Acute kidney injury in low- and middle-income countries: investigations, management and prevention

Acute kidney injury (AKI) is common in the intensive care unit (ICU) and is associated with significant morbidity and mortality. This study is aimed to estimate the prevalence of AKI in ICU and assess its relation with different indication of ICU admission and duration of hospital stay. It was a cross sectional study done in the Intensive Care Unit (ICU) of Chittagong Medical College Hospital (CMCH), in the period of six months from 08/07/2012 to 07/01/2013. Hundred consecutive admitted patients in the ICU were taken as study subject and Acute Kidney Injury Network (AKIN) criteria was applied to evaluate the acute kidney injury among the admitted patients. The total number of ICU patients taken in the study were 100. Among them, 62 (62%) patients were male and 38(38%) of the patients were female. Male to female ratio was 1.6:1. 52(52%) came from urban areas and 48(48%) came from rural areas. Regarding the age distribution of total 100 patients age range was 22 to 81 years. The mean + SD was 53.90 – 14.502 years. Among the 100 patients majority were illiterate to primary level educated which were 42(42%). Maximum were in the income group 10,000-20,000 TK/month which is 45(45%). Among all patients housewives were found in 28(28%) cases, followed by retired from service, service holder and businessman in 20(20%), 12(12%) and 16(16%) cases respectively. Regarding analysis of causes of ICU admission respiratory failure was 31% which was highest, then 13% cases were stroke, 12% were septic shock and accidental injury each, postoperative complications were 8%, poisoning was 7%, GBS was 5%, hepatic encephalopathy was 7% and others was 5%. Among the 100 ICU patients, 28(28%) were found to have AKI. Among them, most of the patients (21.4%) of respiratory failure had AKI, next to it was accidental injury (17.8%), postoperative patients(14.2%), septic shock (14.4%), hepatic encephalopathy(10.7%), poisoning (7.2%) and stroke (3.6%). Regarding the renal function tests the mean + SD of blood urea was 46.64 18.19 mg/dl and it was 2.38 + 1.7mg/dl for serum creatinine. Out of 100 patients 57(57%) were ventilated and 43(43%) were not ventilated. Among the 57 ventilated patients 23(40.4%) had AKI and among the 43 non ventilated patients 4(11.6%) had AKI. Distribution was statistically significant (p<0.05). Among the 100 patients who stayed less than 5 days in the hospital(n=29) had AKI 24.1% of patients, who stayed 5-10 days(n=41) had AKI among 29.4% patients and who stayed >10 days(n=20) had AKI 30% of patients. Distribution of the AKI according to different duration of hospital stay was statistically significant (p<0.05) The prevalence of AKI in the ICU CMCH, according to AKIN criteria is 28%. Early intervention is essential to overcome the development of overt renal failure.
 JCMCTA 2013 ; 24 (2): 36-39

Acute kidney injury (AKI) is a frequent complication after orthotopic liver transplantation (OLT). The incidence of post-operative AKI according to acute kidney injury network criteria can be estimated to be as high as 60% of all patients after liver transplantation [1–3]. Besides increasing morbidity and length of hospitalization, graft survival is significantly reduced, even with only modest increase of serum creatinine (> 0.5 mg/dL, AKIN Stage 1) [3, 4]. Postoperative AKI is also an independent risk factor for mortality during the first year after transplantation [1]. The development of AKI following liver transplantation is multifactorial and influenced by numerous pre-, intraand post-operative factors. During the preoperative period, conditions predisposing for post-operative AKI can be present. The most commonly observed preoperative renal dysfunction is due to the hepato-renal syndrome characterized by arterial vasodilatation mainly in the splanchnic vessel area and severe renal vasoconstriction. Intraoperative factors include long periods of vascular crossclamping, hypotension, high doses of vasopressors and large volume load. Post-operative hypotension and calcineurin inhibitors such as cyclosporine and tacrolimus also support conditions potentially culminating in AKI [4]. Currently, there are no effective measures or treatment strategies available for the prevention or treatment of AKI. The development of effective interventions is hampered by the limited ability of early detection of AKI [5, 6]. In order to develop and evaluate strategies for the prevention and treatment of AKI, there is a great need for early biomarkers. In this issue of Nephrology Dialysis Transplantation, Wagener et al. [7] propose increased urinary neutrophil gelatinase-associated lipocalin (NGAL)/creatinine ratio as an early predictor of AKI following OLT. The data source is a prospective cohort study of 92 patients undergoing OLT at a single centre between 2008 and 2010 (18 living related, 74 deceased). Patients underwent OLT for different reasons (hepatitis C, hepatitis B, nutritive toxic liver cirrhosis, primary sclerosing cholangitis) and showed a modified end stage liver disease score of 21.9 7.4 prior to surgery. Patients did not require renal replacement therapy preoperatively and apparently had intact kidney function according to the serum creatinine (0.99 0.64 mg/dL). Urine samples were collected after induction of anaesthesia prior to incision, immediately after portal reperfusion of the liver graft and then 3, 18 and 24 h later. To compensate for possible urinary dilution or concentration, the results of the NGAL measurements are given as urinary NGAL/creatinine ratio. AKI was defined according to the RIFLE criteria by an increased serum creatinine of >150% after OLT compared to preoperative values. Thirty-seven patients (40.2%) developed AKI during the post-operative period. In those patients, serum creatinine concentration significantly increased at Day 2 after transplantation, whereas urinary NGAL/creatinine ratio already showed a significant increase after 3 h. According to the study, there is a diagnostic benefit of ~2 days using urinary NGAL compared to serum creatinine for the diagnosis of AKI after OLT. Interestingly, in patients with AKI, NGAL already declined between 3 and 18 h after OLT and there was no significant difference between the AKI and nonAKI group after 24 h. This time course suggests that the increase in urinary NGAL/creatinine is specific for the kidney injury during OLT. Just before transplantation, and immediately after reperfusion, there were no differences in urinary NGAL/creatinine concentration between patients with AKI and those without AKI. The investigators conclude that urinary NGAL/creatinine ratio is an early marker of AKI after liver transplantation, which, because of its high sensitivity and specificity, might be a useful surrogate end point of AKI in clinical trials. Urinary NGAL might be a more sensitive marker for AKI, especially in patients after liver transplantation, than serum creatinine because unlike serum creatinine, it is not dependent on drugs, muscle mass or liver metabolism [8]. Urinary NGAL is mainly produced by the distal nephron after injury and is immediately secreted into the urine. In contrast, plasma NGAL is a product of multiple sources. Nevertheless, AKI also triggers increasing amounts of messenger RNA in other tissues than the distal nephron including liver and lung [9]. This might explain why both urinary and plasma NGAL proved to be reliable markers for AKI in children after cardiac surgery with an AUC–ROC of >0.9 [14]. But also in patients with AKI after liver transplantation, it was shown to be of benefit. In a prospective study of

Acute kidney injury (AKI) and delirium are common complications on the intensive care unit (ICU). Few is known about the association of AKI and delirium, as well as about incidence and predictors of delirium in patients with AKI. In this retrospective study, all patients with AKI, as defined by the KDIGO (kidney disease improving global outcome) guideline, treated for more than 24 h on the ICU in an university hospital in 2019 were included and analyzed. Delirium was defined by a NuDesc (Nursing Delirium screening scale) ≥ 2, which is evaluated three times a day in every patient on our ICU as part of daily routine. A total of 383/919 (41.7%) patients developed an AKI during the ICU stay. Delirium was detected in 230/383 (60.1%) patients with AKI. Independent predictors of delirium were: age, psychiatric disease, alcohol abuse, mechanical ventilation, severe shock, and AKI stage II/III (all p < 0.05). The primary cause of illness had no influence on the onset of delirium. Among patients with AKI, the duration of the ICU stay correlated with higher stages of AKI and the presence of delirium (stage I/no delirium: median 1.9 (interquartile range (25th–75th) 1.3–2.9) days; stage II/III/no delirium: 2.6 (1.6–5.5) days; stage I/delirium: 4.1 (2.5–14.3) days; stage II/III/delirium: 6.8 (3.5–11.9) days; all p < 0.01). Delirium, defined as NuDesc ≥ 2 is frequent in patients with AKI on an ICU and independently predicted by higher stages of AKI.

Acute kidney injury (AKI) comprises several syndromes that are associated with a sudden decrease in renal function. AKI is a common condition especially among critically ill patients. It is typically multifactorial and of great prognostic significance. The incidence of AKI has increased while the associated mortality rate has remained unchanged over the last years. Recent definitions of AKI, namely the Risk, Injury, Failure, Loss of renal function and End-stage kidney disease (RIFLE) classifycation or the Acute Kidney Injury Network (AKIN) criteria, incorporate serum creatinine and urine output as the principal markers to define and detect AKI. However, elevated serum creatinine or oliguria were demonstrated to detect AKI at late stages of renal injury when preventive strategies may be less effective. Therefore, there has recently been a great scientific interest in obtainng valuable markers for early AKI detection. In the last 5 years numerous new markers such as neutrophil-gelatinase associated lipo-calin, interleukin-18, cystatin C and kidney injury molecule 1 in the urine and/or serum have been studied and proposed as early detection markers of AKI. Persistently, these markers performed well in initial pilot trials. However, these promising results could often not be confirmed in later, larger multicentre trials and limitation of these biomarkers in the early diagnosis of renal injury were discovered. Furthermore, as AKI is multi-factorial and heterogeneous in origin, it seems likely that not one single marker but a panel of biomarkers will be required to detect all subtypes of AKI early during their evolution. This has initiated proteomic studies to develop panels of biomarkers which may facilitate early detection of AKI. The present review will focus on the most important clinical studies evaluating the ability of single AKI biomarkers and on those in clinical proteomics that attempted to establish panels of biomarkers in urine for early and accurate AKI diagnosis and prognosis.

Acute kidney injury (AKI), impairment of kidney function requires special attention in intensive care unit’s (ICU), because if multiorgan failure affect the kidney, it carries a greater risk for worse outcome and furthermore survivors have higher risk then normal population for chronic renal failure. It was reported that they also have higher mortality and morbidity rates compared to normal population (Kellum, 2008 & Shiffle, 2006). Acute tubular necrosis (ATN) is the primary causes of AKI in hospital and ICU and sepsis, ischemic or toxic insults were reported as the most common reason for ATN. The rates of AKI have been reported in hospitalized patients to be between 3.2%-20% and in ICUs this rate rises up to 22% and even to 67% depending on the population studied and the definition used (Murugan 2011). Based on the administrative data, the incidence of severe AKI (defined requiring dialysis) from 1988 to2002 has increased from 4 to 27 per 100000 population. But fortunately in hospital mortality, has decreased from 41.3 to28 % (p<0.001) (Waikar, 2008). Likewise a progressive 2.8% annual increase in incidence of AKI and progressive 3.8% annual decrease in AKI associated mortality(95%CI:-4.7 to-2.12:p<0.001) was observed from 1996-2005 in a large database in Australia and New Zealand (Pisoni, 2008&Bagshaw, 2007). Despite the fact that mortality might be decreasing in ICU patients with AKI, it is still high and reported to be up to 43-88%. Mortality rate becomes even higher when patients require renal replacement therapy (Kellum, 2008). Interestingly, it was reported that irreversible AKI requiring chronic dialysis therapy increased from 3.7% in 1984 to 18.2% in 1995 in surviving patients. Even higher number of patients (33-68%) at discharge whose kidney failed to recover and who needed long term dialysis. This changing renal outcome in the survivors of ICU acquired AKI cases might be related to increasing number of older patients, several co morbid conditions, more severe AKI cases than before and in addition, complication of the more aggressive renal replacement therapies currently used (Shiffle, 2006). Since AKI in critical ill patients have high mortality rate and even if patients survive, they are at risk for End Stage Renal Disease (ESRD) and higher mortality than the normal population, it is important to recognize the clinical picture of AKI and to institute prevention as early as possible. Thus, physician should be alarmed and be ready for early intervention in this particular group of patients. With the introduction of the RIFLE

Acute kidney injury (AKI) is a frequent and serious clinical condition which is associated with poor outcomes, including high mortality rate. Classically, it was considered as an acute condition, potentially reversible with full restitution if patient survives the acute phase of the disease. However, recent epidemiologic and observational studies underscore the association of an episode of AKI with long-term adverse outcomes such as chronic kidney disease, end-stage renal disease, cardiovascular events, and premature death. The increasing incidence of AKI, the association with severe in-hospital complications and long-term outcomes and death, the rise in costs, and the potentially preventable nature of AKI make it as a major public health issue, raising the interest of investigators in the field. Focusing on avoidance of the syndrome or its complications, the burden of the disease that is estimated in more than 13 million people/year all around the world could be effectively reduced. In this special issue devoted to AKI, the potential protective effects of diverse interventions were explored in five basic research studies. Y.-Y. Chen et al. explored the effect of 2-methoxyestradiol against ischemia/reperfusion injury. The protective effect of the angiotensin-receptor blocker olmesartan in rats exposed to tacrolimus is addressed by N. O. Al-Harbi et al. The influence of acute superoxide radical scavenging on systemic hemodynamic and kidney function was investigated by Z. Miloradovic et al. in a model of induced postischemic AKI. Z. O. Ibraheem et al. evaluated the impact of high fructose feeding in rat model of gentamicin induced nephrotoxicity. Finally, W. Zhang et al. addressed the feasibility and efficacy of hypoxia preconditioning to enhance MSC-based therapy of AKI. Contrast induced nephropathy (CIN) was addressed in three clinical studies. The beneficial effect of atorvastatin and rosuvastatin administered at high doses and before iodinated contrast administration was addressed by M. Peruzzi et al. concluding that they have a consistent and beneficial preventive effect on CIN and may actually halve its incidence. The incidence of CI-AKI and ERD in patients who received iodixanol (isoosmolar) versus iohexol (low-osmolar) during angiography for cardiac indication was examined by H.-R. Chua et al. who found advanced age, emergent cardiac conditions, and critical illness as stronger predictors of CI-AKI. J. Malyszko et al. sought cytokine midkine as a potential early marker of renal injury after contrast administration. In a series of critically ill patients with AKI, C.-M. Zheng et al. found that anion gap value predicts short-term mortality in patients with metabolic acidosis and AKI, whereas the strong ion gap value predicts both short-term and long-term mortality among such patients. Dr. H. E. Liu et al. explored genetic polymorphisms of ERCC1 and TP53 as risk factors for cisplatin- and carboplatin-induced nephrotoxicity. Dr. B. B. Albino et al. wondered whether the duration of extended dialysis was associated with complications in AKI patients. The frequency of TGF-β and IFN-γ genotype as risk factors for AKI and death in ICU patients is explored by C. C. Grabulosa et al. who found no association with these outcomes. S. N. Fernandez et al. compared the efficacy of heparin and citrate for anticoagulation in critically ill children on CRRT and found that citrate is a safe and effective anticoagulation method. In a large cohort of AKI patients V.-C. Wu et al. found a decreasing risk of long-term ESRD and mortality in patients surviving an episode of AKI-requiring dialysis, AKI nonrequiring dialysis, and no AKI, respectively. Finally, pathophysiology of cisplatin-induced AKI and nephrotoxicity of contrast media were reviewed by A. Ozkok and C. L. Edelstein and M. Andreucci et al., respectively. We hope this special issue on AKI collaborates in raising the awareness on this clinical condition that challenges not only nephrologists and intensivists who mostly deal with patients with AKI but also primary care physicians, clinicians, surgeons, radiologists, and those who are “in the right place at the right time” to prevent the onset of AKI or, even more, the disease leading to AKI. Raul Lombardi Emmanuel A. Burdmann Alejandro Ferreiro Fernando Liano

Acute kidney injury (AKI), previously called acute renal failure, is characterized by an abrupt increase in the concentration of serum creatinine (SCr) and nitrogenous waste products and by the inability of the kidney to appropriately regulate fluid and electrolyte homeostasis. The incidence of AKI in children has increased over the last decades, and the etiology of AKI has evolved from primary renal disease to multifactorial causes due to major advances in the medical management of critical illnesses, such as solid organ and stem cell transplantation, corrective surgery for congenital heart disease, sepsis, and septic shock. AKI is not just a marker of illness severity in children, but has a direct association with poor outcomes. Even when the definitions and characterization of AKI in children have advanced significantly over the past two decades, the diagnosis of AKI is still made with surrogate markers of glomerular filtration rate, such as SCr and urine output [1,2]. There are improved consensus multidimensional AKI definitions, namely the pRIFLE, AKIN and The KDIGO AKI definition and staging criteria being used worldwide, but with significant limitations. SCr continues to be quite limited as a marker of kidney dysfunction: it is often inaccurate in patients with low muscle mass, fluid overload or prior chronic kidney disease. Furthermore, SCr shows a demonstrable rise in concentration many hours to days after insult to the kidney, making it an insensitive, late and unmodifiable functional AKI marker. Thus, creatinine-based AKI diagnosis is often delayed, rendering treatments to mitigate or prevent AKI ineffective. There is a strong ongoing research effort to identify novel serum and urinary AKI biomarkers that reflect early kidney injury development and severity before loss of kidney function, with the hope that earlier “sub-clinical” AKI diagnosis can lead to earlier initiation of AKI treatment, or to changes in clinical management to mitigate the adverse effects of AKI until renal function recovery occurs [3,4]. Some of these promising serum and urine biomarkers are CyC and NGAL, IL-18, KIM-1, and LFABP respectively [5]. All of them have shown considerable promise diagnosing AKI earlier than SCr. Given that AKI is a complex and heterogeneous disease, it will probably be best diagnosed by a panel of biomarkers, rather than a single one. In the future, once these biomarker panels have been used widely in clinical practice and linked to clinical outcomes, it is likely that pediatric AKI will become defined by biomarker elevations and not by SCr [6].

Acute kidney injury (AKI) after liver transplantation (LT) is a pressing issue and remains the focus of many researchers. The etiology of AKI is multifactorial, but the main one is ischemia-reperfusion injury to the liver transplant. Numerous preoperative, intraoperative and postoperative risk factors contribute to the development of AKI. The use of standard classifications, such as AKIN, RIFLE and KDIGO, has improved post-transplant AKI diagnosis. However, determination of creatinine levels in the blood enables AKI diagnosis only in the later stages of this syndrome. Therefore, studies are currently underway to find ways of early diagnosis of AKI using biomarkers. Transition to a molecular level not only improves accuracy but also facilitates early diagnosis of AKI. Currently, the diagnostic capabilities of neutrophil gelatinase-associated lipocalin (NGAL) are the most investigated. To date, there are no known measures of preventing post-transplant AKI. Moreover, treatment of this condition cannot be considered satisfactory. Even a mild post-transplant AKI can be fatal. In severe AKI, where renal replacement therapy is used, there is a risk of death in the intensive care unit. More than half of AKI patients develop chronic kidney disease requiring chronic hemodialysis.

Acute kidney injury (AKI) is associated with adverse short-and long-term outcomes. The aim of this study was to evaluate the incidence of AKI and the short-term mortality in patients admitted with acute coronary syndrome (ACS) to a single coronary care unit (CCU) in Tripoli, Libya. We retrospectively studied the medical records of ACS patients admitted to the CCU of a referral cardiology center, during the period from January 1, 2014, to December 31, 2014. AKI was defined according to the AKI network criteria. The incidence of AKI and short-term CCU mortality was compared between different types of ACS. Data of patients with and without AKI were compared using Student's t-test and Chi-squared statistic considering P <0.05 statistically significant. Eighty-four patients with ACS were included in the study; their mean age was 57.6 ± 14.4 years [standard deviation (SD)], 75% were males and their mean stay in the CCU was 4.3 ± 3 days (SD). Of them, 71.4% had ST-elevated myocardial infarction (STEMI), 22.6% had non-STEMI, and 6% had unstable angina. About 41.7% had AKI (19% had AKI Stage 1, 17.9% had AKI Stage 2, and 4.8% had AKI Stage 3). The total CCU mortality was 15.5%; mortality among AKI patients in the CCU was 25.7% compared with 6.12% in the non-AKI patients (P = 0.014). The mortality worsened with increasing severity of AKI. Patients with AKI were older (61.6 ± 15 years) than the non-AKI group (54.7 ± 13 years, P = 0.031), their mean blood pressure at admission was lower, their CCU stay was longer, and they more frequently had coexisting acute decompensated heart failure. In this study of ACS patients, the incidence of AKI was high, the CCU mortality among the AKI patients was 25.7% compared with 6.12% in the non-AKI patients, and the mortality worsened with increasing severity of AKI.

Acute kidney injury (AKI) is a risk factor for increased mortality in critically ill patients. Sustained low efficiency dialysis (SLED) is a new approach in renal replacement therapy (RRT) and it combines the advantages of continuous renal replacement therapy (CRRT) and intermittent haemodialysis (HD). The study was aimed to evaluate the outcome of the hae-modynamically unstable patients with AKI in Bangladesh who were treated with SLED. So far this is the first reported study on SLED in intensive care unit (ICU) in Bangladesh. This quasi-experimental study was conducted in a 10-bed adult ICU of a tertiary care hospital in Bangladesh from June 2012 to May 2013. A total of 153 sessions of SLED were performed on 43 AKI patients. Mean age of the patients was 60.12 ± 15.57 years with male preponder-ance (67.4% were male). Mean APACHE II score was 26.88 ± 6.25. Fourteen patients (32.55%) had de novo AKI. Twenty nine patients (67.4%) had chronic kidney disease (CKD) with baseline mean serum creatinine 2.56 mg/dl, but did not require any RRT before admis-sion in ICU. After giving SLED, AKI of the study patients were completely resolved in 27.9%. Some forty two percent patients became dialysis dependant and 30.23% patients died. Patients who had AKI on CKD became dialysis dependant more often than the patients with de novo AKI (p &lt;0.01). Mortality rate was significantly higher in patients who were on inotrope support (p= 0.017). Otherwise, there was no relation of 28 day mortality with age, prior renal function and mechanical ventilator requirement (p&gt;0.05). Thus, SLED is an excellent renal replacement therapy for the haemodynamically unstable AKI patients of ICU. It is also cost-effective compared to CRRT.

Acute kidney injury (AKI), as defined by the Acute Kidney Injury Network, has been widely investigated in decompensated liver cirrhosis patients. AKI is frequently progressive and independently associated with mortality in these patients. However, in the Asia-Pacific region, the majority of cases of acute-on-chronic liver failure (ACLF) are caused by acute exacerbation of chronic hepatitis B without preexisting cirrhosis. It is not clear whether these patients are at similar risk as those with underlying cirrhosis. We performed a retrospective cohort analysis of hepatitis B-related ACLF patients in a single center from January 2004 through December 2011 and evaluated the occurrence of AKI after admission and its relation to the 3-month mortality of ACLF patients. A total of 439 patients with hepatitis B-related ACLF without preexisting cirrhosis were enrolled, and 158 patients (36.0%) developed AKI during hospitalization. ACLF patients with AKI had higher serum creatinine, bilirubin, and INR values and MELD scores as well as more complications compared to those without AKI (p < 0.01). The occurrence of AKI and its stage affect the 3-month mortality of ACLF patients (p < 0.001), and a greater percentage of AKI was found in non-survivors than survivors (56.7 vs. 27.6%, p < 0.001). The cumulative survival of patient with no AKI, AKI stage 1, 2 and 3 was 77.84, 65.46, 41.38 and 27.03%, respectively. In our study, we observed that AKI was associated with increased 3-month mortality in hepatitis B-related ACLF patients without preexisting cirrhosis. Higher AKI stage predicted a worse prognosis. Our findings support the importance of early identification and timely therapy of AKI in hepatitis B-related ACLF patients.

Acute kidney injury (AKI) complicates the clinical course of hospitalized patients by increasing need for intensive care treatment and mortality. There is only little data about its impact on AML patients undergoing intensive induction chemotherapy. In this study, we analyzed the incidence as well as risk factors for AKI development and its impact on the clinical course of AML patients undergoing induction chemotherapy. We retrospectively analyzed data from 401 AML patients undergoing induction chemotherapy between 2007 and 2019. AKI was defined and stratified according to KIDGO criteria by referring to a defined baseline serum creatinine measured on day 1 of induction chemotherapy. Seventy-two of 401 (18%) AML patients suffered from AKI during induction chemotherapy. AML patients with AKI had more days with fever (7 vs. 5, p = 0.028) and were more often treated on intensive care unit (45.8% vs. 10.6%, p < 0.001). AML patients with AKI had a significantly lower complete remission rate after induction chemotherapy and, with 402 days, a significantly shorter median overall survival (OS) (median OS for AML patients without AKI not reached). In this study, we demonstrate that the KIDGO classification allows mortality risk stratification for AML patients undergoing induction chemotherapy. Relatively mild AKI episodes have impact on the clinical course of these patients and can lead to chronic impairment of kidney function. Therefore, we recommend incorporating risk factors for AKI in decision-making considering nutrition, fluid management, as well as the choice of potentially nephrotoxic medication in order to decrease the incidence of AKI.

Acute kidney injury (AKI) is a relevant complication following thoracoabdominal aortic aneurysm repair (TAAA). Biomarkers, such as secretory leucocyte peptidase inhibitor (SLPI), may enable a more accurate diagnosis. In this study, we tested if SLPI measured in serum is an appropriate biomarker of AKI after TAAA repair. In a prospective observational single-center study including 33 patients (51.5% women, mean age 63.0 ± 16.2 years) undergoing open and endovascular aortic aneurysm repair in 2017, SLPI was measured peri-operatively (until 72 h after surgery). After surgery, the postoperative complications AKI, as defined according to the KDIGO diagnostic criteria, sepsis, death, MACE (major cardiovascular events) and, pneumonia were assessed. In a subgroup analysis, patients with preexisting kidney disease were excluded. Of 33 patients, 51.5% (n = 17) of patients developed AKI. Twelve hours after admission to the intensive care unit (ICU), SLPI serum levels were significantly increased in patients who developed AKI. Multivariable logistic regression revealed a significant association between SLPI 12 hours after admission to ICU and AKI (P = 0.0181, OR = 1.055, 95% CI = 1.009–1.103). The sensitivity of SLPI for AKI prediction was 76.47% (95% CI = 50.1–93.2) and the specificity was 87.5% (95% CI = 61.7–98.4) with an AUC = 0.838 (95% CI = 0.7–0.976) for an optimal cut-off 70.03 ng/ml 12 hours after surgery. In patients without pre-existing impaired renal function, an improved diagnostic quality of SLPI for AKI was observed (Sensitivities of 45.45–91.67%, Specificities of 77.7–100%, AUC = 0.716–0.932). There was no association between perioperative SLPI and the incidence of sepsis, death, MACE (major cardiovascular events), pneumonia. This study suggests that SLPI might be a post-operative biomarker of AKI after TAAA repair, with a superior diagnostic accuracy for patients without preexisting impaired renal function.

Acute kidney injury (AKI) is characterized by a sudden reduction in renal function resulting in the accumulation of nitrogenous compounds such as urea and creatinine in the blood. AKI is classified into three categories: (1) pre-renal disease, (2) intrinsic renal disease, and (3) post-renal disorders. Ischemic injury, nephrotoxic agents, and sepsis are among the major causes of AKI. AKI occurs in approximately 5 % of hospitalized patients or more than 30 % of critically ill patients. In recent years, there have been significant advancements in our understanding of AKI and its impact on outcomes across the medicine. There has been great progress on the definition, diagnosis, risk factors, epidemiology, evaluation, outcomes, and management of AKI in children including continuous renal replacement therapies. There is a strong epidemiologic association between development of AKI and subsequent development and progression of chronic kidney disease (CKD). It is recommended to define AKI according to the RIFLE classification system into risk, injury, and failure. It is also recommended to base the decision when to start continuous renal replacement therapy (CRRT) not only on the severity of AKI but also on the severity of other organ failure. We put forth and highlight the pediatric AKI modified RIFLE definition of AKI, discuss risk factors for pediatric AKI and provide recommendations for the evaluation and treatment of these patients, and identify those children who require CRRT. Renewed knowledge into these aspects of AKI may prove helpful in initiating early therapeutic interventions that can attenuate development of CKD and improve clinical outcomes in children with AKI.

Acute Kidney Injury (AKI) after cardiac surgery is associated with increased mortality, but very few data exist on the ocurrence of AKI associated with Transcatheter Aortic Valve Implantation (TAVI). The objective of this study was to determine the incidence, predictors and prognosis of AKI after percutaneous implantation of the CoreValve aortic valve prosthesis. Methods: Between April 2008 and January 2011, 230 patients with severe aortic stenosis were treated with the CoreValve aortic valve prosthesis. The AKI was defined according to Valve set by the Academic Research Consortium, as the absolute increase in serum creatinine ≥0.3 mg/dl or an increase of over 50% at 72 hours a percutaneous procedure. Were excluded from analysis 7 patients, in 5 patients were unsuccessful procedural and 2 patients had chronic renal failure on dialysis. Results: Of the 223 patients treated with TAVI, 53 patients (23.8%) had chronic renal failure. AKI was identified in 37 patients (16.6%) and none reqired renal replacement therapy. After implantation there was a slight improvement in renal function, baseline serum creatinine decreased from 1.29±0.5 mg/dl to 1.22 mg/dl, P = 0.023 and Glomerular Filtration Rate (GFR) increased from 49.6±22 to 52±23, P = 0.015. There were no differences in the amount of contrast received (197±67 for patients with AKI vs. 180±72 cc for patients without AKI, P = 0.580). In patients with AKI, the mortality at 30 days was 13.5% compared to 1.6% of patients without AKI, P = 0.001 and late mortality after a mean of 16.7±11 months was 18.8% in those patients with AKI compared to 8.2% in those witout AKI, P = 0.068. In the multivariate analysis AKI was an independent predictor of cumulative total mortality (HR = 3.516, 95% CI from 1.098 to 11.255, P = 0.034). The factors associated with development of AKI were males and the presence of stroke prior the procedure. Conclusions: The deterioration of renal function in patients undergoing TAVI with the CoreValve prosthesis is a serious and frequent complication. The occurrence of AKI was associated with increase early mortality and also was a predictor of worse outcomes in the long-term follow-up.