Kidney Disease Research Articles

The Urinary Glycopeptide Profile Differentiates Early Cardiorenal Risk in Subjects Not Meeting Criteria for Chronic Kidney Disease

Early diagnosis and treatment of chronic kidney disease (CKD) is a worldwide challenge. Subjects with albumin-to-creatinine ratio (ACR) ≥ 30 mg/g and preserved renal function are considered to be at no cardiorenal risk in clinical practice, but prospective clinical studies evidence increased risk, even at the high-normal (HN) ACR range (10–30 mg/g), supporting the need to identify other molecular indicators for early assessment of patients at higher risk. Following our previous studies, here we aim to stratify the normoalbuminuria range according to cardiorenal risk and identify the glycoproteins and N-glycosylation sites associated with kidney damage in subclinical CKD. Glycoproteins were analyzed in urine from hypertensive patients within the HN ACR range compared to control group (C; ACR < 10 mg/g) by mass spectrometry. A different cohort was analyzed for confirmation (ELISA) and sex perspective was evaluated. Patients’ follow-up for 8 years since basal urine collection revealed higher renal function decline and ACR progression for HN patients. Differential N-glycopeptides and their N -glycosylation sites were also identified, together with their pathogenicity. N-glycosylation may condition pathological protein deregulation, and a panel of 62 glycoproteins evidenced alteration in normoalbuminuric subjects within the HN range. Haptoglobin-related protein, haptoglobin, afamin, transferrin, and immunoglobulin heavy constant gamma 1 (IGHG1) and 2 (IGHG2) showed increased levels in HN patients, pointing to disturbed iron metabolism and tubular reabsorption and supporting the tubule as a target of interest in the early progression of CKD. When analyzed separately, haptoglobin, afamin, transferrin, and IGHG2 remained significant in HN, in both women and men. At the peptide level, 172 N-glycopeptides showed differential abundance in HN patients, and 26 showed high pathogenicity, 10 of them belonging to glycoproteins that do not show variation between HN and C groups. This study highlights the value of glycosylation in subjects not meeting KDIGO criteria for CKD. The identified N-glycopeptides and glycosylation sites showed novel targets, for both the early assessment of individual cardiorenal risk and for intervention aimed at anticipating CKD progression.

Post-acute and Chronic Kidney Function Outcomes of COVID-19 in Children and Adolescents: An EHR Cohort Study from the RECOVER Initiative.

This study examined the impact of COVID-19 on kidney health in children and adolescents under 21 years old in the United States. Using data from the RECOVER program, we analyzed the health records of 1,864,637 young individuals from 19 hospitals and health institutions between March 2020 and May 2023. The study focused on three groups: those with pre-existing chronic kidney disease (CKD), those who experienced acute kidney injury (AKI) during the initial COVID-19 infection, and those without any prior kidney issues. The results showed that children and adolescents who had COVID-19 were at a higher risk of developing serious kidney problems later on, even if they had no previous kidney conditions. This research highlights the long-term effects of COVID-19 on kidney health in young people and underscores the importance of monitoring kidney function in pediatric COVID-19 patients.

Galectin-8 counteracts folic acid-induced acute kidney injury and prevents its transition to fibrosis

Acute kidney injury (AKI), characterized by a sudden decline in kidney function involving tubular damage and epithelial cell death, can lead to progressive tissue fibrosis and chronic kidney disease due to interstitial fibroblast activation and tissue repair failures that lack direct treatments. After an AKI episode, surviving renal tubular cells undergo cycles of dedifferentiation, proliferation and redifferentiation while fibroblast activity increases and then declines to avoid an exaggerated extracellular matrix deposition. Appropriate tissue recovery versus pathogenic fibrotic progression depends on fine-tuning all these processes. Identifying endogenous factors able to affect any of them may offer new therapeutic opportunities to improve AKI outcomes. Galectin-8 (Gal-8) is an endogenous carbohydrate-binding protein that is secreted through an unconventional mechanism, binds to glycosylated proteins at the cell surface and modifies various cellular activities, including cell proliferation and survival against stress conditions. Here, using a mouse model of AKI induced by folic acid, we show that pre-treatment with Gal-8 protects against cell death, promotes epithelial cell redifferentiation and improves renal function. In addition, Gal-8 decreases fibroblast activation, resulting in less expression of fibrotic genes. Gal-8 added after AKI induction is also effective in maintaining renal function against damage, improving epithelial cell survival. The ability to protect kidneys from injury during both pre- and post-treatments, coupled with its anti-fibrotic effect, highlights Gal-8 as an endogenous factor to be considered in therapeutic strategies aimed at improving renal function and mitigating chronic pathogenic progression.

Prevention of Chronic Kidney Disease and Its Complications in Older Adults.

In an era marked by a global demographic shift towards an aging society, there is a heightened prevalence of chronic kidney disease (CKD) among older adults. The burden of CKD spans from kidney-related complications to impacting psychological well-being, giving rise to depressive symptoms and caregiver burnout. This article delves into CKD prevention strategies within the context of aging, contributing to the discourse by exploring its multifaceted aspects. The prevention of CKD in the older adults necessitates a comprehensive approach. Primary prevention is centered on the modification of risk factors, acknowledging the intricate interplay of various comorbidities. Secondary prevention focuses on early CKD identification. Tertiary prevention aims to address factors contributing to CKD progression and complications, emphasizing the importance of timely interventions. This comprehensive strategy aims to enhance the quality of life for individuals affected by CKD, decelerating the deterioration of functional status. By addressing CKD at multiple levels, this approach seeks to effectively and compassionately care for the aging population.

Intermittent protein restriction before but not after the onset of diabetic kidney disease attenuates disease progression in mice.

High dietary protein intake exacerbates proteinuria in individuals with diabetic kidney disease (DKD). However, studies on the impacts of low protein diet (LPD) on DKD have yielded conflicting results. Furthermore, patient compliance to continuous protein restriction is challenging. The current study aims to investigate the effects of intermittent protein restriction (IPR) on disease progression of DKD. Diabetic KK-Ay mice were used in this study. For the IPR treatment, three consecutive days of LPD were followed by four consecutive days of normal protein diet (NPD) within each week. For early intervention, mice received IPR before DKD onset. For late intervention, mice received IPR after DKD onset. In both experiments, age-matched mice fed continuous NPD served as the control group. Kidney morphology, structure and function of mice in different groups were examined. Intermittent protein restriction before DKD onset ameliorated pathological changes in kidney, including nephromegaly, glomerular hyperfiltration, tubular injuries and proteinuria, without improving glycemic control. Meanwhile, IPR initiated after DKD onset showed no renoprotective effects despite improved glucose homeostasis. Intermittent protein restriction before rather than after DKD onset protects kidneys, and the impacts of IPR on the kidneys are independent of glycemic control. IPR shows promise as an effective strategy for managing DKD and improving patient compliance.

Patient-derived and gene-edited pluripotent stem cells lacking NPHP1 recapitulate juvenile nephronophthisis in abnormalities of primary cilia and renal cyst formation.

Juvenile nephronophthisis is an inherited renal ciliopathy with cystic kidney disease, renal fibrosis, and end-stage renal failure in children and young adults. Mutations in the NPHP1 gene encoding nephrocystin-1 protein have been identified as the most frequently responsible gene and cause the formation of cysts in the renal medulla. The molecular pathogenesis of juvenile nephronophthisis remains elusive, and no effective medicines to prevent end-stage renal failure exist even today. No human cellular models have been available yet. Here, we report a first disease model of juvenile nephronophthisis using patient-derived and gene-edited human induced pluripotent stem cells (hiPSCs) and kidney organoids derived from these hiPSCs. We established NPHP1-overexpressing hiPSCs from patient-derived hiPSCs and NPHP1-deficient hiPSCs from healthy donor hiPSCs. Comparing these series of hiPSCs, we found abnormalities in primary cilia associated with NPHP1 deficiency in hiPSCs. Kidney organoids generated from the hiPSCs lacking NPHP1 formed renal cysts frequently in suspension culture with constant rotation. This cyst formation in patient-derived kidney organoids was rescued by overexpression of NPHP1. Transcriptome analysis on these kidney organoids revealed that loss of NPHP1 caused lower expression of genes related to primary cilia in epithelial cells and higher expression of genes related to the cell cycle. These findings suggested the relationship between abnormality in primary cilia induced by NPHP1 loss and abnormal proliferative characteristics in the formation of renal cysts. These findings demonstrated that hiPSC-based systematic disease modeling of juvenile nephronophthisis contributed to elucidating the molecular pathogenesis and developing new therapies.

Risk factors associated with COVID-19 mortality in Mexico.

On December 31, 2019, one of the most serious pandemics in recent times made its appearance. Certain health conditions, such as obesity and diabetes mellitus, have been described to be related to COVID-19 unfavorable outcomes. To identify factors associated with mortality in patients with COVID-19. Retrospective cohort of 998,639 patients. Patient sociodemographic and clinical characteristics were analyzed, with survivors being compared with the deceased individuals. Cox proportional hazards model was used to identify variables predictive of COVID-19-associated mortality. Among the deceased patients, men accounted for 64.3%, and women, for 35.7%, with the difference being statistically significant. Subjects older than 80 years had a 13-fold higher risk of dying from COVID-19 (95% CI = 12,469, 13,586), while chronic kidney disease entailed a risk 1.5 times higher (95% CI = 1,341, 1,798), and diabetes mellitus involved a risk 1.25 times higher (95% CI = 1.238,1.276). Age, sex, diabetes mellitus and obesity were found to be predictors of COVID-19 mortality. Further research related to chronic obstructive pulmonary disease, cardiovascular diseases, smoking and pregnancy is suggested.

Reframing “Chronicity” with “Urgency” in Chronic Kidney Disease Management

Reframing “Chronicity” with “Urgency” in Chronic Kidney Disease Management

Evaluation of Serum Electrolyte Abnormalities and Kidney Function to Assess Risk of Kidney Disease in Hypertensive Patients at Kenyatta National Hospital

HTN is a known leading cause of kidney disease with over 20% of the population aged 20 years or older with HTN developing CKD. Complications from HTN and kidney disease contribute significantly to global mortality. In Kenya, data from WHO shows that about 4 million individuals suffer from CKD, with many progressing to kidney failure. The aim was to assess serum electrolyte abnormalities and kidney function among hypertensive patients at KNH. The study utilized cross-sectional retrospective data from KNH patient records. The CKD-EPI equation was used to calculate eGFR. Fisher et al.’s equation determined sample size. Data were stratified by variables such as DBP, age, sex, SBP, proteinuria, serum creatinine, urea levels, serum electrolytes, and eGFR. Data collection involved 189 patients: 82 males (43.4%) and 107 females (56.6%), with a median age of 54.00 years. 93 patients (49.20%) were <54 years and 96 (50.80%) were ≥54 years. 78.84% of HTN patients had abnormal serum creatinine levels, and 54.5% had abnormal serum urea levels. 58.7% showed proteinuria. Elevated sodium levels (>145 mmol/l) affected 39.68% of patients, while reduced potassium levels (<3.5 mmol/l) were found in 15.34%. 41.27% had elevated chloride levels above 106 mmol/l. CKD stages varied: 3.2% had G1, 17.5% had G2, 14.8% had G3a, 29.1% had G3b, 16.4% had G4, and 19.0% had G5. Reduced renal function, estimated using GFR, was prevalent among hypertensive patients (79.4%) (95% CI:72.9-82.9), notably those ≥54 years. In conclusion, the risk of progressive kidney disease was high amongst hypertensive patients and this was evident from the proportion of patients who have abnormal kidney function including proteinuria. Early screening and implementation of therapeutic strategies can improve patient’s quality of life.

Unveiling the enigma of acute kidney disease: predicting prognosis, exploring interventions, and embracing a multidisciplinary approach.

Acute kidney disease (AKD) is a critical transitional period between acute kidney injury and chronic kidney disease. The incidence of AKD following acute kidney injury is approximately 33.6%, and it can occur without identifiable preceding acute kidney injury. The development of AKD is associated with increased risks of chronic kidney disease, dialysis, and mortality. Biomarkers and subphenotypes are promising tools to predict prognosis in AKD. The complex clinical situations in patients with AKD necessitate a comprehensive and structured approach, termed "KAMPS" (kidney function check, advocacy, medications, pressure, sick day protocols). We introduce "MAND-MASS," an acronym devised to summarize the reconciliation of medications during episodes of acute illness, as a critical component of the sick day protocols at AKD. A multidisciplinary team care, consisting of nephrologists, pharmacists, dietitians, health educators, and nurses, is an optimal model to achieve the care bundle in KAMPS. Although the evidence for patients with AKD is still lacking, several potential pharmacological agents may improve outcomes, including but not limited to angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide 1 receptor agonists. In conclusion, accurate prognosis prediction and effective treatment for AKD are critical yet unmet clinical needs. Future studies are urgently needed to improve patient care in this complex and rapidly evolving field.

SGLT2 inhibition leads to a restoration of hepatic and circulating metabolites involved in the folate cycle and pyrimidine biosynthesis.

Inhibition of sodium-glucose co-transporter 2 (SGLT2) by Empagliflozin (EMPA) and other 'flozins can improve glycemic control under conditions of diabetes and kidney disease. Though they act on the kidney, they also offer cardiovascular and liver protection. Previously, we found that EMPA decreased circulating triglycerides and hepatic lipid and cholesterol esters in male TallyHo mice fed a high milk fat diet (HMFD). The goal of this study was to determine if the liver protection is associated with a change in metabolic function by characterizing the hepatic and circulating metabolic and lipidomic profiles using targeted LC-MS. In both male and female mice, HMFD feeding significantly altered the circulating and hepatic metabolome compared to low-fat diet (LFD). Addition of EMPA resulted in the restoration of circulating orotate (intermediate in pyrimidine biosynthesis) and hepatic dihydrofolate (intermediate in the folate and methionine cycles) levels in males and acylcarnitines in females. These changes were partially explained by altered expression of rate-limiting enzymes in these pathways. This metabolic signature was not detected when EMPA was incorporated into an LFD suggesting that the restoration requires the metabolic shift that accompanies the HMFD. Notably, the HMFD increased expression of 18/20 circulating amino acids in males and 11/20 in females, and this pattern was reversed by EMPA. Finally, we confirmed that SGLT2 inhibition upregulates ketone bodies including b-hydroxybutyrate. Collectively, this study highlights the metabolic changes that occur with EMPA treatment, and sheds light on the possible mechanisms by which this drug offers liver and systemic protection.

The Complex Immunological Alterations in Patients with Type 2 Diabetes Mellitus on Hemodialysis

It is widely known that diabetes mellitus negatively impacts both the innate immunity (the inflammatory response) and the acquired immunity (the humoral and cellular immune responses). Many patients with diabetes go on to develop chronic kidney disease, which will necessitate hemodialysis. In turn, long-term chronic hemodialysis generates an additional chronic inflammatory response and impairs acquired immunity. The purpose of this paper is to outline and compare the mechanisms that are the basis of the constant aggression towards self-components that affects patients with diabetes on hemodialysis, in order to find possible new therapeutic ways to improve the functionality of the immune system. Our study will take a detailed look at the mechanisms of endothelial alteration in diabetes and hemodialysis, at the mechanisms of inflammatory generation and signaling at different levels and also at the mechanisms of inflammation-induced insulin resistance. It will also discuss the alterations in leukocyte chemotaxis, antigen recognition and the dysfunctionalities in neutrophils and macrophages. Regarding acquired immunity, we will outline the behavioral alterations of T and B lymphocytes induced by diabetes mellitus and chronic hemodialysis.

To Evaluate the Epidemiology, Etiology, Risk Factors and Treatment Management in Chronic Kidney Disease on Children, Adult and Geriatric Patients in a Tertiary Care Teaching Hospital in Nellore, on Study-II

To Evaluate the Epidemiology, Etiology, Risk Factors and Treatment Management in Chronic Kidney Disease on Children, Adult and Geriatric Patients in a Tertiary Care Teaching Hospital in Nellore, on Study-II

Dietary fibre directs microbial tryptophan metabolism via metabolic interactions in the gut microbiota.

Tryptophan is catabolized by gut microorganisms resulting in a wide range of metabolites implicated in both beneficial and adverse host effects. How gut microbial tryptophan metabolism is directed towards indole, associated with chronic kidney disease, or towards protective indolelactic acid (ILA) and indolepropionic acid (IPA) is unclear. Here we used in vitro culturing and animal experiments to assess gut microbial competition for tryptophan and the resulting metabolites in a controlled three-species defined community and in complex undefined human faecal communities. The generation of specific tryptophan-derived metabolites was not predominantly determined by the abundance of tryptophan-metabolizing bacteria, but rather by substrate-dependent regulation of specific metabolic pathways. Indole-producing Escherichia coli and ILA- and IPA-producing Clostridium sporogenes competed for tryptophan within the three-species community in vitro and in vivo. Importantly, fibre-degrading Bacteroides thetaiotaomicron affected this competition by cross-feeding monosaccharides to E. coli. This inhibited indole production through catabolite repression, thus making more tryptophan available to C. sporogenes, resulting in increased ILA and IPA production. The fibre-dependent reduction in indole was confirmed using human faecal cultures and faecal-microbiota-transplanted gnotobiotic mice. Our findings explain why consumption of fermentable fibres suppresses indole production but promotes the generation of other tryptophan metabolites associated with health benefits.

Metabolic MRI With Hyperpolarized 13 C-Pyruvate for Early Detection of Fibrogenic Kidney Metabolism.

Fibrosis is the final common pathway for chronic kidney disease and the best predictor for disease progression. Besides invasive biopsies, biomarkers for its detection are lacking. To address this, we used hyperpolarized 13 C-pyruvate MRI to detect the metabolic changes associated with fibrogenic activity of myofibroblasts. Hyperpolarized 13 C-pyruvate MRI was performed in 2 pig models of kidney fibrosis (unilateral ureteral obstruction and ischemia-reperfusion injury). The imaging data were correlated with histology, biochemical, and genetic measures of metabolism and fibrosis. The porcine experiments were supplemented with cell-line experiments to inform the origins of metabolic changes in fibrogenesis. Lastly, healthy and fibrotic human kidneys were analyzed for the metabolic alterations accessible with hyperpolarized 13 C-pyruvate MRI. In the 2 large animal models of kidney fibrosis, metabolic imaging revealed alterations in amino acid metabolism and glycolysis. Conversion from hyperpolarized 13 C-pyruvate to 13 C-alanine decreased, whereas conversion to 13 C-lactate increased. These changes were shown to reflect profibrotic activity in cultured epithelial cells, macrophages, and fibroblasts, which are important precursors of myofibroblasts. Importantly, metabolic MRI using hyperpolarized 13 C-pyruvate was able to detect these changes earlier than fibrosis-sensitive structural imaging. Lastly, we found that the same metabolic profile is present in fibrotic tissue from human kidneys. This affirms the translational potential of metabolic MRI as an early indicator of fibrogenesis associated metabolism. Our findings demonstrate the promise of hyperpolarized 13 C-pyruvate MRI for noninvasive detection of fibrosis development, which could enable earlier diagnosis and intervention for patients at risk of kidney fibrosis.

Influence of sodium/glucose cotransporter-2 inhibitors on the incidence of acute kidney injury: a meta-analysis.

Sodium/glucose cotransporter-2 inhibitors (SGLT2i) are associated with cardiovascular benefits. The aim of this systematic review and meta-analysis is to summarize the influence of SGLT2i on the incidence of acute kidney injury (AKI), and to ascertain whether it is affected by confounding variables such as age, baseline renal function and concurrent use of renin-angiotensin-aldosterone system inhibitors (RAASi) or mineralocorticoid receptor antagonists (MRA). PubMed, Embase, and Cochrane Library databases were searched for randomized controlled trials comparing the influence of SGLT2i versus placebo/blank treatment on AKI in the adult population. A fixed-effect model was used if the heterogeneity was not significant; otherwise, a randomized-effect model was used. Eighteen studies comprising 98,989 patients were included. Compared with placebo/blank treatment, treatment with SGLT2i significantly reduced the risk of AKI (risk ratio [RR]: 0.78, 95% confidence interval [CI]: 0.71 to 0.84, p < 0.001; I 2 = 0%). Subgroup analysis suggested consistent results in patients with diabetes, chronic kidney disease, and heart failure (for subgroup difference, p = 0.32). Finally, univariate meta-regression suggested that the influence of SGLT2i on the risk of AKI was not significantly modified by variables such as age (coefficient: 0.011, p = 0.39), baseline estimated glomerular filtration rate (coefficient: -0.0042, p = 0.13) or concomitant use of RAASi (coefficient: 0.0041, p = 0.49) or MRA (coefficient: -0.0020, p = 0.34). SGLT2i may be effective in reducing the risk of AKI, and the effect might not be modified by age, baseline renal function and concurrent use of RAASi or MRA.

Exploiting multivariate network meta-analysis: A calibrated Bayesian composite likelihood inference.

Multivariate network meta-analysis has emerged as a powerful tool in evidence synthesis by incorporating multiple outcomes and treatments. Despite its advantages, this method comes with methodological challenges, such as the issue of unreported within-study correlations among treatments and outcomes, which potentially lead to misleading conclusions. In this paper, we proposed a calibrated Bayesian composite likelihood approach to overcome this limitation. The proposed method eliminated the need to specify a full likelihood function while allowing for the unavailability of within-study correlations among treatments and outcomes. Additionally, we developed a hybrid Gibbs sampler algorithm along with the Open-Faced Sandwich post-sampling adjustment to enable robust posterior inference. Through comprehensive simulation studies, we demonstrated that the proposed approach yielded unbiased estimates while maintaining coverage probabilities close to the nominal level. Furthermore, we implemented the proposed method on two real-world network meta-analysis datasets; one comparing treatment procedures for the root coverage and another comparing treatments for anaemia in chronic kidney disease patients.

Sex differences in the association of long-term exposure to heat stress on kidney function in a large Taiwanese population study.

The incidence and prevalence of dialysis in Taiwan are high compared to other regions. Consequently, mitigating chronic kidney disease (CKD) and the worsening of kidney function have emerged as critical healthcare priorities in Taiwan. Heat stress is known to be a significant risk factor for CKD and kidney function impairment. However, differences in the impact of heat stress between males and females remains unexplored. We conducted this retrospective cross-sectional analysis using data from the Taiwan Biobank (TWB), incorporating records of the wet bulb globe temperature (WBGT) during midday (11 AM-2 PM) and working hours (8 AM-5 PM) periods based on the participants' residential address. Average 1-, 3-, and 5-year WBGT values prior to the survey year were calculated and analyzed using a geospatial artificial intelligence-based ensemble mixed spatial model, covering the period from 2010 to 2020. A total of 114,483 participants from the TWB were included in this study, of whom 35.9% were male and 1053 had impaired kidney function (defined as estimated glomerular filtration rate < 60ml/min/1.73m2). Multivariable analysis revealed that in the male participants, during the midday period, the 1-, 3-, and 5-year average WBGT values per 1℃ increase were significantly positively associated with eGFR < 60ml/min/1.73m2 (odds ratio [OR], 1.096, 95% confidence interval [CI] = 1.002-1.199, p = 0.044 for 1year; OR, 1.093, 95% CI = 1.000-1.196, p = 0.005 for 3years; OR, 1.094, 95% CI = 1.002-1.195, p = 0.045 for 5years). However, significant associations were not found for the working hours period. In the female participants, during the midday period, the 1-, 3-, and 5-year average WBGT values per 1℃ increase were significantly negatively associated with eGFR < 60ml/min/1.73m2 (OR, 0.872, 95% CI = 0.778-0.976, p = 0.018 for 1year; OR, 0.874, 95% CI = 0.780-0.978, p = 0.019 for 3years; OR, 0.875, 95% CI = 0.784-0.977, p = 0.018 for 5years). In addition, during the working hours period, the 1-, 3-, and 5-year average WBGT values per 1℃ increase were also significantly negatively associated with eGFR < 60ml/min/1.73m2 (OR, 0.856, 95% CI = 0.774-0.946, p = 0.002 for 1year; OR, 0.856, 95% CI = 0.774-0.948, p = 0.003 for 3years; OR, 0.853, 95% CI = 0.772-0.943, p = 0.002 for 5years). In conclusion, our results revealed that increased WBGT was associated with impaired kidney function in males, whereas increased WBGT was associated with a protective effect against impaired kidney function in females. Further studies are needed to elucidate the exact mechanisms underlying these sex-specific differences.

Risk factors for progression to chronic kidney disease in patients with cardiac valve replacement surgery-associated acute kidney injury

Objective: To explore the risk factors for progression to chronic kidney disease (CKD) in patients with cardiac valve replacement surgery-associated acute kidney injury (AKI). Methods: A retrospective, nested case-control study was conducted at Fuwai Central China Cardiovascular Hospital. The study subjects were patients who underwent cardiac valve replacement surgery from January 1, 2018 to December 31, 2020, with a baseline estimated glomerular filtration rate (eGFR)>60 ml·min-1·(1.73 m2)-1 and postoperative complication of AKI. The patients were followed up for 90 days after discharge from hospital. The endpoint event was defined as progression to CKD 90 days after the occurrence of cardiac valve replacement surgery-associated AKI. The patients were divided into CKD group and non-CKD group based on whether they experienced endpoint event. The baseline clinical data were compared between the two groups. The measurement data with non-normal distribution was represented as M (Q1,Q3). Logistic regression model was used to analyze the risk factors of endpoint event. The receiver-operating characteristic (ROC) curve was drawn to evaluate the performance for predicting CKD in cardiac valve replacement surgery-associated AKI patients. Results: A total of 149 cardiac valve replacement surgery-associated AKI patients (86 males and 63 females) were included in the study, aged (59.0±10.2) years. There were 27 patients (18.1%) who progressed to new-onset CKD 90 days after the occurrence of cardiac valve replacement surgery-associated AKI. Compared with non-CKD group, patients in CKD group had older age [66 (58, 70) vs 59 (53, 64) years], lower baseline eGFR [76.3 (65.8, 98.5) vs 92.7 (78.5, 101.6) ml·min-1·(1.73 m2)-1], higher proportion of preoperative hypertension [51.9% (14/27) vs 27.9% (34/122)] and serum creatinine at discharge [136 (101, 165) vs 86 (65, 104) μmol/L], and the differences were statistically significant (all P<0.05). The multivariate logistic regression analysis results revealed that older age (OR=1.063, 95%CI: 1.001-1.129, P=0.047), preoperative hypertension (OR=3.070, 95%CI: 1.105-8.532, P=0.031) and higher serum creatinine at discharge (OR=1.026, 95%CI:1.013-1.038, P<0.001) were risk factors for progression to CKD in patients with cardiac valve replacement surgery-associated AKI. The clinical risk model including age, preoperative hypertension, preoperative baseline eGFR, and serum creatinine at discharge produced a moderate performance for predicting progression to CKD in patients with cardiac valve replacement surgery-associated AKI [the area under the curve (AUC)=0.865, 95%CI: 0.790-0.940, P<0.001]. Conclusion: Older age, preoperative hypertension and higher serum creatinine at discharge are risk factors for progression to CKD in patients with cardiac valve replacement surgery-associated AKI.

Results of Chemical and Pharmacological Studies of the Mongolian Traditional Prescription "Arur-10"

This study examines ARUR-10, the herbal prescription commonly utilized in Traditional Mongolian Medicine practices for the treatment of kidney disease and the improvement of physical strength. This investigation aims to establish a profile of the biologically active compounds, antioxidant activity, and the anti-inflammatory impact on the kidneys in the traditional ARUR-10 prescription. For this analysis, we used Thin-Layer Chromatography (TLC) to identify phenolic compounds in the traditional prescription. Quantification of these bioactive substances was determined by UV/Vis spectrophotometry. The traditional ARUR-10 prescription, or traditional drug, had a higher polyphenolic content of 12.9±0.361% (gallic acid equivalent) and a sum flavonoid content of 0.33±0.015% (Rutin equivalent). The antioxidant activity was measured using the inhibiting free radical’s DPPH method and evaluated using the IC50 value. The 100 μg/ml concentration inhibited free radicals by 68.47%, whereas 200 μg/ml inhibited them by 83.29%, with an IC50 of 92.4 μg/ml. This study concluded that the traditional ARUR-10 prescription contains many polyphenolic compounds and flavonoids and has antioxidant properties. ARUR-10 has a moderate level of toxicity and no signs of chronic toxicity have been detected. Urine excretion was 1.52 ± 1.23 times higher than in the distilled water group (0.97 ± 0.71). ARUR-10 at doses of 240 mg/kg (1.62±1.14) had a similar effectiveness to Hydrochlorothiazide (1.52±1.23). In the gentamicin-induced nephritis model, ARUR-10 reduced serum creatinine by 42.8%, uric acid by 14.9%, and urea by 32% at doses of 240 mg/kg, compared to the control group that produced the pathological model. It had a protective effect on the kidneys by preserving the tube structure; cell death and cell necrosis were not observed.