Renal fibrosis is a hallmark of progressive chronic kidney disease (CKD), with emerging evidence linking gut microbiota dysbiosis to disease progression. Myeloid-derived suppressor cells (MDSCs) have demonstrated renoprotective effects, yet the impact of fecal microbiota transplantation (FMT) on MDSC-mediated modulation of renal fibrosis remains unclear.

C57BL/6J mice underwent unilateral ureteral obstruction (UUO) to induce renal fibrosis, followed by FMT administration via gavage. Flow cytometry was used to quantify granulocytic (G-MDSCs) and monocytic (M-MDSCs) MDSC populations in peripheral blood, kidney, and spleen. To elucidate the role of MDSCs in FMT-mediated effects, MDSCs were depleted or adoptively transferred in vivo. Renal fibrosis severity and inflammatory cytokine expression were subsequently analyzed.

FMT altered MDSC distribution, increasing M-MDSC accumulation in the blood and kidney. This was associated with downregulation of proinflammatory cytokines and attenuation of renal fibrosis. Adoptive MDSC transfer similarly produced anti-inflammatory and antifibrotic effects, reinforcing their therapeutic role in FMT-mediated renal protection.

FMT enhances M-MDSC-mediated immunomodulation, reducing inflammation and renal fibrosis in UUO-induced CKD. These findings suggest a potential therapeutic strategy targeting the gut-kidney axis in CKD management.

The association between serum soluble Klotho (sKlotho) and chronic kidney disease (CKD) in individuals with diabetes mellitus (DM) remains controversial, and the influence of hypertension on this association is inconclusive.

This study aims to investigate the joint association of sKlotho and hypertension with CKD prevalence in adults with DM.

This cross-sectional study included 3,302 adults with DM from the National Health and Nutrition Examination Survey (2007-2016). Multivariate logistic regression analysis stratified by hypertension was used to assess the association between sKlotho and CKD prevalence. Moreover, the interaction between hypertension and sKlotho on CKD was evaluated.

Among individuals with DM, a significant association between sKlotho levels and CKD prevalence was observed only in those with hypertension. CKD prevalence was significantly lower in individuals with high sKlotho (≥ 806 pg/mL) than in those with low sKlotho (< 806 pg/mL) [adjusted OR = 0.54 (95% CI: 0.41-0.72); p < 0.001]. Moreover, a significant interaction between hypertension and sKlotho on CKD prevalence was observed among adults with DM [Multiplicative scale: OR = 0.65 (95% CI: 0.42-0.99); RERI = -0.80 (95% CI: -1.49 to -0.10); AP = -0.51 (95% CI: -0.90 to -0.12); SI = 0.44 (95% CI: 0.30-0.66)].

Among DM adults, hypertension modified the association between sKlotho levels and CKD prevalence. Both additive and multiplicative interactions were observed between hypertension and sKlotho levels on CKD. The causalities between hypertension, Klotho, and CKD in diabetic patients need further exploration, and underlying mechanisms warrants elucidation.

While there are numerous benefits to tea consumption, its long-term impact on patients with chronic kidney disease (CKD) remains unclear.

Our analysis included 17,575 individuals with CKD from an initial 45,019 participants in the National Health and Nutrition Examination Survey (NHANES) (1999-2018). Individuals with extreme dietary habits, pregnancy, or non-CKD conditions were excluded. Key cohort demographics revealed a mean age of 62.3 years, with 52.1% female participants, and 57.3% identified as non-Hispanic White. A total of 5,835 deaths were recorded during follow-up, including 1,823 cardiovascular-related deaths. Cox and restricted cubic spline regression was used to examine the linear or nonlinear association of tea consumption with mortality. The substitution analysis explored the effects of replacing a specific type of tea with another type of tea. Subgroup analysis stratified by sex, age, body mass index (BMI), diabetes, cancer, cardiovascular disease (CVD), and urinary albumin. Sensitivity analysis was performed to ensure the reliability of our findings.

After adjusting for age, sex, race, education level, marital, annual household income, energy intake, total water intake, protein intake, carbohydrate intake, dietary fiber, sugar beverages, milk whole, total monounsaturated fatty acids, total polyunsaturated fatty acids, total saturated fatty acids, smoking, metabolic equivalent of task for physical activity level (MET-PA), BMI, diabetes, hypertension, urinary albumin, estimated glomerular filtration rate (eGFR), CVD, cancer, serum sodium, serum potassium, and serum phosphorus, setting the individuals without tea consumption record as reference. Consuming up to 4 cups of tea per day was significantly associated with lower all-cause mortality compared with that never drinking tea, among CKD patients at 1-2 stages [Hazard Ratio (HR) = 0.89; 95% Confidence Interval (CI) = 0.79, 0.99; p = 0.04], while the association between tea consumption and CVD mortality didn't reach statistical significance. Dose-response effect was observed, showing that consuming up to three to five cups of tea per day was associated with mitigated risks of all-cause mortality, particularly in early CKD stages (non-linear p > 0.05). A 1 cup per day higher intake of oxidized tea was associated with a 10% lower risk of all-cause mortality in CKD stage 1-2 [HR = 0.90; 95%CI = 0.82, 0.99; p = 0.03]. Replacing 1 cup of green tea with 1 cup of oxidized tea per day was associated with an 8% and 11% lower risk of all-cause mortality [HR = 0.92; 95%CI = 0.86, 0.98; p = 0.01] and CVD mortality [HR = 0.89; 95%CI = 0.80, 1.00; p < 0.05], respectively, in individuals with CKD stages 1-2.

Tea consumption showed protective effects on all-cause mortality in CKD population, with potential benefits observed in terms of both the cups quantity and types of tea consumed. These findings appeared to be more prominent among early stages CKD population.

To assess the link between persistent lipoprotein(a) [Lp(a)] exposure levels and clinical outcomes in patients with acute myocardial infarction (AMI).

This longitudinal cohort study included 1131 AMI patients, categorizing persistent Lp(a) exposure based on measurements at admission and after 1 year. Patients were segmented into four groups using a 300 mg/L Lp(a) threshold: (1) persistent low Lp(a) (lowon admission - lowat 1 year); (2) fortified Lp(a) (lowon admission - highat 1 year); (3) attenuated Lp(a) (highon admission - lowat 1 year); and (4) persistent high Lp(a) (highon admission - highat 1 year). Multivariate Cox regression, subgroup analysis and sensitivity analysis assessed the association between Lp(a) trajectories and major adverse cardiovascular and cerebrovascular events (MACCE), cardiovascular death, non-fatal MI, non-fatal stroke, unplanned revascularization, and all-cause death.

Over a median 50-month follow-up, 343 (35.70%) patients encountered MACCE, and 210 (18.70%) died, including 126 (11.20%) from cardiovascular causes. The group with persistent high Lp(a) faced increased risk of MACCE (HRadjusted, 1.871; 95% CI: 1.474-2.374), non-fatal stroke (HRadjusted, 1.647; 95% CI: 1.031-2.632), unplanned revascularization (HRadjusted, 1.571; 95% CI: 1.008-2.449), and both all-cause (HRadjusted, 1.546; 95% CI: 1.134-2.108) and cardiovascular death (HRadjusted, 2.163; 95% CI: 1.405-3.331), compared to the persistent low Lp(a) group.

In AMI patients, sustained high Lp(a) levels were significantly associated with increased risk of MACCE, non-fatal stroke, unplanned revascularization, and both all-cause and cardiovascular death.

Ion channels, particularly those in the transient receptor potential (TRP) family, play key roles in cellular stress responses like inflammation and apoptosis, significantly impacting renal disease progression. Some channels such as TRPV1, TRPM2, TRPC6 impact renal pathology by mediating detrimental calcium influx, exacerbating oxidative stress, and promoting inflammatory pathways. Their activities are especially pronounced in conditions like ischemia and nephrotoxicity, common in acute kidney injury, and persist into chronic kidney injury, influencing fibrosis and nephron loss. Additionally, potassium and sodium channels like Kir4.1, KATP, and ENaC play critical roles in maintaining electrolyte balance and cellular energy under stress conditions. Further exploration of ion channel functionality and regulation is necessary to clarify their roles in renal disease. This review summarizes the involvement of ion channels in AKI and CKD and examines their potential clinical value in diagnosing and treating kidney disease.

A substantial body of evidence indicates a positive correlation between dyslipidemia and an elevated risk of chronic kidney disease, with renal interstitial fibrosis frequently serving as a common pathway in the advanced stages of chronic kidney disease progression. Hydrogen has anti-inflammatory and antioxidant properties, and magnesium hydride nanoparticle is a material with high hydrogen storage capacity. Magnesium hydride -fortified feed is capable of releasing hydrogen gas steadily and continuously within the digestive tract. A 12-week high-fat diet significantly elevated the serum urea and creatinine levels in mice. In contrast, dietary addition of magnesium hydride demonstrated a notable protective effect against pathological conditions. Additionally, magnesium hydride -fortified feed was found to reduce renal fibrosis and thereby improve renal function. In support of these findings, an in vitro study utilizing human kidney cortical proximal tubule epithelial cells (HK-2 cells) exposed to palmitic acid under conditions mimicking a high-fat diet confirmed the renoprotective effects of magnesium hydride. Furthermore, the primary target phosphatase and tensin homologue deleted on chromosome 10 and the molecular mechanisms underlying the effects of magnesium hydride, specifically its ability to inhibit the transforming growth factor-beta -Smad family member 2 and 3 (Smad2/3) axis through downregulating the expression of phosphatase and tensin homologue deleted on chromosome 10, were elucidated. Additionally, overexpression of Hes family BHLH transcription factor 1 can negate the beneficial effects of magnesium hydride, suggesting that Hes family BHLH transcription factor 1 may serve as an upstream regulatory target in the context of the effects of magnesium hydride. In conclusion, this study demonstrated that magnesium hydride functions as a safe and effective hydrogen source capable of inhibiting the activation of the transforming growth factor-beta/Smad2/3 and protein kinase B/mechanistic target of rapamycin pathways by increasing the expression of phosphatase and tensin homologue deleted on chromosome 10. This mechanism counteracts the progression of high-fat diet-induced chronic renal damage.

We aimed to investigate the association between objectively measured physical activity and the presence and development of albuminuria in individuals recently diagnosed with type 2 diabetes at baseline.

This study was based on data from The Danish Centre for Strategic Research in Type 2 diabetes cohort (N = 832). We assessed moderate to vigorous physical activity (MVPA) and sedentary time by 24-hour dual-monitor accelerometry at baseline and 4-years follow-up and investigated the association with albuminuria, defined as urine albumin/creatinine-ratio (UACR) ≥30 mg/g, measured from a urine sample. The odds ratio (OR) for the presence and development of albuminuria were investigated using multiple logistic regressions.

We found an inverse association between baseline MVPA and both presence (OR: 0.82; 95 % CI: 0.69-0.98) and incidence of albuminuria (OR: 0.74; 95 % CI: 0.59-0.94), independent of known confounding factors. However, sedentary time was not significantly associated with increased development of albuminuria. Moreover, neither decrease in MVPA (OR: 0.79; 95 % CI: 0.42-1.49) nor increase in sedentary time (OR: 1.03; 95 % CI: 0.98-1.09) were significantly associated with development of albuminuria from baseline to 4-years follow-up.

Our findings demonstrate an inverse association between baseline MVPA and development of albuminuria in individuals recently diagnosed with type 2 diabetes. An increase in MVPA from baseline to follow-up inferred 21 % lower incidence of albuminuria after 4-years follow-up, albeit insignificant, likely due to the relatively small sample size at follow-up and the lack of larger changes in physical activity.

NCT02015130.

Renal ischemia-reperfusion injury (RIRI) is a major contributor to acute kidney injury (AKI), associated with high mortality in intensive care units. Hydroxysafflower yellow A (HSYA), with known anti-inflammatory and antioxidant properties, may protect against AKI caused by RIRI.

This study investigates HSYA's mechanisms in AKI protection through transcriptome sequencing and functional validation.

Cell viability under OGD/R conditions was assessed using the lactate dehydrogenase (LDH) assay. The role of HSYA in CCR4-associated pathways was explored by transcriptome analysis, molecular docking, and rescue studies. A mouse RIRI model was established, and serum creatinine and blood urea nitrogen (BUN) were detected to evaluate the degree of renal injury.

HSYA enhanced the viability of HK-2 renal tubular epithelial cells and inhibited OGD/R-induced apoptosis. Transcriptome analysis revealed HSYA's regulatory effects on G protein-coupled receptor (GPCR) pathways, particularly via downregulation of CCR4. Molecular docking predicted a direct interaction between HSYA and CCR4, which was experimentally supported by reduced CCR4 expression. HSYA inhibited IP3R/PLCβ signaling through the p38/JNK pathway, maintained calcium homeostasis, and reduced apoptosis. In vivo, HSYA significantly decreased creatinine and BUN levels, alleviating renal injury; these effects were reversed by the CCR4 agonist CCL17.

HSYA mitigates renal injury by modulating CCR4-associated signaling pathways and stabilizing intracellular calcium levels. This study is the first to propose CCR4 as a direct molecular target of HSYA in the context of RIRI.

Targeting metabolic disorders has emerged as a promising therapeutic strategy in the treatment of chronic kidney disease (CKD). 18β-glycyrrhetinic acid (18β-GA) is known for its metabolic regulatory and antioxidant effects in various diseases. However, the precise effects and underlying mechanisms of 18β-GA on CKD remain unclear.

This study aims to evaluate the therapeutic efficacy of 18β-GA on CKD and to identify the molecular targets of 18β-GA with a particular emphasis on its role in metabolic regulation.

A high-fat diet-induced CKD model was established to investigate the influence of 18β-GA on lipid metabolic disorders, cellular senescence and fibrosis in the kidneys. Co-immunoprecipitation was performed to investigate the impact of 18β-GA on the interaction between transcription factor EB (TFEB) and sirtuin 1 (SIRT1). Additionally, network pharmacology and molecular docking analyses were conducted to identify the specific target proteins of 18β-GA.

18β-GA alleviated renal lipid accumulation, tubular cell senescence and renal interstitial fibrosis in CKD mice. Treatment with 18β-GA largely restored mitochondrial function and attenuated intracellular lipotoxicity and associated cellular senescence by promoting lipophagy in renal tubular cells. Mechanistically, 18β-GA acting as a partial antagonist of peroxisome proliferator-activated receptor gamma (PPARγ) enhanced lipophagy through SIRT1-mediated nuclear translocation of TFEB which induced the expression of microtubule-associated protein light chain 3 (LC3).

Our findings demonstrate that 18β-GA, functioning as a partial antagonist of PPARγ, counteracts CKD progression by activating the SIRT1-TFEB-LC3 signaling axis-mediated lipophagy and thus uncover a novel mechanism by which 18β-GA improves renal lipid metabolism disorders and exerts renoprotective effects. These results highlight the potential of 18β-GA as a promising therapeutic agent for the treatment and prevention of CKD.

Amomum kravanh Pierre ex Gagnep. (BDK) is a Zingiberaceae plant traditionally widely used as a sweet fragrance, and commonly also utilized in minority medicine for various kidney diseases, especially chronic kidney disease (CKD) in Tibetan and Mongolian medicine. However, the underlying mechanisms by which it confers renal protection remain to be fully clarified.

To investigate the renal protective mechanism of which BDK's essential oil exerts in rats with CKD induced by adenine and 5/6 nephrectomy.

Rat models of adenine and 5/6 nephrectomy chronic nephropathy were established, and the therapeutic effects were evaluated by detecting the blood biochemical levels and H&E-/Masson staining and fiber-related factors. Then, the chemical composition of BDK's essential oil and blood components were analyzed using GC-MS. The efficacy of eucalyptol was evaluated by adenine and 5/6 nephrectomy CKD model, with mechanistic studies conducted using RNA-seq, western blot, and metabolomic approaches.

The blood biochemical levels and histopathological analyses (H&E-/Masson's staining) revealed that the BDK's essential oil significantly enhanced renal function and ameliorated kidney tissue fibrosis. Furthermore, GC-MS analysis identified 33 components in the essential oil of BDK, with eucalyptol being the predominant chemical component at 74.07 %. Eucalyptol is capable of entering the bloodstream in its prototypical form. Then, the efficacy and mechanism of eucalyptol were confirmed by adenine/5/6 nephrectomy CKD models, and based on RNA-seq analysis, we found that eucalyptol could significantly improve kidney function and fibrosis of kidney tissues by blocking TGF-β/smad and NF-κB pathways and inhibit ferroptosis through the Nrf2/HO-1 signaling pathway.

Both BDK's essential oil and its main constituent, eucalyptol, exhibited protective effects against CKD. They both ameliorated oxidative stress, inflammation, and fibrosis in adenine/5/6 nephrectomy rats. Eucalyptol is implicated in ferroptosis and regulation of renal fibrosis via the Nrf2/HO-1 pathway.

Early identification and prevention of ventilator-associated pneumonia (VAP) in patients with mechanical ventilation (MV) through reliable prediction model undergoing a rigorous and standardized process is essential for clinical decision-making.

This study aims to externally validate the VAP prediction model previously developed by a tertiary hospital in Northwestern China, using data from different time periods or hospitals, and to develop a web-based model calculator for clinical application to evaluate the model's prediction performance and generalizability.

We prospectively collected MV patients data from the ICUs of two tertiary hospitals in Northwestern China for external validation of the model. Temporal and geographical validation were performed at the hospital where the model was developed and another hospital, respectively. The area under the receiver operating characteristic curve (AUC), Howsmer-Lemeshow test, calibration curve and decision curve analysis (DCA) were used to evaluate the model's discrimination, calibration and clinical applicability, respectively. A web-based model calculator was further developed and applied to MV patients in one of the hospitals to obtain the prediction probabilities of VAP risk. Model performance was evaluated using a confusion matrix and diagnostic tests.

The temporal and geographical validation cohorts included 416 and 410 patients, and the AUCs were 0.814 and 0.800, respectively. The Hosmer-Lemeshow tests (both P > 0.05) and calibration curves showed a relatively high consistency. The DCA revealed the model threshold probabilities in the temporal (2.0 % to 50.0 %) and geographical validation (5.0 % to 70.0 %). The web-based model calculator (https://vapnomogram.shinyapps.io/VAPDynNomapp/) was applied to 202 patients in clinical practice. The cut-off value of the prediction probability was 0.096, with an accuracy of 0.911, a sensitivity of 0.900, a specificity of 0.912, and a positive and negative predictive value of 0.529 and 0.988, respectively.

The VAP prediction model showed relatively stable and relaible clinical prediction performance and generalizability, with a clinical application and promotion value.

The population with cardiovascular-kidney-metabolic (CKM) syndrome has a higher risk of cardiovascular events. Chinese visceral adiposity index (CVAI), an index of both visceral obesity and surrogate insulin resistance, has been linked to cardiovascular events. However, the nature of this relationship remains unclear in individuals with CKM syndrome.

All data came from the China Health and Retirement Longitudinal Study (CHARLS). The association between CVAI and cardiovascular events risk was explored using Cox regression models, restricted cubic spline (RCS) curves, and multiple sensitivity analyses. To compare the predictive abilities of various indices, receiver operating characteristic (ROC) analyses were employed.

7744 participants were in final analysis. During 9 year follow-up, 1679 cases of cardiovascular disease (CVD), 1,255 cases of heart disease, and 604 cases of stroke were recorded. Cox regression analyses revealed that per-SD (standard deviation) increase in CVAI, the risk of CVD, heart disease, and stroke increased by 22% (95% CI 1.13-1.32), 22% (95% CI 1.13-1.32), and 32% (95% CI 1.19-1.47). In participants at CKM stage 3 with CVD, a J-shaped curve was observed in the RCS analyses (P non-linearity = 0.036). Subgroup analysis revealed an interaction between age and each 10-unit increase in CVAI in CVD (P interaction = 0.0173) and stroke risk (P interaction = 0.028). The AUC (area under curve) value for CVAI was highest compared to other indicators (all DeLong Test P values < 0.05).

This research demonstrates a higher CVAI was linked to increased cardiovascular risk in individuals with CKM syndrome stage 0-3. Monitoring CVAI can help identify high-risk individuals early and improve the effectiveness of disease management.

Understanding the impact of psychosocial factors and pain management on cardiovascular disease (CVD) risk and life expectancy in patients with chronic kidney disease (CKD) is critical for developing targeted interventions. We aimed to assess the associations of social isolation, loneliness, and pain risk with incident CVD in patients with CKD and to evaluate the impact of these factors on the life expectancy of CKD patients.

This prospective cohort study comprised 34,381 CKD patients from the UK Biobank. Loneliness and social isolation were measured using two-item and three-item scales, respectively. The risk of pain spreading score (ROPS) was determined by summing responses to six items based on mood, trauma, sleep, neuroticism, and anthropometric measurement. The Cox proportional hazards regression model was used to evaluate CVD risk by estimating hazard ratios (HRs) and 95 % confidence intervals (CIs).

Higher levels of loneliness (HR2 vs. 0 = 1.32, 95 % CI = 1.22-1.44), social isolation (HR2+ vs. 0 = 1.11, 95 % CI = 1.04-1.19), and higher ROPS (HRhigh vs low risk = 1.34, 95 % CI = 1.28-1.40) were associated with a higher risk of CVD in CKD patients (P-trend<0.001 for all). Significant interactions between loneliness and ROPS were observed, suggesting a synergistic effect on CVD risk. Moreover, loneliness, social isolation, and elevated ROPS were significantly associated with reduced life expectancy among patients with CKD.

The study findings suggest that addressing social isolation and loneliness, along with effective pain management, is crucial for reducing the risk of CVD and improving life expectancy in patients with CKD.

Chronic kidney disease (CKD) and its progression to end-stage renal disease (ESRD) represent significant global health challenges, contributing to increased morbidity and mortality. Despite the potential diagnostic value of ATR-FTIR spectroscopic analysis of serum in CKD, research in this area remains limited. This study addressed this gap by aiming to explore the spectral profiles of sera obtained from hemodialysis patients and healthy controls. We investigated serum spectral profiles from 21 hemodialysis patients and 21 age/sex-matched controls using ATR-FTIR spectroscopy in the mid-infrared region (4000-400 cm-1). Spectroscopic analysis revealed elevated spectral intensity in ESRD samples compared to controls. Principal Component Analysis (PCA) successfully distinguished ESRD from control samples across multiple spectral regions (1480-900 cm-1, 1800-900 cm-1, and combined 3000-2800/1800-900 cm-1). Partial Least Squares Discriminant Analysis (PLS-DA) demonstrated enhanced group separation, with the optimized PLS model achieving perfect classification metrics (100% accuracy, sensitivity, and specificity). The combined spectral region models exhibited superior diagnostic performance compared to other regions. The analysis identified key molecular biomarkers associated with ESRD, including alterations in lipids, protein structures (represented by amide I and II bands), carbohydrates, nucleic acids, and immunoglobulins, which correlate with known biochemical changes in CKD pathophysiology. These findings demonstrate that ATR-FTIR spectroscopy with multivariate analysis is a rapid, cost-effective screening tool for CKD. The identified spectral biomarkers provide insights into disease-related biochemical alterations, adding valuable data to the research in this field.

The American Heart Association recently released an updated algorithm for evaluating cardiovascular health (CVH), Life's Essential 8 (LE8). However, few studies have examined the association of LE8 with risk of cardiovascular disease (CVD) and mortality among individuals with chronic kidney disease (CKD). We investigated whether LE8 was associated with subsequent risk of CVD and mortality in the Chinese population of adults with CKD.

This prospective study included 18,716 adults (55.4 ± 14.0 years, 77.9 % men) with CKD free of CVD at baseline from the Kailuan study. A LE8 score (range 0-100 points) was constructed based on diet, physical activity, smoking, sleep duration, body mass index, blood lipids, blood glucose, and blood pressure. Incident CVD and mortality were identified by electronic health records and registers. Multivariable Cox regression models were used to compute hazard ratios (HRs) and 95 % confidence intervals (CIs).

During a median follow-up of 14.0 and 14.4 years, 2117 cases of CVD and 4190 deaths were documented. After adjusting for potential confounders, comparing the high LE8 score (80-100 points) to the low LE8 score (<50 points), the multivariable HRs (95 % CIs) were 0.28 (0.20, 0.40) for CVD, 0.14 (0.06, 0.34) for myocardial infarction, 0.35 (0.25, 0.50) for total stroke, and 0.68 (0.56, 0.83) for all-cause mortality, respectively.

Among patients with CKD, greater adherence to CVH, as defined by LE8, was significantly associated with a lower risk of CVD and all-cause mortality.

Cardiovascular disease is one of the leading causes of death worldwide. Even while receiving adequate pharmacological treatment for their hypertension, people are nonetheless at greater risk for cardiovascular disease. There is growing evidence that the gut microbiota may have major positive and negative effects on blood pressure and illnesses related with it as more study into this topic is conducted. Trimethylamine n-oxide (TMAO) and short-chain fatty acids (SCFA) are two major by-products of the gut microbiota. TMAO is involved in the formation of other coronary artery diseases, including atherosclerosis and hypertension, while SCFAs play an important role in controlling blood pressure. Numerous investigations have confirmed the established link between dietary salt intake and hypertension. Reducing sodium in the diet is linked to lower rates of cardiovascular disease morbidity and mortality as well as lower rates of blood pressure and hypertension. In both human and animal research, high salt diets increase local and systemic tissue inflammation and compromise gut architecture. Given that the gut microbiota constantly interacts with the immune system and is required for the correct maturation of immune cells, it is scientifically conceivable that it mediates the inflammatory response. This review highlights the therapeutic possibilities for focusing on intestinal microbiomes as well as the potential functions of the gut microbiota and its metabolites in the development of hypertension.

Negatively charged polystyrene microspheres (NCMs) have been demonstrated as a novel and effective therapy for managing hard-to-heal diabetic foot ulcers (DFUs). However, one limitation of this therapy is that the protocol is based on daily application, which sometimes does not fit local protocols of wound care. Thus, we aimed to analyze the safety and efficacy of a new dose regimen. We conducted a randomized blinded controlled trial in a specialized diabetic foot unit between May 2019 and February 2021 with a total of 30 patients who had neuropathic or neuroischemic DFUs that had not responded after four weeks of standard treatment. Patients were randomized consecutively into a group that received daily application (control) or one that received applications three times per week (experimental). The clinical outcomes were evaluated using the Wollina score and wound-area reduction (WAR) weekly during a treatment period of 28 days. The histological outcomes were assessed using a soft-tissue punch biopsy (3 mm) at 0, 14, and 28 days to evaluate cellular proliferation. The Wollina scores were higher at the end of treatment by week 4 in both groups, but the differences were not significant between groups. The averages were 6 (5, 7) points in Experimental group (EG) and 6 (6,7) points in Control group (CG) (p = 0.848). Wound area reduction at day 28 was 53.57 [37.43, 79.16] % in the CG and 79.37 [42.74, 93.57] % in the EG, without differences among groups (p = 0.305). Cellular proliferation was similar in both groups at day 28. Application three times per week showed similar clinical and histological outcomes to those of daily application, both dose regimens demonstrated significant improvement of granulation tissue formation and WAR during the treatment.

Chronic kidney disease (CKD) is a chronic health problem whose prevalence is increasing. Nutrition and nutrition-related factors, one of the modifiable risk factors for CKD, are of primary importance. The key to planning optimal nutritional therapy is accurately determining energy requirements and total energy expenditure. Many health problems can accompany CKD, such as protein-energy malnutrition, sarcopenia, etc, and increase the mortality rate. This study aims to present the specific factors affecting energy expenditure specific to CKD in line with the current literature, to discuss the methods used to determine energy expenditure, and to examine these methods according to groups receiving and not receiving renal replacement therapy (hemodialysis, peritoneal dialysis, and renal transplantation).

Sarcopenia, characterized by loss of muscle mass and strength, has been linked to various health outcomes, including chronic kidney disease (CKD). This study aims to investigate the association of sarcopenia index, based on serum creatinine and cystatin C levels, with incident CKD in middle-aged and older adults.

This study extracted data from a nation cohort, including age ≥45 years adults without CKD at baseline. Sarcopenia index was calculated based on serum creatinine and cystatin C levels, and incident CKD was assessed through follow-up surveys. Cox proportional hazards regression models were used to analyze the association between sarcopenia index and incident CKD, adjusting for potential confounders, with hazard ratio (HR) with 95 % confidence interval (95 % CI) reported.

A total of 8618 participants were included in the analysis. The median age was 61.0 years, and 44.7 % were male. During a mean follow-up period of 5.0 years, 514 cases of incident CKD were identified. After adjusting for covariates, compared with participants in the lowest tertile, the corresponding CKD HRs (95 % CIs) for participants in the medium and highest tertile were 0.701 (95 % CI: 0.558-0.880, P = 0.002), 0.784 (95 % CI: 0.618-0.994; P = 0.045). Restricted cubic spline curves revealed that incident rate decreased with increase in sarcopenia index.

This study provides national longitudinal evidence on the association of higher sarcopenia index with lower incident CKD. Our findings suggest that sarcopenia index may be a useful biomarker for predicting the risk of CKD in this population.

Triglyceride deposit cardiomyovasculopathy (TGCV) is a rare cardiovascular disorder caused by defective intracellular lipolysis of triglyceride, resulting in heart failure and diffuse narrowing atherosclerosis. Recently, the registry of TGCV patients in Japan revealed that the 3-year overall survival rate was 80.1% and the 5-year overall survival rate was 71.8%. In this study, the effect on mortality of chronic kidney disease (CKD), diabetes malleus (DM), hypertension (HT), and dyslipidemia (DL) was analyzed using this retrospective registry of TGCV patients. The 3-year survival rate was 71.3% in the CKD group and 91.7% in the non-CKD group, and the 5-year survival rate was 61.8% in CKD group and 84.4% in the non-CKD group. The Kaplan-Meier analysis revealed that CKD is a risk factor for mortality in TGCV patients (p = 0.006). Although TGCV patients with CKD were older than those without CKD, Cox proportional hazard model analyses including age indicated that CKD has a significant association of the prognosis of TGCV patients (hazard ratio 2.33 [1.12-4.86], p = 0.024). DM, HT, and DL did not increase mortality in TGCV patients, although these risk factors were established in the general population. TGCV might cause cardiac disorders and kidney disease at the same time, because podocyte foot process disorder in the glomeruli might be caused by TGCV itself, while CKD should be a risk factor for mortality in TGCV patients as is true in the general population. In conclusion, CKD is a major risk factor for mortality in TGCV patients and thus should be paid attention to in these patients.

Patients with chronic kidney disease are at high and very high risk of cardiovascular disease. As estimated glomerular filtration rate declines, the incidence and severity of risk factors, complications, and atherosclerotic cardiovascular events increase. In this scenario, tailored assessment is the key to evaluate the severity of chronic kidney disease and estimate cardiovascular disease risk. Personalized stratification differentiates patients with chronic kidney disease without diabetes mellitus or established atherosclerotic cardiovascular disease in their management and beneficial treatment. Exercise intensity assessment and prescription is suggested to propose specific and safe recommendations for physical activity, training, and cardiac rehabilitation. Programs are based on a combination of endurance and resistance exercise and should be adapted to very high risk chronic kidney disease and haemodialysis patients and after kidney transplantation. Appropriate management of cardiovascular complications in these patients, such as risk factors, heart failure, arrhythmias, and coronary artery disease, is essential to ensure the best treatment and improve the prognosis. Therefore, we propose a critical and comprehensive review to suggest how to manage patients with chronic kidney disease in clinical practice and, specifically, with regard to cardiovascular risk assessment, exercise training prescription, and management of complications.

Fatigue is a common symptom in kidney failure and impacts on health-related quality of life. Educational interventions involving energy conservation strategies have effectively reduced fatigue in people with other chronic diseases.

To evaluate the effectiveness of an energy conservation education intervention for people with kidney failure receiving haemodialysis (EVEREST).

A two-arm parallel group study with haemodialysis shift randomisation.

Recruitment commenced in April 2022 and included 126 participants receiving haemodialysis who met the eligibility criteria. They were randomised based on haemodialysis shifts. The intervention group received a structured energy conservation education program plus usual care over 12 weeks. The control group received the usual care. The energy conservation education program consisted of three individual face-to-face educational sessions, one booster session, and a booklet. Outcomes were fatigue, other chronic kidney disease (CKD) symptoms, occupational performance, and health-related quality of life. Data were collected at baseline, week 4, week 8, and week 12. Intention-to-treat analysis was used.

Participants who received the energy conservation education program showed a significant reduction in fatigue severity (mean difference [MD] = -1.88, 95 % confidence intervals [CI] [-2.36 to -1.40], p < .001), fatigue interference (MD = -1.52, 95 % CI [-2.02 to -1.02], p < .001), number of fatigue days (MD = -1.12, 95 % CI [-1.60 to -0.64], p < .001), and percent of day fatigued (MD = -18.47, 95 % CI [-23.60 to -13.34], p < .001) at week 8 compared to the control group. At week 12, medium to large effect sizes for fatigue severity (effect size [ES] = 2.37, p < .001), fatigue interference (ES = 1.68, p < .001), number of fatigue days (ES = 0.74, p < .001), and percent of day fatigued (ES = 2.10, p < .001) were observed in the intervention group compared to the control group. Similarly, significant improvements were detected in the CKD symptom (ES = 1.49, p < .001), occupational performance (ES = 1.17, p < .001), and satisfaction with the performance (ES = 1.59, p < .001) in the intervention group compared to the control group. A significant effect was seen for health-related quality of life in the intervention group [physical health (ES = 2.14, p < .001) and mental health (ES = 2.06, p < .001)] at week 12 compared to the control group.

The energy conservation education program was successful in reducing fatigue in the haemodialysis population. This simple approach enabled individuals to improve everyday activities, reduce other CKD symptoms and improve health-related quality of life. Nurses could incorporate the energy conservation education program into routine practice in haemodialysis units.

The trial was registered in ClinicalTrials.gov (Trial registration ID NCT04360408) on April 23, 2020.

Educational intervention about energy conservation for those on haemodialysis reduced fatigue and improved daily activities and health-related quality of life.

Patients with chronic kidney disease (CKD) are at risk of progressive loss of kidney function, heart failure, and cardiovascular death despite current proven therapies, including renin-angiotensin system inhibitors (RASi), sodium glucose co-transporter-2 inhibitors (SGLT2i), and statin-based regimens. RASi and SGLT2i reduce risk of CKD progression irrespective of primary cause of kidney disease, suggesting they target final common pathways. Targeting aldosterone overactivity with a nonsteroidal mineralocorticoid receptor antagonist (MRA) also reduces cardiorenal risk in patients with albuminuric diabetic kidney disease already treated with RASi. Together, these observations provide the rationale for trials to assess effects of inhibiting the aldosterone pathway in a broader range of patients with CKD, including those with non-diabetic causes of CKD or low albuminuria. Aldosterone synthase inhibitors (ASi) have emerged as an alternative to MRAs for aldosterone pathway inhibition. Phase II data from 586 patients with albuminuric CKD have shown that 10 mg of an ASi, vicadrostat (BI 690517), reduced urine albumin-to-creatinine ratio by ∼40% compared with placebo, with or without concurrent empagliflozin treatment. MRA and ASi increase risk of hyperkalaemia. Combining their use with an SGLT2i may mitigate some of this risk, improving tolerability, and allowing a wider range of patients to be treated (including those with higher levels of blood potassium than in previous trials). The EASi-KIDNEY (NCT06531824) double-blind placebo-controlled trial will test this approach by assessing the safety and cardiorenal efficacy of vicadrostat in combination with empagliflozin in ∼11 000 patients with CKD. It will be sufficiently large to assess effects in patients with and without diabetes separately.

Chronic kidney disease (CKD) is a globally prevalent and highly lethal condition, often accompanied by dilated cardiomyopathy (DCM), which increases the risk of cardiac complications. Early detection of DCM in CKD patients remains challenging, despite established research demonstrating the relationship between CKD and cardiac abnormalities.

We retrieved expression matrices for DCM (GSE57338, GSE29819) and CKD (GSE104954) from GEO and a DCM scRNA-seq dataset (GSE145154). These were analyzed for differential gene expression and WGCNA. KEGG and GO analyses were performed on shared differentially expressed genes in DCM and CKD. Potential drugs for DCM were identified using CMAP. Machine learning methods LASSO, SVM-RFE, and RF were used to find biomarkers and develop a diagnostic nomogram for CKD-associated DCM, validated with external datasets. Single-gene GSEA was conducted to understand model gene mechanisms in CKD-associated DCM. Immune cell infiltration was analyzed with CIBERSORT, and single-cell sequencing examined model gene distribution and expression in the heart.

Our examination of the expression matrix datasets associated with DCM and CKD revealed 115 key model genes that are shared by the two disorders as well as 47 genes that are differently expressed. These 47 differentially expressed genes were primarily linked to immune regulation and inflammation, according to enrichment analysis. CMAP analysis suggested withaferin-a, droxinostat, fluorometholone, and others as potential DCM treatments. Machine learning identified MNS1 and HERC6 as significant CKD-associated DCM biomarkers. A diagnostic nomogram using these genes was developed, showing strong discriminative power and clinical utility. MNS1 and HERC6 are implicated in metabolism, inflammation, immunity, and heart function. Immune cell infiltration analysis indicated dysregulation in DCM, with MNS1 and HERC6 correlating with immune cells. Single-cell sequencing showed MNS1 and HERC6 expression in endothelial cells and fibroblasts, respectively.

We identified MNS1 and HERC6 as biomarkers and developed a new diagnostic nomogram based on them for the timely diagnosis of CKD patients presenting with DCM complications. This study's findings offer novel insights into potential diagnostic methods and therapeutic strategies regarding the coexistence of CKD and DCM.

To investigate the relationships between dynamic changes in metabolic syndrome (MetS) components and chronic kidney disease (CKD) risk.

Data from the UK Biobank, including baseline assessments from 2006 to 2010, repeat assessments in 2012-2013, and linked national health records, were analyzed. MetS components consisted of abdominal obesity, elevated blood pressure (BP), fasting blood glucose (FBG), serum uric acid (SUA), and lipid abnormalities. The Kaplan-Meier method and log-rank test were used to analyze CKD incidence and group differences. Cox regression models assessed the association between dynamic changes in MetS components and CKD risk.

The study enrolled 455,060 participants (45.7% male, 18.4% aged 65 years or older) with a median follow-up of 12.68 years. Those with MetS had a significantly higher 10-year CKD cumulative incidence probability of CKD than those without MetS (4.14% VS 1.14%). Multivariate analysis showed all baseline metabolic abnormalities were linked to CKD risk with HRs from 1.40(1.35-1.45) to 1.85 (1.78-1.92), and MetS strongly associated with CKD (HR: 2.31). CKD risk rose with more MetS components and progression stages. Notably, with FBG being the exception, the four MetS components that shifted from normal at baseline to abnormal at follow - up were associated with elevated CKD risk, with HRs (95% CI) ranging from 1.21 (1.00-1.48) to 1.73 (1.34-2.24). Participants with high baseline SUA, even if it normalized at follow - up, still faced a 1.30 - fold higher CKD risk (95% CI: 1.25-1.35), distinct from other components. For those developing one and ≥ 2 new MetS components at follow - up, the CKD risk HRs (95% CI) were 1.49 (1.00-2.35) and 2.26 (1.21-4.24) respectively.

MetS and its component changes are significantly associated with CKD risk, in a dose - response pattern. Incorporating SUA into MetS assessments enhances risk identification, especially noting females' higher susceptibility to elevated SUA. Dynamic monitoring of MetS components is crucial for assessing and predicting CKD risk.

Not applicable.

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with several comorbidities. Although chronic kidney disease (CKD) has been recognized as one such comorbidity, the effect of CKD on survival in patients with COPD remains uncertain. This study investigated the clinical impact of CKD in patients with COPD, accounting for clinically characteristics and 6-min walking test (6MWT) results.

Patients with COPD who completed the 6MWT and a 3-year follow-up were retroactively enrolled in the study. Data on clinical information, 6MWT parameters, and outcomes were collected and analyzed.

Among the 141 patients with COPD enrolled, 33 (23.4 %) had comorbid CKD. Patients with CKD were significantly older and more likely to experience heart failure, mortality, and FEV1 decline than patients without CKD. Multivariate analysis revealed that 6-min walking distance <350 m (odds ratio [OR]: 3.65, 95 % confidence interval [CI]: 1.05-12.06, p = 0.041) and CKD (OR: 4.66, 95 % CI: 1.30-16.76, p = 0.018) were independent risk factors for mortality.

Comorbid CKD was associated with an increased mortality rate and rapid FEV1 decline in patients with COPD. Patients with COPD and comorbid CKD may require intensive monitoring during treatment.

Chronic kidney disease (CKD) is a global health challenge marked by progressive renal decline and increased mortality. The interplay between CKD and hypothyroidism, particularly nonthyroidal low-triiodothyronine (T3) syndrome, exacerbates disease progression, driven by HPT axis dysfunction and reduced Klotho levels due to the Wnt/β-catenin pathway activation. This study explored Klotho as a link between CKD and hypothyroidism using an adenine-induced CKD aged mouse model. Exogenous T3 and baicalein (BAI), targeting the Wnt pathway, were used to upregulate Klotho expression. Combined T3 and BAI treatment significantly increased Klotho levels, surpassing individual effects, and suppressed key signaling molecules (TGF, NFκB, GSK3), mitigating renal fibrosis and CKD complications, including cardiovascular disorders and dyslipidemia. This bidirectional approach, enhancing Klotho via T3 and sustained Wnt pathway inhibition, offers a novel and effective strategy for CKD management, particularly in elderly patients with hypothyroidism.

Although dipstick urinalysis has been widely used as part of health screening for employees, its efficacy in predicting renal function decline in healthy workers has not been elucidated.

We conducted a 10-year follow-up study of 33,139 Japanese healthy workers to determine the association between dipstick urinalysis results (urinary protein levels) and the development of adverse kidney outcomes (rapid eGFR decline and low eGFR) and to assess the predictive accuracy of dipstick urinalysis for the 10-year incidence of adverse kidney outcomes.

Trace (±) and positive (1+, 2+, and 3+) dipstick proteinuria were found in 2.8% and 0.8% of the total, respectively. They had a significantly increased risk of adverse kidney outcomes than those who were negative. The sensitivity of dipstick urinalysis to discriminate between those with and without adverse kidney outcomes within 10 years was extremely low (0.01-0.07), while its specificity was nearly perfect (0.97-1.00). The sensitivity and specificity were robust to varying cutoffs (± or 1+) and to testing once or twice.

Workers who have at least one trace or positive result on dipstick urinalysis are more likely to have declining renal function within 10 years than those who do not. The specificity of almost 1.0 suggests that this noninvasive, inexpensive test will not miss workers whose renal function is expected to decline within the next 10 years. Occupational health staff should compile a list of workers with trace and positive results and ensure that those on the list take the necessary actions, such as retests and hospital visits, in a timely manner.

Chronic kidney disease (CKD) is a progressive, irreversible condition that causes kidney damage and has systemic repercussions. The aim of the present study was to summarize the literature on the clinical and nutritional repercussions of dialysis.

Searches were conducted of the PubMed/MEDLINE, Scopus, and Embase databases for relevant articles published up to April 2023. The eligibility criteria were studies published in the English language involving male and female patients between 18 and 80 years of age diagnosed with CKD and undergoing dialysis. No restrictions were imposed regarding year of publication. The outcomes of interest were nutritional and clinical status.

A total of 9.266 records were retrieved, 20 of which were included in the qualitative synthesis and 14 were included in the meta-analysis. The samples ranged from 11 to 601 patients and mean age was 57.6 ± 7.69 years. Time on dialysis ranged from 36 months to 14.48 years. Greater increases in body weight [MD 9.70, CI 7.58-11.82, Z = 8.96, p < 0.0001], arm muscle area [MD 2.36, CI 1.05-3.67, Z = 3.52, p = 0.0004], phase angle [MD0.81, CI0.50-1.12, Z = 5.16, p < 0.00001], creatinine [MD1.93, CI 1.67-2.20, Z = 14.43, p < 0.00001], albumin [MD1.35, CI 0.88-1.82, Z = 5.61, p < 0.00001], urea [MD11.13, CI 4.67-17.59, Z = 3.37, p = 0.0007], and Kt/v [MD-0.97,CI-2.30-0.35, Z = 1.44, p = 0.15] were found in male patients undergoing dialysis compared to female patients. Heterogeneity among the studies ranged from 0 to 85%.

Dialysis exerts an impact on the nutritional status of patients with CKD, especially men. Therefore, monitoring clinical-nutritional variables is of fundamental importance in this population.

Machine learning (ML) has gained attention in diabetes management, particularly for predicting and diagnosing diabetic kidney disease (DKD). However, systematic evidence on its performance remains limited. This study evaluates the predictive and diagnostic accuracy of ML in DKD to support the development of tailored prevention strategies and non-invasive diagnostic tools.

A systematic search of PubMed, Embase, Web of Science, and Cochrane (up to April 14, 2024) identified relevant studies. Risk of bias was assessed using tools for predictive models, and meta-analysis included subgroup analyses based on task type, dataset, and model type.

A total of 34 studies were included, with 19 on DKD risk prediction and 15 on diagnosis. For prediction, the pooled c-index was 0.81 (95% CI 0.79-0.83), sensitivity 0.81 (95% CI 0.74-0.86), and specificity 0.82 (95% CI 0.73-0.89). For diagnosis, the pooled c-index was 0.81 (95% CI 0.79-0.83), sensitivity 0.81 (95% CI 0.78-0.84), and specificity 0.75 (95% CI 0.72-0.79).

ML shows promising accuracy in DKD prediction and diagnosis, offering a viable tool for early screening and risk assessment.

Background: Solid organ transplant (SOT) recipients are living longer and, consequently, more of them require elective total hip arthroplasty (THA) to restore mobility and improve quality of life. Because these patients are chronically immunosuppressed and often burdened by multiple comorbidities, their peri-operative risk profile may differ substantially from that of the general THA population. This study aimed to evaluate risk factors associated with acute medical and surgical complications, implant survivorship, and overall mortality in patients with a history of SOT who underwent THA. Methods: A total of 173 THA procedures were reviewed in patients with previous SOT. Among them, 64 had undergone liver transplantation (LT), 83 had received renal transplants (RT), and 26 had experienced more than one type of organ transplant (MT). Kaplan-Meier survival analysis was employed to estimate median survival. Complications were examined using univariate analysis through mixed-effects logistic regression, while Cox regression was utilized to assess mortality risk. The median follow-up period extended to 99 months. Results: The proportion of patients experiencing at least one acute medical event was 27% in the LT group, 33% in the RT group, and 38% in the MT group, with no statistically significant difference between groups (p = 0.5). American Society of Anesthesiologists Class (ASA) 4 (Odds Ratio (OR) = 28; p = 0.006) and treatment with bisphosphonates (OR = 2.25; p = 0.03) were associated with higher risk of acute medical complications. Increased age at the time of SOT was linked to a reduced likelihood of surgical complications (OR = 0.94, p = 0.008), as was older age at the time of undergoing THA (OR = 0.92, p = 0.001). The observed rates of reoperation and implant revision were 3% and 1%, respectively. The estimated patient survivorship rates at 1, 5, and 10 years were 98.6, 82, and 58.4%, respectively. Older age at SOT (Hazard Ratio (HR) = 1.06, p < 0.001), at THA (HR = 1.08, p < 0.001), ASA 4 at THA (HR = 7.57, p = 0.02), and atrial fibrillation (AFib) (HR = 3.13, p = 0.02) were associated with higher mortality. Conclusions: ASA 4 and bisphosphonates were associated with a higher risk of acute medical complications, whereas older age was associated with lower surgical complications. Additionally, older age, ASA 4, and AFib were associated with higher mortality.

Hepatitis C virus (HCV) infection increases the risk of mortality and morbidity among chronic kidney disease (CKD) patients. However, the advancement of HCV treatment has made this viral infection curable. Thus, the main objective of this study was to comprehend the HCV genotype (GT) distribution and the efficacy of direct-acting antivirals (DAAs) among CKD patients in West Bengal.

Over five years (January 2017 to December 2021), 310 HCV sero-reactive patients were enrolled in this observational prospective study. HCV RNA was quantified using qRT-PCR. The partial amplification of the core (405 bp) and NS5B (389 bp) region was performed by nested RT-PCR followed by Sanger sequencing for HCV genotype analysis using the NCBI genotyping tool. The phylogenetic tree was constructed using the MEGA-X tool.

The occurrence of HCV RNA positivity was 50.64% (n = 157), and of these 157 patients, 141 (89.81%) completed the DAAs treatment. The most important observation of the study was the prevalence of uncommon HCV genotype GT-1c (67.52%) followed by 1a, 4a, 3a, 1b, and 3b among CKD patients. The overall DAAs efficacy between January 2017 and December 2018 was ~ 97%, and in January 2019 and December 2021, ~ 95% among CKD patients. At the same time, in these two phases, DAAs efficacy among GT-1c-infected CKD patients was ˜ 96% and ˜ 93%, respectively.

The prevalence of GT-1c among CKD patients was unusual in this geographic region. The overall efficacy of DAAs among the CKD population was encouraging. However, the downtrend of the DAAs efficacy in GT-1c may increase concern among this high-risk group in the future.

Not applicable.

Rhabdomyolysis is one of the leading causes of acute kidney injury (AKI) and is infrequently associated with chronic kidney disease (CKD). CKD appears in diabetes mellitus and arterial hypertension, as a result of other systemic diseases and glomerulonephritis. In this study, we present two cases (one with CKD and one with AKI) that are caused by a genetic defect. A genetic examination was performed in both patients, proving that the patient with CKD has a genetic defect in the RYR1 gene, which is observed in patients with malignant hyperthermia. Meanwhile, the patient with AKI has a homozygous pathogenic variant in SLC2A9, which is associated with urinary urate wasting and is characterized by asymptomatic hypouricemia and AKI after exercise. The first case is chronic rhabdomyolysis, as the patient is an athlete and performs heavy daily exercise. The second case is AKI without prior kidney damage or symptoms. Both patients did not undergo a kidney biopsy. In the first case, changes in daily routine without extreme physical exercise led to the recovery of normal kidney function. The second patient recovered from AKI without sequelae. These two cases are an example of "thinking outside the box" with respect to how genetic diseases and defects can cause kidney damage, both chronic and acute.

Diabetic kidney disease (DKD) is a common microvascular complication and the main cause of death in diabetic patients. Metabolic disorders can accelerate the occurrence and development of DKD through a variety of ways, Recent studies have found that Clusterin (Clu) levels are associated with renal dysfunction and can be used as a biomarker of renal tubular injury, while preclinical studies reveal its renoprotective function. This article reviews the molecular mechanisms of Clu in the interaction between various cells in DKD. In addition, we discuss the latest research progress of Clu in the field of DKD. This review aims to explore Clu as a potential therapeutic target for DKD and provide some guidance for future clinical treatment.

To estimate the incidence of comorbidities in persons with HIV (PWH) with a stable viral load (VL) of ≤50 copies/mL and evaluate the likelihood of treatment switch (TS) according to the new development of dyslipidaemia (DP), kidney disease and a weight change that determined overweight.

We carried out six case-control studies nested within the Icona Foundation Study cohort with the outcome of TS of the current regimen (due to intolerance/toxicity or simplification) and investigated the incident comorbidities. Conditional logistic regression models were employed.

Overall, the median age of study participants was 45 years (IQR: 36-52), 19% were female, 48% were MSM and 17% were migrants. DP was confirmed to be the most frequent incident comorbidity [138 events; incidence rate (IR) = 28.4%; 95% CI: 22.7%-34%], followed by estimated glomerular filtration rate (eGFR) deterioration and BMI elevation. None of the studied factors was associated with the risk of TS because of simplification. TS because of toxicity was predicted by incident DP [adjusted OR (aOR) = 2.49, 95% CI: 1.19-5.19, P = 0.02] and by a decline in eGFR of >10 mL/min/1.73 m2 (aOR = 1.51, 95% CI: 0.98-2.32, P = 0.06). The association with DP was stronger in participants who were receiving a boosted PI-based regimen at baseline (aOR = 3.38, 95% CI: 1.11-10.30, P = 0.03). Therapy discontinuation because of toxicity/simplification has remained common in PWH with VL of ≤50 copies/mL in recent years.

The onset of DP and a decline in eGFR was associated with discontinuations due to toxicity. Interventions aiming to mitigate the risk of developing lipid abnormalities in PWH are likely to also reduce the number of ART changes, which can potentially affect future drug options.

The comparison between online hemodiafiltration (online HDF) and expanded hemodialysis (HDx) remains undetermined. This systematic review and meta-analysis were conducted to provide comparative evidence on the molecule clearance, efficacy, and all-cause mortality of HDx versus online HDF in patients with end-stage kidney disease (ESKD).

A comprehensive search was conducted up to September 10, 2024, using various electronic databases PubMed, Cochrane Library, Scopus, Web of Science, and Ovid MEDLINE with adherence to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Risk ratios (RR) for binary outcomes and standardized mean differences (Hedge's g) were used for continuous outcomes.

The meta-analysis included eight studies, consisting of 614 patients in total. No statistical difference in all-cause mortality was found between HDx and online HDF (RR 0.97; 95% Cl 0.62-1.53, p = 0.91, I2 = 0%). Online HDF revealed a decrease in β2-microglobulin clearance (Hedges's g = - 0.61, 95% CI - 1.04 to - 0.18, p = 0.01), with no differences in creatinine, phosphate, and urea clearance. Prolactin clearance favored online HDF (Hedge's g = - 1.49, 95% Cl - 3.36 to 0.37, p = 0.12) but the pooled estimate remained insignificant, with high heterogeneity (I2 = 90.87%).

Overall, both modalities are found to be effective, but online HDF revealed superior efficacy with potential advantages in middle-molecule clearance. Further standardized, randomized, and high-quality trials are required not only to confirm these findings but also to address the substantial heterogeneity found in the clearance of prolactin, myoglobulin, and albumin loss.

PROSPERO registration number: CRD42024622632.