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Few reports have investigated the predictive value of urinary cadmium (UCd) and telomere length on renal function impairment. Therefore, we constructed nomogram models, using a cross-sectional survey to analyze the potential function of UCd and telomere length in renal function impairment risk. We randomly selected two community populations in Shanxi, China, and general information of the subjects was collected through face-to-face questionnaire surveys. Venous blood of subjects was collected to detect absolute telomere length (ATL) by real-time quantitative chain reaction (RT-PCR). Collecting urinary samples detected UCd and urinary N-acetyl-β-d-glucosaminidase (UNAG). Estimated glomerular filtration rate (eGFR) was obtained based on serum creatinine (SCr). Nomogram models on risk prediction analysis of renal function impairment was constructed. After adjusting for other confounding factors, UCd ( β  = 0.853, 95% confidence interval (CI): 0.739 ~ 0.986) and ATL ( β  = 1.803, 95%CI: 1.017 ~ 1.154) were independent risk influencing factors for increased UNAG levels, and the risk factors for eGFR reduction were UCd ( β  = 1.011, 95%CI: 1.187 ~ 1.471), age ( β  = 1.630, 95%CI: 1.303 ~ 2.038), and sex ( β  = 0.181, 95%CI: 0.105 ~ 0.310). Using UCd, ATL, sex, and age to construct the nomogram, and the C-statistics 0.584 (95%CI: 0.536 ~ 0.632) and 0.816 (95%CI: 0.781 ~ 0.851) were obtained by internal verification of the calibration curve, C-statistics revealed nomogram model validation was good and using decision curve analysis (DCA) confirmed a good predictive value of the nomogram models. In a nomogram model, ATL, UCd, sex, and age were detected as independent risk factors for renal function impairment, with UCd being the strongest predictor.

Background At present, the clinical methods for preventing and treating contrast-induced nephropathy (CIN) are limited, and statins can play a better role during this process. So, we aimed to assess the atorvastatin on renal function in nephropathy patients after percutaneous coronary intervention (PCI). Methods In this work, 100 elderly patients with coronary heart disease (CHD) were selected into an experimental group (Exp group, 50 cases, 40 mg/d po atorvastatin) and a control group (Ctrl group, 50 cases, 10 mg/d po atorvastatin). The renal function indicators, blood routine indicators, and the incidence of adverse reactions (ARs) were compared between patients in Exp and Ctrl groups. Results After surgery, the levels of serum creatinine (SCr), blood urea nitrogen (BUN), cystatin C (CysC), high-sensitivity C-reactive protein (hs-CRP), and interleukin (IL6) in patients in the Exp group were much lower, and the levels of estimated glomerular filtration rate (eGFR) and superoxide dismutase (SOD) were higher (all P  < 0.05). Meanwhile, the incidences of ARs during hospitalization between patients in the Exp and Ctrl groups were all 8%, showing no observable difference ( P  > 0.05). Compared with conventional doses of atorvastatin, high-dose atorvastatin can effectively prevent renal function damage in patients with CIN, decrease the inflammation and oxidative stress in patients, and will not increase the risk of ARs during hospitalization. Conclusion Taken together, high-dose atorvastatin can be applied in treating patients with CHD after PCI due to its excellent efficacy and high safety.

We investigate the relationship between the changes of serum 25-hydroxyvitamin D3 (25(OH)D3) and vasohibin-1 (VASH-1) and renal function injury in patients with type 2 diabetic nephropathy. In this study, 143 patients with diabetic nephropathy (DN) were selected as DN group, and 80 patients with type 2 diabetes mellitus were selected as T2DM group. The serum 25 (OH) D3, VASH-1, blood glucose index, inflammation index and renal function index were compared between the two groups. According to the urinary microalbumin/creatinine ratio (UACR), the DN group was divided into microalbuminuria group (UACR range≥30.0mg/g and <300.0mg/g) and macroalbuminuria group (UACR≥300.0mg/g) for stratified comparison. The correlation between 25-hydroxyvitamin D3, VASH-1 and inflammation index and renal function index was analyzed by simple linear correlation analysis. The level of 25 (OH) D3 in DN group was significantly lower than that in T2DM group (P<0.05). The levels of VASH-1, CysC, BUN, Scr, 24h urine protein, serum CRP, TGF-β1, TNF-α and IL-6 in DN group were higher than those in T2DM group (P<0.05). The level of 25 (OH) D3 in DN patients with massive proteinuria was significantly lower than that in DN patients with microalbuminuria. The level of VASH-1 in DN patients with massive proteinuria was higher than that in DN patients with microalbuminuria (P<0.05). There was a negative correlation between 25 (OH) D3 and CysC, BUN, Scr, 24h urine protein, CRP, TGF-β1, TNF-α, IL-6 in patients with DN (P<0.05). VASH-1 was positively correlated with Scr, 24h urinary protein, CRP, TGF-β1, TNF-α and IL-6 in patients with DN (P<0.05). The level of serum 25 (OH) D3 in DN patients was considerably decreased, and the level of VASH-1 was increased, which was related to the degree of renal function injury and inflammatory response.

Objectives: To investigate the effect of atorvastatin on inflammatory factors, hemorheology, and renal function damage in patients with diabetic nephropathy (DN). Methods: One hundred and six DN patients who were treated in our hospital between June 2018 and August 2019 were selected and randomly grouped into observation group and control group, 53 each group. Patients in the control group were given the conventional treatment; patients in the observation group were given atorvastatin treatment on the basis of the conventional treatment. They were treated for three months. The hemorheology indexes (whole blood viscosity, erythrocyte aggregation index, and fibrinogen (FIB)), renal function damage indexes (macrophage migration inhibitory factor (MIF), vascular cell adhesion molecule (VCAM)-1, Secreted frizzled-related protein-5 (SFRP5), and mAIb/Cr) and inflammatory factor related indexes (C-reactive protein (CRP), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α)) were compared between the two groups before and after three months of treatment. Results: After three months of treatment, the hemorheology indexes, renal function damage indexes, and inflammatory factors related indexes in the two groups changed. Compared with the control group, the whole blood viscosity, erythrocyte aggregation index, FIB, MIF, VACM-1, mAIb/Cr, CRP, IL-1, and TNF-α levels in the observation group significantly decreased, while the levels of SERP-5 significantly increased; the differences were statistically significant (P<0.05). Conclusion: Atorvastatin can effectively alleviate the renal function damage in patients with DN, reduce the level of serum inflammatory factors, and improve hemorheology, which has a good clinical application value for DN patients. doi: https://doi.org/10.12669/pjms.37.5.4045 How to cite this:Li R, Shi T, Xing E, Qu H. Atorvastatin calcium tablets on inflammatory factors, hemorheology and renal function damage indexes in patients with diabetic nephropathy. Pak J Med Sci. 2021;37(5):1392-1396. doi: https://doi.org/10.12669/pjms.37.5.4045 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background Xanthii Fructus was used in the treatment of rhinitis and related nasal disease. It is the most commonly used chemically active component in compounds formulated for the treatment of rhinitis. However, poisoning, resulting in serious consequences, can easily occur owing to cocklebur overdose, improper processing, or usage without processing. Case presentation We reported on a 55-year-old man who experienced allergic rhinitis for 2.5 years. He ingested unprocessed Xanthii Fructus for 2 months as treatment. However, he developed anorexia; nausea; abdominal pain; general weakness; hiccups; oliguria and anuria; significantly elevated serum alanine aminotransferase, aspartate aminotransferase, and creatinine levels; and abnormalities in blood coagulation series. Nutritional support; daily drugs for liver protection, gastric protection, inflammation reduction; fresh plasma; and cryoprecipitate infusion were administered. Continuous venovenous hemodialysis (Prismaflex ST100) was also administered. However, the patient’s multiple organ failure gradually worsened, ultimately leading to death. Conclusion Xanthii Fructus poisoning affects multiple systems, and its clinical manifestations are complex. Therefore, it is easily misdiagnosed and missed. Along with careful inquiry of medical and medication history, early diagnosis and intervention are vital for a successful treatment. It is also important to educate people and create awareness about this poisoning. Therefore, this intractable case has great clinical significance.

Alcohol use disorder (AUD) is a spectrum of high risk behaviors including alcohol abuse and dependence. Chronic kidney disease (CKD) is progressive loss of renal function for more or equal to 3 months or presence of any irreversible kidney damage. Common risk factors of CKD have been identified, but the impact of alcohol consumption on kidney function is controversial. The study aims to investigate the relationship between alcohol use disorder and CKD on a national scale. This retrospective cohort study was conducted using Taiwan's National Health Insurance research database. Patients aged 20 years or older, without CKD and with the diagnosis of AUD (ICD-9-CM codes 303.X; 305.0, V113) from years 2000 to 2013 were enrolled. Control cohort was selected to match the demographics of the target population. Patients were followed until the end of 2013 or earlier if they developed CKD, died, or lost follow up. Baseline characteristics and comorbidities were identified for risk stratification. We identified 11639 patients in the AUD cohort and 46556 patients in the control cohort. Compared to patients in the control cohort, those in the AUD group were more likely to have multiple comorbidities (p < 0.001 for all comorbidities). After adjustment of age, gender, baseline comorbidities, and nonsteroidal anti-inflammatory drug use, the diagnosis of AUD was associated with an increased risk of CKD development (aHR = 1.62, 95% CI, 1.46-1.81). During the mean follow up periods of 6.47 (standard deviation (SD) = 3.80) years for the AUD cohort and 7.23 (SD = 3.75) years for the control cohort, the overall incidence density of CKD was significantly higher in patients with AUD than those in the control cohort (3.48 vs 6.51 per 1000 person-years, aHR = 1.68, 95% CI, 1.50-1.87). Kaplan-Meier analysis showed that the AUD cohort had a higher cumulative incidence of CKD than the control cohort (log-rank test, p value < 0.001). Patients with AUD had higher risks of CKD in all the stratified groups, except for the subgroup with age over 65 years old. Our study suggested that AUD was associated with an increased incidence of newly diagnosed CKD by nearly two folds. Young age, in particular, had a higher association between AUD and CKD. Considering the preventable nature of AUD, establishing effective health policies is imperative to reduce high-risk alcohol behaviors and thereby prevent alcohol-related kidney disease. Further prospective studies are warranted to further elucidate the causation of AUD on kidney function.

Probiotics are well-known therapeutic agents for managing constipation and have been used to improve chronic kidney disease (CKD) progression. However, heat-killed probiotics on CKD remain inadequately explored. This study aimed to evaluate the probiotic potential of lactic acid bacteria derived from natural sources and to investigate the effects of both live and heat-killed Leuconostoc mesenteroides (Ln.m) on renal and gastrointestinal functions in CKD mice. Ln.m was selected from acid and bile salt intolerance tests, non-hemolytic activity, and antibiotic sensitivity. CKD mice demonstrated significantly elevated blood urea nitrogen (BUN) and creatinine levels compared to control mice ( p  < 0.001 and p  < 0.01). Treatment with live and heat-killed Ln.m significantly reduced BUN and creatinine levels in CKD mice ( p < 0.01 and p < 0.05). Additionally, kidney damage observed in CKD mice compared to control mice, including glomerular necrosis, tubular dilatation, inflammation, and fibrosis, was significantly alleviated following live and heat-killed Ln.m treatments. CKD-induced gastrointestinal dysfunction was characterized by an imbalance in Firmicutes/Bacteroidota populations, increased colonic uremic toxin ( p  < 0.01), reduced fecal short-chain fatty acids (SCFAs) ( p < 0.05), and constipation. Treatment with live and heat-killed Ln.m restored gut microbiota, decreased uremic toxin ( p  < 0.001), increased SCFAs ( p  < 0.05), and alleviated constipation. In summary, both live and heat-killed Ln.m effectively alleviated gastrointestinal dysfunction and renal damage in CKD mice, primarily through modulation of the intestinal environment. These findings highlight the therapeutic potential of live and heat-killed Ln.m as the gastrointestinal dysfunction treatment in CKD.

To explore the mechanism by which Astragalus membranaceus and Salvia miltiorrhiza (AS) regulates the “metabolic- transcriptional” co-expression network to improve Hypertensive renal damage (HRD). Spontaneously hypertensive rats (SHRs) were used to establish the model of HRD. The structure and function of the kidney were observed following AS intervention. We identified various metabolites in the kidneys using UHPLC-MS/MS and observed renal mRNA expression through RNA sequencing. The “metabolism-transcription” coexpression network was further constructed, and the target metabolites and target genes of AS were ultimately screened and validated. AS significantly reduced blood pressure, improved renal function and alleviated renal pathological damage in SHRs. A total of 596 target mRNAs of AS were identified. Of note, 254 of these mRNAs were expressed in 25 pathways that were closely related to metabolic processes. Additionally, the target metabolites of AS were determined, predominantly enriched in 8 pathways, including linoleic acid metabolism, cholesterol metabolism, choline metabolism in cancer, and the synthesis and degradation of ketone bodies, etc. In addition, the target metabolites and target mRNAs of AS were co-enriched in 3 specific pathways of linoleic acid metabolism, cholesterol metabolism, taurine and hypotaurine metabolism, involving 7 different metabolites and 18 differentially expressed (DE) mRNAs. The 7 metabolites exhibited high AUC prediction values, and the verification and sequencing results of the 4 genes were basically consistent. Conclusion The mechanisms by which AS improves HRD may be closely related to the regulation of linoleic acid metabolism, cholesterol metabolism and taurine and hypotaurine metabolism pathways as well as the relevant target genes.

The kidney has large regenerative capacity, but this is compromised when kidney damage is excessive and renal tubular epithelial cells (TECs) undergo SNAI1-driven growth arrest. Here we investigate the role of IL11 in TECs, kidney injury and renal repair. IL11 stimulation of TECs induces ERK- and p90RSK-mediated GSK3β inactivation, SNAI1 upregulation and pro-inflammatory gene expression. Mice with acute kidney injury upregulate IL11 in TECs leading to SNAI1 expression and kidney dysfunction, which is not seen in Il11 deleted mice or in mice administered a neutralizing IL11 antibody in either preemptive or treatment modes. In acute kidney injury, anti-TGFβ reduces renal fibrosis but exacerbates inflammation and tubule damage whereas anti-IL11 reduces all pathologies. Mice with TEC-specific deletion of Il11ra1 have reduced pathogenic signaling and are protected from renal injury-induced inflammation, fibrosis, and failure. In a model of chronic kidney disease, anti-IL11 therapy promotes TEC proliferation and parenchymal regeneration, reverses fibroinflammation and restores renal mass and function. These data highlight IL11-induced mesenchymal transition of injured TECs as an important renal pathology and suggest IL11 as a therapeutic target for restoring stalled endogenous regeneration in the diseased kidney. Repair processes in kidney are impaired in severe disease. Here, the authors show that in kidney failure, genetic or pharmacologic inhibition of IL11 releases the brake on regeneration, reverses tissue damage and restores kidney function.

Friedhelm Hildebrandt, Agata Smogorzewska and colleagues show that mutations in the DNA repair gene FAN1 cause karyomegalic interstitial nephritis. These findings implicate deficient DNA damage response signaling in the pathophysiology of renal fibrosis. Chronic kidney disease (CKD) represents a major health burden 1 . Its central feature of renal fibrosis is not well understood. By exome sequencing, we identified mutations in FAN1 as a cause of karyomegalic interstitial nephritis (KIN), a disorder that serves as a model for renal fibrosis. Renal histology in KIN is indistinguishable from that of nephronophthisis, except for the presence of karyomegaly 2 . The FAN1 protein has nuclease activity and acts in DNA interstrand cross-link (ICL) repair within the Fanconi anemia DNA damage response (DDR) pathway 3 , 4 , 5 , 6 . We show that cells from individuals with FAN1 mutations have sensitivity to the ICL-inducing agent mitomycin C but do not exhibit chromosome breakage or cell cycle arrest after diepoxybutane treatment, unlike cells from individuals with Fanconi anemia. We complemented ICL sensitivity with wild-type FAN1 but not with cDNA having mutations found in individuals with KIN. Depletion of fan1 in zebrafish caused increased DDR, apoptosis and kidney cysts. Our findings implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms contributing to renal fibrosis and CKD.