Association Of Acute Kidney Injury Research Articles

Eight-year national multicenter experience on the use of glucarpidase as effective rescue therapy for delayed methotrexate elimination after high-dose methotrexate cycles administered in children with hemato-oncological diseases

BackgroundHigh-dose methotrexate (HDMTX) for cancer treatment can be complicated by delayed methotrexate elimination (DME) and associated acute kidney injury (AKI). This study evaluated glucarpidase for the treatment of DME and HDMTX-AKI in pediatric hemato-oncology patients. MethodsThis multicenter, retrospective study reviewed the medical records of pediatric patients (1–18 years) with ALL or NHL, who were given glucarpidase as rescue therapy for DME or HDMTX-AKI at 13 Italian AIEOP centers between January 1, 2015, and June 30, 2023. Patients also received uniform supportive therapy, per study protocols and guidelines, to prevent and treat AKI. ResultsData were available for 42/44 patients given glucarpidase, following i.v. HDMTX as monotherapy (non-high risk ALL [non-HR ALL], n=24), or within combined intensive chemotherapy blocks (HR-ALL, n=13; NHL, n=5). Median time to glucarpidase infusion was 53hours (range 32–72). Most patients required glucarpidase during the first cycle of HDMTX. Glucarpidase led to a rapid decrease in plasma MTX levels (median 72.53%; range 12.62%–94.57%). Median time for complete elimination of MTX and its metabolites was 216hours (range 120–672). Recovery of renal function (return of serum creatinine to ≤1.5 times baseline value) took a median 18 days (range 4–72). Of the 22/42 patients (52%) re-challenged with HDMTX (at 40–100% of recommended dose), none experienced DME and all completed per-protocol number of HDMTX cycles. ConclusionsOur experience shows that glucarpidase is effective and well tolerated for the treatment of DME and HDMTX-AKI in pediatric patients with hemato-oncologic diseases.

Renal medullary perfusion differs from that in renal cortex in patients with sepsis associated acute kidney injury and correlates with renal function prognosis: A prospective cohort study.

Renal perfusion status remains poorly studied at the bedside during sepsis associated acute kidney injury (AKI). The aim of the study is to examine renal cortical and medullary perfusion using renal contrast enhanced ultrasound (CEUS) in septic patients. In this single-center, prospective longitudinal study, septic patients were enrolled. Renal ultrasonography was performed within 24 hours of ICU admission (D1), then repeated at D3, D5 and D7. Each measurement consisted of three destruction replenishment sequences that were recorded for delayed analysis with dedicated software (Vuebox). Renal cortex and medulla perfusion were quantified by measuring time to peak (TTP). Receiver operating characteristic (ROC) analysis was used to evaluate 28-day renal prognosis. The study included 149 septic patients, including 70 non-AKI patients and 79 AKI patients. Both renal cortical and medullary TTP was longer in the AKI group than in the non-AKI group. The difference of TTP between renal cortex and medulla in AKI group was higher than that in the non-AKI group (p = 0.000). Medullary TTP on day 3 had the best performance in predicting the prognosis of 28-day renal function (AUC 0.673, 95% confidence interval 0.528-0.818, p = 0.024), and its cut-off value was 45 s with a sensitivity 52.2% and a specificity of 82.1%. Cortical TTP on day 3 also had the performance in predicting the prognosis of 28-day renal function (AUC 0.657, 95% confidence interval 0.514-0.800, p = 0.039), and its cut-off value was 33 s with a sensitivity 78.3% and a specificity of 55.0%. Renal medullary perfusion alterations differ from those in cortex, with the medulla is worse. Simultaneous and dynamic assessment of cortical and medullary microcirculatory flow alterations necessary. TTP on day 3, especially medullary TTP, seems to be a relatively stable and useful indicator, which correlates with 28-day renal function prognosis in septic patients. Early correction of renal cortical and medullary perfusion alterations reduces the incidence of adverse renal events.

Macroscopic hematuria-associated severe acute kidney injury triggered by kidney stone formation in a patient with thin basement membrane and no history of microscopic hematuria.

Macroscopic hematuria (MH)-associated acute kidney injury (AKI) is a rare condition that causes acute tubular damage due to severe glomerular bleeding with MH. A 66-year-old Japanese woman with no significant past medical history was referred for severe kidney injury with oliguric MH. Her prior medical checkup results showed no occult blood in her urine. Seven days earlier, she had experienced transient severe acute right lumbar back pain. On admission, her serum urea nitrogen was 147mg/dL, serum creatinine (sCr) 18.3mg/dL, urinary red blood cells (RBCs) > 100/hpf, urinary protein 28.8g/gCr, with no hydronephrosis in either kidney, but two stones were found in the right kidney and right ureteropelvicjunction. At the start of her hemodialysis, the patient was treated with high-dose steroids because of suspected rapidly progressive glomerulonephritis. A renal biopsy of the left kidney showed acute tubular injury with massive RBC casts filling the tubular lumen. Glomerulitis was not detected, but electron microscopy revealed diffuse glomerular thin basement membrane (TBM). Despite immediate steroid discontinuation, the patient's renal function and MH improved, and she was weaned from hemodialysis. The stones resolved 2months after onset, but microscopic hematuria persisted for 7months post-onset. The sCr level was fixed at 1.1mg/dL 20months post-onset. This is the first report of MH-AKI in a TBM without the risk of MH-AKI development, such as bleeding tendency or iron overload. In this TBM, a colic attack of the renal urinary tract induced glomerular bleeding, and intolerance to hematuria may have caused severe tubular damage.

8192 A Two-Cycle Clinical Audit Testing Inpatient Management Of Hypophosphatemia In A UK District Hospital

Abstract Disclosure: J. Porto: None. E. Ssemmondo: None. N. Obike: None. A. Abobaker: None. R. March: None. N. Tun: None. T. Pawlak: None. Objective: A clinical audit was conducted to assess if there was any improvement in management of hypophosphatemia among patients admitted to the medical wards using the local Trust protocol, following structured edcational sessions to the junior doctors covering medical wards. Design and methodology: The 2 cycles of the audit were conducted between March 2020 and September 2021 in Scarborough district Hospital. The clinical notes of 52 patients (20 in the first cycle and 32 in the re-audit) with hypophosphatemia were reviewed. These were identified using the electronic laboratory results of patients within the study period. The aspects of the trust protocol for management of hypophosphatemia that were audited; documentation of symptoms associated with low phosphate levels, cardiac monitoring in severe hypophosphatemia, identification of the likely cause of hypophosphatemia, the presence or absence of associated acute kidney injury (AKI) and initiation of phosphate replacement. The results of the first audit were presented at the local hospital clinical governance meeting (August 2020). Following this, 2 teaching sessions and 2-case based discussion on hypophosphatemia were organised for all the doctors in the department of medicine. The re-audit was subsequently conducted after the fourth teaching session. The proportions of each audited item were compared between the first audit and the re-audit using Fisher exact probability test. Results:25% of patients in the first audit had severe hypophosphatemia compared to 28% in the re-audit. In patients with severe hypophosphataemia, only 33.3% had cardiac monitoring during the re-audit cycle compared to 60% in the first cycle, and the difference was not statistically significant (p=0.58). There was significant improvement in the documentation of symptoms of hypophosphataemia amongst inpatients during the re-audit cycle compared with the initial cycle; 62.5% vs only 10% (P 0.002). Most patients had an underlying cause of the hypophosphatemia identified (80% and 62.5%-first and second cycle respectively). AKI was associated with hypophosphataemia in 15% & 34.4% (P 0.2) in the first and second cycles respectively. Despite low phosphate levels, 25% and 28.1% at the initial audit and the second cycle respectively did not receive any form of phosphate replacement. Conclusion: The two-cycle clinical audit showed that the teaching sessions on management of hypophosphatemia increased the awareness of the importance to document whether the patients were symptomatic or asymptomatic following the drop in their phosphate levels, which can help to identify patients at risk of developing complications, such as cardiac arrythmias. However, these sessions were not sufficient to improve overall management of patients with low phosphate levels. Presentation: 6/1/2024

Circ_001653 alleviates sepsis associated-acute kidney injury by recruiting BUD13 to regulate KEAP1/NRF2/HO-1 signaling pathway

BackgroundThe kidney is exceptionally vulnerable during sepsis, often resulting in sepsis-associated acute kidney injury (SA-AKI), a condition that not only escalates morbidity but also significantly raises sepsis-related mortality rates. Circular RNA circ_001653 has been previously reported to be upregulated in the serum of SA-AKI patients, while the role and underlying mechanism of circ_001653 in SA-AKI remains unknown. In this study, we aimed to explore the functional role and the molecular mechanism of circ_001653 in the pathogenesis of SA-AKI.MethodsLPS-stimulated HK-2 cells and ligation and perforation of cecum (CLP)-induced rats were used as in vitro and in vivo models of SA-AKI. The target gene expression levels were measured using qRT-PCR and western blot. Renal function (BUN, sCr, uNGAL, and uKIM-1), and renal pathological changes were detected in septic mice. TUNEL and EdU assays were conducted to measure apoptosis and proliferation rates in vitro. DCFH-DA staining was used to detect ROS levels in vitro and in vivo. Oxidative stress markers (SOD, GSH-Px, MDA, and SOD), and inflammation markers (IL-1β, IL-6, and TNF-α) were determined using commercial kits both in vitro and in vivo. Additionally, gain-and-loss-of-function assays and mechanistic experiments were conducted to explore the regulatory role of circ_001653 in SA-AKI pathogenesis.ResultsData showed that circ_001653 expression was high in LPS-stimulated HK-2 cells and CLP-induced rat renal tissue and was mainly localized in the cytoplasm. Notably, circ_001653 silencing alleviated SA-AKI by reducing apoptosis and alleviating oxidative stress and inflammation in HK-2 cells and renal tissue of rats. Mechanistically, it was found that circ_001653 alleviated SA-AKI by recruiting BUD13 to activate the KEAP1/Nrf2/HO-1 signaling pathway.ConclusionsTo summarize, our study is the first to reveal elevated expression of circ_001653 in sepsis-associated AKI, and its downregulation effectively attenuates AKI by reducing apoptosis, inflammation, and oxidative stress. Mechanistically, circ_001653 exerts its effects by recruiting BUD13 to activate the KEAP1/Nrf2/HO-1 signaling pathway. These findings suggest circ_001653 as a potential therapeutic target for the drug development of sepsis-associated AKI.

Ferroptosis and inflammation are modulated by the NFIL3-ACSL4 axis in sepsis associated-acute kidney injury

Sepsis-associated acute kidney injury (SA-AKI) increases the risk of death in patients with sepsis, and its major pathological change is the death of renal tubular cells. However, the mechanism of its occurrence remains unclear. Sepsis can lead to circadian dysregulation, and the rhythm gene NFIL3 has been reported to regulate lipid metabolism. There is compelling evidence that has demonstrated that lipid peroxidation can cause cellular ferroptosis. In this study, we established the in vitro and in vivo models of SA-AKI and confirmed the presence of ferroptosis of the renal tubular epithelial cells in SA-AKI. In addition, analysis of the GEO database showed that NFIL3 was highly expressed in sepsis patients and was highly correlated with the key molecule of ferroptosis, ACSL4. The in vitro and in vivo data suggested that NFIL3 was involved in ferroptosis and inflammation in SA-AKI. Subsequently, loss-of-function experiments revealed that NFIL3 knockdown attenuated ferroptosis and inflammation in renal tubular epithelial cells by downregulating ACSL4 expression, thus protecting SA-AKI. In conclusion, this study is the first to illustrate the involvement of the rhythm gene NFIL3 in SA-AKI, providing new insights and potential therapeutic targets for SA-AKI.

Cardiopulmonary Bypass Blood Flow Rates and Major Adverse Kidney Events in Cardiac Surgery: A Propensity Score-adjusted Before–After Study

ObjectiveCardiac surgery associated-acute kidney injury (CSA-AKI) is a common and serious postoperative complication of cardiac surgery, which is associated with increased postoperative morbidity and mortality. This study aimed to explore the association between CPB blood flow rate (CPB-BFR) and major adverse kidney events at day 30 (MAKE30). DesignRetrospective single-center before-after observational study. Patients were divided in two groups according to CPB flow rates: a first group with an institutional protocol targeting a CPB-BFR >2.2 L/min/m² (low CPB-BFR group), and a second group with a modified institutional protocol targeting a CPB-BFR >2.4 L/min/m² (high CPB-BFR group). The primary outcome was MAKE 30, defined as the composite of death, renal replacement therapy or persistent renal dysfunction. SettingThe data were collected from clinical routines in university hospital. ParticipantsAdult patients who underwent elective and urgent cardiac surgery without severe chronic renal failure, for whom CPB duration was ≥90 minutes. Interventions533 patients were included (low CPB-BFR group n=270, high CPB-BFR group n=263). Measurements and Main ResultsA significant decrease in MAKE 30 was observed in the high CPB-BFR group (3% vs. 8%; OR 0.779, 95% CI [0.661;0.919]; P<0.001) mainly mediated by a lower 30-day mortality in the high CPB-BFR group (1% vs. 5%; OR 0.697, 95% CI [0.595;0.817]; P= 0.001), as was renal replacement therapy (1% vs. 4%; OR 0.739, 95% CI [0.604;0.904]; P=0.016). ConclusionsIn patients undergoing cardiac surgery, increased CPB-BFR was associated with a reduction in MAKE 30 including mortality and renal replacement therapy.

Association of Acute Kidney Injury with Bronchopulmonary Dysplasia in Preterm Infants.

Bronchopulmonary dysplasia (BPD) is among the most common complications of prematurity and is associated with high morbidity and mortality rates. Acute kidney injury (AKI) is also commonly observed in premature infants and significantly increases morbidity and mortality. Studies have shown that systemic changes in AKI may also trigger lung damage. This study aimed to determine the effects of AKI on the development of BPD in preterm infants with a postconceptional age of ≤32 weeks and/or birth weight of ≤1500 grams. The relationship between demographic features and accompanying perinatal and postnatal morbidities among the patients was investigated. The incidence of BPD in infants with AKI was 52.6% (10 of 19 infants) and 38.3% (61 of 140 infants) in infants without AKI. In infants who developed BPD, the rate of AKI did not vary notably between babies born at ≤28 weeks and those born at >28 weeks [n=9, 17.3% (9 of 52 infants) and n= 1, 5.3%, (1 of 19 infants) respectively] of gestation (p>0.05). AKI was associated with a greater need for resuscitation at birth, a greater need for invasive mechanical ventilation, fewer ventilatorfree days, and a higher incidence of sepsis, patent ductus arteriosus, and necrotizing enterocolitis in premature infants. It was also more frequently associated with fluid-electrolyte imbalance, blood pressure, and hemodynamic disorders in the first postnatal week. The rate of BPD development was higher in infants with AKI, but this disparity was not statistically notable (p>0.05).

Renal resistive index by point of care ultrasound to predict sepsis associated acute kidney injury in critically ill children.

Sepsis associated acute kidney injury (AKI) is linked with adverse outcomes in the PICU. Doppler-based renal resistive index (RRI) has shown promising results in adults for prediction of AKI. We aimed to explore the performance of RRI in children with sepsis. This prospective observational study (March - November 2022) included children aged 1-12years with sepsis admitted to the PICU. RRI and urine neutrophil gelatinase associated lipocalin (NGAL) were measured within 12h of admission. Children were followed up for 3days. AKI (new and persistent) was defined as any child with KDIGO stage 2 or 3 AKI on day 3. We enrolled 90 children but included 79 in final analysis. Two thirds (n = 53, 67%) had septic shock. Median (IQR) age was 6.2years (4.1-9.2). RRI decreased with increasing age. Twenty-six (33%) children had AKI on day 3. Mean (SD) RRI was higher in the AKI group [0.72 (0.08) vs. 0.65 (0.07), p < 0.001].The area under ROC curve for RRI to detect AKI among the 1-4year old group was 0.75 (95% CI:0.51, 0.98; p = 0.05) and among the 5-12year old group was 0.76 (0.62, 0.89; p = 0.001). An RRI 0.71 predicted AKI with 100% sensitivity and 46.2% specificity among the 1-4-year-old group and RRI 0.69 predicted it with 70% sensitivity and 77.5% specificity in the 5-12-year-old group. RRI and eGFR at admission were independent predictors of AKI on multivariable analysis. Urine NGAL 94.8ng/ml predicted AKI with 76.9% sensitivity and 77.4% specificity and AUROC was 0.74 (0.62, 0.86) among the 1-12-year-old group. RRI values varied with age. RRI showed good diagnostic accuracy to detect new/persistent AKI on day 3 in children with sepsis; however, it was less precise as an independent predictor.

Incidence of postoperative acute kidney injury is twice as high in men than women following radical colorectal surgery — key findings from PROSACC, a posthoc analysis of a global, multicenter, randomized controlled trial

Acute kidney injury (AKI) affects approximately 8% of the general surgical population. Additionally, AKI increases the risk for morbidity and mortality by 8- and 3-fold respectively. It was earlier believed that women had a greater risk for postoperative AKI. However, recent literature indicates that the incidence of AKI is actually higher in hospitalized men than women (2.2 odds ratio). Hence the male sex is currently discussed to be a risk factor for AKI. We therefore hypothesized that the incidence of postoperative AKI will be higher amongst men than women after radical colorectal surgery. We conducted a posthoc analysis (PROSACC: Propofol or Sevoflurane Anesthesia in Colon Cancer, NCT05585866) on the database from the CAN-study (Cancer and Anesthesia: Survival After Radical Surgery, NCT01975064). The CAN-study included cancer patients undergoing radical surgery at several sites in China, Croatia, Poland, and Sweden. Patients included in PROSACC were those undergoing colorectal surgery at any predefined site. Primary outcome was incidence of AKI by changes in plasma creatinine, secondary outcome was AKI in association to gender (women/men). The KDIGO criteria was used for classifying AKI on postoperative days 1-3 and 4-10. Database management and statistical analysis was performed by Uppsala Research Centre. Men vs women AKI outcome at day 1-3 and 4-10 was statistically compared with the Pearson’s chi-square test. A total of 3254 patients (n=1900 men; n=1354 women) were included in the analysis with their preoperative plasma creatinine. Demographics showed that of the women, 39% had hypertension, 12% had diabetes and 2% had preexisting kidney disease. In comparison, amongst the men, 24% had hypertension, 9% had diabetes and 1% preexisting kidney disease. Postoperative plasma creatinine values were obtainable from the database in 2741 patients (n=1578 men; n=1163 women) on postoperative day 1-3. One hundred and ninety patients (7%) of this group had developed AKI. Separated by gender, 6% of the women (n=72) and 8% of the men (n=118) had established AKI according to KDIGO (p=0.190). Plasma creatinine values were obtainable in 986 patients (n=582 men; n=404 women) on postoperative day 4-10 whereas 87 patients (9%) in this group had developed AKI. Separated by gender, 6% of the women (n=23) but 11% of the men (n=64) had established AKI at this timepoint (p=0.004). With this posthoc analysis of a global, multicenter, randomized controlled trial we conclude that the incidence of postoperative AKI is twice as high in men compared with women after 4-10 postoperative days following radical colorectal surgery. Since the women had higher rate of pronounced preoperative risk factors yet still had lower incidence of AKI, this study aligns with the conclusion that the male sex is a risk factor for postoperative AKI. Funded by the Swedish Research Council (2014–02569 and 2014–07606). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cystatin c as an early marker of cardiac surgery associated-acute kidney injury in children in Nigeria

Cystatin c as an early marker of cardiac surgery associated-acute kidney injury in children in Nigeria

4 A Case of Metformin Toxicity in a Patient with Contrast Associated Acute Kidney Injury (AKI)

4 A Case of Metformin Toxicity in a Patient with Contrast Associated Acute Kidney Injury (AKI)

Selenium binding protein 1 protects renal tubular epithelial cells from ferroptosis by upregulating glutathione peroxidase 4

Ferroptosis is a form of programmed cell death involved in various types of acute kidney injury (AKI). It is characterized by inactivation of the selenoprotein, glutathione peroxidase 4 (GPX4), and upregulation of acyl-CoA synthetase long-chain family member 4 (ACSL4). Since urinary selenium binding protein 1 (SBP1/SELENBP1) is a potential biomarker for AKI, this study investigated whether SBP1 plays a role in AKI. First, we showed that SBP1 is expressed in proximal tubular cells in normal human kidney, but is significant downregulated in cases of AKI in association with reduced GPX4 expression and increased ACSL4 expression. In mouse renal ischemia-reperfusion injury (I/R), the rapid downregulation of SBP1 protein levels preceded downregulation of GPX4 and the onset of necrosis. In vitro, hypoxia/reoxygenation (H/R) stimulation in human proximal tubular epithelial (HK-2) cells induced ferroptotic cell death in associated with an acute reduction in SBP1 and GPX4 expression, and increased oxidative stress. Knockdown of SBP1 reduced GPX4 expression and increased the susceptibility of HK-2 cells to H/R-induced cell death, whereas overexpression of SBP1 reduced oxidative stress, maintained GPX4 expression, reduced mitochondrial damage, and reduced H/R-induced cell death. Finally, selenium deficiency reduced GPX4 expression and promoted H/R-induced cell death, whereas addition of selenium was protective against H/R-induced oxidative stress. In conclusion, SBP1 plays a functional role in hypoxia-induced tubular cell death. Enhancing SBP1 expression is a potential therapeutic approach for the treatment of AKI.

Comparison Efficacy between Percutaneous Nephrostomy and Double J Stent in Management of Obstructive Uropathy

Background: The prevalence of urolithiasis and associated acute kidney injury (AKI) has seen a notable increase in recent decades, particularly in developing countries such as Pakistan, which falls within the "stone forming belt" region. This rise has underscored the need for effective management strategies for obstructive uropathy, a potentially reversible condition if timely intervention is provided. However, the literature reveals a divergence in treatment approaches between different regions and among healthcare professionals, with no universally recommended treatment for relieving the obstructed system. Objective: This study aimed to evaluate and compare the efficacy of percutaneous nephrostomy (PCN) versus Double J stent (DJS) in the management of obstructive uropathy secondary to urolithiasis in patients with elevated serum creatinine levels. Methods: Conducted as a randomized controlled trial at the Jinnah Postgraduate Medical Center Karachi from January 2023 to December 2023, the study included patients aged 20 to 50 years with obstructive uropathy secondary to urolithiasis and serum creatinine above or equal to 2.0 mg/dL. Exclusion criteria encompassed obstructive uropathy due to bladder outlet obstruction, uncontrolled coagulopathy, and lack of consent. Participants were randomized into two groups for either PCN or DJS placement, with pre-operative and post-procedure serum creatinine and urea levels measured at multiple intervals. Data analysis was performed using SPSS version 25. Results: The study enrolled 30 patients in the PCN group and 30 in the DJS group. Efficacy rates for PCN and DJS were 93.3% (28 out of 30) and 76.7% (23 out of 30), respectively. Stratified analysis revealed no statistically significant differences in efficacy based on age, gender, or duration of illness, although a trend favoring PCN was observed in patients over 40 years and those treated within 5-10 days of illness onset. Conclusion: While both PCN and DJS are effective interventions for obstructive uropathy secondary to urolithiasis, PCN showed a non-significantly higher overall efficacy. These findings suggest a potential preference for PCN in certain patient subsets, though further research with larger sample sizes and multi-center trials is needed to substantiate these observations.

Risk Factors Analysis of AKI in Patients with Primary Non-small Cell Lung Cancer Treated with PD-1/PD-L1 Inhibitor.

To investigate the risk factors of Programmed Cell Death Protein 1 (PD-1), Programmed Cell Death Ligand 1(PD-L1) inhibitor associated acute kidney injury (AKI) in patients with primary non-small cell lung cancer (NSCLC) and construct a predictive model. 120 NSCLC patients were selected as the research subjects and their clinical data were collected. Patients were divided into AKI and Non-AKI (N-AKI) group based on the development of AKI. Exploring the risk factors of PD-1P/D-L1 inhibitor related AKI in NSCLC patients using multivariate logistic regression analysis and visualized the logistic regression analysis to obtain a nomogram model. Meanwhile, evaluate the predictive value of the model. The results of multivariate analysis showed that the presence of extrarenal immune related adverse reactions (irAEs) is a risk factor for PD-1/PD-L1 inhibitor related AKI in NSCLC patients; At the same time, the risk of developing PD-1/PD-L1 inhibitor related AKI in NSCLC patients increases with increasing serum creatinine (SCr) and C-reactive protein (CRP) levels, decreasing baseline estimated glomerular filtration rate (eGFR) levels (P < .05). The analysis results of receiver operator characteristic curve (ROC), calibration curve, and decision curve show that the model has good discrimination and accuracy, and can achieve a high clinical benefit rate. Primary NSCLC patients with extrarenal irAEs, high levels of SCr and CRP, and low levels of eGFR have a higher risk of AKI after PD-1/PD-L1 inhibitor treatment. Establishing a predictive model with high accuracy is more conducive to early detection of high-risk patients. DOI: 10.52547/ijkd.7964.

Risk Factors Analysis of AKI in Patients with Primary Non-small Cell Lung Cancer Treated with PD-1/PD-L1 Inhibitor.

To investigate the risk factors of Programmed Cell Death Protein 1 (PD-1), Programmed Cell Death Ligand 1(PD-L1) inhibitor associated acute kidney injury (AKI) in patients with primary non-small cell lung cancer (NSCLC) and construct a predictive model. 120 NSCLC patients were selected as the research subjects and their clinical data were collected. Patients were divided into AKI and Non-AKI (N-AKI) group based on the development of AKI. Exploring the risk factors of PD-1P/D-L1 inhibitor related AKI in NSCLC patients using multivariate logistic regression analysis and visualized the logistic regression analysis to obtain a nomogram model. Meanwhile, evaluate the predictive value of the model. The results of multivariate analysis showed that the presence of extrarenal immune related adverse reactions (irAEs) is a risk factor for PD-1/PD-L1 inhibitor related AKI in NSCLC patients; At the same time, the risk of developing PD-1/PD-L1 inhibitor related AKI in NSCLC patients increases with increasing serum creatinine (SCr) and C-reactive protein (CRP) levels, decreasing baseline estimated glomerular filtration rate (eGFR) levels (P < .05). The analysis results of receiver operator characteristic curve (ROC), calibration curve, and decision curve show that the model has good discrimination and accuracy, and can achieve a high clinical benefit rate. Primary NSCLC patients with extrarenal irAEs, high levels of SCr and CRP, and low levels of eGFR have a higher risk of AKI after PD-1/PD-L1 inhibitor treatment. Establishing a predictive model with high accuracy is more conducive to early detection of high-risk patients. DOI: 10.52547/ijkd.7964.

Ceftazidime-avibactam induced renal disorders: past and present.

With the increasing prevalence of multidrug-resistant Gram-negative bacterial pathogens worldwide, antimicrobial resistance has become a significant public health concern. Ceftazidime-avibactam (CAZ-AVI) exhibited excellent in vitro activity against many carbapenemase-producing pathogens, and was widely used for the treatment of various complicated infections. CAZ-AVI is well tolerated across all dosing regimens, and its associated acute kidney injury (AKI) in phase II/III clinical trials is rare. However, recent real-world studies have demonstrated that CAZ-AVI associated AKI was more frequent in real-world than in phase II and III clinical trials, particularly in patients receiving concomitant nephrotoxic agents, with critically ill patients being at a higher risk. Herein, we reviewed the safety data related to renal impairment of CAZ-AVI, and discussed its pharmacokinetic/pharmacodynamic targets and dosage adjustment in patients with impaired renal function. This review aimed to emphasize the importance for healthcare professionals to be aware of this adverse event of CAZ-AVI and provide practical insights into the dosage optimization in critically ill patients with renal dysfunction.

Risk Factors for Teicoplanin-Associated Acute Kidney Injury in Patients with Hematological Malignancies: Focusing on Concomitant Use of Tazobactam/Piperacillin.

Patients with hematological malignancies (HM) often receive tazobactam/piperacillin (TAZ/PIPC) and glycopeptide antibiotics for febrile neutropenia. The effect of concomitant use of TAZ/PIPC on risk of teicoplanin (TEIC)-associated acute kidney injury (AKI) remains unclear. We investigated the impact of concomitant TAZ/PIPC use on TEIC-associated AKI in HM patients and identified the risk factors. In this retrospective, single-center, observational cohort study, 203 patients received TEIC, 176 of whom satisfied the selection criteria and were divided into TEIC cohort (no TAZ/PIPC; n = 118) and TEIC + TAZ/PIPC cohort (n = 58). AKI was defined as serum creatinine increase ≥0.3 mg/dL within 48 h or ≥50% from baseline. Incidence of AKI in TEIC cohort before and after propensity score matching was 9.3 and 5.9%, respectively, and that in TEIC + TAZ/PIPC cohort was 10.3 and 11.8%. AKI incidence and risk were not significantly different between two cohorts before (p = 0.829; odds ratio (OR) 1.122, 95% confidence interval (CI) 0.393-3.202) and after matching (p = 0.244; OR 2.133, 95% CI 0.503-9.043). Logistic regression analysis with factors clinically or mechanistically potentially related to TEIC-associated AKI, including concomitant TAZ/PIPC use, as independent variables identified baseline hemoglobin level as the only significant risk factor for TEIC-associated AKI (p = 0.011; OR 0.484, 95% CI 0.276-0.848). In HM patients treated with TEIC, concomitant TAZ/PIPC use did not increase AKI risk whereas lower hemoglobin levels had higher risk for TEIC-associated AKI development, suggesting the necessity to monitor serum creatinine when using TEIC in patients with anemia.

Vancomycin associated acute kidney injury in patients with infectious endocarditis: a large retrospective cohort study.

Background: Vancomycin remains the cornerstone antibiotic for the treatment of infective endocarditis (IE). Vancomycin has been associated with significant nephrotoxicity. However, vancomycin associated acute kidney injury (AKI) has not been evaluated in patients with IE. We conducted this large retrospective cohort study to reveal the incidence, risk factors, and prognosis of vancomycin-associated acute kidney injury (VA-AKI) in patients with IE. Methods: Adult patients diagnosed with IE and receiving vancomycin were included. The primary outcome was VA-AKI. Results: In total, 435 of the 600 patients were enrolled. Of these, 73.6% were male, and the median age was 52 years. The incidence of VA-AKI was 17.01% (74). Only 37.2% (162) of the patients received therapeutic monitoring of vancomycin, and 30 (18.5%) patients had reached the target vancomycin trough concentration. Multiple logistic regression analysis revealed that body mass index [odds ratio (OR) 1.088, 95% CI 1.004, 1.179], duration of vancomycin therapy (OR 1.030, 95% CI 1.003, 1.058), preexisting chronic kidney disease (OR 2.291, 95% CI 1.018, 5.516), admission to the intensive care unit (OR 2.291, 95% CI 1.289, 3.963) and concomitant radiocontrast agents (OR 2.085, 95% CI 1.093, 3.978) were independent risk factors for VA-AKI. Vancomycin variety (Lai Kexin vs. Wen Kexin, OR 0.498, 95% CI 0.281, 0.885) were determined to be an independent protective factor for VI-AKI. Receiver operator characteristic curve analysis revealed that duration of therapy longer than 10.75 days was associated with a significantly increased risk of VA-AKI (HR 1.927). Kidney function was fully or partially recovered in 73.0% (54) of patients with VA-AKI. Conclusion: The incidence of VA-AKI in patients with IE was slightly higher than in general adult patients. Concomitant contrast agents were the most alarmingly nephrotoxic in patients with IE, adding a 2-fold risk of VA-AKI. In patients with IE, a course of vancomycin therapy longer than 10.75 days was associated with a significantly increased risk of AKI. Thus, closer monitoring of kidney function and vancomycin trough concentrations was recommended in patients with concurrent contrast or courses of vancomycin longer than 10.75 days.

Comparison of 4 Predictive Scoring Methods as Assessment Tools for Cardiac Surgery Associated-Acute Kidney Injury in Post Coronary Artery Bypass Surgery Patients: A Single-Center Retrospective Study

Comparison of 4 Predictive Scoring Methods as Assessment Tools for Cardiac Surgery Associated-Acute Kidney Injury in Post Coronary Artery Bypass Surgery Patients: A Single-Center Retrospective Study