Effect of phosphatase and tensin homolog-induced putative kinase 1/ E3 ubiquitin ligase Parkin mediated mitochondrial autophagy on chronic kidney disease myocardial injury and the intervention mechanism of Shenshuai recipe.

OBJECTIVE: To study whether Shenshuai recipe (, SSR) can play a protective role on chronic kidney disease myocardial injury model through phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/E3 ubiquitin ligase Parkin (Parkin) mitochondrial autophagy pathway. METHODS: Forty-eight nephrectomized rats were randomly divided into six groups: sham-operated group, model group, Benazepril group, low, medium and high-dose groups of SSR. The rats were given the cor-responding intervention for six weeks, then were sacrificed. Serum was examined by enzyme linked immunosorbent assay (ELISA). Cardiac ultrasound was used to detect cardiac function in 5/6 nephrectomized rats. Myocardial tissue was examined by light and electron microscopy; PINK1, Parkin, microtubule-associated protein1 light chain 3 II (LC3B), sequestosome 1 (P62), BECN1 (Beclin-1) and dynamin-related protein 1 (Drp-1) were measured by real time polymerase chain reaction (RT-PCR), Western blot (WB) and immunohistochemistry (IHC). RESULTS: The expression levels of blood urea nitrogen (BUN) and creatinine (SCr) in the model group were significantly higher than those in the sham-operated group, indicating that modeling was successful. SSR can protect myocardium by reducing the relative expression of creatine kinase myocardial isoenzyme and hypersensitivity cardiac troponin I (P<0.05). SSR can improve cardiac function in rats after ultrasound testing. SSR can improve the pathological manifestations of myocardial tissue after Masson staining. SSR can increase the number of autophagosomes and autophagiclysosomes in 5/6 nephrectomized rats (P<0.05). Determined by RT-PCR, WB and IHC, SSR can increase the relative expression of PINK1, Parkin, and LC3B (P<0.05), and decrease the relative expression of P62, Beclin-1 and Drp-1 (P<0.05). CONCLUSIONS: The PINK1/Parkin mitochondrial autophagy pathway in myocardial tissues in 5/6 nephrectomy CKD myocardial injury rats was inhibited. SSR can activate PINK1/Parkin mitochondrial autophagy to enhance mitochondrial autophagy, and play a protective role in myocardial tissues.

Estimated glomerular filtration rate in clinical practice: Consensus positioning of the Brazilian Society of Nephrology (SBN) and Brazilian Society of Clinical Pathology and Laboratory Medicine (SBPC/ML) / Estimativa da taxa de filtração glomerular na prática clínica: posicionamento consensual da Sociedade Brasileira de Nefrologia (SBN) e Sociedade Brasileira de Patologia Clínica e Medicina Laboratorial (SBPC/ML)

ABSTRACT Chronic kidney disease (CKD) represents one of today's main public health problems. Serum creatinine measurement and estimation of the glomerular filtration rate (GFR) are the main tools for evaluating renal function. There are several equations to estimate GFR, and CKD-EPI equation (Chronic Kidney Disease - Epidemiology) is the most recommended one. There are still some controversies regarding serum creatinine measurement and GFR estimation, since several factors can interfere in this process. An important recent change was the removal of the correction for race from the equations for estimating GFR, which overestimated kidney function, and consequently delayed the implementation of treatments such as dialysis and kidney transplantation. In this consensus document from the Brazilian Societies of Nephrology and Clinical Pathology and Laboratory Medicine, the main concepts related to the assessment of renal function are reviewed, as well as possible existing controversies and recommendations for estimating GFR in clinical practice.

RESUMO A doença renal crônica (DRC) representa um dos principais problemas de saúde pública da atualidade. A dosagem da creatinina sérica e a estimativa da taxa de filtração glomerular (TFG) são as principais ferramentas para avaliação da função renal. Para a estimativa da TFG, existem diversas equações, sendo a mais recomendada a CKD-EPI (Chronic Kidney Disease - Epidemiology). Existem ainda algumas controvérsias com relação à dosagem da creatinina sérica e da estimativa da TFG, uma vez que vários fatores podem interferir nesse processo. Uma importante mudança recente foi a retirada da correção por raça das equações para estimativa da TFG, que superestimavam a função renal, e consequentemente retardavam a implementação de tratamentos como diálise e transplante renal. Neste documento de consenso da Sociedade Brasileira de Nefrologia e Sociedade Brasileira de Patologia Clínica e Medicina Laboratorial são revisados os principais conceitos relacionados à avaliação da função renal, possíveis controvérsias existentes e recomendações para a estimativa da TFG na prática clínica.

Coronary Plaque Characteristics in Patients With Chronic Kidney Failure: Impact on Cardiovascular Events and Mortality.

BACKGROUND: In patients with coronary artery disease, coronary plaques with high-risk features and low-attenuation plaque burden are independent measures associated with major adverse cardiovascular events (MACEs). Patients with chronic kidney failure may have different coronary artery disease characteristics. The aim was to assess the association of coronary plaque characteristics and coronary artery disease extent with MACE and all-cause mortality in patients with chronic kidney failure. METHODS: Potential kidney transplant candidates who underwent coronary computed tomography angiography as part of the cardiac screening program before kidney transplantation were included. We evaluated high-risk plaques and diameter stenosis semiqualitatively and quantified coronary artery calcium score and plaque burden (percentage atheroma volume). RESULTS: In 484 patients with chronic kidney failure and few or no symptoms of coronary artery disease (mean age, 53±12 years; 62% men; 32% on dialysis), 56 (12%) patients suffered MACE and 69 (14%) patients died during a median follow-up of 4.9 years. High-risk plaques were present in 39 (70%) patients with MACE. Median calcified plaque burden was 3.7% in patients with MACE versus 0.2% in patients without MACE. The median low-attenuation plaque burden was 0.3% versus 0.03%, respectively. In semiqualitative analyses, the presence of high-risk plaque and a higher coronary artery calcium score were associated with increased risk of MACE (hazard ratio (HR), 2.0 [95% CI, 1.0-3.7]; P=0.040; HR, 1.2 [95% CI, 1.0-1.3]; P=0.014), respectively. Neither were associated with all-cause mortality. In quantified analysis, increasing levels of both calcified and low-attenuation plaque burdens were associated with risk of MACE (HR, 2.6 [95% CI, 1.8-3.7]; P<0.001; HR, 2.6 [95% CI, 1.5-4.5]; P=0.001 [per variable doubling, respectively]) and all-cause mortality (HR, 1.6 [95% CI, 1.2-2.1]; P=0.002; HR, 1.8 [95% CI, 1.1-3.0]; P=0.028, respectively). CONCLUSIONS: In patients with chronic kidney failure, calcified and low-attenuation plaque burdens were independently associated with MACE and all-cause mortality, while high-risk plaques and coronary artery calcium score were only associated with MACE. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01344434.

Efficacy and safety of ketoanalogue supplementation combined with protein-restricted diets in advanced chronic kidney disease: a systematic review and meta-analysis.

BACKGROUND: The benefits and harms of protein-restricted diets supplemented with ketoanalogues in patients with chronic kidney disease (CKD) remain uncertain. We aimed to evaluate the effects of ketoanalogues supplemented to protein-restricted diets in patients with advanced CKD. METHODS: We conducted systematic literature searches of PubMed, Embase, Scopus, and Cochrane Library up to June 3, 2024. Randomized controlled trials comparing ketoanalogue supplementation with a low- or very low-protein diet versus a low-protein diet alone in stages 3-5 CKD patients were selected. Outcomes included glomerular filtration rate (GFR), end-stage kidney disease (ESKD), all-cause mortality, and blood levels of urea nitrogen, calcium, phosphorus, and albumin. Triceps skin fold, mid-arm muscle circumference, lean body mass, and subjective global assessment were also evaluated. The protocol for this systematic review was registered in the International Prospective Register of Systematic Reviews (PROSPERO; registration number CRD42023465754). RESULTS: A total of 16 trials comprising 1344 participants were identified, with a median follow-up of 13 months. Compared to a low-protein diet alone, ketoanalogues supplemented to a protein-restricted diet resulted in a significantly higher GFR, decreased levels of urea nitrogen and phosphorus, and increased levels of calcium. Furthermore, ketoanalogues combined with a protein-restricted diet showed a marginally lower risk of ESKD in participants without diabetes. No significant differences were observed in all-cause mortality, albumin, mid-arm muscle circumference, lean body mass, and subjective global assessment. CONCLUSIONS: For stages 3-5 CKD patients, ketoanalogues combined with a protein-restricted diet may help postpone initiation of dialysis, improve calcium-phosphate homeostasis, and slow GFR decline, while maintaining a similar nutritional status and survival. Larger, long-term studies are needed to confirm these potential benefits, especially in CKD patients with diabetes.

Tuberous Sclerosis Complex and the kidneys: what nephrologists need to know / Complexo da Esclerose Tuberosa e rins: o que os nefrologistas devem saber

Abstract Tuberous sclerosis complex (TSC) is an autosomal dominant disease characterized by the development of hamartomas in the central nervous system, heart, skin, lungs, and kidneys and other manifestations including seizures, cortical tubers, radial migration lines, autism and cognitive disability. The disease is associated with pathogenic variants in the TSC1 or TSC2 genes, resulting in the hyperactivation of the mTOR pathway, a key regulator of cell growth and metabolism. Consequently, the hyperactivation of the mTOR pathway leads to abnormal tissue proliferation and the development of solid tumors. Kidney involvement in TSC is characterized by the development of cystic lesions, renal cell carcinoma and renal angiomyolipomas, which may progress and cause pain, bleeding, and loss of kidney function. Over the past years, there has been a notable shift in the therapeutic approach to TSC, particularly in addressing renal manifestations. mTOR inhibitors have emerged as the primary therapeutic option, whereas surgical interventions like nephrectomy and embolization being reserved primarily for complications unresponsive to clinical treatment, such as severe renal hemorrhage. This review focuses on the main clinical characteristics of TSC, the mechanisms underlying kidney involvement, the recent advances in therapy for kidney lesions, and the future perspectives.

Resumo O complexo da esclerose tuberosa (CET) é uma doença autossômica dominante caracterizada pelo desenvolvimento de hamartomas no sistema nervoso central, coração, pele, pulmões e rins e outras manifestações, incluindo convulsões, tubérculos corticais, linhas de migração radial, autismo e deficiência cognitiva. A doença está associada a variantes patogênicas nos genes TSC1 ou TSC2, resultando na hiperativação da via mTOR, um importante regulador do crescimento e metabolismo celular. Consequentemente, a hiperativação da via mTOR leva à proliferação anormal do tecido e ao desenvolvimento de tumores sólidos. O envolvimento renal no CET é caracterizado pelo desenvolvimento de lesões císticas, carcinoma de células renais e angiomiolipomas renais, que podem progredir e causar dor, sangramento e perda da função renal. Nos últimos anos, houve uma mudança notável na abordagem terapêutica do CET, especialmente no tratamento das manifestações renais. Os inibidores de mTOR surgiram como a principal opção terapêutica, enquanto intervenções cirúrgicas como nefrectomia e embolização são reservadas principalmente para complicações que não respondem ao tratamento clínico, como hemorragia renal grave. Esta revisão se concentra nas principais características clínicas do CET, nos mecanismos subjacentes ao envolvimento renal, nos recentes avanços na terapia para lesões renais e nas perspectivas futuras.

Impact of Chronic Kidney Disease and Gout on End-Stage Renal Disease in Type 2 Diabetes: Population-Based Cohort Study.

Background: We examined the impact of gout on the end-stage renal disease (ESRD) risk in patients with type 2 diabetes mellitus (T2DM) and determined whether this association differs according to chronic kidney disease (CKD) status. Methods: Using the Korean National Health Insurance Service, this nationwide cohort study enrolled 847,884 patients with T2DM who underwent health checkups in 2009. Based on the presence of CKD (estimated glomerular filtration rate <60 mL/min/1.73 m2) and gout (two outpatient visits or one hospitalization within 5 years), patients were classified into four groups: CKD-Gout-, CKD- Gout+, CKD+Gout-, and CKD+Gout+. Patients with incident ESRD were followed up until December 2018. Results: Among 847,884 patients, 11,825 (1.4%) experienced progression to ESRD. ESRD incidence increased in the following order: 0.77 per 1,000 person-years (PY) in the CKD-Gout- group, 1.34/1,000 PY in the CKD-Gout+ group, 8.20/1,000 PY in the CKD+Gout- group, and 23.06/1,000 PY in the CKD+Gout+ group. The presence of gout modified the ESRD risk in a status-dependent manner. Hazard ratios (HR) were 1.49 (95% confidence interval [CI], 1.32 to 1.69) and 2.24 (95% CI, 2.09 to 2.40) in patients without and with CKD, respectively, indicating a significant interaction (P<0.0001). The CKD+Gout+ group had a markedly higher risk of developing ESRD (HR, 18.9; 95% CI, 17.58 to 20.32) than the reference group (CKD-Gout-). Conclusion: Gout substantially enhances the risk of ESRD, even in the absence of CKD. Concurrent CKD and gout synergistically increase the risk of ESRD. Therefore, physicians should carefully screen for hyperuricemia to prevent progression to ESRD.

Management of chronic kidney disease: a Hong Kong consensus recommendation.

Chronic kidney disease (CKD) imposes a significant burden on healthcare systems worldwide, and diabetes is a major risk factor for CKD. There is currently no consensus in Hong Kong regarding the prioritisation of early identification and intervention for CKD. A comprehensive and Hong Kong-specific diabetes and CKD treatment guideline is also lacking. A multidisciplinary group of experts discussed issues surrounding the current management of CKD and reviewed evidence in the context of local experience to support recommendations. The experts used a modified Delphi approach to finalise recommendations. Consensus was regarded as ≥75% acceptability among all expert panel members. The panel members finalised 14 CKD-focused consensus statements addressing disease definition, screening, disease monitoring, lifestyle management, and treatment strategies. The recommendations provided are relevant to the Hong Kong healthcare setting and can be used as a guide by physicians across various specialties to facilitate the appropriate management of CKD.

Financial Benefits of Renal Dose-Adjusted Dipeptidyl Peptidase-4 Inhibitors for Patients with Type 2 Diabetes and Chronic Kidney Disease.

BACKGRUOUND: Dipeptidyl peptidase-4 (DPP4) inhibitors are frequently prescribed for patients with type 2 diabetes; however, their cost can pose a significant barrier for those with impaired kidney function. This study aimed to estimate the economic benefits of substituting non-renal dose-adjusted (NRDA) DPP4 inhibitors with renal dose-adjusted (RDA) DPP4 inhibitors in patients with both impaired kidney function and type 2 diabetes. METHODS: This retrospective cohort study was conducted from January 1, 2012 to December 31, 2018, using data obtained from common data models of five medical centers in Korea. Model 1 applied the prescription pattern of participants with preserved kidney function to those with impaired kidney function. In contrast, model 2 replaced all NRDA DPP4 inhibitors with RDA DPP4 inhibitors, adjusting the doses of RDA DPP4 inhibitors based on individual kidney function. The primary outcome was the cost difference between the two models. RESULTS: In total, 67,964,996 prescription records were analyzed. NRDA DPP4 inhibitors were more frequently prescribed to patients with impaired kidney function than in those with preserved kidney function (25.7%, 51.3%, 64.3%, and 71.6% in patients with estimated glomerular filtration rates [eGFRs] of ≥60, <60, <45, and <30 mL/min/1.73 m2, respectively). When model 1 was applied, the cost savings per year were 7.6% for eGFR <60 mL/min/1.73 m2 and 30.4% for eGFR <30 mL/min/1.73 m2. According to model 2, 15.4% to 51.2% per year could be saved depending on kidney impairment severity. CONCLUSION: Adjusting the doses of RDA DPP4 inhibitors based on individual kidney function could alleviate the economic burden associated with medical expenses.

Trimethylamine N-oxide: a meta-organismal axis linking the gut and fibrosis.

BACKGROUND: Tissue fibrosis is a common pathway to failure in many organ systems and is the cellular and molecular driver of myriad chronic diseases that are incompletely understood and lack effective treatment. Recent studies suggest that gut microbe-dependent metabolites might be involved in the initiation and progression of fibrosis in multiple organ systems. MAIN BODY OF THE MANUSCRIPT: In a meta-organismal pathway that begins in the gut, gut microbiota convert dietary precursors such as choline, phosphatidylcholine, and L-carnitine into trimethylamine (TMA), which is absorbed and subsequently converted to trimethylamine N-oxide (TMAO) via the host enzyme flavin-containing monooxygenase 3 (FMO3) in the liver. Chronic exposure to elevated TMAO appears to be associated with vascular injury and enhanced fibrosis propensity in diverse conditions, including chronic kidney disease, heart failure, metabolic dysfunction-associated steatotic liver disease, and systemic sclerosis. CONCLUSION: Despite the high prevalence of fibrosis, little is known to date about the role of gut dysbiosis and of microbe-dependent metabolites in its pathogenesis. This review summarizes recent important advances in the understanding of the complex metabolism and functional role of TMAO in pathologic fibrosis and highlights unanswered questions.

Mineralocorticoid Receptor Antagonism Prevents Aortic Plaque Progression and Reduces Left Ventricular Mass and Fibrosis in Patients With Type 2 Diabetes and Chronic Kidney Disease: The MAGMA Trial.

BACKGROUND: Persistent mineralocorticoid receptor activation is a pathologic response in type 2 diabetes and chronic kidney disease. Whereas mineralocorticoid receptor antagonists are beneficial in reducing cardiovascular complications, direct mechanistic pathways for these effects in humans are lacking. METHODS: The MAGMA trial (Mineralocorticoid Receptor Antagonism Clinical Evaluation in Atherosclerosis) was a randomized, double-blind, placebo-controlled trial in patients with high-risk type 2 diabetes with chronic kidney disease (not receiving dialysis) on maximum tolerated renin-angiotensin system blockade. The primary end point was change in thoracic aortic wall volume, expressed as absolute or percent value (ΔTWV or ΔPWV), using 3T magnetic resonance imaging at 12 months. Secondary end points were changes in left ventricle (LV) mass; LV fibrosis, measured as a change in myocardial native T1; and 24-hour ambulatory and central aortic blood pressures. Tertiary end points included plasma proteomic changes in 7596 plasma proteins using an aptamer-based assay. RESULTS: A total of 79 patients were randomized to placebo (n=42) or 25 mg of spironolactone daily (n=37). After a modified intent-to-treat, including available baseline data of study end points, patients who completed the trial protocol were included in the final analyses. At the 12-month follow-up, the average change in PWV was 7.1±10.7% in the placebo group and 0.87±10.0% in the spironolactone group (P=0.028), and ΔTWV was 1.2±1.7 cm3 in the placebo group and 0.037±1.9 cm3 in the spironolactone group (P=0.022). Change in LV mass was 3.1±8.4 g in the placebo group and -5.8±8.4 g in the spironolactone group (P=0.001). Changes in LV T1 values were significantly different between the placebo and spironolactone groups (26.0±41.9 ms in the placebo group versus a decrease of -10.1±36.3 ms in the spironolactone group; P=6.33×10-4). Mediation analysis revealed that the spironolactone effect on thoracic aortic wall volume and myocardial mass remained significant after adjustment for ambulatory and central blood pressures. Proteomic analysis revealed a dominant effect of spironolactone on pathways involving oxidative stress, inflammation, and leukocyte activation. CONCLUSIONS: Among patients with diabetes with moderate to severe chronic kidney disease at elevated cardiovascular risk, treatment with spironolactone prevented progression of aortic wall volume and resulted in regression of LV mass and favorable alterations in native T1, suggesting amelioration of left-ventricular fibrosis. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02169089.

Prevalence of Fabry disease in patients with left ventricular hypertrophy and renal involvement (PrEFaCe). / Prevalencia de la enfermedad de Fabry en los pacientes con hipertrofia ventricular izquierda e insuficiencia renal (PrEFaCe).

INTRODUCTION AND AIMS: Fabry disease (FD) causes glycosphingolipid accumulation in the vascular endothelium, with predominantly cardiac and renal involvement. Its prevalence in patients with concomitant involvement of these two organs is unknown. The objective of the study was to determine the prevalence of FD in patients with left ventricular hypertrophy and any degree of chronic kidney disease. PATIENTS AND METHODS: Patients with ventricular thickness ≥13mm and kidney disease from 29 Spanish hospitals were included. Sociodemographic variables and target organ involvement of FD were collected. Laboratory determinations of EF were carried out, with an enzymatic activity test±genetic test in men and direct genetic test in women. RESULTS: Eight hundred ninety-eight patients with left ventricular hypertrophy and chronic kidney disease were included. The presence of heart failure and cardiorenal syndrome was common (46.1% and 40.1%). Three patients (2 men and 1 woman) were diagnosed with FD, based on the presence of a pathogenic variant in the GLA gene and classic signs of FD, resulting in a prevalence of 0.33% (CI 95% 0.06-1%). Six patients (0.66%) presented genetic variants of unknown significance, without showing classic signs of FD, while in 13 patients (3.2%) performing the blood test was impossible. CONCLUSIONS: FD is an important cause of left ventricular hypertrophy and chronic kidney disease. Genetic diagnosis is crucial for avoiding biases and ensuring accurate identification of FD, especially in women. The results support the inclusion of this disease in the differential diagnosis of patients with ventricular hypertrophy ≥13mm and chronic kidney disease.

Effects of cold and hot temperatures on the renal function of people with chronic disease.

OBJECTIVES: This study investigated the effects of hot and cold temperature on the renal function of people with chronic diseases, such as diabetes, hypertension, and chronic kidney disease, using large-scale clinical data. METHODS: We used retrospective cohort data from the Clinical Data Warehouse of the Seoul St Mary's Hospital, which contains clinical, diagnostic, laboratory, and other information about all patients who have visited the hospital since 1997. We obtained climate data from the Automated Synoptic Observing System of the Korea Meteorological Administration. The heat index was used as a measuring tool to evaluate heat exposure by indexing the actual heat that individuals feel according to temperature and humidity. The estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. To investigate changes in renal function trends with heat index, this study used generalized additive mixed models. RESULTS: Renal function decreased linearly with increasing heat index after approximately 25°C, which was considered the flexion point of temperature. A linear decrease in the eGFR was observed with the effects of 0 to 5 lag days. Although there was a correlation observed between the decrease in eGFR and temperatures below -10°C, the results did not indicate statistical significance. CONCLUSIONS: The results of our study provide scientific evidence that high temperatures affect the renal function of people with chronic diseases. These results can help prevent heat-related morbidity by identifying those who are more likely to develop renal disease and experience worsening renal function.

Admixture Mapping of Chronic Kidney Disease and Risk Factors in Hispanic/Latino Individuals From Central America Country of Origin.

BACKGROUND: Chronic kidney disease (CKD) is highly prevalent in Central America, and genetic factors may contribute to CKD risk. To understand the influences of genetic admixture on CKD susceptibility, we conducted an admixture mapping screening of CKD traits and risk factors in US Hispanic and Latino individuals from Central America country of origin. METHODS: We analyzed 1023 participants of HCHS/SOL (Hispanic Community Health Study/Study of Latinos) who reported 4 grandparents originating from the same Central America country. Ancestry admixture findings were validated on 8191 African Americans from WHI (Women's Health Initiative), 3141 American Indians from SHS (Strong Heart Study), and over 1.1 million European individuals from a multistudy meta-analysis. RESULTS: We identified 3 novel genomic regions for albuminuria (chromosome 14q24.2), CKD (chromosome 6q25.3), and type 2 diabetes (chromosome 3q22.2). The 14q24.2 locus driven by a Native American ancestry had a protective effect on albuminuria and consisted of 2 nearby regions spanning the RGS6 gene. Variants at this locus were validated in American Indians. The 6q25.3 African ancestry-derived locus, encompassing the ARID1B gene, was associated with increased risk for CKD and replicated in African Americans through admixture mapping. The European ancestry type 2 diabetes locus at 3q22.2, encompassing the EPHB1 and KY genes, was validated in European individuals through variant association. CONCLUSIONS: US Hispanic/Latino populations are culturally and genetically diverse. This study focusing on Central America grandparent country of origin provides new loci discovery and insights into the ancestry-of-origin influences on CKD and risk factors in US Hispanic and Latino individuals.

Sarcopenia as a predictor of mortality in kidney transplant recipients: A 5-year prospective cohort study with propensity score matching.

BACKGROUND: Sarcopenia is known to bring about adverse outcomes in elderly populations and dialysis patients. However, whether it is a risk factor in kidney transplant recipients (KTRs) has not yet been established. In the present study, the association of sarcopenia with mortality was investigated in KTRs. METHODS: We conducted a single-center prospective cohort study and recruited KTRs who were more than 1-year posttransplant from August 2017 to January 2018. The participants were followed for 5 years, and the Kaplan-Meier method and Cox proportional hazards model were used to assess patient survival. RESULTS: A total of 212 KTRs with a median age of 54 years and median transplant vintage of 79 months were enrolled in this study. Among them, 33 (16%) had sarcopenia according to the Asia Working Group for Sarcopenia 2019 at baseline. During the 5-year follow-up period, 20 (9.4%) died, 5 returned to dialysis after graft loss, and 4 were lost to follow-up. The 5-year overall survival rate was 90%. After 1:1 propensity score matching, a matched cohort with 60 KTRs was generated. The overall survival rate was significantly lower in the sarcopenia group compared to the non-sarcopenia group (p = 0.025, log-rank test). Furthermore, mortality risk was significantly higher in the sarcopenia group compared to the non-sarcopenia group (hazard ratio = 7.57, 95% confidence interval = 0.94-62). CONCLUSION: Sarcopenia was a predictor of mortality in KTRs. KTRs with suboptimal muscle status who were at risk for poor survival could have a clinical benefit by interventions for sarcopenia.

Predictive Role of Resilience and Hope on Adherence to Treatment in Hemodialysis Patients.

Objective: To determine the predictive role of resilience and hope on adherence to treatment in hemodialysis patients hospitalized in two hospitals affiliated to Shiraz University of Medical Sciences (Shiraz, Iran). Methods: This is a descriptive-analytical study that was conducted in 2021-2022 on 120 patients treated in hemodialysis sections in Namazi and Shahid Faqihi teaching hospitals. Sampling was conducted using a stratified random method. Demographic information questionnaires, Connor and Davidson's resilience, Snyder's hope and adherence to kidney patients' treatment questionnaires were used to collect the data. Results: The finds showed that the levels of resilience, hope, and adherence to treatment had hight level. More specifically, it was indicated that the mean and standard deviation for the total resilience score, the hope variable, and adherence to total treatment was 75.45±14.34, 40.43±3.66, and 80.12±18.20, respectively; which have maximum possible scores of 100, 48 and 100. Thus, it can be said that no correlation was observed between resilience and adherence to treatment variables (p>0.05); hope variable and adherence to treatment (p>0.05), and adherence to treatment with hope and resilience variables (p>0.05). However, hope and resilience variables showed a direct and weak correlation with each other (r=0.36, p<0.05); that is, patients who had more hope indicated better resilience as well. Conclusion: Although in this study we found that the resilience and hope variables were not able to predict the treatment adherence, hope and resilience indicated a direct and weak correlation. It is recommended that nurses should pay more attention to hope and resilience of hemodialysis patients in order to promote their health.

[Renoprotective treatments : renin-angiotensin-aldosterone system blockade and beyond]. / Néphroprotection médicamenteuse : au-delà du blocage du système rénine-angiotensine.

RENOPROTECTIVE TREATMENTS: RENIN-ANGIOTENSINALDOSTERONE SYSTEM BLOCKADE AND BEYOND. Patients with chronic kidney disease (CKD) require both etiological and symptomatic treatments to slow renal function decline. Reductions of protein and salt intakes are required. Pharmacological treatments combines blockade of the renin-angiotensin system, sodium-glucose co-transporter type 2 inhibitors and mineralocorticoid receptor antagonists in most diabetic patients. The albumin creatinine ration (ACR) in morning spot urine samples is now a therapeutic target both in diabetic and non-diabetic CKD patients.

NÉPHROPROTECTION MÉDICAMENTEUSE : AU-DELÀ DU BLOCAGE DU SYSTÈME RÉNINE-ANGIOTENSINE. Au-delà du traitement étiologique éventuel d'une maladie rénale chronique (MRC), et du contrôle de l'ensemble des facteurs de risque vasculaire, un traitement symptomatique est nécessaire pour ralentir le déclin de la fonction rénale. La prise en charge diététique permet de limiter les apports en protéines et en sel. Le traitement pharmacologique comporte nécessairement une association d'un bloqueur du système rénine-angiotensine-aldostérone, le plus souvent un inhibiteur du co-transport sodiumglucose de type 2 (SGLT2i) et chez certains diabétiques un antagoniste des récepteurs des minéralocorticoïdes (ARM). Le rapport albuminurie/créatininurie (RAC) sur un échantillon d'urine devient une cible thérapeutique aussi bien chez les non-diabétiques que chez les diabétiques.

[Chronic kidney disease : a genuine public health burden]. / La maladie rénale chronique : un authentique fardeau de santé publique.

CHRONIC KIDNEY DISEASE: A GENUINE PUBLIC HEALTH BURDEN. Chronic kidney disease (CKD) is a frequent pathology. It requires regular screening and, once diagnosed, specific follow-up. Complications are serious, as end-stage CKD needs renal replacement therapy, and cardiovascular events are common. Over and above its complications, CKD also impacts the quality of life of patients.

"LA MALADIE RÉNALE CHRONIQUE : UN AUTHENTIQUE FARDEAU DE SANTÉ PUBLIQUE. La maladie rénale chronique (MRC) est une pathologie fréquente. Il est nécessaire de la dépister régulièrement, puis de mettre en place un suivi spécifique lorsqu'elle est diagnostiquée. Ses complications sont graves, car à un stade dit terminal, la MRC nécessite un traitement de suppléance rénale, et les événements cardiovasculaires sont fréquents. Au-delà des complications cliniques, la MRC impacte également la qualité de vie des patients."

[Chronic kidney disease: how to benefit form coordinated care?] / Maladie rénale chronique : bien connaître le parcours de soins sur son territoire.

CHRONIC KIDNEY DISEASE: HOW TO BENEFIT FORM COORDINATED CARE? Chronic kidney disease (CKD) is a major goal of public health. At each stage of CKD, from screening to renal replacement therapy, coordinated care at geographic level or population-based may contribute to enhance effectiveness and efficiency. Kidney transplantation, home-dialysis and conservative treatment must be prioritized.

MALADIE RÉNALE CHRONIQUE : BIEN CONNAÎTRE LE PARCOURS DE SOINS SUR SON TERRITOIRE. Du point de vue du système de soins, la maladie rénale chronique (MRC) est un modèle de maladie chronique. Aux différents stades de l'évolution de la MRC, du dépistage à la suppléance, une coordination du parcours sur chaque territoire et une approche populationnelle des différents acteurs ­ MSP, CPTS, structures hospitalières... ­ contribuent à l'efficacité et l'efficience des soins. L'éducation thérapeutique est centrale pour permettre au patient d'être assuré, rassuré, en gagnant en autonomie. La greffe, la dialyse autonome et le traitement conservateur sont prioritaires.

[Detection and diagnosis of chronic kidney disease to take action as early as stage 3]. / Dépistage et diagnostic de la maladie rénale chronique pour agir dès le stade 3.

DETECTION AND DIAGNOSIS OF CHRONIC KIDNEY DISEASE TO TAKE ACTION AS EARLY AS STAGE 3. The prevalence of chronic kidney disease (CKD) is constantly increasing. The considerable impact of CKD on all-cause mortality, cardiovascular morbidity and on health economy makes it a real public health issue. Early detection helps to prevent progression to advanced stages of the disease. Targeted screening in populations at risk is recommended, with the use of 3 tests: serum creatinine, estimation of GFR and measurement of albumin/creatinine ratios. Once diagnosed, management of CKD involves nephroprotective measures such as blood pressure management, correction of metabolic complications, and prevention of drug toxicity. The general practitioner has a central role in the screening and initial management of CKD.

DÉPISTAGE ET DIAGNOSTIC DE LA MALADIE RÉNALE CHRONIQUE POUR AGIR DÈS LE STADE 3. La prévalence de la maladie rénale chronique (MRC) est en constante augmentation. L'impact considérable de la MRC sur la mortalité toutes causes, sur la morbidité cardiovasculaire et sur l'économie de la santé en fait un véritable enjeu de santé publique. Le dépistage précoce permet de prévenir la progression vers des stades avancés de la maladie. Le dépistage ciblé chez les populations à risque est recommandé, avec l'utilisation de trois tests : créatininémie, estimation du débit de filtration glomérulaire (DFG) et mesure du rapport albumine/créatinine (RAC). Une fois diagnostiquée, la prise en charge de la MRC implique des mesures de néphroprotection telles que la gestion de la pression artérielle, la correction des complications métaboliques et la limitation de la toxicité médicamenteuse. Le médecin généraliste joue un rôle central dans le dépistage et la prise en charge initiale de la MRC.