Introduction: Since the breakout of COVID-19 in December 2019, the virus has already affected and taken millions of lives over the past year. There is still much to learn about this disease. It has been postulated that the human kidney is a potential pathway for COVID-19 due to the presence of the ACE2 receptors found in the surfaces of kidney cells. Some studies that demonstrated acute tubular necrosis and lymphocyte infiltration among post mortem COVID-19 patients, concluding that the virus could directly damage the kidney, increasing the risk of the development of Acute Kidney Injury (AKI) among patients with COVID-19. This study investigated the incidence and severity of AKI among hospitalized COVID-19 patients and the association of the degree of AKI with regards to the severity and outcomes of COVID-19 patients. Methods: This was a single-center cross-sectional study retrospective chart review of COVID-19 patients who developed AKI. Descriptive statistics were used to summarize the general and clinical characteristics of the patients. Frequency and proportion were used for categorical variables. Shapiro-Wilk test was used to determine the normality distribution of continuous variables. Continuous quantitative data that met the normality assumption was described using mean and standard deviation, while those that did not were described using median and range. Continuous variables which are normally distributed were compared using the One-way ANOVA, while those variables that are not normally distributed were compared using the Kruskal-Wallis H test. For categorical variables, the Chi-square test was used to compare the outcomes. If the expected percentages in the cells are less than 5%, Fisher's Exact Test was used instead. Results: A total of 1441 COVID-19 in-patients from March 1, 2020 to March 1, 2021 were reviewed, 59 of whom were excluded. Among the adults with COVID-19 who developed AKI, 60% were in stage I, 10% in stage II, and 30% in stage III. The incidence of AKI among COVID-19 in-patients at Makati Medical Center was 13.10% (95% CI 11.36% - 14.99%). Among the 181 patients, 79 (43.65%, 95% CI 36.30 - 51.20) had died. The mortality rate is 22.02% for Stage I, 50% for Stage II, and 85.19% for Stage III. The median length of hospital stay was 12 days, ranging from 1 day up to 181 days. Full renal recovery on discharge was observed only in one-third of the patients. It was observed in 44.95% of those in Stage I, 27.78% of those in Stage II, and 5.56% of those in Stage III. Conclusion The study demonstrated that the incidence of AKI in hospitalized COVID-19 patients was 13.1% (95% CI 11.36% - 14.99%), which was lower than previously reported. This could be attributed to the longer study period wherein, to date, we have a better understanding of the disease and had already established a standard of care for treatment for the disease attributing to the decreased incidence of AKI among COVID-19 patients than what was initially reported. The development of AKI has a direct correlation with the degree of infection. Among patients who developed AKI, 20% required renal replacement therapy. Overall development of AKI increases the risk of mortality among hospitalized COVID-19 patients. The stage of AKI has a direct correlation with regards to mortality and has an indirect relationship with regards to renal recovery.
Acute Kidney Injury ; COVID-19 ; Renal Replacement Therapy ; Mortality

Objective: The objective of the study is to determine the association of renal impairment (AKI or CKD) with IL-6 levels on mortality, intubation, and length of hospitalization among COVID-19 positive patients. Methods: This is a retrospective cohort study involving chart review of COVID-19 patients with IL-6 levels and admitted from May 2020 to April 2021. The KDIGO criteria was used for determining renal impairment. The subsequent data processing and analysis was carried out using the statistical software, Stata 13. Results: A total of 1,120 charts were included with patients classified as having AKI (33%), CKD (14%), and no renal impairment (58%). Overall mortality and need for intubation were 27% and 30%, respectively, with average length of stay at 12 days. The IL-6 values were divided into low (0 to less than 51 pg/mL), intermediate (51 to 251 pg/mL), and high (greater than 251 pg/mL) tertiles, which showed acceptable sensitivity and specificity for mortality and need for intubation. Conclusion The presence of renal impairment (CKD or AKI) with increasing IL-6 levels had an effect of increasing risk of adverse outcomes; however, within tertile groups, the presence of renal impairment did not significantly change the risk of adverse outcomes. The tertile groups have acceptable sensitivity and specificity for clinical use.
Interleukin-6 ; Acute Kidney Injury ; Renal Insufficiency, Chronic

BACKGROUND

Pregnancy-related acute kidney injury (PR-AKI) is an underdiagnosed yet serious public health obstetric complication with high risk of maternal and fetal morbidity and mortality. Several studies have varied reports as to its incidence since there is no validated diagnostic criteria. As of date, there is a lack in published studies on the prevalence and clinical profiles of PR-AKI in the Philippines.

To determine the prevalence of PR-AKI and investigate their clinical profiles and outcomes in a tertiary hospital.

This single-center, cross-sectional, retrospective study included all admitted patients with PR-AKI from January 2019 to December 2021. Prevalence was determined and clinical data and outcomes were obtained and analyzed through review of electronic records.

A total of 49 out of 1374 patients had PR-AKI with a prevalence of 3.57% while prevalence of AKI with underlying CKD was 0.22%. The mean age was at 30 ± 6 years and most were primigravid (51.02%). Most of the patients affected had no pre-existing comorbidities (57.14%) and no known maternal comorbidities (59.18%) prior to the admission. The top causes of PR-AKI were pre-eclampsia/eclampsia (53.06%), blood loss (24.48%) and sepsis/septic shock (22.45%) mostly occurring during the third trimester (69.39%). The mean highest creatinine level was at 1.99 ± 2.01 mg/dL. Only 18.37% had oliguria while hemodialysis was done in only 6.12%. ICU admission rates were at 26.53%. Intrauterine fetal demise was seen in 12.24% of cases. PR-AKI had a 6.12% mortality rate. However, most were discharged with normal creatinine (89.8%).

R-AKI is a serious complication with significant burden even in previously healthy individuals. Prompt diagnosis is essential for a more favorable maternal and fetal outcome as well as improvement of kidney function to baseline.

BACKGROUND AND OBJECTIVES

Acute kidney injury (AKI) is a common complication of critical illness that often leads to increased mortality and morbidity. Biomarkers detect AKI earlier, providing a window of opportunity for timely intervention. Of the recent biomarkers in literature, the cell cycle arrest biomarkers tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor binding protein-7 (IGFBP-7) were found to be superior in predicting AKI. Our study aimed to evaluate the diagnostic performance of urine TIMP-2/IGFBP-7 in its ability to predict AKI and major adverse kidney events within 30 days (MAKE30) among high-risk patients for AKI. MAKE30 is a composite outcome comprised of all-cause mortality, use of renal replacement therapy (RRT), or persistent renal dysfunction at hospital discharge truncated at 30 days.

We conducted a prospective, cross-sectional study which included 135 adult, non-COVID ICU patients. Baseline urine TIMP-2/IGFBP-7 results were used to dichotomize the population into low risk (< 0.3 ng/mL) or high risk (≥ 0.3 ng/mL) for AKI. Participants were then observed for 30 days and monitored for MAKE30 outcomes. ROC curves were created to calculate the sensitivity, specificity, NPV, PPV, and the AUC of the 0.3 ng/mL cut-off to predict the AKI and MAKE30.

Urine TIMP-2/IGFBP-7 cutoff of 0.3 ng/mL predicted AKI with a sensitivity of 82.4%, specificity of 79.2%, PPV of 57.1%, NPV of 93% and AUC of 0.81. MAKE30 was detected with a sensitivity of 62.8%, specificity of 76.1%, PPV of 55.1%, NPV of 81.4% and AUC of 0.69. Elevated levels of urine TIMP-2/IGFBP-7 were found to be associated with AKI (p <0.01), MAKE30 (p <0.01) and all of its subcomponents. Survival or discharge after 30 days were found to be associated with lower urine TIMP-2/IGFBP-7 levels (p <0.01).

Urine TIMP-2/IGFBP-7, at its current cutoff at 0.3 ng/mL, can predict the likelihood of developing AKI and major adverse kidney events among high-risk patients for AKI. It can serve as a useful adjunct to existing methods, such as serum creatinine, in the early diagnosis and prognosis of acute kidney injury and expanding the therapeutic window to prevent disease progression and improve outcomes.

The present study was aimed to investigate whether Gasdermin D (GSDMD)-mediated pyroptosis participated in lipopolysaccharide (LPS)-induced sepsis-associated acute kidney injury (AKI), and to explore the role of caspase-1 and caspase-11 pyroptosis pathways in this process. The mice were divided into four groups: wild type (WT), WT-LPS, GSDMD knockout (KO) and KO-LPS. The sepsis-associated AKI was induced by intraperitoneal injection of LPS (40 mg/kg). Blood samples were taken to determine the concentration of creatinine and urea nitrogen. The pathological changes of renal tissue were observed via HE staining. Western blot was used to investigate the expression of pyroptosis-associated proteins. The results showed that the concentrations of serum creatinine and urea nitrogen in the WT-LPS group were significantly increased, compared with those in the WT group (P < 0.01); whereas serum creatinine and urea nitrogen in the KO-LPS group were significantly decreased, compared with those in the WT-LPS group (P < 0.01). HE staining results showed that LPS-induced renal tubular dilatation was mitigated in GSDMD KO mice. Western blot results showed that LPS up-regulated the protein expression levels of interleukin-1β (IL-1β), GSDMD and GSDMD-N in WT mice. GSDMD KO significantly down-regulated the protein levels of IL-1β, caspase-11, pro-caspase-1, caspase-1(p22) induced by LPS. These results suggest that GSDMD-mediated pyroptosis is involved in LPS-induced sepsis-associated AKI. Caspase-1 and caspase-11 may be involved in GSDMD cleavage.
Animals ; Mice ; Acute Kidney Injury ; Caspase 1 ; Caspases/metabolism* ; Creatinine ; Lipopolysaccharides ; Mice, Knockout ; Nitrogen ; Sepsis ; Urea ; Gasdermins/metabolism*

Acute kidney injury (AKI) is a common critical disease clinically with high morbility and mortality and some survival patients also progress to chronic kidney disease. Renal ischemia-reperfusion (IR) is one of the main causes of AKI, in which, its repair and potential fibrosis, apoptosis, inflammation and phagocytosis play important roles. During the progression of IR-induced AKI, the expression of erythropoietin homodimer receptor (EPOR)₂ and EPOR and β common receptor formed heterodimer receptor (EPOR/βcR) is changed dynamically. Moreover, (EPOR)₂ and EPOR/βcR may synergistically participate in renoprotection at the stage of AKI and early repair, whereas at the late stage of AKI, the (EPOR)₂ induces renal fibrosis and the EPOR/βcR facilitates repair and remodelling. The underlying mechanism, signaling pathways and the different effect turning point of (EPOR)₂ and EPOR/βcR have not been well defined. It has been reported that EPO, according to its 3D structure, derived helix B surface peptide (HBSP) and cyclic HBSP (CHBP) only bind to EPOR/βcR. Synthesized HBSP, therefore, provides an effective tool to distinguish the different roles and mechanisms of both receptors, with the (EPOR)₂ promoting fibrosis or the EPOR/βcR leading to repair/remodelling at the late stage of AKI. This review discusses the similarities and differences of (EPOR)₂ and EPOR/βcR in their impacts on apoptosis, inflammation and phagocytosis in AKI, repair and fibrosis post IR, associated mechanisms, signaling pathways and outcomes.
Humans ; Receptors, Erythropoietin ; Acute Kidney Injury ; Apoptosis ; Inflammation ; Phagocytosis ; Reperfusion Injury

This paper reported a case of poisoning caused by ingestion of Amanita neoovoidea. The patient experienced nausea, vomiting, oliguria, acute renal function injury, and was discharged after symptomatic support treatment and blood purification treatment. Given the different toxicity of different mushrooms, species identification of poisonous mushrooms can help clinicians in diagnosis and treatment.
Humans ; Amanita ; Acute Kidney Injury

OBJECTIVES: Abdominal aortic aneurysm is a pathological condition in which the abdominal aorta is dilated beyond 3.0 cm. The surgical options include open surgical repair (OSR) and endovascular aneurysm repair (EVAR). Prediction of acute kidney injury (AKI) after OSR is helpful for decision-making during the postoperative phase. To find a more efficient method for making a prediction, this study aims to perform tests on the efficacy of different machine learning models. METHODS: Perioperative data of 80 OSR patients were retrospectively collected from January 2009 to December 2021 at Xiangya Hospital, Central South University. The vascular surgeon performed the surgical operation. Four commonly used machine learning classification models (logistic regression, linear kernel support vector machine, Gaussian kernel support vector machine, and random forest) were chosen to predict AKI. The efficacy of the models was validated by five-fold cross-validation. RESULTS: AKI was identified in 33 patients. Five-fold cross-validation showed that among the 4 classification models, random forest was the most precise model for predicting AKI, with an area under the curve of 0.90±0.12. CONCLUSIONS Machine learning models can precisely predict AKI during early stages after surgery, which allows vascular surgeons to address complications earlier and may help improve the clinical outcomes of OSR.
Humans ; Aortic Aneurysm, Abdominal/complications* ; Endovascular Procedures/methods* ; Retrospective Studies ; Blood Vessel Prosthesis Implantation/adverse effects* ; Acute Kidney Injury/etiology* ; Machine Learning ; Treatment Outcome ; Postoperative Complications/etiology* ; Risk Factors

Sepsis-induced uncontrolled systemic inflammatory response syndrome (SIRS) is a critical cause of multiple organ failure. Acute kidney injury (AKI) is one of the most serious complications associated with an extremely high mortality rate in SIRS, and it lacked simple, safe, and effective treatment strategies. Leontopodium leontopodioides (Willd.) Beauv (LLB) is commonly used in traditional Chinese medicine for the treatment of acute and chronic nephritis. However, it remains unclear whether lipopolysaccharide (LPS) affects LPS-induced AKI. To identify the molecular mechanisms of LLB in LPS-induced HK-2 cells and mice, LLB was prepared by extraction with 70% methanol, while a lipopolysaccharide (LPS)-induced HK-2 cell model and an AKI model were established in this study. Renal histopathology staining was performed to observe the morphology changes. The cell supernatant and kidney tissues were collected for determining the levels of inflammatory factors and protein expression by ELISA, immunofluorescence, and Western blot. The results indicated that LLB significantly reduced the expression of IL-6 and TNF-α in LPS-induced HK-2 cells, as well as the secretion of IL-6, TNF-α, and IL-1β in the supernatant. The same results were observed in LPS-induced AKI serum. Further studies revealed that LLB remarkably improved oxidative stress and apoptosis based on the content of MDA, SOD, and CAT in serum and TUNEL staining results. Notably, LLB significantly reduced the mortality due to LPS infection. Renal histopathology staining results supported these results. Furthermore, immunofluorescence and Western blot results confirmed that LLB significantly reduced the expression of the protein related to the NF-κB signaling pathway and NLRP3, ASC, and Caspase-1 which were significantly increased through LPS stimulation. These findings clearly demonstrated the potential use of LLB in the treatment of AKI and the crucial role of the NF-κB/NLRP3 pathway in the process through which LLB attenuates AKI induced by LPS.
Animals ; Mice ; NF-kappa B/metabolism* ; Lipopolysaccharides/adverse effects* ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Interleukin-6/metabolism* ; Acute Kidney Injury/metabolism* ; Kidney ; Systemic Inflammatory Response Syndrome/pathology*

Humans ; Aged ; Acute Kidney Injury ; Risk Factors ; Creatinine