4,3%) were colonized with ESBL-producing E. coli and 6 (2,4%) with ESBL-producing K. pneumoniae, which were compared with age- and sex-matched ESBL-E non carriers. While no significant differences were found between ESBL-producing E. coli carriers and non-carriers, gut bacteriobiota α-diversity was decreased in ESBL-K. pneumoniae faecal carriers compared both with non-carriers (p = 0.05), and with ESBL-producing E. coli carriers. The presence of Sellimonas intestinalis was associated with the absence of ESBL-producing E. coli fecal carriage. Campylobacter ureolyticus, Campylobacter hominis, bacteria belonging to Clostridium cluster XI and Saccharomyces sp. were associated with the absence of ESBL-producing K. pneumoniae faecal carriage. Conclusions The composition of the gut microbiota differs between ESBL-producing E. coli and K. pneumoniae faecal carriers suggesting that microbial species should be taken into account when investigating the role of gut microbiota in resistance to gut colonization with ESBL-E. Trial registration number: NCT04131569, date of registration: October 18, 2019