Cystatin C is a biomarker for predicting acute kidney injury in patients with acute-on-chronic liver failure

AIM:To investigate serum cystatin C level as an early biomarker for predicting acute kidney injury(AKI)in patients with acute-on-chronic liver failure(ACLF).METHODS:Fifty-six consecutive patients with hepatitis B virus-related ACLF who had normal serum creatinine(Cr)level(<1.2 mg/dL in men,or<1.1 mg/dL in women)were enrolled in the Liver Failure Treatment and Research Center of Beijing 302 Hospital between August 2011 and October 2012.Thirty patients with chronic hepatitis B(CHB)and 30 healthy controls in the same study period were also included.Measurement of serum cystatin C(CysC)was performed by a particle-enhanced immunonephelometry assay using the BN Prospec nephelometer system.The ACLF patients were followed during their hospitalization period.RESULTS:In the ACLF group,serum level of CysC was 1.1±0.4 mg/L,which was significantly higher(P<0.01)than those in the healthy controls(0.6±0.3mg/L)and CHB patients(0.7±0.2 mg/L).During the hospitalization period,eight ACLF patients developed AKI.Logistic regression analysis indicated that CysC level was an independent risk factor for AKI development(odds ratio=1.8;95%CI:1.4-2.3,P=0.021).The cutoff value of serum CysC for prediction of AKI in ACLF patients was 1.21 mg/L.The baseline CysC-based estimated glomerular filtration rate(eGFR CysC)was significantly lower than the creatinine-based eGFR(eGFR CG and eGFR MDRD)in ACLF patients with AKI,suggesting that baseline eGFR CysC represented early renal function in ACLF patients while the Cr levels were still within the normal ranges.CONCLUSION:Serum CysC provides early prediction of renal dysfunction in ACLF patients with a normal serum Cr level.

Acute kidney injury in acute-on-chronic liver failure is different from in decompensated cirrhosis

AIM To evaluate the differences in acute kidney injury(AKI) between acute-on-chronic liver failure(ACLF) and decompensated cirrhosis(DC) patients. METHODS During the period from December 2015 to July 2017, 280 patients with hepatitis B virus(HBV)-related ACLF(HBV-ACLF) and 132 patients with HBV-related DC(HBV-DC) who were admitted to our center were recruited consecutively into an observational study. Urine specimens were collected from all subjects and the levels of five urinary tubular injury biomarkers were detected,including neutrophil gelatinase-associated lipocalin(NGAL), interleukin-18(IL-18), liver-type fatty acid binding protein(L-FABP), cystatin C(CysC), and kidney injury molecule-1(KIM-1). Simultaneously, the patient demographics, occurrence and progression of AKI, and response to terlipressin therapy were recorded. All patients were followed up for 3 mo or until death after enrollment. RESULTS AKI occurred in 71 and 28 of HBV-ACLF and HBV-DC patients, respectively(25.4% vs 21.2%, P = 0.358). Among all patients, the levels of four urinary biomarkers(NGAL, CysC, L-FABP, IL-18) were significantly elevated in patients with HBV-ACLF and AKI(ACLF-AKI), compared with that in patients with HBV-DC and AKI(DC-AKI) or those without AKI. There was a higher proportion of patients with AKI progression in ACLF-AKI patients than in DC-AKI patients(49.3% vs 17.9%, P = 0.013). Fortythree patients with ACLF-AKI and 19 patients with DC-AKI were treated with terlipressin. The response rate of ACLFAKI patients was significantly lower than that of patients with DC-AKI(32.6% vs 57.9%, P = 0.018). Furthermore, patients with ACLF-AKI had the lowest 90 d survival rates among all groups(P < 0.001).CONCLUSION AKI in ACLF patients is more likely associated with structural kidney injury, and is more progressive, with a poorer response to terlipressin treatment and a worse prognosis than that in DC patients.

Intestinal expressions of eNOSmRNA and iNOSmRNA in rats with acute liver failure

AIM: To observe the gene expression change of eNOSmRNA and iNOSmRNA in the small and large intestines with acute liver failure (ALF), and to reveal the biological function of NO on the pathogenesis of ALF and multiple organs dysfunction at the molecular level. METHODS: Sixty male Wistar rats were selected, weighing from 250g to 350g, and divided into 5 groups randomly: SO, ALF (6h, 12h), L-Arg, L-NAME, L-Arg and L-NAME, each group with 10 rats. The dose of L-Arg was 300mg.kg(-1), and L-NAME was 30mg.kg(-1), the reagents diluted by normal saline were injected through tail vein 30 minutes pre and post operation. The rats in the ALF group were respectively sacrificed postoperatively at 6h, 12h, and the rats in the other groups were sacrificed postoperatively at 6h. The tissues of small and large intestines were harvested in 4% paraforaldehyde containing the reagent of DEPC and fixed at 6h, embedded in paraffin, and 4 microm section was cut. The expression of eNOSmRNA and iNOSmRNA in these tissues was determined with in situ hybridization, and analyzed with the imaging analysis system of CMM-3 and SPSS statistical software. RESULTS: The expression of eNOSmRNA in the large intestine and iNOSmRNA in the small and large intestines increased significantly at 6h after ALF, but the expression of iNOSmRNA in the small and large intestines reduced notably at 12h after ALF (P【0.05); the expression of eNOSmRNA in the large intestine and iNOSmRNA in the small and large intestines decreased significantly with the reagents of L-Arg at 6h ALF, but the expression of eNOSmRNA and iNOSmRNA in the small and large intestines decreased totally with the reagents of L-NAME or association with L-Arg 6h ALF. CONCLUSION: The expression of eNOSmRNA in the large intestine increased notably at the early stage of ALF, NO induced by the enzyme of eNOS from the transplantation of eNOSmRNA can protect the function of the large intestine, the high expression of iNOSmRNA is involved in the damaged function of the small and large intestines. NO precursor can reduce the expression of iNOSmRNA in the small and large intestines and the damage to intestines; NOS inhibitor or association with NO pre-cursor can totally lower the expression of eNOSmRNA and iNOSmRNA in the small and large intestines, it cannot notably influence the NOS inhibitor in the gene expression of eNOSmRNA and iNOSmRNA to supply the additional NO precursor.

Prognostic impact of atrial fibrillation on clinical outcomes of acute coronary syndromes,heart failure and chronic kidney disease

Atrial fibrillation(AF) is the most common type of sustained arrhythmia,which is now on course to reach epidemic proportions in the elderly population. AF is a commonly encountered comorbidity in patients with cardiac and major non-cardiac diseases. Morbidity and mortality associated with AF makes it a major healthcare burden. The objective of our article is to determine the prognostic impact of AF on acute coronary syndromes,heart failure and chronic kidney disease. Multiple studies have been conducted to determine if AF has an independent role in the overall mortality of such patients. Our review suggests that AF has an independent adverse prognostic impact on the clinical outcomes of acute coronary syndromes,heart failure and chronic kidney disease.

Fetal kidney stem cells ameliorate cisplatin induced acute renal failure and promote renal angiogenesis

AIM: To investigate whether fetal kidney stem cells(f KSC) ameliorate cisplatin induced acute renal failure(ARF) in rats and promote renal angiogenesis.METHODS: The f KSC were isolated from rat fetuses of gestation day 16 and expanded in vitro up to 3rd passage. They were characterized for the expression of mesenchymal and renal progenitor markers by flow cytometry and immunocytochemistry, respectively. The in vitro differentiation of f KSC towards epithelial lineage was evaluated by the treatment with specific induction medium and their angiogenic potential by matrigel induced tube formation assay. To study the effect of f KSC in ARF, f KSC labeled with PKH26 were infused in rats with cisplatin induced ARF and, the blood and renal tissues of the rats were collected at different time points. Blood biochemical parameters were studied to evaluate renal function. Renal tissues were evaluated for renal architecture, renal cell proliferation and angiogenesis by immunohistochemistry, renal cell apoptosis by terminal deoxynucleotidyl transferase nickend labeling assay and early expression of angiogenic molecules viz. vascular endothelial growth factor(VEGF), hypoxia-inducible factor(HIF)-1α and endothelial nitric oxide synthase(eN OS) by western blot.RESULTS: The fK SC expressed mesenchymal markers viz. CD29, CD44, CD73, CD90 and CD105 as well asrenal progenitor markers viz. Wt1, Pax2 and Six2. They exhibited a potential to form CD31 and Von Willebrand factor expressing capillary-like structures and could be differentiated into cytokeratin(CK)18 and CK19 positive epithelial cells. Administration of fK SC in rats with ARF as compared to administration of saline alone, resulted in a significant improvement in renal function and histology on day 3(2.33 ± 0.33 vs 3.50 ± 0.34, P < 0.05) and on day 7(0.83 ± 0.16 vs 2.00 ± 0.25, P < 0.05). The infused PKH26 labeled fK SC were observed to engraft in damaged renal tubules and showed increased proliferation and reduced apoptosis(P < 0.05) of renal cells. The kidneys of fK SC as compared to saline treated rats had a higher capillary density on day 3 [13.30 ± 1.54 vs 7.10 ± 1.29, capillaries/high-power fields(HPF), P < 0.05], and on day 7(21.10 ± 1.46 vs 15.00 ± 1.30, capillaries/HPF, P < 0.05). In addition, kidneys of fK SC treated rats had an upregulation of angiogenic proteins hypoxia-inducible factor-1α, VEGF and eN OS on day 3(P < 0.05).CONCLUSION: Our study shows that fK SC ameliorate cisplatin induced ARF in rats and promote renal angiogenesis, which may be an important therapeutic mechanism of these stem cells in the disease.

Page Kidney: A Case of Acute or Chronic Renal Failure &Refractory HTN Presenting after Renal Biopsy

Page Kidney is a relatively rare cause of Acute Renal Failure (ARF) presenting as accelerated and uncontrolled hypertension secondary direct compression of the renal parenchyma by an extrinsic source. This case report describes a 44-year-old male with advanced acute renal failure requiring hemodialysis, hypertension, and initial suspicion for thrombotic thrombocytopenic purpura who developed a case of Page Kidney following retroperitoneal hematoma following a renal biopsy. The patient was medically managed with intravenous nifedipine until blood pressure stabilized after improvement of the hematoma. Usually hematomas are self-resolving, however rarely they can result in the Page phenomenon—extrinsic compression of the affected kidney by the hematoma resulting in a picture that is similar to acute renal failure (ARF). This case highlights the importance of early medical management of blood pressure control after renal compression has been identified.

A case study report of acute renal failure associated with Nigella sativa in a diabetic patient

1 Introduction Nigella sativa, known as black seed, has analgesic, anti-inflammatory, antioxidant and anticancer effects. It has been shown to reduce the development of kidney failure when given prior to the use of nephrotoxic drugs particularly due to its antioxidant action. However, as far as the authors could ascertain, there is no human study in literature showing these effects. Here we present a case of acute renal failure after the use of N. sativa, rather than exhibiting antioxidant or antidiabetic effects.

Experimental research on TECA-I bioartificial liver support system to treat canines with acute liver failure

AIM: To evaluate the efficacy and safety of the TECA-I bioartificial liver support system (BALSS) in treating canines with acute liver failure (ALF). METHODS: Ten canines with ALF induced by 80% liver resection received BALSS treatment (BALSS group). Blood was perfused through a hollow fiber tube containing 1X10(10) porcine hepatocytes.Four canines with ALF were treated with BALSS without porcine hepatocytes (control group), and five canines with ALF received drug treatment (drug group). Each treatment lasted 6 hours. RESULTS: BALSS treatment yielded beneficial effects for partial liver resection induced ALF canines with survival and decreased plasma ammonia, ALT, AST and BIL. There was an obvious decrease in PT level and increase in PA level, and there were no changes in the count of lymphocytes, immunoglobulins (IgA, IgG and IgM) and complement (C3 and C4) levels after BALSS treatment. In contrast, for the canines with ALF in non-hepatocyte BALSS group (control group) and drug group, there were no significant changes in ammonia, ALT, AST, BIL, PT and PA levels. ALF canines in BALSS group, control group and drug group lived respectively an average time of 108.0h +/- 12.0h, 24.0h +/- 6.0h and 20.4h +/- 6.4h,and three canines with ALF survived in BALSS group. CONCLUSION: TECA-I BALSS is efficacious and safe for ALF canines induced by partial liver resection.

Relationship between acute kidney injury before thoracic endovascular aneurysm repair and in-hospital outcomes in patients with type B acute aortic dissection

Objective Acute kidney injury （AKI） frequently occurs after catheter-based interventional procedures and increases mortality. However, the implications of AKI before thoracic endovascular aneurysm repair （TEVAR） of type B acute aortic dissection （AAD） remain unclear. This study evaluated the incidence, predictors, and in-hospital outcomes of AKI before TEVAR in patients with type B AAD. Methods Between 2009 and 2013, 76 patients were retrospectively evaluated who received TEVAR for type B AAD within 36 h from symptom onset. The patients were classified into no-AKI vs. AKI groups, and the severity of AKI was further staged according to kidney disease： im- proving global outcomes criteria before TEVAR. Results The incidence of preoperative AKI was 36.8%. In-hospital complications was significantly higher in patients with preoperative AKI compared with no-AKI （50.0% vs. 4.2%, respectively; P 〈 0.001）, including acute renal failure （21.4% vs. O, respectively; P 〈 0.001）, and they increased with severity of AKI （P 〈 0.001）. The maximum levels of body tem- perature and white blood cell count were significantly related to maximum serum creatinine level before TEVAR. Multivariate analysis showed that systolic blood pressure on admission （OR： 1.023; 95% CI： 1.003-1.044; P ： 0.0238） and bilateral renal artery involvement （OR： 19.076; 95% CI： 1.914 190.164; P = 0.0120） were strong predictors of preoperative AKI. Conclusions Preoperative AKI frequently occurred in patients with type B AAD, and correlated with higher in-hospital complications and enhanced inflammatory reaction. Systolic blood pressure on admission and bilateral renal artery involvement were major risk factors for AKI before TEVAR.

Acute kidney injury spectrum in patients with chronic liver disease:Where do we stand?

Acute kidney injury (AKI) is a common complication of liver cirrhosis and is of the utmost clinical and prognostic relevance. Patients with cirrhosis, especially decompensated cirrhosis, are more prone to develop AKI than those without cirrhosis. The hepatorenal syndrome type of AKI (HRS–AKI), a spectrum of disorders in prerenal chronic liver disease, and acute tubular necrosis (ATN) are the two most common causes of AKI in patients with chronic liver disease and cirrhosis. Differentiating these conditions is essential due to the differences in treatment. Prerenal AKI, a more benign disorder, responds well to plasma volume expansion, while ATN requires more specific renal support and is associated with substantial mortality. HRS–AKI is a facet of these two conditions, which are characterized by a dysregulation of the immune response. Recently, there has been progress in better defining this clinical entity, and studies have begun to address optimal care. The present review synopsizes the current diagnostic criteria, pathophysiology, and treatment modalities of HRS–AKI and as well as AKI in other chronic liver diseases (non-HRS–AKI) so that early recognition of HRS–AKI and the appropriate management can be established.

Causal relationship between hypoalbuminemia and acute kidney injury

Our meta-analysis published in 2010 provided evidence that low levels of serum albumin （hypoalbuminemia） are a signifcant independent predictor of acute kidney injury （AKI） and death following AKI. Since then, a large volume of additional data from observational clinical studies has been published further evaluating the relationship between serum albumin and AKI occurrence. This is an updated review of the literature to re-evaluate the hypothesis that hypoalbuminemia is independently associated with increased AKI risk. Eligible studies published from September 2009 to December 2016 were sought in PubMed （MEDLINE） and forty-three were retained, the great majority being retrospective observational cohort studies. These included a total of about 68000 subjects across a diverse range of settings, predominantly cardiac surgery and acute coronary interventions, infectious diseases, transplant surgery, and cancer. Appraisal of this latest data set served to conclusively corroborate and confirm our earlier hypothesis that lower serum albumin is an independent predictor both of AKI and death after AKI, across a range of clinical scenarios. The body of evidence indicates that hypoalbuminemia may causally contribute to development of AKI. Furthermore, administration of human albumin solution has the po-tential to prevent AKI; a randomized, controlled study provides evidence that correcting hypoalbuminemia may be renal-protective. Therefore, measurement of serum albumin to diagnose hypoalbuminemia may help identify high-risk patients who may beneft from treatment with exogenous human albumin. Multi-center, prospective, randomized, interventional studies are warranted, along with basic research to define the mechanisms throughwhich albumin affords nephroprotection.

Cardiorenal biomarkers in acute heart failure

Managing patients with heart failure （HF） is a challenging task within itself, but the presence of associated worsening renal function can greatly increase mortality and morbidity. Early diagnosis and treatment is the key to prevent re-hospitalizations and reduce healthcare costs. Biomarkers have long been established as highly sensitive and specific tools in diagnosing and prognosticating patients with HF. Reflecting distinct pathophysiological events and ongoing cellular insult, biomarkers have been proven superior to conventional laboratory tests. Availability of better assays and rapid analysis has allowed the use of biomarkers as point-of-care tests in the emergency department and at the patient＇s bed-side. Acute HF patients often go on to develop worsening renal function, termed as acute cardiorenal syndrome. The growing breadth of studies has shown the implications of combining multiple biomarkers to better chart outcomes and produce desirable results in such patients.

Challenges facing early detection of acute kidney injury in the critically ill

Recent advances in the detection of acute kidney injury(AKI) afford the possibility of early intervention. Proteomics and genomics have identified many markers of tubular cell injury, some of which are manifest in the urine. One trial has used novel injury biomarkers to recruit patients to an intervention prior to an elevation in plasma creatinine. This trial and other recent studies have shown that the use of biomarkers of injury will depend on the time the patient presents following insult to the kidney, the likely cause of that insult, and the pre-injury renal function of that patient. The definition of AKI is likely to change in the near future to include a measure of injury. We anticipate novel therapies becoming available following successful trials that utilize the methodology of early intervention following an elevated injury biomarker.

A rat model for acute hepatic failure

OBJECTIVE: To develop a surgical model of acute hepatic failure.METHODS: Hepatectomy was performed in rats according to the method described by Higgins andAnderson. Ninety percent liver resection (removing the left lateral, median, and right lateral lobes)(n=7) and 95% liver resection leaving only half of the caudate lobe (n=13) were performed.Hypoglycemia was corrected by giving 20% glucose in the drinking water, coupled with repeatedintraperitoneal injection of 5% glucose adapted to glycemia. While the survival rate, alanine transaminase(ALT) and bilirubin were observed.RESULTS: 95% liver resection decreased survival rates of the rats from 86% (90% liver resection) to23% (P【0. 05), and increased bilirubin levels (4.04±2.84 mg/dL vs. 1.25±1.85 mg/dL [90%liver resection]).CONCLUSION: 95% liver resection is a good rat model for acute hepatic failure.

Hepatoprotective effect of nitric oxide in experimental model of acute hepatic failure

AIM: To evaluate the effect of nitric oxide (NO) on the development and degree of liver failure in an animal model of acute hepatic failure (AHF).

Prevalence and outcome of acute kidney injury,as defined by the new Kidney Disease Improving Global Outcomes guideline,in very low birth weight infants

AIMTo evaluate the prevalence, risk factors and outcome of acute kidney injury （AKI） in very low birth weight （VLBW） infants. METHODSIn this retrospective study of VLBW infants, we analyzed the prevalence of AKI, as defined by changes in serum creatinine and urine output, associated risk factors and outcomes.RESULTSA total of 293 VLBW infants （mean gestational age 28.7 wk） were included, of whom 109 weighed less than 1000 g at birth. The overall prevalence of AKI was 11.6% （22% in infants with a birth weight under 1000 g and 5.4% those heavier）. A total of 19 （55%） affected infants died, with a mortality rate of 58% in infant less than 1000 g and 50% in those heavier. After adjusting for confounding variables, only necrotizing enterocolitis （NEC） remained associated with AKI, with odds ratio of 4.9 （95%CI： 1.9-18.6）. Blood pressure and glomerular filtration rate （GFR） were not different between affected infants and the others upon discharge from hospital. A normal GFR was documented in all affected infants at one year of age.CONCLUSION Using Kidney Disease Improving Global Outcomes defnition of AKI, it occurred in over 10% of VLBW infants, more commonly in infants with lower birth weight. NEC was an independent associated risk factor. Renal function, as defined by GFR, was normal in all surviving affected infants 10 to 12 mo later.

Histopathological characteristics and causes of kidney graft failure in the current era of immunosuppression

BACKGROUND The histopathological findings on the failing kidney allograft in the modern era is not well studied. In this study, we present our experience working with kidney transplant recipients with graft failure within one year of the biopsy.AIM To report the histopathological characteristics of failed kidney allografts in the current era of immunosuppression based on the time after transplant, cause of the end-stage renal disease and induction immunosuppressive medications.METHODS In a single-center observational study, we characterized the histopathological findings of allograft biopsies in kidney transplant recipients with graft failure within one year after the biopsy.RESULTS We identified 329 patients with graft failure that met the selection criteria between January 1, 2006 and December 31, 2016. The three most common biopsy findings were interstitial fibrosis and tubular atrophy(IFTA, 53%), acute rejection (AR, 43%) and transplant glomerulopathy(TG, 33%). Similarly, the three most common causes of graft failure based on the primary diagnosis were AR(40%),TG(17%), and IFTA(13%). Most grafts failed within two years of post-transplant(36%). Subsequently, approximately 10%-15% of grafts failed every two years: >2-4 years(16%), > 4-6 years(13%), > 6-8 years(11%), > 8-10 years(9%) and > 10 years(16%). AR was the most common cause of graft failure in the first six years(48%), whereas TG was the most prevalent cause of graft failure after 6 years(32%) of transplant.CONCLUSION In the current era of immunosuppression, AR is still the most common cause of early graft failure, while TG is the most prevalent cause of late graft failure.

Effects of Chinese patent medicine Niaoduqing on adenineinduced chronic renal failure in rats

The authors made rat model of chronic renal failure by feeding the animals with foodcontaining 0.5 % adenine and treated with Niaoduqing(NDQ),a Chinese patent medicine,whichcomposed of Rhizoma Rhei,Radix Glycyrrhizae,Radix Paeoniae Alba,etc.The rats were divid-ed into four groups:model control,normal control;and two NDQ-treated groups with high andlow doses separately.The blood tests including urea nitrogen(BUN),serum creatinine(Scr),red blood cell(RBC),hemoglobin (Hb) hematocrit (HCT),sodium (Na),potassium (K),cal-cium(Ca)and phosphate(P)levels were performed atthe fourth week and the eighth week,thetime of sacrifice.The results showed that in the NDQ-treated groups the mean levels of BUN andScr were lower and the mean values of RBC,Hb and HCT,higher than those in the untreatedcontrol group.In the NDQ-treated groups,hyperphosphatemia and hypocalcemia of rats im-proved,the deposited crystals of adenine metabolite and the proliferation of fibroid tissue in kid-ney decreased.These findings indicate that NDQ can ameliorate the symptoms of chronic renalfailure and delay the progress of this disease.

Correlation of oxygen free radical items between blood and kidney of chronic renal failure rat

The correlation of oxygen free radical items between blood and kidney of 5/6 nephrectomy-induced chronic renal failure rats was studied. It was found that oxygen free radicals played an important role in the impairment of remnant kidney,and antioxidant vitamin E could protect remnant kidney from the impairment caused by oxygen free radicals,and that,both in normal and chronic renal failure conditions,plasma lipid peroxides and vitamin E concentration and superoxide dismutase activity of red blood cells correlated very well with corresponding items of remnant kidney.These results suggested that blood oxygen free radical items could reflect renal oxygen free radical metabolic status in chronic renal failure patients.

Incidence and peri-operative risk factors for development of acute kidney injury in patients after cardiac surgery:A prospective observational study

BACKGROUND Patients admitted to intensive care unit(ICU) after cardiac surgery develop acute kidney injury(AKI) immediately post-operation. We hypothesized that AKI occurs mainly due to perioperative risk factors and may affect outcome.AIM To assess peri-operative risk factors for AKI post cardiac surgery and its relationship with clinical outcome.METHODS This was an observational single center, tertiary care setting study, which enrolled 206 consecutive patients, admitted to ICU after cardiac surgery. Patients were followed-up until ICU discharge or death, in order to determine the incidence of AKI, perioperative risk factors for AKI and its association with outcome.Univariate and multivariate logistic regression analysis was performed to assess predictor variables for AKI development.RESULTS After ICU admission, 55 patients(26.7%) developed AKI within 48 h. From the logistic regression analysis performed, high EuroScore Ⅱ(OR: 1.18;95%CI: 1.06-1.31, P = 0.003), white blood cells(WBC) pre-operatively(OR: 1.0;95%CI: 1.0-1.0, P = 0.002) and history of chronic kidney disease(OR: 2.82;95%CI: 1.195-6.65, P = 0.018) emerged as independent predictors of AKI among univariate predictors. AKI that developed AKI had longer duration of mechanical ventilation [1113(777–2195) vs 714(511–1020) min, P = 0.0001] and ICU length of stay [70(28–129) vs 26(21–51) h, P = 0.0001], higher rate of ICU-acquired weakness(16.4% vs 5.3%, P =0.015), reintubation(10.9% vs 1.3%, P = 0.005), dialysis(7% vs 0%, P = 0.005), delirium(36.4% vs 23.8%, P = 0.001) and mortality(3.6% vs 0.7%, P = 0.046).CONCLUSION Patients present frequently with AKI after cardiac surgery. EuroScore Ⅱ, WBC count and chronic kidney disease are independent predictors of AKI development. The occurrence of AKI is associated with poor outcome.