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Sepsis is defined as organ dysfunction resulting from the host’s deleterious response to infection. One of the most common organs affected is the kidneys, resulting in sepsis associated acute kidney injury (SA-AKI) that contributes to the morbidity and mortality of sepsis. A growing body of knowledge has illuminated the clinical risk factors, pathobiology, response to treatment, and elements of renal recovery that have advanced our ability to prevent, detect, and treat SA-AKI. Despite these advances, SA-AKI remains an important concern and clinical burden, and further study is needed to reduce the acute and chronic consequences. This review summarizes the relevant evidence, with a focus on the risk factors, early recognition and diagnosis, treatment, and long term consequences of SA-AKI. In addition to literature pertaining to SA-AKI specifically, pertinent sepsis and acute kidney injury literature relevant to SA-AKI was included.

Acute kidney injury (AKI) has emerged as a major public health problem that affects millions of patients worldwide and leads to decreased survival and increased progression of underlying chronic kidney disease (CKD). Recent consensus criteria for definition and classification of AKI have provided more consistent estimates of AKI epidemiology. Patients, in particular those in the ICU, are dying of AKI and not just simply with AKI. Even small changes in serum creatinine concentrations are associated with a substantial increase in the risk of death. AKI is not a single disease but rather a syndrome comprising multiple clinical conditions. Outcomes from AKI depend on the underlying disease, the severity and duration of renal impairment, and the patient's renal baseline condition. The development of AKI is the consequence of complex interactions between the actual insult and subsequent activation of inflammation and coagulation. Contrary to the conventional view, recent experimental and clinical data argue against renal ischemia–reperfusion as a sine qua non condition for the development of AKI. Loss of renal function can occur without histological signs of tubular damage or even necrosis. The detrimental effects of AKI are not limited to classical well-known symptoms such as fluid overload and electrolyte abnormalities. AKI can also lead to problems that are not readily appreciated at the bedside and can extend well beyond the ICU stay, including progression of CKD and impaired innate immunity. Experimental and small observational studies provide evidence that AKI impairs (innate) immunity and is associated with higher infection rates.

Acute kidney injury (AKI) is a heterogeneous clinical syndrome that has multiple aetiologies, variable pathogenesis and diverse outcomes. However, these heterogeneities are not reflected in current approaches to the diagnosis and, to some degree, treatment of AKI. For example, congestive heart failure and dehydration can produce identical changes in serum creatinine level and urine output (parameters that are used to define AKI); however, they differ vastly in their physiological contexts and demand completely opposite treatments. AKI is often still considered to be a homogeneous clinical entity, which implies a uniform pathogenesis and a well-defined prognosis. As a consequence, efforts to find effective AKI treatments have been hampered by a lack of clear clinical classifications for various types of AKI. In addition, subclassification of AKI into subclinical phenotypes -- for example, on the basis of protein biomarkers and other in vitro diagnostics that take into account disease aetiology and underlying pathogenesis -- might be necessary to develop therapeutic approaches that effectively target the widely differing pathomechanisms of AKI. In this Review, we discuss the major subtypes of AKI that are associated with sepsis, major surgery, renal hypoperfusion and nephrotoxin exposure --situations that are typically seen in the intensive care setting. We consider differences and similarities in their phenotype, pathogenesis and outcomes and how this information might be used to guide treatment.

The timing of renal replacement therapy (RRT) for severe acute kidney injury is highly debated when no life-threatening complications are present. We assessed whether a strategy of delayed versus early RRT initiation affects 28-day survival in critically ill adults with severe acute kidney injury. In this systematic review and individual patient data meta-analysis, we searched MEDLINE (via PubMed), Embase, and the Cochrane Central Register of Controlled Trials for randomised trials published from April 1, 2008, to Dec 20, 2019, that compared delayed and early RRT initiation strategies in patients with severe acute kidney injury. Trials were eligible for inclusion if they included critically ill patients aged 18 years or older with acute kidney injury (defined as a Kidney Disease: Improving Global Outcomes [KDIGO] acute kidney injury stage 2 or 3, or, where KDIGO was unavailable, a renal Sequential Organ Failure Assessment score of 3 or higher). We contacted the principal investigator of each eligible trial to request individual patient data. From the included trials, any patients without acute kidney injury or who were not randomly allocated were not included in the individual patient data meta-analysis. The primary outcome was all-cause mortality at day 28 after randomisation. This study is registered with PROSPERO (CRD42019125025). Among the 1031 studies identified, one study that met the eligibility criteria was excluded because the recruitment period was not recent enough, and ten (including 2143 patients) were included in the analysis. Individual patient data were available for nine studies (2083 patients), from which 1879 patients had severe acute kidney injury and were randomly allocated: 946 (50%) to the delayed RRT group and 933 (50%) to the early RRT group. 390 (42%) of 929 patients allocated to the delayed RRT group and who had available data did not receive RRT. The proportion of patients who died by day 28 did not significantly differ between the delayed RRT group (366 [44%] of 837) and the early RRT group (355 [43%] of 827; risk ratio 1·01 [95% CI 0·91 to 1·13], p=0·80), corresponding to an overall risk difference of 0·01 (95% CI −0·04 to 0·06). There was no heterogeneity across studies (I2=0%; τ2=0), and most studies had a low risk of bias. The timing of RRT initiation does not affect survival in critically ill patients with severe acute kidney injury in the absence of urgent indications for RRT. Delaying RRT initiation, with close patient monitoring, might lead to a reduced use of RRT, thereby saving health resources. None.

Despite overall improvement in the outcomes of hematopoietic-cell transplantation, kidney injury is a frequent complication. The author reviews the causes, diagnosis, and management of renal complications and disorders after hematopoietic-cell transplantation. Each year, approximately 50,000 patients worldwide undergo hematopoietic-cell transplantation. This procedure, which is used to treat a wide range of malignant and nonmalignant diseases, may involve either a myeloablative or reduced-intensity conditioning regimen; the use of alternative allogeneic donors (i.e., haploidentical or mismatched donors); cells from bone marrow, cord blood, or peripheral-blood stem cells; and new immunomodulatory agents to prevent graft-versus-host disease (GVHD) 1 (Table 1). Despite the overall improvement in outcomes after hematopoietic-cell transplantation, kidney injury remains a frequent complication and contributes to the morbidity and mortality associated with the procedure. 2 – 11 The onset of acute kidney injury and chronic . . .

ObjectivesTo propose an improvement on the current classification of renal dysfunction in cirrhosis. Clinicians caring for patients with cirrhosis recognize that the development of renal dysfunction is associated with significant morbidity and mortality. While most cases of renal dysfunction in cirrhosis are functional in nature, developed as a result of changes in haemodynamics, cardiac function, and renal auto-regulation, there is an increasing number of patients with cirrhosis and structural changes in their kidney as a cause of renal dysfunction. Therefore, there is a need for a newer classification to include both functional and structural renal diseases.DesignA working party consisting of specialists from multiple disciplines conducted literature search and developed summary statements, incorporating the renal dysfunction classification used in nephrology. These were discussed and revised to produce this proposal.SettingMulti-disciplinary international meeting.PatientsNone.InterventionsLiterature search using keywords of cirrhosis, renal dysfunction, acute kidney injury (AKI), chronic kidney injury (CKD), and hepatorenal syndrome.ResultsAcute kidney injury will include all causes of acute deterioration of renal function as indicated by an increase in serum creatinine of >50% from baseline, or a rise in serum creatinine of ≥26.4µmol/L (≥0.3mg/dL) in <48hours. Chronic renal disease will be defined as an estimated glomerular filtration rate (GFR) of <60ml/min calculated using the Modification of Diet in Renal Disease 6 (MDRD6) formula, recognising that the MDRD6 formula is not perfect for the cirrhotic patients and this may change as improved means of estimating GFR becomes available. Acute on chronic kidney disease will be defined as AKI superimposed on existing chronic renal disease using the above definitions for AKI and CKD.ConclusionsAccepting this new classification will allow studies into the epidemiology, incidence, prevalence, natural history and the development of new treatments for these subtypes of renal dysfunction in cirrhosis.

Background Current classification for acute kidney injury (AKI) in critically ill patients with sepsis relies only on its severity-measured by maximum creatinine which overlooks inherent complexities and longitudinal evaluation of this heterogenous syndrome. The role of classification of AKI based on early creatinine trajectories is unclear. Methods This retrospective study identified patients with Sepsis-3 who developed AKI within 48-h of intensive care unit admission using Medical Information Mart for Intensive Care-IV database. We used latent class mixed modelling to identify early creatinine trajectory-based classes of AKI in critically ill patients with sepsis. Our primary outcome was development of acute kidney disease (AKD). Secondary outcomes were composite of AKD or all-cause in-hospital mortality by day 7, and AKD or all-cause in-hospital mortality by hospital discharge. We used multivariable regression to assess impact of creatinine trajectory-based classification on outcomes, and eICU database for external validation. Results Among 4197 patients with AKI in critically ill patients with sepsis, we identified eight creatinine trajectory-based classes with distinct characteristics. Compared to the class with transient AKI, the class that showed severe AKI with mild improvement but persistence had highest adjusted risks for developing AKD (OR 5.16; 95% CI 2.87–9.24) and composite 7-day outcome (HR 4.51; 95% CI 2.69–7.56). The class that demonstrated late mild AKI with persistence and worsening had highest risks for developing composite hospital discharge outcome (HR 2.04; 95% CI 1.41–2.94). These associations were similar on external validation. Conclusions These 8 classes of AKI in critically ill patients with sepsis, stratified by early creatinine trajectories, were good predictors for key outcomes in patients with AKI in critically ill patients with sepsis independent of their AKI staging.

Background The definition of sepsis-associated acute kidney injury (SA-AKI) was updated in 2023. This study aims to describe the epidemiology of SA-AKI using updated consensus definition and to evaluate clinical outcomes. Methods The study was a retrospective cohort analysis conducted at two academic medical centers. Adult patients admitted to intensive care units (ICU) between 2010 and 2022 were included and categorized as SA-AKI, sepsis alone, or AKI alone. SA-AKI was further classified by time of onset (early < 2 days from sepsis diagnosis vs. late 2–7 days following sepsis diagnosis) and presence of septic shock. Clinical outcomes included hospital mortality and major adverse kidney events (MAKE = death, kidney replacement therapy, or reduced kidney function from baseline) at discharge. Results 187,888 adult ICU patients were included, and SA-AKI was found in nearly half of sepsis patients and about 1 in 6 ICU admissions. 1 in 4 patients with SA-AKI died during hospitalization and 37.7% experienced at least one MAKE by hospital discharge. Compared to sepsis or AKI alone, SA-AKI was associated with higher mortality (adjusted HR 1.59; 95% CI 1.51–1.66) and higher odds of MAKE (adjusted OR 3.35; 95% CI 3.19–3.51). The early clinical phenotype of SA-AKI was most common, with incident AKI decreasing daily from sepsis onset. The presence of septic shock significantly worsened outcomes. Conclusions Applying updated consensus definitions highlights the high prevalence of SA-AKI in the ICU and its significant associated morbidity and mortality. Outcomes differ based on clinical phenotypes, including the timing of SA-AKI onset and the presence of shock.

ObjectivePrognostic stratification of patients with cirrhosis is common clinical practice. This study compares the prognostic accuracy (28-day and 90-day transplant-free mortality) of the acute-on-chronic liver failure (ACLF) classification (no ACLF, ACLF grades 1, 2 and 3) with that of acute kidney injury (AKI) classification (no AKI, AKI stages 1, 2 and 3).DesignThe study was performed in 510 patients with an acute decompensation of cirrhosis previously included in the European Association for the Study of the Liver–Chronic Liver Failure consortium CANONIC study. ACLF was evaluated at enrolment and 48 h after enrolment, and AKI was evaluated at 48 h according to Acute Kidney Injury Network criteria.Results240 patients (47.1%) met the criteria of ACLF at enrolment, while 98 patients (19.2%) developed AKI. The presence of ACLF and AKI was strongly associated with mortality. 28-day transplant-free mortality and 90-day transplant-free mortality of patients with ACLF (32% and 49.8%, respectively) were significantly higher with respect to those of patients without ACLF (6.2% and 16.4%, respectively; both p<0.001). Corresponding values in patients with and without AKI were 46% and 59%, and 12% and 25.6%, respectively (p<0.0001 for both). ACLF classification was more accurate than AKI classification in predicting 90-day mortality (area under the receiving operating characteristic curve=0.72 vs 0.62; p<0.0001) in the whole series of patients. Moreover, assessment of ACLF classification at 48 h had significantly better prognostic accuracy compared with that of both AKI classification and ACLF classification at enrolment.ConclusionsACLF stratification is more accurate than AKI stratification in the prediction of short-term mortality in patients with acute decompensation of cirrhosis.

Background Acute kidney injury (AKI) is common in patients in the intensive care unit (ICU) and may be present on admission or develop during ICU stay. Our objectives were (a) to identify factors independently associated with the development of new AKI during early stay in the ICU and (b) to determine the risk factors for non-recovery of AKI. Methods We retrospectively analysed prospectively collected data of patients admitted to a multi-disciplinary ICU in a single tertiary care centre in the UK between January 2014 and December 2016. We identified all patients without AKI or end-stage renal failure on admission to the ICU and compared the outcome and characteristics of patients who developed AKI according to KDIGO criteria after 24 h in the ICU with those who did not develop AKI in the first 7 days in the ICU. Multivariable logistic regression was applied to identify factors associated with the development of new AKI during the 24–72-h period after admission. Among the patients with new AKI, we identified those with full, partial or no renal recovery and assessed factors associated with non-recovery. Results Among 2525 patients without AKI on admission, the incidence of early ICU-acquired AKI was 33.2% (AKI I 41.2%, AKI II 35%, AKI III 23.4%). Body mass index, Sequential Organ Failure Assessment score on admission, chronic kidney disease (CKD) and cumulative fluid balance (FB) were independently associated with the new development of AKI. By day 7, 69% had fully recovered renal function, 8% had partial recovery and 23% had no renal recovery. Hospital mortality was significantly higher in those without renal recovery. Mechanical ventilation, diuretic use, AKI stage III, CKD, net FB on first day of AKI and cumulative FB 48 h later were independently associated with non-recovery with cumulative fluid balance having a U-shape association. Conclusions Early development of AKI in the ICU is common and mortality is highest in patients who do not recover renal function. Extreme negative and positive FB were strong risk factors for AKI non-recovery.