Occurrence Of Chronic Kidney Disease Research Articles

Relationship between the longitudinal trajectory of the triglyceride-glucose index and the development of CKD: an 8-year retrospective longitudinal cohort study

BackgroundThe triglyceride-glucose (TyG) index, a simple surrogate marker of insulin resistance, is significantly associated with chronic kidney disease (CKD). However, there is limited research on the longitudinal trajectory of TyG index over time and its relationship with CKD.ObjectiveTo analyse the characteristics of the longitudinal trajectory of the TyG index over time and its association with the development of CKD in a health check-up population.MethodsParticipants who underwent at least three annual health check-ups at the Health Management Center of Sichuan Provincial People’s Hospital from 2015 to 2022 were included in this retrospective cohort study. The TyG index was calculated as ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. The latent class mixed model (LCMM) was used to identify the TyG index trajectory of the study population. A Cox proportional hazard model was used to estimate the CKD incidence risk in different quartile groups and the association of changes in the TyG index trajectory with the development of CKD.ResultsA total of 4,921 participants were included in this study, and they were divided into four groups according to the quartiles of the baseline TyG index: Q1 (5.43-6.66), Q2 (6.67-7.04), Q3 (7.05-7.43), and Q4 (7.43-9.97). There was no difference in the risk of CKD occurrence among the TyG groups. Three different TyG index trajectories were identified in this study: a high-level group, middle-level stable group and low-level stable group, respectively. The incidence rate of CKD in the high-level TyG index trajectory group was 2.399 times greater than that in the low-level stable trajectory group (HR=2.399, 95% CI 1.167-4.935).ConclusionIndividuals with long-term exposure to high TyG index levels had a significantly greater risk of CKD. Routine monitoring of the TyG index and its longitudinal trend will aid in the risk stratification of CKD in the general population and will be helpful for CKD prevention and targeted management.

Metabolome-wide Mendelian randomization reveals causal effects of betaine and N-acetylornithine on impairment of renal function.

Chronic kidney disease (CKD) is a common public health problem, which is characterized as impairment of renal function. The associations between blood metabolites and renal function remained unclear. This study aimed to assess the causal effect of various circulation metabolites on renal function based on metabolomics. We performed a two-sample Mendelian randomization (MR) analysis to estimate the causality of genetically determined metabolites on renal function. A genome-wide association study (GWAS) of 486 metabolites was used as the exposure, while summary-level data for creatinine-based estimated glomerular filtration rate (eGFR) or CKD occurrence were set the outcomes. Inverse variance weighted (IVW) was used for primary causality analysis and other methods including weight median, MR-egger, and MR-PRESSO were applied as complementary analysis. Cochran Q test, MR-Egger intercept test, MR-PRESSO global test and leave-one-out analysis were used for sensitivity analysis. For the identified metabolites, reverse MR analysis, linkage disequilibrium score (LDSC) regression and multivariable MR (MVMR) analysis were performed for further evaluation. The causality of the identified metabolites on renal function was further validated using GWAS data for cystatin-C-based eGFR. All statistical analyses were performed in R software. In this MR analysis, a total of 44 suggestive associations corresponding to 34 known metabolites were observed. After complementary analysis and sensitivity analysis, robust causative associations between two metabolites (betaine and N-acetylornithine) and renal function were identified. Reverse MR analysis showed no causal effects of renal function on betaine and N-acetylornithine. MVMR analysis revealed that genetically predicted betaine and N-acetylornithine could directly influence independently of each other. The causal effects of betaine and N-acetylornithine were also found on cystatin-C-based eGFR. Our study provided evidence to support the causal effects of betaine and N-acetylornithine on renal function. These findings required further investigations to conduct mechanism exploration and drug target selection of these identified metabolites.

The Factors Influencing Chronic Kidney Disease Incidence: Database from the Korean National Health Insurance Sharing Service (NHISS).

Background: The global prevalence of chronic kidney disease (CKD) is increasing, with diabetes accounting for the highest proportion. We analyzed the influence of clinical factors on the incidence of CKD according to the renal function, primary focusing on patients with diabetes. Methods: We used the Sample Cohorts Database provided by the National Health Insurance Sharing Service (NHISS) in Korea. Participants aged ≥ 40 years who underwent a health checkup in 2009 were categorized into six groups based on their eGFR values (<60 mL/min, 60-89 mL/min, ≥90 mL/min) and the presence of diabetes. And all patients with CKD at 2009 screening were excluded. The participants were tracked from 2010 to 31 December 2019. The CKD incidence rate according to the eGFR values and the effect of the accompanying factors on CKD incidence were confirmed. Results: 148,089 people without CKD were analyzed. The CKD incidence rate was highest in those with eGFR < 60 mL/min with diabetes and lowest in those with eGFR ≥ 90 mL/min without diabetes. The CKD incidence rates were similar between the eGFR < 60 mL/min group without diabetes and the eGFR 60-89 mL/min group with diabetes. Compared to under 44 years of age, the hazard ratio of CKD incidence was 8 times higher in over 75 years of age. Men had a 1.7-fold higher risk of developing CKD than women. Current smoker, hypertension, dyslipidemia, myocardial infarction history, and atrial fibrillation and flutter increased the risk of CKD incidence. Age, diabetes, and baseline eGFR are important factors in the occurrence of CKD. As age increases, the risk of developing CKD in men increases compared to women. Conclusions: These results will be helpful in predicting risk groups for CKD and establishing strategies to lowering CKD incidence.

Early prediction of chronic kidney disease based on ensemble of deep learning models and optimizers

Recent studies have proven that data analytics may assist in predicting events before they occur, which may impact the outcome of current situations. In the medical sector, it has been utilized for predicting the likelihood of getting a health condition such as chronic kidney disease (CKD). This paper aims at developing a CKD prediction framework, which forecasts CKD occurrence over a specific time using deep learning and deep ensemble learning approaches. While a great deal of research focuses on disease detection, few studies contribute to disease prediction before it may occur. However, the performance of previous work was not competitive. This paper tackles the under-explored area of early CKD prediction through a high-performing deep learning and ensemble framework. We bridge the gap between existing detection methods and preventive interventions by: developing and comparing deep learning models like CNN, LSTM, and LSTM-BLSTM for 6–12 month CKD prediction; addressing data imbalance, feature selection, and optimizer optimization; and building an ensemble model combining the best individual models (CNN-Adamax, LSTM-Adam, and LSTM-BLSTM-Adamax). Our framework achieves significantly higher accuracy (98% and 97% for 6 and 12 months) than previous work, paving the way for earlier diagnosis and improved patient outcomes.

Machine learning models for predicting the onset of chronic kidney disease after surgery in patients with renal cell carcinoma

BackgroundPatients with renal cell carcinoma (RCC) have an elevated risk of chronic kidney disease (CKD) following nephrectomy. Therefore, continuous monitoring and subsequent interventions are necessary. It is recommended to evaluate renal function postoperatively. Therefore, a tool to predict CKD onset is essential for postoperative follow-up and management.MethodsWe constructed a cohort using data from eight tertiary hospitals from the Korean Renal Cell Carcinoma (KORCC) database. A dataset of 4389 patients with RCC was constructed for analysis from the collected data. Nine machine learning (ML) models were used to classify the occurrence and nonoccurrence of CKD after surgery. The final model was selected based on the area under the receiver operating characteristic (AUROC), and the importance of the variables constituting the model was confirmed using the shapley additive explanation (SHAP) value and Kaplan-Meier survival analyses.ResultsThe gradient boost algorithm was the most effective among the various ML models tested. The gradient boost model demonstrated superior performance with an AUROC of 0.826. The SHAP value confirmed that preoperative eGFR, albumin level, and tumor size had a significant impact on the occurrence of CKD after surgery.ConclusionsWe developed a model to predict CKD onset after surgery in patients with RCC. This predictive model is a quantitative approach to evaluate post-surgical CKD risk in patients with RCC, facilitating improved prognosis through personalized postoperative care.

Familial primary calcific band-shaped keratopathy with late onset systemic disease: a case series and review of the literature

BackgroundFamilial calcific band-shaped keratopathy (BSK) is a very rare disease, with no underlying cause. There is no underlying disease in this form of the disease. This article introduces a family with seven children, three of whom were diagnosed with familial primary calcific BSK. One of them developed a systemic disease 38 years after ocular manifestation.Case presentationIn this case report, three Iranian siblings from a family with familial calcific band-shaped keratopathy (BSK) are introduced. Systemic and ocular examinations performed on these patients indicated the occurrence of chronic kidney disease in the older child, a 41-year-old woman, 38 years after ocular manifestation. The examinations conducted on the other two siblings revealed no pathological findings. The 41-year-old sister and 37-year-old brother underwent unilateral deep anterior lamellar keratoplasty (DALK), while the 33-year-old sister underwent bilateral superficial keratectomy (SK).ConclusionConsidering the late onset of systemic disease in one of the siblings diagnosed with familial calcific band-shaped keratopathy (BSK), it is crucial to emphasize the necessity of long-term follow-up for these patients and their families.

Blockade of aryl hydrocarbon receptor restricts omeprazole-induced chronic kidney disease.

Chronic kidney disease (CKD) is the 16th leading cause of mortality worldwide. Clinical studies have raised that long-term use of omeprazole (OME) is associated with the morbidity of CKD. OME is commonly used in clinical practice to treat peptic ulcers and gastroesophageal reflux disease. However, the mechanism underlying renal failure following OME treatment remains mostly unknown and the rodent model of OME-induced CKD is yet to be established. We described the process of renal injury after exposure to OME in mice; the early renal injury markers were increased in renal tubular epithelial cells (RTECs). And after long-term OME treatment, the OME-induced CKD mice model was established. Herein, aryl hydrocarbon receptor (AHR) translocation appeared after exposure to OME in HK-2 cells. Then for both in vivo and in vitro, we found that Ahr-knockout (KO) and AHR small interfering RNA (siRNA) substantially alleviated the OME-induced renal function impairment and tubular cell damage. Furthermore, our data demonstrate that antagonists of AHR and CYP1A1 could attenuate OME-induced tubular cell impairment in HK-2 cells. Taken together, these data indicate that OME induces CKD through the activation of the AHR-CYP axis in RTECs. Our findings suggest that blocking the AHR-CYP1A1 pathway acts as a potential strategy for the treatment of CKD caused by OME. KEY MESSAGES: We provide an omeprazole-induced chronic kidney disease (CKD) mice model. AHR activation and translocation process was involved in renal tubular damage and promoted the occurrence of CKD. The process of omeprazole nephrotoxicity can be ameliorated by blockade of the AHR-CYP1A1 axis.

Severity and Remission of Metabolic Dysfunction-Associated Fatty/Steatotic Liver Disease With Chronic Kidney Disease Occurrence.

The association of the severity of hepatic steatosis in metabolic dysfunction-associated fatty liver disease (MAFLD)/metabolic dysfunction-associated steatotic liver disease (MASLD) and the remission of MAFLD/MASLD with CKD occurrence is unclear. The study enrolled 79 540 participants from the Kailuan cohort. Hepatic steatosis was diagnosed by ultrasound. MAFLD/MASLD was defined as hepatic steatosis combined with metabolic dysfunction and MASLD further excluded alcohol or other causes of liver disease. Chronic kidney disease (CKD) was defined as estimated glomerular filtration rate<60 mL/min per 1.73 m2 or positive proteinuria (≥1+). Hazard ratio (HR) was calculated by Cox regression models. After a median follow-up of 12.9 years, CKD occurred in 20 465 participants. After adjusting for potential confounders, MAFLD was associated with a higher risk of CKD compared with non-MAFLD (HR, 1.12 [95% CI, 1.09-1.16]), and this risk increased with increasing severity of hepatic steatosis (P-trend<0.001). Consistent findings were observed when MASLD was used as the exposure. Compared with persistent non-MAFLD, no statistical difference was found in the risk of CKD in MAFLD remission (HR, 1.04 [95% CI, 0.95-1.15]); however, MASLD remission still had a higher risk of CKD compared with persistent non-MASLD (HR, 1.15 [95% CI, 1.03-1.27]). When grouped according to the prior severity of hepatic steatosis, there was no statistically significant difference in risk of CKD in mild-MAFLD/MASLD remission compared with persistent non-MAFLD/MASLD, but moderated/severe-MAFLD/MASLD remission still had a higher risk. The risk of CKD in patients with MAFLD/MASLD increased with the severity of hepatic steatosis. Even after remission of the disease, patients with MAFLD/MASLD with prior moderate to severe hepatic steatosis still had a higher risk of CKD.

Comparing the Performance of Machine Learning Models in Predicting the Risk of Chronic Kidney Disease

Background: Chronic kidney disease (CKD) poses a significant health burden worldwide, affecting approximately 10 - 15% of the global population. As one of the leading non-communicable diseases, CKD is a major cause of morbidity and mortality. Early identification of CKD is crucial for reducing its adverse effects on patient health. Prompt detection can significantly lessen the harmful consequences and enhance health outcomes for individuals with CKD. Objectives: This study aimed to evaluate and compare the effectiveness of various machine learning models in predicting the occurrence of CKD. Methods: The study involved the collection of data from a sample of 400 patients. We applied the well-established cross-industry standard process (CRISP) methodology for data mining to analyze the data. As part of this process, we efficiently handled missing data using the mode approach and addressed outliers through the interquartile range (IQR) method. We utilized sophisticated techniques, such as CatBoost (CB), random forest (RF), and artificial neural network (ANN) models to predict outcomes. For evaluation, we used the receiver operating characteristic (ROC) curve and calculated the area under the curve (AUC). Results: An analysis of 400 patient records in this study identified that variables like serum creatinine, packed cell volume, specific gravity, and hemoglobin were most influential in predicting CKD. The results indicated that the CB and RF models surpassed the ANN in predicting the disease. Ten critical predictors were pinpointed for accurate disease prediction. Conclusions: The ensemble models in this study not only showcased remarkable speed but also demonstrated superior accuracy. These findings suggest the potential of ensemble models as an effective tool for enhancing predictive performance in similar studies.

A Prospective Study of the Association Between Plasma Calprotectin Levels and New-Onset CKD in the General Population

IntroductionSystemic inflammation has been associated with chronic kidney disease (CKD). In this study, we aimed to investigate a potential association between the plasma biomarker of inflammation calprotectin and new-onset CKD in a population-based cohort study. MethodsIndividuals without CKD at baseline (n=4,662) who participated in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) prospective population-based cohort study in the Netherlands were included. Baseline plasma calprotectin levels were assessed in samples that had been stored at -80°C. Occurrence of new-onset CKD was defined as a composite outcome of an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73m2, urinary albumin excretion (UAE) >30 mg/24-h, or both. ResultsBaseline median [IQR] plasma calprotectin levels were 0.49 [0.35-0.68] mg/l and baseline median eGFR was 95.9 [IQR: 85.0-105.7] ml/min/1.73m2. After median follow-up of 8.3 [7.8-8.9] years, 467 participants developed new-onset CKD. Baseline plasma calprotectin levels were significantly associated with an increased risk of new-onset CKD (hazard ratio [HR] per doubling 1.28 [95% CI: 1.14-1.44], P<0.001), independent of potentially confounding factors (HR 1.14 [95% CI: 1.01-1.29], P=0.034), except for baseline hs-CRP (HR 1.05 [0.91-1.21], P=0.494). In secondary analyses, the association between plasma calprotectin and occurrence of UAE >30 mg/24-h remained significant (HR 1.17 [1.02-1.34], P=0.027), but not significantly so for the incidence of eGFR <60 ml/min/1.73m2 as individual outcome (HR 1.15 [0.92-1.43], P=0.218). ConclusionHigher plasma calprotectin levels are associated with an increased risk of developing CKD in the general population. This association is mitigated after adjustment for hs-CRP, and more pronounced with new-onset CKD defined by UAE.

Risk factors of chronic kidney disease in cisplatin-based hyperthermia intraperitoneal chemotherapy

Purpose Cisplatin is commonly prescribed in hyperthermic intraperitoneal chemotherapy (HIPEC) for peritoneal malignancy. Acute kidney injury (AKI) is regarded as a common complication after HIPEC combined with cytoreductive surgery (CRS). However, post-HIPEC chronic kidney disease (CKD) is scarce and less investigated. This study aims to investigate the incidence of CKD following cisplatin-based HIPEC and to analyse the associated risk factors. Materials and Methods From January 2016 to August 2021, a total of 55 patients treated with CRS and cisplatin-based HIPEC for peritoneal carcinomatosis were categorized retrospectively into groups, with and without CKD. Demographics, comorbidity, surgery, postoperative management, and complications were collected to evaluate risk factors for cisplatin-based HIPEC-related CKD. Univariate and multivariate analyses were conducted to confirm the correlation between different variables and CKD occurrence. Results Of the 55 patients, 24 (43.6%) patients developed AKI and 17 (70.8%) patients of these AKI patients progressed to CKD. Multivariate regression analysis identified intraoperative use of parecoxib (Odds Ratio (OR) = 4.39) and intraoperative maximum temperature > 38.5°C (OR = 6.40) as major risk factors for cisplatin-based HIPEC-related CKD occurrence. Though type II diabetes mellitus and intraoperative complications were the independent risk factors of AKI following cisplatin-based HIPEC, but they were not shown in CKD analysis. Conclusion Intraoperative use of parecoxib during cisplatin-based HIPEC emerged as a significant risk factor for postoperative CKD. Clinicians should exercise caution in prescribing parecoxib during HIPEC procedures. Additionally, maintaining intraoperative body temperature below 38.5°C might be crucial to mitigate the risk of CKD development. This study underscores the importance of identifying and preventing specific risk factors to improve long-term renal outcomes in patients undergoing cisplatin-based HIPEC.

Prediction of the risk of 3-year chronic kidney disease among elderly people: a community-based cohort study

Objective We conducted a community-based cohort study to predict the 3-year occurrence of chronic kidney disease (CKD) among population aged ≥60 years. Method Participants were selected from two communities through randomized cluster sampling in Jiading District of Shanghai, China. The two communities were randomly divided into a development cohort (n = 12012) and a validation cohort (n = 6248) with a 3-year follow-up. Logistic regression analysis was used to determine the independent predictors. A nomogram was established to predict the occurrence of CKD within 3 years. The area under the curve (AUC), the calibration curve and decision curve analysis (DCA) curve were used to evaluate the model. Result At baseline, participants in development cohort and validation cohort were with the mean age of 68.24 ± 5.87 and 67.68 ± 5.26 years old, respectively. During 3 years, 1516 (12.6%) and 544 (8.9%) new cases developed CKD in the development and validation cohorts, respectively. Nine variables (age, systolic blood pressure, body mass index, exercise, previous hypertension, triglycerides, fasting plasma glucose, glycated hemoglobin and serum creatinine) were included in the prediction model. The AUC value was 0.742 [95% confidence interval (CI), 0.728–0.756] in the development cohort and 0.881(95%CI, 0.867–0.895) in the validation cohort, respectively. The calibration curves and DCA curves demonstrate an effective predictive model. Conclusion Our nomogram model is a simple, reasonable and reliable tool for predicting the risk of 3-year CKD in community-dwelling elderly people, which is helpful for timely intervention and reducing the incidence of CKD.

Energy depletion by cell proliferation sensitizes the kidney epithelial cells to injury.

Acute kidney injury activates both proliferative and antiproliferative pathways, the consequences of which are not fully elucidated. If an initial proliferation of the renal epithelium is necessary for the successful repair, the persistence of proliferation markers is associated with the occurrence of chronic kidney disease. We hypothesized that proliferation in stress conditions impacts cell viability and renal outcomes. We found that proliferation is associated with cell death after various stresses in kidney cells. In vitro, the ATP/ADP ratio oscillates reproducibly throughout the cell cycle, and cell proliferation is associated with a decreased intracellular ATP/ADP ratio. In vivo, transcriptomic data from transplanted kidneys revealed that proliferation was strongly associated with a decrease in the expression of the mitochondria-encoded genes of the oxidative phosphorylation pathway, but not of the nucleus-encoded ones. These observations suggest that mitochondrial function is a limiting factor for energy production in proliferative kidney cells after injury. The association of increased proliferation and decreased mitochondrial function was indeed associated with poor renal outcomes. In summary, proliferation is an energy-demanding process impairing the cellular ability to cope with an injury, highlighting proliferative repair and metabolic recovery as indispensable and interdependent features for successful kidney repair.NEW & NOTEWORTHY ATP depletion is a hallmark of acute kidney injury. Proliferation is instrumental to kidney repair. We show that ATP levels vary during the cell cycle and that proliferation sensitizes renal epithelial cells to superimposed injuries in vitro. More proliferation and less energy production by the mitochondria are associated with adverse outcomes in injured kidney allografts. This suggests that controlling the timing of kidney repair might be beneficial to mitigate the extent of acute kidney injury.

Sensorineural Hearing Loss in Patients With Chronic Kidney Disease: A Comprehensive Review.

This article aims to ascertain the prevalence of loss of hearing in patients with chronic kidney disease (CKD) and also to examine potential causes of sensorineural hearing loss (SNHL) in patients suffering from CKD. It has been discovered in recent years that there is a relationship between the occurrence of SNHL and CKD. Nowadays many people are suffering from CKD. These patients deal with several otorhinolaryngological issues, such as SNHL, candidiasis, epistaxis, halitosis, dysgeusia, xerostomia, and lip and thyroid malignancies. One of the most frequent otorhinolaryngological complications is audiovestibular system impairment. There are various proposed mechanisms for the appearance of loss of hearing in people suffering from CKD. The kidney and the inner ear have multiple functional and structural similarities, which may be the cause of these problems in CKD patients. In addition, changes in the homeostasis of water and electrolytes can affect the endolymphatic fluid and result in endolymphatic hydrops. Finally, some medications, like aminoglycosides and loop diuretics, are well known for their ototoxicity and are utilized to treat patients with CKD. Only a small number of population-based research have so far been able to show a connection between CKD and audiovestibular system impairment. Some investigationhasshown that CKD patients are more likely than healthy people to experience vestibular impairment. The quality of life of a patient can be reduced by hearing loss. People with hearing loss experience communication issues in daily life, which negatively affects their cognitive and psychosocial functioning. Social isolation and a poor quality of life in terms of health can all result from hearing loss. In addition, decreased renal function has also been linked to poor quality of life, hospitalization, and cognitive dysfunction.

A systematic analysis of chronic kidney disease burden attributable to lead exposure based on the global burden of disease study 2019

AimAs an important toxic heavy metal, lead exposure can lead to the occurrence of chronic kidney disease (CKD). However, the analysis of its disease burden pattern on a global scale is lacking. This study aimed to analyze the CKD burden attributable to lead exposure globally, regionally and temporally, as well as to examine the role of socio-economic factors. MethodThis study used data from the Global Burden of Disease (GBD) study 2019. We obtained the global burden of CKD caused by lead exposure between 1990 and 2019, and stratified this burden according to factors such as gender, age, GBD regions, and countries. From 1990 to 2019, the changing trend of the disease burden of CKD attributed to lead exposure was estimated using Joinpoint regression model with the average annual percent change (AAPC) estimated. Finally, the relationship between country-level socio-economic factors and lead exposure related CKD burden was explored using a panel data model analysis. ResultsIn 2019, worldwide, there were 52.94 thousand deaths (95 % uncertainty interval (UI): 31.64, 76.23) and 1225.2 thousand disability-adjusted life years (DALYs) (95 % UI: 707.88, 1818) of CKD caused by lead exposure, accounting for 3.71 % of total CKD deaths and 2.95 % of total CKD DALYs. The age-standardized death and DALY rates per 100,000 population were 0.68 (95 % UI: 0.40, 0.98) and 15.02 (95 % UI: 8.68, 22.26) respectively, indicating an upward trend and stable trend between 1990 and 2019. However, the age-standardized rates attributed to lead exposure showed a wide variability across regions, with the highest rates in Central Latin America and the lowest in Eastern Europe. Moreover, the results of panel model analysis indicated that GDP growth was positively associated with lead exposure related CKD death rate and DALY rate. However, there were inverse associations between life expectancy at birth and hospital beds (per 1000 people) with lead exposure-related CKD DALY rate. ConclusionIn summary, a significant burden of CKD can be attributed to lead exposure, with noticeable regional discrepancies. Findings here are valuable to deploy efficient measures at curbing lead exposure worldwide.

TRF-003634 alleviates adriamycin-induced podocyte injury by reducing the stability of TLR4 mRNA.

Podocyte injury plays a key role in the production of proteinuria and is closely related to the progression of chronic kidney disease (CKD). Alleviating podocyte injury is beneficial to prevent the occurrence and development of CKD. tRNA-derived RNA fragments (tRFs) are associated with podocytes injury processes such as protein binding, cell adhesion, synapses, the actin cytoskeleton. Our previous data showed that tRF-003634 tightly correlated with podocyte injury, while its effect remains unclear. This study aimed to investigate the role of tRF-003634 in podocyte injury and the potential mechanisms. The expression level of tRF-003634, nephrin, podocin and tRF-003634 targeted toll-like receptor 4 (TLR4) in podocytes and kidney tissues were examined by quantitative real-time PCR (qRT-PCR), western blot and immunohistochemistry. The biochemical indices were monitored and renal pathological changes were assessed by hematoxylin and eosin PAS staining. Furthermore, potential target genes of tRF-003634 were screened using high-throughput mRNA sequencing, and then confirmed by RNA pulse-chase analysis. The results showed that tRF-003634 was downregulated in adriamycin (Adr)-induced podocyte injury. Overexpression of tRF-003634 increased the expression of nephrin and podocin in vivo and in vitro and alleviated podocyte injury. Meanwhile, overexpression of tRF-003634 alleviated proteinuria and renal pathological damage. In addition, high-throughput sequencing after overexpression of tRF-003634 showed that TLR4 might be a downstream target gene. tRF-003634 can alleviate podocyte injury by reducing the stability of TLR4 mRNA, possibly by competing with TLR4 mRNA to bind to YTH domain-containing protein 1 (YTHDC1). In conclusion, tRF-003634 was underexpressed in Adr-induced podocyte injury, and its overexpression alleviated podocyte injury in vitro and in vivo by reducing the stability of TLR4 mRNA.

POSTER: MPN-409 Associations of JAK2 Mutant Allele Burden With Occurrence of CKD (Chronic Kidney Disease) and Dynamics of Kidney Function Over Time in Patients With Chronic Myeloproliferative Neoplasms

POSTER: MPN-409 Associations of JAK2 Mutant Allele Burden With Occurrence of CKD (Chronic Kidney Disease) and Dynamics of Kidney Function Over Time in Patients With Chronic Myeloproliferative Neoplasms

MPN-409 Associations of JAK2 Mutant Allele Burden With Occurrence of CKD (Chronic Kidney Disease) and Dynamics of Kidney Function Over Time in Patients With Chronic Myeloproliferative Neoplasms

MPN-409 Associations of JAK2 Mutant Allele Burden With Occurrence of CKD (Chronic Kidney Disease) and Dynamics of Kidney Function Over Time in Patients With Chronic Myeloproliferative Neoplasms

Chronic kidney disease prediction model using machine learning approach

&lt;p&gt;Chronic disease (CD) such as kidney disease and causes severe challenging issues to the people all around the world. Chronic kidney disease (CKD) and diabetes mellitus (DM) are considered in this paper. Predicting the diseases in earlier stage, gives better preventive measures to the people. Healthcare domain leads to tremendous cost savings and improved health status of the society. The main objective of this paper is to develop an algorithm to predict CKD occurrence using machine learning (ML) technique. The commonly used classification algorithms namely logistic regression (LR), random forest (RF), conditional random forest (CRF), and recurrent neural networks (RNN) are considered to predict the disease at an earlier stage. The proposed algorithm in this paper uses medical code data to predict disease at an earlier stage.&lt;/p&gt;

The occurrence of chronic kidney disease among African American aged 65 years and above in the United States

This paper focuses on chronic kidney disease (CKD) among African American adults over 65 years old in the USA. CKD is a progressive illness that affects more than 800 million people worldwide, with a higher prevalence among older individuals, women, racial minorities, and those with comorbidities such as diabetes mellitus and hypertension. African Americans have a higher prevalence of CKD, along with risk factors such as obesity, diabetes, and hypertension. The paper investigates the occurrence of CKD in this population and explores the etiology of the disease, including non-modifiable risk factors like genetics and modifiable risk factors such as hypertension and metabolic factors.