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Background Chronic kidney disease (CKD) can lead to serious conditions such as anemia and cardiovascular disease, posing a growing global health challenge. End-stage renal disease (ESRD) requires treatments such as dialysis or kidney transplantation. Despite the widespread impact and rising prevalence of CKD and ESRD, comprehensive data remains limited in India. This study seeks to investigate the clinical, socio-demographic, and etiological profiles of CKD patients undergoing hemodialysis at a tertiary care hospital, with the goal of enhancing understanding and improving patient care. Methodology This retrospective cohort study, conducted at a tertiary care center, included 500 CKD patients undergoing hemodialysis, with comprehensive medical records. Data collected covered demographics (age, sex, education, and occupation), CKD etiology, disease duration, hemodialysis duration, viral marker status, blood transfusions, and vascular access details. With continuous variables reported as mean ± standard deviation (SD) and categorical variables as counts (percentages), statistical analysis was carried out using SPSS version 21 (IBM Corp., Armonk, New York, USA). The connections were examined using the Pearson Chi-square test, with P≤0.05 being deemed significant. Results The study revealed that hypertension was the primary cause of CKD in 58% of patients, followed by diabetes mellitus in 13%. A significant 93% of patients tested negative for viral markers such as human immunodeficiency virus (HIV), hepatitis C virus (HCV), and hepatitis B surface antigen (HBsAg). Hemodialysis duration varied, with 68% of patients undergoing dialysis for one to five years. Most patients had two (40%) or three (58%) dialysis sessions per week, and 84% had only one arteriovenous (AV) fistula surgery. Blood transfusions were common, with 62% of patients receiving between one and five transfusions. The gender distribution showed more males (372) than females (201), and the majority of patients were aged between 41 and 60 years. Conclusion This study highlights the importance of early detection and management of CKD, emphasizing preventive health measures, enhanced diagnostic capabilities, and sufficient resource allocation to reduce the disease burden. It also calls for further research into unknown CKD causes and strategies to improve patient care and outcomes.

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Background: Elastin degradation and severe calcification in the medial layer of the vessel wall, known as medial arterial calcification (MAC), is typical in the aging population and patients with metabolic disorders, such as diabetes and chronic kidney disease (CKD). We have previously reported that ethylene diamine tetraacetic acid (EDTA) delivery to the site of calcification can be achieved by tagging nanoparticles with an elastin antibody that recognizes explicitly damaged elastin, and such systemic therapy can remove focal calcium deposits from the calcified arteries in CKD rodent model. The current study aims to test whether heavy calcification seen throughout arterial tree and kidneys in CKD can be reversed with nanoparticle therapy. Methods: Thirty healthy male Sprague-Dawley rats weighing approximately 300 g, were placed on an adenine diet for 21 non-consecutive days to induce kidney failure, followed by daily vitamin D3 (VitD3) injections for 4 sequential days to cause severe calcification throughout the cardiovascular system and kidneys. DiR-dye loaded and elastin antibody conjugated albumin nanoparticles were used to confirm the targeting of nanoparticles to the calcification area. The rats were divided into two groups for targeted removal of calcification starting at day 7 of the last doses of VitD3. The experimental group received biweekly IV injections of anti-elastin antibody conjugated EDTA loaded human serum albumin nanoparticles (EDTA-HSA-El-Ab NPs), while the sham controls received blank nanoparticles (Blank-HSA-El-Ab NPs) (5 injections in total). Micro-computed tomography (microCT) was used to analyze the extent of calcification. Reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry studies were performed for osteogenic markers, including bone morphogenic protein 2 (BMP2), runt-related transcription factor 2 (RUNX2), and tissue non-specific alkaline phosphatase (TNAP). For comparison, aortic ring organ cultures from healthy rats were treated with high phosphate to induce calcification in vitro, and then they were treated with EDTA. Human calcified femoral arteries were also treated ex vivo with EDTA-HSA-EL-Ab NPs to test if nanoparticles remove heavy calcification. Results: EDTA-loaded nanoparticles that specifically target degraded elastin reversed existing heavy mineral deposits in arteries, as per elemental calcium analysis (124.161±34.410 µg Ca per mg of the dry aorta in Blank-HSA-El-Ab NPs vs. 100.520±19.131 µg in EDTA-HSA-El-Ab NPs group, P=0.04) and microCT (object volume, 129.001±37.785 vs. 29.815±24.169 mm3, P=0.0005). The reversal of aortic calcification was accompanied by a significant reduction of bone-associated mRNA expression of BMP2 and RUNX2 (P=0.01). Immunohistochemistry studies corroborated RT-PCR results, showing a reduction of BMP2 and RUNX2 stains in the vessel wall. The rat aortic ring culture study also showed similar results, where osteogenic genes (BMP2, RUNX2) and proteins (BMP2, RUNX2, TNAP) were suppressed upon reversal of calcification with EDTA (P=0.001). We also show ex vivo reversal of human femoral artery calcification by microCT (calcium intensity: untreated, 57.721±28.551 vs. day 6 of treatment, 5.441±3.615, P=0.01) by EDTA nanoparticle therapy. Conclusions: This is the first study showing the removal of calcium from heavily calcified arteries by using intravenous targeted EDTA therapy. Such therapy also reversed vascular smooth muscle cell osteoblastic transition and apoptosis in the arterial tissue, thereby potentially creating an environment for suitable tissue repair.

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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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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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Tubulointerstitial fibrosis (TIF) is present with chronic kidney disease (CKD). Vinpocetine (Vinpo) is used for treating cerebrovascular deficits, exhibiting some kidney-beneficial effects; however, its role in TIF is uncertain. So, the aim of this study was to investigate its potential impact on adenine-induced fibrotic CKD and explore the underlying mechanistic aspects. Eighteen male Wistar rats were categorized into three groups (n = 6 each). Group I was kept as controls and given saline; group II received adenine (300 mg/kg, twice weekly, i.p.) for induction of the CKD model; and group III was administered Vinpo (20 mg/kg/d, orally) concurrently with adenine. All treatments were administered for 4 weeks. Vinpo revealed an improvement in renal function and an alleviation of inflammation triggered by adenine via diminishing serum tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) levels. Further, Vinpo repressed the epithelial-mesenchymal transition (EMT) with preserved E-cadherin mRNA expression and lowered gene and immune expression of fibronectin and vimentin, respectively, besides attenuating the elevated G2/M arrest-related molecules (renal Ki67 protein contents and p21 gene expression). Renal pathological alterations caused by adenine were attenuated upon Vinpo administration. Interestingly, Vinpo suppressed abnormal renal ß-catenin immunoreactivity, Snail 1, and MMP-7 gene expression while simultaneously restored Klotho protein expression by downregulating DNA methyltransferase 1 enzyme (DNMT1) protein expression in the kidney. These data indicated that Vinpo effectively mitigated EMT and G2/M arrest-induced renal fibrosis in adenine-induced CKD rats by targeting DNMT1-associated Klotho suppression, subsequently inhibiting ß-catenin and its fibrotic downstream genes.

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Methotrexate (MTX) is a commonly used immunosuppressant and chemotherapeutic agent, widely prescribed for autoimmune diseases such as psoriasis, rheumatoid arthritis, and certain malignancies. It functions by inhibiting dihydrofolate reductase, leading to impaired DNA synthesis and cell proliferation. While generally well-tolerated, MTX has a narrow therapeutic index, and its adverse effects can be severe, including hepatotoxicity, pulmonary toxicity, and hematological complications such as pancytopenia. Pancytopenia involves the reduction of all three blood cell lines and can result in significant morbidity and mortality. The risk of MTX toxicity is notably higher in patients with renal impairment, as the kidneys are the primary route of drug excretion. Renal dysfunction can lead to the accumulation of MTX, enhancing its toxicity. Numerous studies and case reports have highlighted the risks of MTX toxicity, especially in patients with renal impairment. Pancytopenia can present insidiously, with symptoms such as mucosal ulcers, fever, and generalized weakness, making early detection crucial. We report a case of a male patient in his late 40s with a complex medical history, including psoriasis, insulin-dependent type 2 diabetes mellitus, chronic kidney disease (CKD) stage 3b, and coronary artery disease (CAD). The patient presented to the emergency department with a one-week history of fever, generalized weakness, mouth sores, and a five-day history of bilateral lower limb swelling and pain. Vital signs were stable, but physical examination revealed pallor, large ulcerative lesions in the buccal mucosa, and erythematous, scaly lesions on the lower limbs. The patient's medication history included methotrexate, which he had stopped two months prior but was inadvertently resumed at an increased dose two weeks prior to presentation. Laboratory findings revealed pancytopenia with worsening trends, prompting a bone marrow biopsy that showed hypocellular marrow. The patient's CKD likely exacerbated the MTX toxicity due to impaired drug clearance, leading to pancytopenia. Treatment included intravenous leucovorin, blood and platelet transfusions, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Despite initial critical presentation, the patient showed significant improvement, with recovery of blood counts and resolution of symptoms. He was discharged with stable hemoglobin, platelet, and white blood cell counts.

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This document reports a brief update to the previously published protocol of the MinDial study.Trial registration German Clinical Trials Register DRKS00029691. Registered on 12 Sept. 2022, https://drks.de/search/en/trial/DRKS00029691 .

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Estudios Multicéntricos como Asunto , Ensayos Clínicos Controlados Aleatorios como Asunto , Diálisis Renal , Insuficiencia Renal Crónica , Humanos , Insuficiencia Renal Crónica/terapia , Insuficiencia Renal Crónica/epidemiología , Insuficiencia Renal Crónica/diagnóstico , Factores de Riesgo , Alemania/epidemiología , Resultado del Tratamiento , Medición de Riesgo , Factores de Tiempo

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OBJECTIVE: This study aimed to investigate the effect of the soluble Klotho (sKlotho)/Wnt/ß-catenin signaling pathway on vascular calcification in rat models of chronic kidney disease (CKD) and the intervention effect of Shenyuan granules. METHODS: Rats with 5/6 nephrectomy and high phosphorus feeding were used to establish the vascular calcification model. The rats were given gradient doses of Shenyuan granules aqueous solution and calcitriol solution by gavage for 8 weeks, which were divided into experimental group and positive control group. RESULTS: The 5/6 nephrectomy combined with high phosphorus feeding induced thoracic aortic calcification in rats. Shenyuan granules intervention increased the serum sKlotho level, inhibited the mRNA and protein expression of Wnt1, ß-catenin, and Runx2 in the thoracic aorta, and alleviated thoracic aortic media calcification in rats. CONCLUSION: Shenyuan granules may partially regulate the Wnt/ß-catenin signaling pathway via serum sKl to interfere with the expression of Runx2, thereby improving vascular calcification in CKD.

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Medicamentos Herbarios Chinos , Glucuronidasa , Proteínas Klotho , Insuficiencia Renal Crónica , Calcificación Vascular , Vía de Señalización Wnt , beta Catenina , Animales , Masculino , Ratas , Aorta Torácica/metabolismo , Aorta Torácica/patología , beta Catenina/metabolismo , Subunidad alfa 1 del Factor de Unión al Sitio Principal/metabolismo , Modelos Animales de Enfermedad , Medicamentos Herbarios Chinos/farmacología , Medicamentos Herbarios Chinos/uso terapéutico , Glucuronidasa/metabolismo , Glucuronidasa/genética , Proteínas Klotho/metabolismo , Nefrectomía , Ratas Sprague-Dawley , Insuficiencia Renal Crónica/metabolismo , Insuficiencia Renal Crónica/complicaciones , Calcificación Vascular/metabolismo , Calcificación Vascular/etiología , Calcificación Vascular/patología , Vía de Señalización Wnt/efectos de los fármacos , Proteína Wnt1/metabolismo , Proteína Wnt1/genética

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Introduction According to a 2023 poll by the International Society of Nephrology, 850 million individuals worldwide suffer from chronic kidney disease (CKD) and hemodialysis (HD) is the primary treatment for 69% of the patients with CKD. While HD effectively regulates fluid balance and electrolyte levels, patients often face challenges such as weakness, exhaustion, and cognitive changes, which impact their quality of life. Sleep-related issues, including poor quality, excessive morning sleepiness, insomnia, and restless leg syndrome (RLS), are particularly common among HD patients. These disturbances stem from various factors, including psychological discomfort and biochemical imbalances. Dialysis shifts, despite their importance, remain poorly studied regarding their impact on sleep and biochemical parameters. Our study aims to address these gaps, exploring how different dialysis shifts affect sleep quality and biochemical parameters. Our hypothesis suggests that the particular dialysis shift that hemodialysis patients undergo has an impact on the quality of sleep, with various groups exhibiting varying degrees of sleep disturbance. Simultaneously, we believe that the time of dialysis shifts could influence biochemical parameter variations, which in turn could affect the quality of sleep in hemodialysis patients. Methodology This cross-sectional study focuses on assessing sleep problems and analyzing biochemical variables among hemodialysis (HD) patients in Georgia. A total of 150 participants were selected from morning, afternoon, and evening dialysis shifts, with strict inclusion criteria and exclusion criteria. Assessment procedures involved questionnaires on sleep quality, restless leg syndrome (RLS), daytime sleepiness, and severity of insomnia. Biochemical variables were obtained from the hospital records. Statistical analyses were performed using Graph Pad Prism software (GraphPad, San Diego, USA), including ANOVA and Chi-square tests for association between biochemical variables and dialysis shifts, as well as logistic regression for assessing the influence of biochemical variables on insomnia and poor sleep quality. The significance level was set at 95%. Results Results showed that patients in the afternoon shift undergo longer sessions of hemodialysis compared to other shifts. Notably, a larger proportion of morning shift patients reported poor sleep quality, while a smaller fraction of evening shift patients experienced insomnia. There were no significant associations between dialysis shift and excessive morning sleepiness or restless leg syndrome. Potassium emerged as the sole biochemical variable exhibiting an association with all three dialysis shifts. Biochemical parameters showed no discernible impact on insomnia or poor sleep quality. Conclusion Our findings suggest an association between poor sleep quality and insomnia with dialysis shifts. Hemodialysis does influence potassium levels. However, biochemical variables like sodium, potassium, calcium, phosphorus, vitamin D3, parathyroid gland hormone (PTH), and hemoglobin do not seem to affect poor sleep quality and insomnia. Further research is needed to explore potential sleep issues with nocturnal shifts and to assess if creatinine and chloride have any influence on poor sleep quality. It is important to acknowledge dialysis shift as a contributor to sleep problems, emphasizing the need for targeted interventions to enhance the quality of life for these patients.

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Background: Renal artery pseudoaneurysm (RAP) is one of the most stressful and life-threatening complications of partial nephrectomy, the standard treatment for small renal cell carcinoma. The use of a monopolar soft coagulation system for hemostasis during robot-assisted partial nephrectomy (RAPN) is expected to prevent post-surgical RAP development. In this study, we aimed to investigate how the use of a soft coagulation system in RAPN reduces postoperative pseudoaneurysms and changes renal function over time. Methods: The incidence of pseudoaneurysms and postoperative renal function were compared in 208 partial nephrectomies performed between May 2016 and March 2023 at a single institution, with propensity score matching to balance patient backgrounds. Outcomes were analyzed using multivariate logistic or linear regression analyses. Results: In total, 80 matched pairs were analyzed. One (1.2%) and eighteen (22.5%) pseudoaneurysms were found in the soft coagulation users and non-users, respectively (P<0.001). Compared to the non-user group, postoperative estimated glomerular filtration rates (eGFRs) in the user group were 89% vs. 96% (P<0.001), 87% vs. 93% (P=0.009), and 88% vs. 92% (P=0.15) at 1, 3, and 12 months, respectively. Subsequent multivariate analyses showed a lower incidence of pseudoaneurysms in the user group with an odds ratio of 0.05 [95% confidence interval (CI): 0.01 to 0.44; P=0.007], and no significant difference in the rate of change in renal function at 12 months postoperatively (-1.1%, 95% CI: -5.5% to 3.3%; P=0.61). Conclusions: The use of a soft coagulation system reduces pseudoaneurysm occurrence after partial nephrectomy. Although renal function decreased in the short-term for the use group, no long-term differences were observed.

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AIMS: Calciprotein particles (CPPs) are circulating calcium and phosphate nanoparticles associated with development of vascular calcification (VC) in chronic kidney disease (CKD). Although recent studies have been focusing on associations of CPPs with presence of VC in CKD, insights in the underlying processes and mechanisms by which CPPs might aggravate VC and vascular dysfunction in vivo are currently lacking. Here, we assessed overall burden of abdominal VC in healthy kidney donors and CKD patients, and subsequently performed transcriptome profiling in vascular tissue obtained from these subjects, linking outcome to CPP counts and calcification propensity. METHODS AND RESULTS: Calcification scores were quantified in renal arteries, iliac arteries and abdominal aorta, using computed tomography (CT) scans of kidney donors and CKD patients. Vascular tissue was collected from kidney donors (renal artery) and CKD patients (iliac artery), after which bulk RNA sequencing and gene set enrichment analysis (GSEA) was performed on a subset of patients. Calcification propensity (crystallization time, T50) was measured using nephelometry, and CPP counts with microparticle flow cytometric analysis. Increased calcification scores (based on CT) were found in CKD patients compared to kidney donors. Transcriptome profiling revealed enrichment for processes related to endothelial activation, inflammation, extracellular matrix (ECM) remodelling and ossification in CKD vascular biopsies compared to kidney donors. Calcification propensity was increased in CKD, as well as CPP counts, of which the latter significantly associated with markers of vascular remodelling. CONCLUSIONS: Our findings reveal that CKD is characterized by systemic VC with increased calcification propensity and CPP counts. Transcriptome profiling showed altered vascular gene expression with enrichment for endothelial activation, inflammation, ECM remodelling and ossification. Moreover, we demonstrate for the first time that vascular remodelling processes are associated with increased circulating CPP counts. Interventions targeting CPPs are promising avenues for alleviating vascular remodelling and VC in CKD.

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OBJECTIVES: Kidney diseases are considered silent killers due to the lack of well-defined symptoms. Public knowledge about chronic kidney disease (CKD) management has been shown to decrease the risk of CKD onset and progression to end-stage renal disease and renal failure. The main objective of this study was to assess the knowledge of kidney function, CKD symptoms, etiology, prevention and treatment in the general population. METHODS: A cross-sectional study using a validated questionnaire was conducted in Jordan to assess public knowledge of CKD. Public knowledge of CKD was assessed using a questionnaire consisting of 32 knowledge questions, including risk factors, symptoms, treatment, protective measures and kidney function. The knowledge level was classified according to the total score: poor (0-50%), intermediate (51-70%) and good/high (71-100%). Multiple regression analysis was performed to compare knowledge scores (KS) and predict associations with the participants' baseline characteristics. RESULTS: The level of knowledge about CKD among the 2181 participants was intermediate. The KS was significantly higher among participants with health issues such as hypertension, diabetes and heart problems, first-degree relatives working in the medical field, majors relevant to health, married, employed, highly educated, high-income and smokers. The main sources of knowledge about CKD were health professionals, TV shows, books and magazines. Multiple regression analysis showed an association between KS and age, sex, functional status, educational level and field, income, smoking status, having a family member/spouse work in the medical field, and knowledge source. CONCLUSIONS: The public level of knowledge about CKD management is greatly influenced by participants' health and social factors. Thus, improving public knowledge and perception through education and the media will significantly reduce CKD prevalence and incidence.

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Public awareness and educating the public about chronic kidney diseases (CKDs) is essential because of the high prevalence, and increased awareness can contribute to early detection, management and potentially slow down the progression of CKD.Creating awareness of the risk factors for CKD enables health policy developers to adopt preventive measures.CKD can significantly affect quality of life, and public awareness campaigns can emphasize the impact of CKD on overall well-being, motivating individuals to prioritize kidney health.

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Conocimientos, Actitudes y Práctica en Salud , Insuficiencia Renal Crónica , Humanos , Estudios Transversales , Jordania/epidemiología , Masculino , Femenino , Insuficiencia Renal Crónica/epidemiología , Adulto , Persona de Mediana Edad , Encuestas y Cuestionarios , Adulto Joven , Factores de Riesgo , Anciano , Adolescente

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AIMS: The new nomenclature of steatotic liver disease (SLD) including metabolic dysfunction-associated SLD (MASLD), MASLD and increased alcohol intake (MetALD), and alcohol-associated liver disease (ALD) has recently been proposed. We aimed to elucidate the relationship between each category of SLD and chronic kidney disease (CKD). METHODS: We investigated the effects of various SLDs on the development of CKD, defined as estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or positive for urinary protein, during a 10-year period in 12 138 Japanese subjects (men / women, 7984/4154; mean age, 48 years) who received annual health examinations including abdominal ultrasonography. RESULTS: The prevalences of SLD without metabolic dysfunction (SLD-MD[-]), MASLD, MetALD, and ALD were 1.7%, 26.3%, 4.9%, and 1.9%, respectively. During the follow-up period, 1963 subjects (16.2%) (men / women, 1374 [17.2%]/589 [14.2%]) had new onset of CKD. Multivariable Cox proportional hazard model analyses after adjustment of age, sex, eGFR, current smoking habit, diabetes mellitus, hypertension, and dyslipidemia showed that the hazard ratios (HR [95% confidence interval]) for the development of CKD in subjects with MASLD (1.20 [1.08-1.33], p = 0.001) and those with ALD (1.41 [1.05-1.88], p = 0.022), but not those with MetALD (1.11 [0.90-1.36], p = 0.332), were significantly higher than the HR in subjects with non-SLD. Interestingly, subjects with SLD-MD[-] had a significantly lower HR (0.61 [0.39-0.96], p = 0.034) than that in subjects with non-SLD. The addition of the novel classification of SLDs into traditional risk factors for the development of CKD significantly improved the discriminatory capacity. CONCLUSIONS: MASLD and ALD, but not SLD-MD[-], are independently associated with the development of CKD.

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AIM AND BACKGROUND: Chronic kidney disease (CKD) is associated with increased cardiovascular morbidity and mortality. This study aimed to assess the frequency of cardiac abnormalities across different stages of CKD, providing insights into the relationship between renal dysfunction and cardiac abnormalities. MATERIAL AND METHODS: A cross-sectional observational study was conducted at Lahore General Hospital's Nephrology Department, enrolling 356 non-dialysis CKD patients (stages I-V) over one year. Participants aged 18-65 years with CKD duration of three months or more were included. Exclusion criteria encompassed dialysis dependency, transplantation, acute kidney injury, and various cardiac conditions. Detailed echocardiographic evaluation of cardiac structure and function was noted. RESULTS: This study included 356 patients with CKD across stages I-V, with the majority in stages III (44.7%) and IV (36.5%). Significant variations were observed in age (p<0.000), hypertension prevalence (p=0.004), and smoking status. Haemoglobin, calcium, and phosphate levels differed significantly across stages (p<0.001). Echocardiographic findings revealed significant differences: left ventricular hypertrophy frequency increased from 12.5% in stages I-II to 60.0% in stage V (p=0.001); diastolic dysfunction worsened, with grades 2-3 dysfunction increasing from 6.2% in stages I-II to 51.4% in stage V (p=0.000); systolic dysfunction increased with reduced ejection fraction (<45%) more common in advanced stages (p=0.000); global longitudinal strain worsened from -18.47% to -15.34% (p=0.000); left atrial volume index and pulmonary hypertension also increased significantly (p=0.049). CONCLUSION: This study demonstrates a significant correlation between the progression of CKD and the severity of echocardiographic abnormalities. As CKD advances, structural and functional cardiac abnormalities increase, underscoring the importance of early cardiac evaluation and intervention to improve cardiovascular outcomes in non-dialysis-dependent CKD patients.

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AIM AND BACKGROUND: This study aimed to evaluate the quality of life (QoL) in end-stage kidney disease (ESRD) patients on maintenance hemodialysis through the Missoula-Vitas Quality of Life Index-15 (MVQOLI-15) to identify factors affecting their well-being. MATERIALS AND METHODS: A cross-sectional study was conducted at the Dialysis Unit of the Nephrology Department, Nishtar Hospital Multan. Over six months, 140 eligible patients were enrolled using non-probability consecutive sampling. Participants aged 18-80 years on maintenance hemodialysis for at least six months were evaluated using the MVQOLI-15 questionnaire assessing symptoms, function, interpersonal, well-being, and transcendence dimensions of QoL. Data were analyzed using the IBM SPSS Statistics for Windows, Version 26 (Released 2019; IBM Corp., Armonk, New York). Inferential statistical tests, including the t-test for comparing two groups and analysis of variance (ANOVA) for comparing multiple groups, were utilized to determine the significance of differences in QoL scores among different demographic and clinical categories. P-values less than 0.05 were considered statistically significant. RESULTS: The study analyzed 140 hemodialysis patients, with a mean age of 52.41 ± 16.31 years and an average hemodialysis duration of 4.55 ± 2.46 years. Most participants were aged 61-80 years (35.7%), had secondary education (44.3%), and were married (67.1%). QoL scores, measured using the MVQOLI, indicated mean values for symptoms at 4.51 ± 10.71, function at 5.77 ± 8.04, interpersonal at 7.49 ± 13.67, well-being at -13.60 ± 7.11, transcendence at 8.24 ± 13.12, and a total score of 16.24 ± 2.75. Significant findings include the following: females had higher symptom scores (p=0.001) and lower well-being scores (p=0.000); younger patients (<30 years) had higher function scores (p=0.054); patients on hemodialysis three times per week had higher function scores (p=0.006); patients taking 1 to 3 pills per day had higher transcendence scores (p=0.000); unmarried patients had higher symptoms scores (p=0.064) and lower well-being scores (p=0.004); and illiterate patients had higher symptoms (p=0.005) and transcendence scores (p=0.034). In total score, patients on hemodialysis once per week reported significantly better scores (p=0.011). CONCLUSION: This study highlights varied QoL experiences among hemodialysis patients, with transcendence scoring the highest and well-being, the lowest. Demographic factors such as age, gender, and education level significantly impact the QoL dimensions. Understanding these findings can guide personalized interventions to improve the well-being of hemodialysis patients.

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This study aimed to close an evidence gap concerning the relative efficacy of finerenone versus SGLT2is in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D). Canagliflozin was selected as a proxy for the SGLT2i class. Patient-level data of two randomized controlled trials (RCTs) of finerenone (FIDELIO-DKD and FIGARO-DKD) were used alongside aggregated data from CREDENCE, an RCT of canagliflozin. To account for meaningful between-study heterogeneity between each finerenone trial and CREDENCE, a matching-adjusted indirect comparison of a range of efficacy outcomes was undertaken for each finerenone study versus CREDENCE. These results were meta-analyzed, enabling the estimation of the relative effects of finerenone against canagliflozin. For the cardiorenal composite endpoint, the hazard ratio (HR) comparing finerenone to canagliflozin was 1.07 (95% CI: 0.83 to 1.36). The corresponding HRs for all-cause mortality, end-stage kidney disease and cardiovascular death were 0.99 (95% CI: 0.73 to 1.34), 1.03 (95% CI: 0.68 to 1.55) and 0.94 (95% CI: 0.64 to 1.37), respectively. The absence of statistically significant differences was consistent throughout the main analysis and a range of sensitivity analyses. Based on this study, using a large sample of data and adjusted for meaningful differences between the baseline characteristics of the included RCTs, there was no statistically significant evidence indicating a difference in the efficacy of finerenone compared to canagliflozin in the treatment of CKD in patients with T2D.

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Background: Chronic kidney disease (CKD) is a major public health burden and is often undiagnosed in the primary care setting. Untested and untreated, this often leads to renal failure and dialysis. Materials and Methods: This was a cross-sectional study of adults aged 20 years and over, diagnosed with type 2 diabetes mellitus and/or hypertension, with no previous history or record of CKD, and attending three chronic disease clinics in the Eastern Regional Health Authority (ERHA). Patients were screened for risk of CKD by using the albumin creatinine ratio. The eGFR was calculated based on serum creatinine by using the CKD Epidemiology Collaboration (EPI) 2009 equation. Results: In total, 430 patients agreed to participate with 61.2% of response rate. Of the 385 with complete data, 357 (92%) were detected as having a high risk for CKD; older patients (>66 years) and those with both diabetes and hypertension had high proportions of risk for CKD. There were significant associations between age, systolic hypertension, and the severity of risk for CKD. Conclusion: CKD is common at the primary care level among adults with NCDs in Trinidad, with many patients having been left out without being tested for CKD. Primary care physicians must take this into consideration in caring for NCD patients.

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The uremic toxin indoxyl sulfate (IS) has been related to the development of various medical conditions notably chronic kidney disease (CKD). Hence, quantification of this biomarker in biological fluids may be a diagnostic tool to evaluate renal system functionality. Numerous analytical methods including liquid chromatography, gas chromatography, spectroscopy, and electrochemical techniques have since been used to analyze IS in different biological fluids. The current review highlights the relevant studies that assessed IS with a special focus on sample preparation, which is essential to reduce or eliminate the effect of endogenous components from the matrix in bioanalysis.

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Aims: Chronic kidney disease (CKD) is a risk factor for the development of cardiovascular diseases, e.g., atherosclerosis and calcific aortic valve disease, leading inevitably to valve replacement surgery. CKD patients with bioprosthetic cardiovascular grafts, in turn, have a higher risk of premature graft degeneration. Peroxisome proliferator-activated receptor gamma (PPARγ) activation by pioglitazone has cardio-renal protective properties, and research using a heterotopic valve implantation model has shown anti-degenerative effects of PPARγ activation on bioprosthetic valved grafts (BVG) in rats. The present work aims to analyze a potential protective effect of pioglitazone treatment on BVG in an adenine-induced rat model of CKD. Methods and Results: BVG of Sprague Dawley rats were heterotopically implanted in Wistar rats in an infrarenal position for 4 and 8 weeks. Animals were distributed into three groups for each time point: 1) control group receiving standard chow, 2) CKD group receiving 0.25% adenine and 3) CKD + pioglitazone group (300 mg per kg of 0.25% adenine chow). BVG function was analyzed by echocardiography. Plasma analytes were determined and explanted grafts were analyzed by semi-quantitative real-time PCR, Western blot analysis, histology and immunohistology.PPARγ activation significantly reduced CKD-induced calcification of aortic and valvular segments of BVG by 44% and 53%, respectively. Pioglitazone treatment significantly also reduced CKD-induced intima hyperplasia by 60%. Plasma analysis revealed significantly attenuated potassium and phosphate levels after pioglitazone treatment. Moreover, PPARγ activation led to significantly decreased interleukin-6 gene expression (by 57%) in BVG compared to CKD animals. Pioglitazone treatment leads to functional improvement of BVG. Conclusion: This study broadens the understanding of the potential value of PPARγ activation in cardio-renal diseases and delineates pioglitazone treatment as a valuable option to prevent bioprosthetic graft failure in CKD. Further mechanistic studies, e.g., using small molecules activating PPARγ signaling pathways, are necessary for the evaluation of involved mechanisms. Additionally, the translation into pre-clinical studies using large animals is intended as the next research project.