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Severe preeclampsia is a disorder of pregnancy, characterized by increased blood pressure (>140/90 mmHg) and proteinuria (≥ 300 mg/24 hours) at later than 20 weeks of gestation. Particularly in underdeveloped nations, severe preeclampsia and eclampsia have a significant negative impact on the health of expectant mothers, fetuses, and newborns. The HELLP (hemolysis, increased liver enzymes, low platelets) syndrome is thought to be a subset of preeclampsia, a group of hypertensive disorders of pregnancy that also includes eclampsia. Compared to preeclampsia alone, maternal and fetal problems are more severe in HELLP. There can be a diagnostic dilemma that arises when attempting to differentiate HELLP from its numerous imitators to determine the appropriate course of treatment. Here, we present a rare case of a pregnant woman presenting with preeclampsia complicated by manifestations and investigations suggestive of HELLP syndrome with acute kidney injury (AKI), retinal detachment, and symptoms of DIC (disseminated intravascular coagulation), which can be grievous to the mother as well as the fetus.

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Acute kidney injury (AKI) has a high rate of morbidity, death, and medical expenses, making it a worldwide public health problem. There are still few viable treatment plans for AKI despite medical advancements. A subclass of non-coding RNAs with over 200 nucleotides in length, long non-coding RNAs (lncRNAs) have a wide range of biological roles. Lately, lncRNAs have become important mediators of AKI and prospective biomarkers. However, current studies show that, via constructing the lncRNA/microRNA/target gene regulatory axis, abnormal expression of lncRNAs has been connected to significant pathogenic processes associated with AKI, such as the inflammatory response, cell proliferation, and apoptosis. In order to compete with mRNAs for binding to the same miRNAs and affect the expression of transcripts targeted by miRNAs, lncRNAs may function as competing endogenous RNAs (ceRNAs). The most widely used approach for researching the biological roles of lncRNAs is the construction of ceRNA regulation networks. Our goal in this article is to deliver an updated review of lncRNAs in AKI and to provide more knowledge on their possible applications as therapeutic targets and AKI biomarkers.

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Introduction This study aimed to assess plasma cystatin C (CysC) as a marker of acute kidney injury (AKI) in patients undergoing extracorporeal shock wave lithotripsy (ESWL). We compared serum levels of CysC, C-reactive protein (CRP), and creatinine before and after ESWL. The study results may have implications for early detection of AKI and prevention of progression to chronic kidney disease. Methodology This prospective observational study included 105 adult participants and was conducted from August 2022 to July 2024. ESWL was the only modality of treatment. Results Forty-eight (46%) patients developed AKI after ESWL. Patients with AKI had significantly higher post-ESWL mean plasma CysC levels than patients without AKI (121 ± 0.25 vs. 0.94 ± 0.22 mg/dL, respectively; P = 0.001). The mean serum CRP levels after ESWL were significantly higher in patients who developed AKI compared with those who did not (4.36 ± 1.63 vs. 2.64 ± 0.95 mg/dL, respectively; P = 0.001). Conclusions In patients with renal stone disease, serum creatinine, serum CRP, and plasma CysC can be used as markers of acute renal injury after ESWL.

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Introduction: Blood transfusions are essential for managing blood loss in surgical patients but can lead to life-threatening reactions. This report presents a severe transfusion reaction in a postoperative total knee arthroplasty (TKA) patient, emphasizing the need for vigilant monitoring and timely intervention. Case Report: A 70-year-old male with a history of bilateral knee pain underwent right-sided TKA. Preoperative evaluations were normal. Post-surgery, significant blood loss led to a one-pint packed red blood cell transfusion. The patient developed fever, chills, palpitations, and rapid breathing, indicating a transfusion reaction. Despite immediate treatment, the patient's condition deteriorated, requiring ICU admission. Complications included acute kidney injury (AKI), metabolic acidosis, thrombocytopenia, pleural effusion, and aspiration pneumonitis. Multiple organ dysfunction syndrome (MODS) developed, necessitating hemodialysis. Despite comprehensive care, the patient passed away. Conclusion: This case highlights the critical need for rigorous pre-transfusion screening, vigilant monitoring, and immediate intervention in managing severe transfusion reactions in postoperative TKA patients. Comprehensive patient care strategies are essential to mitigate the multifocal complications associated with transfusion reactions. Additional research is needed to understand and prevent such life-threatening reactions.

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BACKGROUND: The role of the geriatric nutritional risk index (GNRI) as a prognostic factor in intensive care unit (ICU) patients with acute kidney injury (AKI) remains uncertain. OBJECTIVES: The aim of this study was to investigate the impact of the GNRI on mortality outcomes in critically ill patients with AKI. METHODS: For this retrospective study, we included 12,058 patients who were diagnosed with AKI based on ICD-9 codes from the eICU Collaborative Research Database. Based on the values of GNRI, nutrition-related risks were categorized into four groups: major risk (GNRI < 82), moderate risk (82 ≤ GNRI < 92), low risk (92 ≤ GNRI < 98), and no risk (GNRI ≥ 98). Multivariate analysis was used to evaluate the relationship between GNRI and outcomes. RESULTS: Patients with higher nutrition-related risk tended to be older, female, had lower blood pressure, lower body mass index, and more comorbidities. Multivariate analysis showed GNRI scores were associated with in-hospital mortality. (Major risk vs. No risk: OR, 95% CI: 1.90, 1.54-2.33, P < 0.001, P for trend < 0.001). Moreover, increased nutrition-related risk was negatively associated with the length of hospital stay (Coefficient: -0.033; P < 0.001) and the length of ICU stay (Coefficient: -0.108; P < 0.001). The association between GNRI scores and the risks of in-hospital mortality was consistent in all subgroups. CONCLUSIONS: GNRI serves as a significant nutrition assessment tool that is pivotal to predicting the prognosis of critically ill patients with AKI.

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Epidermal growth factor receptor (EGFR), which is referred to as ErbB1/HER1, is the prototype of the EGFR family of receptor tyrosine kinases which also comprises ErbB2 (Neu, HER2), ErbB3 (HER3), and ErbB4 (HER4). EGFR, along with other ErbBs, is expressed in the kidney tubules and is physiologically involved in nephrogenesis and tissue repair, mainly following acute kidney injury. However, its sustained activation is linked to several kidney pathologies, including diabetic nephropathy, hypertensive nephropathy, glomerulonephritis, chronic kidney disease, and renal fibrosis. This review aims to provide a summary of the recent findings regarding the consequences of EGFR activation in several key renal pathologies. We also discuss the potential interplay between EGFR and the reno-protective angiotensin-(1-7) (Ang-(1-7), a heptapeptide member of the renin-angiotensin-aldosterone system that counter-regulates the actions of angiotensin II. Ang-(1-7)-mediated inhibition of EGFR transactivation might represent a potential mechanism of action for its renoprotection. Our review suggests that there is a significant body of evidence supporting the potential inhibition of EGFR/ErbB, and/or administration of Ang-(1-7), as potential novel therapeutic strategies in the treatment of renal pathologies. Thus, EGFR inhibitors such as Gefitinib and Erlinotib that have an acceptable safety profile and have been clinically used in cancer chemotherapy since their FDA approval in the early 2000s, might be considered for repurposing in the treatment of renal pathologies.

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The aberrant expression of SET8, a histone methyltransferase that mediates H4 lysine 20 mono-methylation (H4K20me1), is implicated in the pathogenesis of various tumors, however, its role in acute kidney injury (AKI) is unknown. Here we showed that SET8 and H4K20me1 were upregulated in the murine kidney with AKI induced by cisplatin, along with increased renal tubular cell injury and apoptosis and decreased expression of E-cadherin and Phosphatase and Tensin Homolog (PTEN). Suppression of SET8 by UNC0379 improved renal function, attenuated tubule damage, and restored expression of PTEN, but not E-cadherin. UNC0379 was also effective in lessening cisplatin-induced DNA damage response (DDR) as indicated by reduced expression of γ-H2AX, p53, p21, and alleviating cisplatin-impaired autophagy as shown by retained expression of Atg5, Beclin-1, and CHMP2A and enhanced levels of LC3-II in the kidney. Consistently, inhibition of SET8 with either UNC0379 or siRNA mitigated apoptosis and DDR, and restored autophagy, along with PTEN preservation in cultured renal proximal tubular epithelial cell (TKPTs) exposed to cisplatin. Further studies showed that inhibition of PTEN with Bpv or siRNA potentiated cisplatin-induced apoptosis, DDR, and hindered autophagy, and conversely, alleviated by overexpression of PTEN in TKPTs. Finally, blocking PTEN largely abolished the inhibitory effect of UNC0379 on apoptosis. Taken together, these results suggest that SET8 inhibition protects against cisplatin-induced AKI and renal cell apoptosis through a mechanism associated with the preservation of PTEN, which in turn inhibits DDR and restores autophagy.

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Background: The cardiac surgery-associated acute kidney injury (CSA-AKI) occurs in up to 1 out of 3 patients. Off-pump coronary artery bypass grafting (OPCABG) is one of the major cardiac surgeries leading to CSA-AKI. Early identification and timely intervention are of clinical significance for CSA-AKI. In this study, we aimed to establish a prediction model of off-pump coronary artery bypass grafting-associated acute kidney injury (OPCABG-AKI) after surgery based on machine learning methods. Methods: The preoperative and intraoperative data of 1,041 patients who underwent OPCABG in Chest Hospital, Tianjin University from June 1, 2021 to April 30, 2023 were retrospectively collected. The definition of OPCABG-AKI was based on the 2012 Kidney Disease Improving Global Outcomes (KDIGO) criteria. The baseline data and intraoperative time series data were included in the dataset, which were preprocessed separately. A total of eight machine learning models were constructed based on the baseline data: logistic regression (LR), gradient-boosting decision tree (GBDT), eXtreme gradient boosting (XGBoost), adaptive boosting (AdaBoost), random forest (RF), support vector machine (SVM), k-nearest neighbor (KNN), and decision tree (DT). The intraoperative time series data were extracted using a long short-term memory (LSTM) deep learning model. The baseline data and intraoperative features were then integrated through transfer learning and fused into each of the eight machine learning models for training. Based on the calculation of accuracy and area under the curve (AUC) of the prediction model, the best model was selected to establish the final OPCABG-AKI risk prediction model. The importance of features was calculated and ranked by DT model, to identify the main risk factors. Results: Among 701 patients included in the study, 73 patients (10.4%) developed OPCABG-AKI. The GBDT model was shown to have the best predictions, both based on baseline data only (AUC =0.739, accuracy: 0.943) as well as based on baseline and intraoperative datasets (AUC =0.861, accuracy: 0.936). The ranking of importance of features of the GBDT model showed that use of insulin aspart was the most important predictor of OPCABG-AKI, followed by use of acarbose, spironolactone, alfentanil, dezocine, levosimendan, clindamycin, history of myocardial infarction, and gender. Conclusions: A GBDT-based model showed excellent performance for the prediction of OPCABG-AKI. The fusion of preoperative and intraoperative data can improve the accuracy of predicting OPCABG-AKI.

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Acute kidney injury (AKI) is a debilitating, multi-etiological disease that is commonly seen in clinical practice and in the emergency department. In this review, we introduce the definition, symptoms, and causes of poisoning-related AKI; we also discuss its mechanisms, risk factors, and epidemiology, as well as elaborate on the relevant laboratory tests. Subsequently, we discuss the treatment strategies for toxin- and substance-related AKI caused by Glafenin, antimicrobial agents, lithium, contrast media, snake venom, herbicides, ethylene glycol, synthetic cannabinoids, cocaine, heroin, and amphetamines. Finally, for a comprehensive overview of poisoning-related AKI, we review the management, prevention, and outcomes of this condition.

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We recently reported the case of a patient who experienced three consecutive episodes of acute kidney injury, all of them following a "Brazilian" hair-straightening treatment. The cream used for the straightening procedure contained glyoxylic acid. To examine possible underlying mechanisms causing kidney injury, four groups of mice were exposed to topical application of (i) the straightening product, (ii) a cream containing 10% glyoxylic acid, (iii) a cream containing 10% glycolic acid or (iv) a control cream. Application of glycolic acid slightly increased urine oxalate excretion, while glyoxylic acid and the straightening product dramatically increased urine oxalate excretion and caused calcium oxalate nephropathy after transcutaneous absorption. Thus, glyoxylic acid was presumptively absorbed through the skin, metabolized to oxalate and promoted crystallization of calcium oxalate in urine. Hence, cosmetic products containing glyoxylic acid may induce acute kidney injury and should be discontinued. Further studies are needed to investigate the metabolism of glycolic acid and glyoxylic acid following topical application.

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Introduction: Mesoamerican nephropathy (MeN) is a chronic kidney disease (CKD) which may be caused by recurrent acute kidney injury (AKI). We investigated urinary quinolinate-to-tryptophan ratio (Q/T), a validated marker of nicotinamide adenine dinucleotide (NAD+) biosynthesis that is elevated during ischemic and inflammatory AKI, in a sugarcane worker population in Nicaragua with high rates of MeN. Methods: Among 693 male sugarcane workers studied, we identified 45 who developed AKI during the harvest season. We matched them 1:1 based on age and job category with 2 comparison groups: (i) "no kidney injury," active sugarcane workers with serum creatinine (sCr) <1.1 mg/dl; and (ii) "CKD," individuals no longer working in sugarcane due to their CKD, who had additional 1:1 matching for sCr. We measured urine metabolites using liquid chromatography coupled tandem mass spectrometry (LC-MS/MS) and compared Q/T and other metabolic features between the AKI and comparison groups. Results: Urine Q/T was significantly higher in workers with AKI than in those with no kidney injury (median interquartile Range [IQR]: 0.104 [0.074-0.167] vs. 0.060 [0.045-0.091], P < 0.0001) and marginally higher than in workers with CKD (0.086 [0.063-0.142], P = 0.059). Urine levels of the NAD+ precursor nicotinamide were lower in the AKI group than in comparison groups. Conclusion: Workers at risk for MeN who develop AKI demonstrate features of impaired NAD+ biosynthesis, thereby providing new insights into the metabolic mechanisms of injury in this population. Therapeutic use of oral nicotinamide, which may ameliorate NAD+ biosynthetic derangement and fortify against kidney injury, should be investigated to prevent AKI in this setting.

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Background: The incidence of postoperative acute kidney injury (AKI) is high due to insufficient perfusion in patients with heart failure. Heart failure patients with preserved ejection fraction (HFpEF) have strong heterogeneity, which can obtain more accurate results. There are few studies for predicting AKI after coronary artery bypass grafting (CABG) in HFpEF patients especially using machine learning methodology. Methods: Patients were recruited in this study from 2018 to 2022. AKI was defined according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria. The machine learning methods adopted included logistic regression, random forest (RF), extreme gradient boosting (XGBoost), gaussian naive bayes (GNB), and light gradient boosting machine (LGBM). We used the receiver operating characteristic curve (ROC) to evaluate the performance of these models. The integrated discrimination improvement (IDI) and net reclassification improvement (NRI) were utilized to compare the prediction model. Results: In our study, 417 (23.6%) patients developed AKI. Among the five models, random forest was the best predictor of AKI. The area under curve (AUC) value was 0.834 (95% confidence interval (CI) 0.80-0.86). The IDI and NRI was also better than the other models. Ejection fraction (EF), estimated glomerular filtration rate (eGFR), age, albumin (Alb), uric acid (UA), lactate dehydrogenase (LDH) were also significant risk factors in the random forest model. Conclusions: EF, eGFR, age, Alb, UA, LDH are independent risk factors for AKI in HFpEF patients after CABG using the random forest model. EF, eGFR, and Alb positively correlated with age; UA and LDH had a negative correlation. The application of machine learning can better predict the occurrence of AKI after CABG and may help to improve the prognosis of HFpEF patients.

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BK polyomavirus (BKPyV) is a ubiquitous human polyomavirus and a major infection after kidney transplantation, primarily due to immunosuppression. BKPyV reactivation can manifest as viruria in 30%-40%, viremia in 10%-20%, and BK polyomavirus-associated nephropathy (BKPyVAN) in 1%-10% of recipients. BKPyVAN is an important cause of kidney graft failure. Although the first case of BKPyV was identified in 1971, progress in its management has been limited. Specifically, there is no safe and effective antiviral agent or vaccine to treat or prevent the infection. Even in the current era, the mainstay approach to BKPyV is a reduction in immunosuppression, which is also limited by safety (risk of de novo donor specific antibody and rejection) and efficacy (graft failure). However, recently BKPyV has been getting more attention in the field, and some new treatment strategies including the utilization of viral-specific T-cell therapy are emerging. Given all these challenges, the primary focus of this article is complications associated with BKPyV, as well as strategies to mitigate negative outcomes.

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Studies evaluating Cisplatin-induced nephrotoxicity in minorities are limited. We conducted a retrospective review of adult patients receiving cisplatin from 2019 to 2023 at an inner-city hospital. Renal indices were obtained at baseline and after cycles 1, 2, and 3 of Cisplatin. A total of 93 patients were included, 46% were male. Median age was 57 years. About 40% were Black, 13% White, and 42% Hispanic. About 54% were uninsured. About 16% of the patients developed AKI after cycle 1 of cisplatin, 5% after cycle 2%, and 17% after cycle 3. There was no statistically significant correlation between race, sex, BMI and development of cisplatin-induced AKI. Repeated measures ANOVA test indicated a statistically significant and cumulative rise in creatinine level following cisplatin therapy [Wilks' Lambda = 0.003, F(1,26)=13.7, η2 = 0.44]. Our study in a minority, low socioeconomic population highlights the progressive kidney injury following each cycle of cisplatin therapy. Further studies targeting this specific population are warranted to develop tailored interventions.

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Acute kidney injury (AKI) is one of the most frequent and prognostic-relevant complications of cardiogenic shock (CS) complicating myocardial infarction (MI). Mechanical circulatory assist devices (MCS) like left ventricular Impella microaxial pump have increasingly been used in the last decade for stabilization of hemodynamics in those patients. Moreover, a protective effect of Impella on renal organ perfusion could recently be demonstrated. However, data identifying early risk predictors for developing AKI during Impella support in CS are rare. Data of hemodynamics and renal function from 50 Impella patients (January 2020 and February 2022) with MI-related CS (SCAI stage C), were retrospectively analyzed using e.g. multivariate logistic regression analysis as well as Kaplan-Meier curves and Cox regression analysis. 30 patients (60%) developed AKI. Central venous pressure as an indicator for venous congestion (OR 1.216, p = 0.02), GFR at admission indicating existing renal damage (OR 0.928, p = 0.002), and reduced central venous oxygen saturation (SvO2) as a marker for decreased tissue perfusion (OR 0.930, p = 0.029) were independently associated with developing an AKI. The 30-day mortality rate was significantly higher in patients with AKI stage 3 (Stage 1: 0%, Stage 2: 0%, Stage 3; 41.6%, p = 0.014) while AKI stage 3 (HR 0.095, p = 0.026) and norepinephrine dosage (HR 1.027, p = 0.008) were independent predictors for 30-day mortality. AKI as a complication of MI-related CS occurs frequently with a major impact on prognosis. Venous congestion, reduced tissue perfusion, and an already impaired renal function are independent predictors of AKI. Thus, timely diagnostics and a focused treatment of the identified factors could improve prognosis and outcome.

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BACKGROUND: Macrophages are the main inflammatory cells involved in kidney injury and play a significant role in the development of acute kidney injury (AKI) and progression of chronic kidney disease (CKD). Emodin is believed to stabilize macrophage homeostasis under pathological conditions. The objective of this study aimed to explore the underlying mechanisms and effects of Emodin on M1 macrophages. METHODS: Network pharmacology methods were used to predict target proteins associated with renal injury and identify the pathways affected by emodin. RAW264.7 macrophages were induced into M1 polarization using LPS and then treated with emodin at 20, 40, and 80 µM. The effects of emodin on cell viability, cytokines (IL-1ß, IL-6, TNF-α), M1 macrophage markers (F4/80 + CD86+), and the EGFR/MAPK pathway were evaluated. Additionally, we transfected RAW264.7 cells with an EGFR shRNA interference lentivirus to assess its effects on RAW264.7 cells function and MAPK pathway. After RAW264.7 cells were passaged to expanded culture and transfected with EGFR-interfering plasmid, macrophages were induced to polarize towards M1 with LPS and then treated with 80 µM emodin. CKD modeling was performed to test how emodin is regulated during CKD. RESULTS: There are 15 common targets between emodin and kidney injury, of which the EGFR/MAPK pathway is the pathway through which emodin affects macrophage function. Emodin significantly reduced the levels of IL-6, IL-1ß and TNF-α (p < 0.05) and the ratio of M1 macrophage surface markers F4/80 + CD86+ (p < 0.01) in the supernatant of RAW264.7 cells in a dose-dependent manner. Furthermore, the inhibitory effect of emodin on RAW264.7 cells was achieved by interfering with the EGFR/MAPK pathway. Moreover, emodin also affected the mRNA and protein expression of EGFR and Ras, leading to a decrease in the rate of M1 macrophages, thus inhibiting the pro-inflammatory effect of M1 macrophages. The addition of emodin reduced the rate of M1 macrophages in CKD and inhibited the further polarization of M1 macrophages, thus maintaining the pro-inflammatory and anti-inflammatory homeostasis in CKD, and these effects were achieved by emodin through the control of the EGRF/ERK pathway. CONCLUSION: Emodin attenuates M1 macrophage polarization and pro-inflammatory responses via the EGFR/MAPK signalling pathway. And the addition of emodin maintains pro- and anti-inflammatory homeostasis, which is important for maintaining organ function and tissue repair.

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Acute kidney injury (AKI) is one of the most important lethal factors for patients admitted to intensive care units (ICUs), and timely high-risk prognostic assessment and intervention are essential to improving patient prognosis. In this study, a stacking model using the MIMIC-III dataset with a two-tier feature selection approach was developed to predict the risk of in-hospital mortality in ICU patients admitted for AKI. External validation was performed using separate MIMIC-IV and eICU-CRD. The area under the curve (AUC) was calculated using the stacking model, and features were selected using the Boruta and XGBoost feature selection methods. This study compares the performance of a stacking model using two-tier feature selection with a model using single-tier feature selection (XGBoost: 85; Boruta: 83; two-tier: 0.91). The predictive effectiveness of the stacking model was further validated by using different datasets (Validation 1: 0.83; Validation 2: 0.85) and comparing it with a simpler model and traditional clinical scores (SOFA: 0.65; APACH IV: 0.61). In addition, this study combined interpretable techniques and causal inference to analyze the causal relationship between features and predicted outcomes.

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Acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise (ALPE) is a rare condition characterized by severe loin pain and patchy renal ischemia following vigorous exercise. Moreover, its diagnosis relies on clinical manifestations. Here, we present the case of a 16-year-old male with recurrent abdominal pain attributed to ALPE. He developed recurrent abdominal pain after he started playing handball, and no definite cause could be identified despite a thorough examination. His symptoms worsened when he resumed handball practice after a one-month interruption. This case underscores the varied presentations of ALPE and the importance of considering it in the differential diagnosis of recurrent abdominal pain, particularly following strenuous exercise. Moreover, caution should be exercised when resuming exercise after periods of detraining, as this may predispose individuals to ALPE. Healthcare providers should be vigilant in recognizing and managing this condition, especially in individuals with recent exercise initiation following detraining.

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The novel coronavirus disease 2019 (COVID-19) is an infectious disease caused by SARS-CoV-2 and associated with a wide spectrum of clinical manifestations ranging from asymptomatic carrier states to fulminant respiratory distress and multiple organ dysfunction. The intravascular arterial and venous thrombotic phenomena are one of the most prevalent and devastating consequences and tend to occur in patients with a severe disease state. Here we present a 45-year-old male with a medical history of essential hypertension (HTN) who presented with severe left flank pain accompanied by dry cough and fever for five days. He was found to have acute kidney injury (AKI) with concomitant renal infarction in computed tomography angiography (CTA) in the setting of a COVID-19 infection. He was eventually managed with novel oral anticoagulation (NOAC) and was discharged after a short hospital stay. Follow-up thereafter showed stable baseline renal function with no relevant symptoms.