Kidney & blood pressure research最新文献

Background Renal artery stenosis (RAS) is characterized by reduced renal perfusion, activating the renin-angiotensin-aldosterone system (RAAS), which can lead to secondary hypertension, ischemic nephropathy, and cardiac destabilization syndrome. These conditions have significant healthcare implications. Renovascular hypertension (RVH) in RAS patients can be managed through medical therapy and revascularization, either endovascular or surgical. While renal artery stenting (RAS) was once viewed as the most effective treatment for atherosclerotic renovascular disease, recent trials suggest no significant difference in RVH management between medical therapy alone and combined with renal artery stenting. However, certain subgroups have exhibited favorable outcomes in blood pressure control post-stenting. Summary This comprehensive review synthesizes data, including findings from the HERCULES trial, which showed a reduction in blood pressure from 162.3±18.5/77.7±11.5 mmHg to 145.7±20.7/75.4±11.0 mmHg over 36 months (P<0.0001). Additionally, the ASPIRE-2 study demonstrated significant decreases in blood pressures from 168±25/82±13 mmHg to 149±25/77±12 mmHg at 24 months (P<0.001). The review delves into the prevalence, pathophysiology, clinical manifestations, diagnosis, and treatment of RAS-related RVH, specifically analyzing the efficacy and safety of renal artery stenting. Key Messages The analysis indicates that renal artery stenting may be particularly advantageous for certain patient subgroups, enhancing blood pressure outcomes and overall clinical status. Nevertheless, the criteria for selecting candidates for this intervention remain under debate. Future research should focus on high-risk RAS patients to explore long-term benefits and refine the utilization of renal artery stents, ultimately improving RVH management.

Introduction: There is an increasing prevalence of chronic kidney disease (CKD) in Malaysia; hence, identifying factors associated with the early stage of CKD is crucial for preventive measures. This study investigated the association between various factors and their interaction in a multi-ethnic Malaysian cohort.

Methods: A nested case-control analysis was conducted on 3,160 eligible participants with renal profile data from The Malaysian Cohort project. CKD status was determined by estimated glomerular filtration rate using the Chronic Kidney Disease Epidemiology Collaboration equation. Multiple logistic regression analysis using the likelihood ratio method was used to identify the factors and their interaction with CKD.

Results: This study suggested five factors associated with CKD: gender, ethnicity, physical activity, atherogenic plasma index (AIP), and systolic blood pressure. There was an interaction between AIP and gender, with increased odds of CKD among men with high AIP.

Conclusions: As CKD is mainly asymptomatic until it is in the later stages, these five factors serve as valuable tools for predicting CKD and enhancing the identification of at-risk individuals, particularly among men with elevated AIP. Future studies should focus on using these factors, especially in preventing new CKD cases and their progression.

Introduction: Urine proteomics plays an important role in the screening of biomarkers for infant diseases. However, there is no unified standard for the selection of urine samples for urine proteomics. It is also unclear whether there are differences in proteomics between whole urine and urine supernatant. Therefore, the urine of preterm infants was used as the research sample to explore the differences in protein profiles between the whole urine and urine supernatant of preterm infants by proteomics.

Methods: Urine samples were collected from five preterm infants with a gestational age of <28 weeks at their corrected gestational age of 37 weeks. Each preterm urine was divided into whole urine and supernatant. Urine protein was extracted and analyzed by liquid chromatography-tandem mass spectrometry.

Results: The two groups of urine samples did not show significant clustering in the principal component analysis. A total of 2,607 proteins were detected in the two groups of urine samples, of which 82 proteins were unique to whole urine samples and 56 proteins were unique to urine supernatant samples. The molecular functions, the main biological processes, and subcellular localization of the differential proteins were analyzed. In other neonatal-related diseases, there was no significant difference in protein enrichment between whole urine and urine supernatant.

Conclusions: This study analyzed the differences between whole urine and urine supernatant in urine proteomics of preterm infants. In neonatal-related diseases, there is no significant difference in urinary protein biomarkers between whole urine and urine supernatant.

Background: Inflammatory rheumatic diseases regularly require the use of disease-modifying antirheumatic drugs (DMARDs). The use of DMARDs in patients with end-stage chronic kidney disease (CKD stage 5D) is particularly challenging due to the lack of systematic studies available for this patient population. This narrative review aimed to address the aspect of DMARD therapy in CKD 5D.

Summary: The current article is a narrative review. References were sourced from the following databases: PubMed, Web of Science, Cochrane Library, and Scopus. The search period spanned from 1975 to 2024. There is a notable lack of systematic data on this topic. The available literature was reviewed to provide insights, despite the limited availability of comprehensive studies. Individuals with terminal kidney disease can presumably be safely treated with leflunomide, mycophenolic acid, sulfasalazine, azathioprine, belimumab, and anti-CD20. For all other substances, there are either significant restrictions, insufficient data, or inadequate experience.

Key messages: Some conventional and biologic DMARDs are available for the management of inflammatory rheumatic diseases in CKD stage 5D. It is essential to consider the limitations on kidney function, as they can significantly affect the pharmacokinetics of medications. Consequently, slightly more frequent checkups are recommended when using the defined preparations.

Introduction: End-stage kidney disease patients on maintenance hemodialysis (HD) are prone to increase cardiovascular and non-cardiovascular mortality at long and short interdialytic intervals of an intermittent thrice-weekly schedule. Variations in fluid and electrolyte status during and in dialysis-free periods may predispose patients to sudden cardiac death (SCD). We studied SCD in HD in relation to the interdialytic interval in patients on a twice-weekly HD schedule.

Methods: An ambispective cohort study was done and data of HD patients on a twice-weekly schedule were collected from January 2009 to December 2017. The primary outcome was cardiovascular mortality and the secondary outcome was an estimate of the standard mortality ratio (SMR) at each 12-h period interval of the HD schedule. Deaths were categorized as SCD, non-SCD, and non-cardiac death as per standard definitions.

Results: Of 413 participants, 289 died. The rate of cardiovascular death accounted for 121 (42%), and non-cardiac death was 168 (58.1%). SCD was the most common cardiovascular event, accounting for 83 (28.7%) of overall mortality. SCD is more likely to occur in the first 12 h after dialysis following the 3-day-long interdialytic interval (SMR: 1.68) and in the 12 h before the next dialysis session after a short interval (SMR: 1.39).

Conclusion: Occurrence of SCD was higher at two different time points, i.e., 12-h period from the starting with the dialysis procedure and 12-h period before the start of the next session of HD at the end of a short interval.

Background: Patients diagnosed with chronic kidney disease (CKD) are at a higher risk of encephalopathy, a condition exacerbated by the presence of various chronic diseases. Hypertension is a significant risk factor for brain damage in the general population but is limitedly discussed in patients with CKD. Brain magnetic resonance imaging (MRI) is an excellent tool for evaluating cerebral white matter lesions. Most previous studies showed the association between hypertension and cerebral white matter lesions in the general population but were less focused on CKD patients. Therefore, the present study aims to investigate the effect of hypertension on the cerebral white matter lesions of brain MRI in patients with CKD.

Methods: In this retrospective study, we enrolled 1,749 CKD patients who underwent brain MRIs to evaluate their brain lesions in Kaohsiung Medical University Hospital. The cerebral white matter hyperintensities (WMHs) on MRI were evaluated according to the Fazekas scale, including separate periventricular and deep white matter lesions from grade 0 to grade 3. The multivariable ordinal regression model was analyzed to determine the independent association between hypertension or blood pressure and cerebral WMHs with adjustment of controlling age, sex, education, comorbidities (hyperlipidemia, cerebrovascular disease, chronic heart failure), laboratory data (hemoglobin, albumin, triglyceride, estimated glomerular filtration rate).

Results: Hypertension was associated with the Fazekas scale of periventricular lesions in multivariable-adjusted ordinal regression analysis (odds ratio [OR] 1.63, 95% confidence interval [CI] 1.15-2.30) after full adjustment. However, the hypertension comorbidities did not associate with the Fazekas scale of deep white matter lesions in the fully adjusted model (OR 1.24, 95% CI [0.89-1.75]). A positive association between blood pressure (per 10 mm Hg increase) and the Fazekas scale was mainly on diastolic blood pressure rather than systolic blood pressure.

Conclusions: In CKD patients, hypertension was associated with brain white matter damage; in particular, Fazekas scale of periventricular lesions. Further study is needed to evaluate adequate blood pressure control to decrease the risk of brain damage in CKD patients.

Introduction: CFHR5 nephropathy is considered a subtype of C3 glomerulopathy. It was originally described in Greek Cypriot families and it is characterized by the time with the development of microscopic hematuria and proteinuria associated with a fast progression toward ESKD, especially in men. These symptoms present an autosomal dominant inheritance pattern and are associated with the exon 2 to 3 duplication of the CFHR5 gene.

Case presentation: Here, we describe a novel clinical phenotype associated with a variant of the CFHR5. The affected subjects present the clinical features of autosomal dominant tubulo-interstitial kidney disease. They present with CKD of unknown origin with no hematuria nor proteinuria. Like the classical CFHR5 nephropathy, males have a worse prognosis than females, with a fast progression toward ESKD in the second-third decade of life. Kidney pathology shows severe tubular atrophy and interstitial fibrosis and infiltrate. Arteries involvement is characterized by thickening of the intima layer, while no major alterations are described at the glomerular level. Electron microscopy confirms no interstitial or glomerular filtration barrier alterations.

Conclusion: The exact mechanism behind this phenomenon remains unclear; we hope that our case will encourage further investigation.

Introduction: Chronic kidney disease worsens the prognosis of cardiovascular disease (CVD) and vice versa. This study aimed to evaluate the mortality of patients with a high CVD burden and unplanned start of maintenance hemodialysis (HD).

Methods: A retrospective study was performed at a tertiary cardiological hospital in São Paulo, Brazil. Hospitalized patients ≥18 years old were identified by the public chronic kidney replacement therapy regulatory system between January 1, 2014, and December 31, 2018. In-hospital and post-discharge mortality, along with associated risk factors, were assessed. Death information up to December 31, 2022, was obtained from the state of São Paulo mortality database.

Results: A total of 302 patients with unplanned start of HD were included. The mean age was 65 ± 13 years old; 68% were male. The heart conditions were as follows: 60% chronic heart failure, 27% coronary artery disease, 13% arrhythmia, and 7% valve disease. Comorbidities included: 93% hypertension, 62% diabetes, 31% dyslipidemia, and 27% known CKD. The mortality rate (deaths per 100 patient-years) was 71.4 between 0 and 3 months, 23.0 between 3 and 12 months, and 39.5 over the entire 0 to 12 months period. The factors independently associated with in-hospital death were age, heart valve disease, chronic obstructive pulmonary disease, positive serology for hepatitis B, and need for HD catheter replacement. The factors associated with post-discharge death (mean ± SD follow-up: 6.4 ± 1.4 years) were age, presence of two or more heart diseases, and HD catheter-related infection.

Conclusion: Patients with a high burden of cardiovascular morbidity and an unplanned start of HD exhibit elevated mortality rates. Some factors independently related to poorer outcomes, such as HD catheter-related complications, could potentially be mitigated through adequate pre-dialysis care.

Introduction: Shikonin is the major bioactive compound abundant in Lithospermum erythrorhizon and possesses diverse pharmacological properties. This study aimed to examine shikonin roles in experimental renal ischemia/reperfusion (I/R) injury.

Methods: Renal tissues and blood were collected from experimental renal I/R injury models. Kidney functions, structural injuries, and cellular death were assessed. Markers of endoplasmic reticulum (ER) stress were evaluated by RT-qPCR and Western blotting. The effect of shikonin on Sirt1/Nrf2/HO-1 signaling was detected by Western blotting and immunofluorescence staining. HK-2 cells that underwent hypoxia/reoxygenation (H/R) process were used to perform CCK-8 and flow cytometry.

Results: For in vivo analysis, renal dysfunctions and tissue structural damage induced by I/R were relieved by shikonin. Additionally, shikonin alleviated ER stress-induced apoptosis in I/R mice. For in vitro analysis, shikonin inhibited ER stress-stimulated apoptosis of H/R cells. Mechanistically, shikonin activated Sirt1/Nrf2/HO-1 signaling post-I/R, and inhibition of Sirt1 limited shikonin-mediated protection against ER stress-stimulated apoptosis in both animal and cellular models.

Conclusion: By activating Sirt1/Nrf2/HO-1 signaling, shikonin inhibits apoptosis caused by ER stress and relieves renal I/R injury.

Background: The Wilms' tumor suppressor gene (WT1) is a critical regulator in kidney development and disease pathogenesis. With the identification of at least 36 isoforms in mammals, each potentially playing distinct roles, WT1's complexity is becoming increasingly apparent. The -KTS and +KTS isoforms, in particular, have been implicated in DNA and RNA regulation, respectively. This review consolidates recent insights into WT1's multifaceted role in renal morphogenesis and its implications in kidney diseases.

Summary: Our review highlights WT1's expression during embryonic kidney development and its maintenance in postnatal kidney function. We discuss the association of WT1 mutations with genetic nephropathies like Denys-Drash and Frasier syndromes, emphasizing its genetic significance. Additionally, we explore the implications of WT1 expression alterations in glomerular diseases, such as IgA nephropathy and lupus nephritis, where its role extends beyond a mere biomarker to a potential therapeutic target.

Key messages: The WT1 gene and its protein products are central to understanding kidney morphogenesis and the molecular basis of renal disorders. As our understanding of WT1's regulatory mechanisms expands, so does the potential for developing targeted therapies for kidney diseases. This review calls for further research to elucidate the precise functions of WT1 isoforms and to explore the upstream regulators of WT1 that could offer novel treatment strategies for kidney pathologies. The significance of WT1 in intricate signaling pathways governing kidney health and disease is underscored, highlighting the need for continued investigation into this pivotal gene.