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Introduction: In resource-constrained countries, inadequate access to healthcare and prognostic tools can be the Achilles' heel in effectively managing chronic kidney disease (CKD). There is a significant similarity in the pathogenesis of CKD and liver fibrosis. The role of liver fibrosis (LF) scores in predicting short-term clinical outcomes in hospitalized patients with CKD is unknown. Our study aimed at calculating LF scores and studying the association of liver fibrosis with short-term mortality and morbidity in CKD patients. Methods: Patients aged above 15 years diagnosed with CKD as per the KDIGO criteria were enrolled. LF scores, namely, NFS, GPRI, and FIB-4 scores were calculated. Patients were followed up for a period of 28 days for good and poor composite outcomes, namely, the requirement of hemodialysis, non-invasive ventilation, prolonged hospital stay, and neurological and cardiovascular outcomes including death. Results: Among 163 patients, 70.5% were below 60 years of age, 82.2% were male and 35% were diabetic. At 28-day follow up, 52.1% had poor composite outcome. The AUROC for GPRI and FIB-4 in predicting poor outcomes was 0.783 (95% CI: 0.71-0.855) (p < 0.001) and 0.62 (95% CI: 0.534-0.706) (p = 0.008), respectively. The AUROC for GPRI and NFS in predicting all-cause mortality was 0.735 (95% CI: 0.627-0.843) (p = 0.001) and 0.876 (95% CI, 0.8-0.952) (p < 0.001), respectively. Conclusion: We found a positive association between LF scores and CKD outcomes in hospitalized patients. The LF scores significantly predicted poor outcomes in patients with CKD. Among the scores, GPRI was found to be a stronger predictor in predicting outcomes in both diabetic and non-diabetic patients with CKD. A high GPRI score was also associated with poor outcomes and increased mortality in both diabetics and non-diabetics.

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Integrating sodium-glucose co-transporter 2 inhibitors (SGLT2i) into the treatment for chronic kidney disease (CKD) has marked a significant therapeutic advance in nephrology. Clinical trials such as DAPA-CKD and EMPA-KIDNEY have demonstrated the beneficial effects of SGLT2i in slowing CKD progression and reducing proteinuria. However, the applicability of these results to patients with glomerulonephritis is still unresolved due to various limitations. This manuscript combines the evidence supporting the use of SGLT2i in glomerular diseases, highlights the limitations and strikes a conclusive balance on their role in clinical practice.

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BACKGROUND: Hypertensive crises in children represent critical medical situations characterized by severe hypertension and potential organ damage. Fenoldopam, a dopaminergic medication, offers a viable therapeutic option for managing such clinical scenarios. We aimed to evaluate efficacy and safety of fenoldopam in the management of hypertensive urgencies and emergencies. METHODS: This retrospective analysis focused on pediatric patients affected by acute or chronic kidney disease, aged 1 month-18 years, admitted to the Pediatric Nephrology and the Pediatric Intensive Care Unit at University-Hospital of Padua, Italy, who presented with a hypertensive crisis treated with fenoldopam between March 2010 and December 2022. RESULTS: The study included 74 patients with median age 10 years (interquartile range [IQR] 4-15 years) who received 102 fenoldopam infusions. Seventy-two percent were already receiving antihypertensive treatment before admission. In all cases, fenoldopam was associated with a reduction of blood pressure (BP) after 8 h of treatment, but in 87% of patients reduction of the initial mean arterial pressure (MAP) was higher than 25% of calculated drop pressure. MAP normalized in 26% of cases after 24 h and in 35% after 48 h. Occurrence of hypotension was 7%, while hypokalemia was observed in 13% of cases. Patients who presented a MAP reduction not exceeding 25% of calculated drop pressure received a lower median fenoldopam dose (0.2 mcg/kg/min; IQR 0.1-0.2) compared with patients having a MAP reduction > 25% of calculated drop pressure (0.4 mcg/kg/min; IQR 0.2-0.6; p = 0.002). CONCLUSIONS: Fenoldopam seems effective and safe for the treatment of hypertensive crises in children with kidney disease, at a starting dose of 0.2 mcg/kg/min. Strict BP monitoring is required to identify possible excessive drop pressure in the first hours of infusion.

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BACKGROUND: In patients with chronic kidney disease (CKD), cardiovascular disease is found to be the primary cause of mortality, and after coronary artery bypass grafting (CABG), their prognosis deteriorates. METHODS: We conducted a meta-analysis comparing off-pump CABG versus on-pump CABG in CKD patients. We searched electronic databases, including PubMed, Cochrane, and Google Scholar, using relevant keywords. We included studies comparing off-pump CABG with on-pump CABG in patients with chronic kidney disease, which was defined as an estimated glomerular filtration rate (eGFR) < 60 ml/min per 1.73 m2. Effect estimates were synthesized using a random-effects model and expressed as risk ratios (RR) for dichotomous outcomes and mean difference (MD) for continuous outcomes, with corresponding 95% confidence intervals (CIs). Our primary outcome was short-term mortality. RESULTS: A total of 25 studies, of which 23 were observational and 2 were RCTs, were included in this meta-analysis, comprising 234,585 patients (66,591 in the off-pump group and 167,994 in the on-pump group). Our meta-analysis showed that there was a significantly higher mortality rate in the on-pump CABG group as compared to the off-pump CABG group (RR: 0.73, 95% CI [0.61, 0.88]; P = 0.0006, I2 = 60%). CONCLUSION: Compared with OPCAB, short-term mortality was significantly higher in ONCAB.

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The outcome of this study was to identify 9-year survivors of intertrochanteric fracture at each stage of chronic kidney disease (CKD) and to investigate the risk factors associated with mortality following surgery with proximal femoral nail anti-rotation (PFNA). 443 elderly intertrochanteric fractures underwent PFNA fixation were recruited. Mortality rate was identified until 9 years. We compared the survival time of hip fracture in each stage of CKD. A regression analysis was used to determine the association between risk factors and one-year mortality. The overall median survival time was 7.1 years. The Kaplan-Meier curve was significantly different in each CKD stage especially in CKD5. In addition, the incidence rate of mortality was highest in CKD 5 (17.4%) and the median survival time in CKD 5 was 3.3 years. The multivariate analysis demonstrated that heart disease, operative time > 60 min, presence of pulmonary embolism, and poor to fair Harris hip score were significantly increased mortality. CKD stage 5 is associated with the highest mortality rate and the shortest median time of survival during the 9-year follow up. Patients who have high risk should focus on long-term care planning, including the counseling for their healthcare providers and families.

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Chronic kidney disease (CKD) presents a significant global health challenge, often progressing to end-stage renal disease (ESRD) necessitating renal replacement therapy (RRT). Late referral (LR) to nephrologists before RRT initiation is linked with adverse outcomes. However, data on CKD diagnosis and survival post-RRT initiation in Kazakhstan remain limited. This study aims to investigate the impact of late CKD diagnosis on survival prognosis after RRT initiation. Data were acquired from the Unified National Electronic Health System (UNEHS) for CKD patients initiating RRT between 2014 and 2019. Survival post-RRT initiation was assessed using the Cox Proportional Hazards Model. Totally, 211,655 CKD patients were registered in the UNEHS databases and 9,097 (4.3%) needed RRT. The most prevalent age group among RRT patients is 45-64 years, with a higher proportion of males (56%) and Kazakh ethnicity (64%). Seventy-four percent of patients were diagnosed late. The median follow-up time was 537 (IQR: 166-1101) days. Late diagnosis correlated with worse survival (HR = 1.18, p < 0.001). Common comorbidities among RRT patients include hypertension (47%), diabetes (21%), and cardiovascular diseases (26%). The history of transplantation significantly influenced survival. Regional disparities in survival probabilities were observed, highlighting the need for collaborative efforts in healthcare delivery. This study underscores the substantial burden of CKD in Kazakhstan, with a majority of patients diagnosed late. Early detection strategies and timely kidney transplantation emerge as crucial interventions to enhance survival outcomes.

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INTRODUCTION: Advanced chronic kidney disease (CKD) is common among patients with coronary artery disease (CAD), and angiotensin­converting enzyme inhibitors (ACEI) or angiotensin­receptor blockers (ARB) can improve cardiac and renal function, but whether ACEI/ARB therapy improves long-term prognosis remains unclear among these high-risk patients. Therefore, this research aimed to investigate the relationship between ACEI/ARB therapy and long-term prognosis among CAD patients with advanced CKD. METHODS: CAD patients with advanced CKD were included in five hospitals. Advanced CKD was defined as estimated glomerular filtration rate (eGFR)<30 ml/min per 1.73 m2. Cox regression models and competing risk Fine and Gray models were used to examine the relationship between ACEI/ARB therapy and all-cause and cardiovascular death, respectively. RESULTS: Of 2527 patients, 47.6% population of our cohort was discharged on ACEI/ARB. The overall all-cause and cardiovascular mortality were 38.6% and 24.7%, respectively. Multivariate Cox regression analyses indicated that ACEI/ARB therapy was found to be associated with lower rates of both all-cause mortality (hazard ratio (HR)=0.836, 95% confidence interval (CI): 0.738-0.948, p = 0.005) and cardiovascular mortality (HR = 0.817, 95%CI: 0.699-0.956, p = 0.011). In the propensity-matched cohort, the survival benefit was consistent, and significantly better survival was observed for all-cause mortality (HR = 0.856, 95%CI: 0.752-0.974, p = 0.019) and cardiovascular mortality (HR = 0.830, 95%CI: 0.707-0.974, p = 0.023) among patients treated with ACEI/ARB. CONCLUSION: ACEI/ARB therapy showed a better survival benefit among high-risk CAD patients with advanced CKD at long-term follow-up, which manifested that strategies to maintain ACEI/ARB treatment may improve clinical outcomes among these high-risk populations.

What is the current knowledge on the topic? Advanced CKD is highly prevalent and strongly associated with higher mortality risk and worse outcomes among CAD patients, and patients with advanced CKD have often been excluded from randomized controlled trials, creating an evidence gap for these high-risk CAD patients. ACEI/ARB are beneficial for greater survival among CAD patients, but the effect of ACEI/ARB therapy on long-term prognosis is unclear among CAD patients with advanced CKD.What does this study add to our knowledge? ACEI/ARB treatment showed a better survival benefit among high-risk CAD patients with advanced CKD at long-term follow-up.How might this change clinical pharmacology or translational science? CAD patients with advanced CKD are not only have worse outcomes but also limited in their choice of therapy strategies. Our study may prompt an important reference for the subsequent improvement of long-term prognosis among these high-risk populations.

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Although it has been established that patients with chronic kidney disease and iron deficiency, as indicated by a transferrin saturation of < 20%, are at increased risk of all-cause mortality and cardiovascular events, the optimal management of such patients has not yet been determined. In this post hoc subgroup analysis, we aimed to clarify the effect of ferric citrate hydrate on transferrin saturation in patients with chronic kidney disease and low transferrin saturation (< 20%) undergoing hemodialysis. To accomplish this, we extracted the relevant data on a subset of patients drawn from two previous studies: the ASTRIO study (A Study examining the contribution to Renal anemia treatment with ferric citrate hydrate, Iron-based Oral phosphate binder, UMIN000019176) and a post-marketing surveillance study. The subset of patients used for the present study were those with baseline transferrin saturation < 20%. We found that administration of ferric citrate hydrate increased transferrin saturation and maintained transferrin saturation at approximately 30%. However, because we did not have access to data on all-cause mortality or cardiovascular events, we could not ascertain whether the frequency of these outcomes was reduced in parallel with improvements in transferrin saturation. Further large studies are required.

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Introduction The SARS-CoV-2 virus causes the highly contagious coronavirus disease 2019 (COVID-19), which most commonly manifests as severe acute respiratory syndrome. The virus is part of the Coronaroviridae family, a group of viruses that can cause various diseases, such as the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). The World Health Organization (WHO) declared the outbreak of COVID-19 as a pandemic on March 11, 2020. On February 26, 2020, Romania confirmed the first case of COVID-19, initiating a series of challenges that negatively impacted the lives of thousands of people. The COVID-19 pandemic has had a disproportionate effect on patients at risk of kidney damage. Patients with chronic kidney disease (CKD) are at high risk of SARS-CoV-2 infection and mortality associated with COVID-19. CKD is associated with pronounced immunodeficiency and represents a risk factor for contracting the infection, but also increases the risk of hospitalization, oxygen therapy, and prolonged treatments. The evidence regarding the management of patients with CKD undergoing renal replacement therapy (RRT) infected with SARS-CoV-2 is still misleading. While these are high-risk patients due to the presence of multiple comorbidities, especially cardiovascular, e.g., hypertension, left ventricular hypertrophy, but also diabetes, the question remains whether RRT itself is associated with a worse prognosis in patients infected with SARS-CoV-2, although infections generally induce severe complications in patients with CKD and RRT. Methods This retrospective study aims to analyze the evolution of COVID-19 disease in patients with CKD, focusing on the association with some common comorbidities such as ischemic coronary disease (ICD), obesity, and diabetes. The study included 72 hemodialyzed patients; they were hospitalized between November 2020 and February 2021 at "Sf. Ioan" Clinical Emergency Hospital, Nephrology and Dialysis Clinic; peritoneal dialysis patients were excluded. Results Older age was found to be an important risk factor for death in hemodialyzed patients admitted with COVID-19 infection. Obese patients were found to be at greater risk of mortality. Discussion This study showed that there is a complex relationship between COVID-19 infection and increased mortality in patients with CKD associating ischemic coronary disease, obesity, and diabetes.

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BACKGROUND: Chronic kidney disease (CKD) leads to a high rate of complications requiring hospital admission for advanced management. Therefore, this study aims to analyze the main causes of hospitalization following the initiation of renal replacement therapy (RRT). MATERIALS AND METHODS: This observational and descriptive study utilized a non-probabilistic quota sampling method, reviewing a total of 423 medical records from General Regional Hospital 1 of the Mexican Social Security Institute in Querétaro. The study evaluated the frequency and causality of hospitalizations during a retrospective period from 2018 to 2023. RESULTS: There were 1,162 hospitalization events involving 423 patients; 71.63% of patients started RRT with peritoneal dialysis, while 26% began with hemodialysis. The leading cause of hospitalization was electrolyte imbalance (397; 34.17%), followed by peritonitis associated with peritoneal dialysis (351; 30.21%), change to hemodialysis (270; 23.24%), Tenckhoff catheter dysfunction (209; 17.99%), and fluid overload (205; 17.64%). The group with the highest number of events was renal-related complications, followed by infectious causes. CONCLUSIONS: Hospitalizations in end-stage CKD patients often arise from the complex renal pathophysiology and complications related to acute and decompensated renal function. This condition refers to the kidneys' failure to maintain essential physiological functions despite ongoing treatment, leading to issues such as electrolyte imbalances, fluid overload, and uremic syndrome. To reduce morbidity and mortality, measures such as enhanced training in ambulatory dialysis, improved catheter care, and early infection detection are crucial. A comprehensive approach that addresses both acute issues and preventive strategies is essential for improving clinical outcomes and quality of life for these patients.

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Background and Aims: Chronic kidney disease (CKD) patients undergoing peritoneal dialysis (PD) are susceptible to complications, including iron overload, which can significantly impact their prognosis and overall health. This scoping review aimed to study the prevalence and implications of iron overload in CKD patients undergoing PD. Methods: A comprehensive search was conducted across five databases, leading to the selection of 18 papers for in-depth analysis. These studies collectively involved 381 PD patients, 60.3% were males. Results: No consensus was reached regarding the exact diagnostic cutoff for iron overload. The investigations revealed four main aspects: (1) Seven papers identified various factors contributing to iron overload, emphasizing the role of different iron supplements and magnetic resonance imaging's capability to diagnose iron accumulation in organs; (2) Iron overload in young patients was found to hinder growth; (3) Six studies highlighted the adverse effects of iron overload, with cardiac issues being the most significant; (4) Three studies demonstrated the efficacy of iron-chelating agents, Deferoxamine and Deferasirox, in treating iron overload patients undergoing PD. Overall, the estimated prevalence of liver iron overload in CKD patients on PD ranges from approximately 10% to 28.6%, which is far lower than the prevalence of 75% elegantly shown in HD patients. Conclusion: While iron overload was a significant concern for CKD patients undergoing PD in the past, it is less common in the current era due to advancements in treatments, such as erythropoiesis-stimulating agents. Treatment with specific chelation agents has proven beneficial, but there is also a risk of adverse effects, necessitating meticulous monitoring and timely intervention.

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Introduction: We investigated the efficacy and safety of oral sodium bicarbonate in kidney-transplant recipients and non-transplant patients with chronic kidney disease (CKD), which are currently unclear. Methods: PubMed, Cochrane Library, Embase, and Web of Science were searched for randomized controlled trials investigating the efficacy and safety of sodium bicarbonate versus placebo or standard treatment in kidney-transplant and non-transplant patients with CKD. Results: Sixteen studies of kidney-transplant recipients (two studies, 280 patients) and non-transplant patients with CKD (14 studies, 1,380 patients) were included. With non-transplant patients, sodium bicarbonate slowed kidney-function declines (standardized mean difference [SMD]: 0.49, 95% confidence interval [CI]: 0.14-0.85, p = 0.006) within ≥12 months (SMD: 0.75 [95% CI: 0.12-1.38], p = 0.02), baseline-serum bicarbonate <22 mmol/L (SMD: 0.41 [95% CI: 0.19-0.64], p = 0.0004) and increased serum-bicarbonate levels (mean difference [MD]: 2.35 [95% CI: 1.40-3.30], p < 0.00001). In kidney-transplant recipients, sodium bicarbonate did not preserve graft function (SMD: -0.07 [95% CI: -0.30-0.16], p = 0.56) but increased blood pH levels (MD: 0.02 [95% CI: 0.00-0.04], p = 0.02). No significant adverse events occurred in the kidney-transplant or non-transplant patients (risk ratio [RR]: 0.89, [95% CI: 0.47-1.67], p = 0.72; and RR 1.30 [95% CI: 0.84-2.00], p = 0.24, respectively). However, oral sodium bicarbonate correlated with increased diastolic pressure and worsened hypertension and edema (MD: 2.21 [95% CI: 0.67-3.75], p = 0.005; RR: 1.44 [95% CI: 1.11-1.88], p = 0.007; and RR: 1.28 [95% CI: 1.00-1.63], p = 0.05, respectively). Discussion: Oral sodium bicarbonate may slow kidney-function decline in non-transplant patients with CKD taking sodium bicarbonate supplementation for ≥12 months or a baseline serum bicarbonate level of <22 mmol/L, without preserving graft function in kidney-transplant recipients. Sodium bicarbonate may increase diastolic pressure, and elevate a higher incidence of worsening hypertension and edema. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42023413929.

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Testosterone's biological functions are extensive, influencing reproductive and systemic health. It plays a vital role in sexual functions, muscle protein synthesis, bone metabolism, fat distribution, and cardiovascular health. The hormone also affects mood, cognitive function, and erythropoiesis, underscoring its importance in both physical and mental health. Testosterone deficiency, or male male hypogonadism, is increasingly recognized as a significant health issue affecting various bodily systems, also in the context of chronic kidney disease (CKD). Recent research indicates a complex interplay between testosterone levels and renal health, suggesting that male male hypogonadism may both impact and be impacted by CKD. The latter is characterized by a gradual loss of kidney function, affects millions globally and is often associated with diabetes mellitus, arterial hypertension, and autoimmune diseases. Men with CKD frequently experience lower testosterone levels, which can exacerbate muscle wasting, reduce quality of life, and increase cardiovascular risk. Overall, low testosterone levels in CKD patients are associated with increased morbidity and mortality. Several mechanisms explain the relationship between CKD and testosterone deficiency. The uremic environment in CKD disrupts the hypothalamic-pituitary-gonadal axis, impairing hormone production. Nutritional deficiencies and chronic inflammation common in CKD patients further suppress gonadal function. The consequences of low testosterone in CKD are profound, with studies suggesting that testosterone replacement therapy (TRT) might improve clinical outcomes, though the long-term effects and causal relationships remain under investigation. The potential benefits of TRT in CKD patients might be significant. TRT can enhance muscle mass and strength, address anemia by stimulating erythropoiesis, improve bone density, and possibly offer cardiovascular benefits by improving body composition and insulin sensitivity. General symptoms of male hypogonadism, such as deteriorated psychological, sexual and physical wellbeing, can be improved by TRT. However, these benefits must be weighed against potential risks. TRT may exacerbate fluid retention, arterial hypertension, or exacerbate existing heart failure, particularly in CKD patients with pre-existing cardiovascular comorbidities. Additionally, concerns about the progression of renal disease via several testosterone affected pathways involving renal tubular integrity exist, highlighting the need for careful patient selection and monitoring. Understanding this relationship is crucial for developing comprehensive treatment strategies that address both renal and endocrine dysfunctions, highlighting the need for integrated patient care, which means good collaboration between subspecialists like nephrologists, endocrinologists, urologists and primary care providers, aiming to improve outcomes and quality of life while mitigating adverse effects.

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BACKGROUND: The aim of this study was to investigate the association between systemic immune-inflammation index (SII) and all-cause mortality in individuals with chronic kidney disease (CKD). PATIENTS AND METHODS: This prospective cohort study was carried out among 9303 participants with CKD from the National Health and Nutrition Examination Survey cycles spanning 1999 to 2018. The mortality data were ascertained by linking participant records to the National Death Index up to December 31, 2019. Complex sampling-weighted multivariate Cox proportional hazards models were employed to estimate the association between SII level and all-cause mortality, providing hazard ratios (HR) and 95% confidence intervals (CI). A restricted cubic spline analysis was conducted to explore potential nonlinear correlation. Subgroup analyses and sensitivity analyses were also conducted. RESULTS: During a median follow-up period of 86 months, 3400 (36.54%) all-cause deaths were documented. A distinctive "J"-shaped relationship between SII level and all-cause mortality was discerned among individuals with CKD, with the nadir observed at an SII level of 478.93 within the second quartile. After adjusting for potential covariates, the risk of all-cause mortality escalated by 13% per increment of one standard deviation of SII, once SII exceeded 478.93 (HR = 1.13; 95% CI = 1.08-1.18). An elevated SII was associated with an increased risk of all-cause mortality among patients with CKD (Q4 vs. Q2: HR = 1.23; 95% CI = 1.01-1.48). Subgroup analyses indicated that the correlation between SII and CKD mortality was particularly pronounced among participants over 60 years old and individuals with diabetes. Sensitivity analyses revealed a linear positive association between SII and all-cause mortality after removing the extreme 5% outliers of SII. CONCLUSIONS: A distinctive "J"-shaped relationship between SII level and all-cause mortality was identified among individuals with CKD. Further research is warranted to validate and expand upon these findings.

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We previously demonstrated hepatic, cardiac, and skin inflammation in a high-fat diet-induced steatotic liver disease (SLD) model. However, the molecular mechanism in the kidneys in this model remains unclear. It has been recently reported that SGLT2 inhibitors improve chronic kidney disease (CKD). Therefore, we used this model to evaluate the effects of tofogliflozin on renal lipid metabolism and inflammation. Male 8-10-week-old C57Bl/6 mice were fed a high-fat/high-cholesterol/high-sucrose/bile acid (HF/HC/HS/BA) diet with 0.015% tofogliflozin (Tofo group) or an HF/HC/HS/BA diet alone (SLD group). After eight weeks, serum lipid profiles, histology, lipid content, and mRNA/microRNA and protein expression levels in the kidney were examined. The Tofo group showed significant reductions in body (26.9 ± 0.9 vs. 24.5 ± 1.0 g; p < 0.001) and kidney weight compared to those of the SLD group. Renal cholesterol (9.1 ± 1.6 vs. 7.5 ± 0.7 mg/g; p < 0.05) and non-esterified fatty acid (NEFA) (12.0 ± 3.0 vs. 8.4 ± 1.5 µEq/g; p < 0.01) were significantly decreased in the Tofo group. Transmission electron microscopy revealed the presence of fewer lipid droplets. mRNA sequencing analysis revealed that fatty acid metabolism-related genes were upregulated and NFκB signaling pathway-related genes were downregulated in the Tofo group. MicroRNA sequencing analysis indicated that miR-21a was downregulated and miR-204 was upregulated in the Tofo group. Notably, the expression of PPARα, which has been known to be negatively regulated by miR-21, was significantly increased, leading to enhancing ß-oxidation genes, Acox1 and Cpt1 in the Tofo group. Tofogliflozin decreased renal cholesterol and NEFA levels and improved inflammation through the regulation of PPARα and miR-21a.

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BACKGROUND: Inherited tubulopathies are rare kidney diseases with few data available in the literature regarding their long-term renal prognosis. This study aimed to evaluate the prevalence of kidney failure in adults with confirmed genetic tubulopathy and to describe the corresponding clinical and genetic findings. METHODS: In this observational cohort study, we focused on genetic tubulopathies assumed to impact kidney function. In all adult patients genetically diagnosed in our laboratory between 2001 and 2019, we estimated Glomerular Filtration Rate (eGFR) at diagnosis using the Modification of diet in renal disease (MDRD) formula. Kidney failure was defined as an eGFR < 60 ml/min/1.73 m2. RESULTS: A total of 2145 patients underwent genetic testing, confirming a genetic tubulopathy in 1031 cases (48%). We identified 116 patients out of 885 with available data with kidney failure, mostly diagnosed with Dent disease and distal renal tubular acidosis (respectively, 31% and 20%), followed by familial hypomagnesemia with hypercalciuria and nephrocalcinosis and renal hypophosphatemia/infantile hypercalcemia. Renal prognosis appeared particularly impacted in familial hypomagnesemia with hypercalciuria and nephrocalcinosis and Dent disease, while preserved in Gitelman syndrome. CONCLUSION: In this cohort, 13% of adults with genetic tubulopathy had kidney failure at diagnosis, with this rate varying greatly according to tubulopathies and suggesting a significant impact on renal prognosis. Even in adults, genetic analyses yield a good diagnostic rate in selected patients, and should be performed as soon as possible, in order to improve the renal management of patients and their relatives.

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Background: A potential independent association between arterial stiffness (AS) and the development of new-onset chronic kidney disease (CKD) has not been thoroughly examined. Patients and methods: A total of 6929 participants were collected from the Kailuan study. All participants were free of CKD at the baseline. The participants were divided into four groups based on their brachial-ankle pulse wave velocity (baPWV) values. Cox regression models were used to analyze the relationship between baPWV values and the risk of new-onset CKD. Results: Over the course of a 10.06-year follow-up period, a total of 962 cases of new-onset CKD were documented. Cox proportional hazards analyses showed that a higher baPWV quartile was linked to an increased risk of new-onset CKD. Conclusions: Brachial-ankle pulse wave velocity has a strong correlation with the development of new-onset CKD. Therefore, baPWV can be considered an innovative indicator for predicting the occurrence of new-onset CKD.

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BACKGROUND: The HIV Organ Policy Equity (HOPE) Act allows individuals living with HIV to accept organs from donors with HIV. This practice widens the pool of available organs, but also presents important virological questions, including the potential for HIV superinfection of the recipient, viral persistence in the kidney, and loss of virological control. METHODS: We addressed these questions by performing in-depth longitudinal viral sequence analyses on urine, blood, and urine-derived renal epithelial cells from twelve recipients of HIV+ kidney allografts. RESULTS: We amplified donor-derived HIV-1 env sequences in 5 out of 12 recipients post-transplant. These donor-derived env sequences were amplified from recipient urine, urine-derived renal epithelial cells, and plasma between 12 and 96-hours post-transplant and remained detectable up to 16-days post-transplant. Env sequences were also detected in kidney biopsies taken from the allografts before implantation in 6 out of the 12 transplant cases, indicating the presence of donor virus within the organ. One recipient had a viremic episode 3.5 years after transplantation as a result of ART interruption. Only recipient strain viral sequences were detected in blood, suggesting that the donor virus, if still present, was not reactivated during the temporary ART withdrawal. CONCLUSIONS: This study demonstrates that the HIV env sequences in a donor kidney can be amplified from biopsies taken from the allograft before implantation and can be detected transiently in blood and urine samples collected from the organ recipients post-transplantation.

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Chronic kidney disease (CKD) is a major cause of death and disability worldwide. It is usually diagnosed at early levels because of its slow progression. Treatment should consider CKD complications (such as electrolyte level imbalance, vascular calcification, and bone mineral disorders), as well as the development of CKD itself. Large-scale studies have shown that current treatment guidelines are nearly ineffective and fail to achieve treatment goals. Guidelines have not paid as much attention to magnesium (Mg) as the other electrolytes, while Mg has a significant role in the treatment goals of CKD. Hypomagnesemia is the only electrolyte imbalance that is equally prevalent in all stages of CKD. A lower plasma Mg level in each stage of CKD is associated with a higher risk of CKD progression and cardiac events. Magnesium exerts its effects both directly and via other ions. Mg supplementation increases insulin sensitivity while reducing proteinuria and inflammation. It lowers blood pressure and inhibits vascular calcification primarily because of its effects on calcium and phosphate, respectively. Vitamin D supplementation for low-active vitamin D in CKD patients increases vascular calcification and cardiac events, but magnesium supplementation enhances vitamin D levels and activity without increasing the risk of cardiac events. However, careful attention is required due to the potential threats of hypermagnesemia, particularly in advanced CKD stages. Starting magnesium supplementation early in patients' treatment plans will result in fewer side effects and more advantages. More original research is needed to determine its optimal dose and serum levels.