International Journal of Nephrology and Renovascular Disease最新文献

Introduction: The causes of chronic kidney disease (CKD) in people living in Sub-Saharan Africa await identification. Also, whether cardiovascular risk and disease extent differ among patients with different CKD etiologies is uncertain.

Methods: In this prospective cross-sectional study, we examined the presumed causes of chronic kidney disease (CKD) and their relationships with cardiovascular risk and disease in 743 consecutive patients from a sub-Saharan low-income population.

Results: Hypertensive nephropathy (HNP) (60.2%), diabetic nephropathy (DNP) (24.4%), HIV associated CKD (20.0%) and glomerular disease (13.6%) comprised the major CKD etiologies upon enrolment at the hospital nephrology clinic. Pulse pressure was larger in patients with concurrent HNP and DNP than in those with HNP only (p<0.001). Pulse pressure and systolic blood pressure were larger in HNP or/and DNP patients than those with HIV associated CKD and glomerular disease (p=0.04 to <0.001). Cardiovascular disease was more prevalent in patients with HNP and concurrent HNP and DNP than those from other etiologic categories (p<0.05). HNP and DNP were associated with pulsatile pressures (pulse pressure and systolic blood pressure) independent of one another (p<0.01). In adjusted product of coefficient mediation analysis, mean arterial or distending pressure accounted fully for the potential impact of HNP on pulsatile pressures (103.9-115.7%) but not for that of DNP on the respective pressures (-2.0%-(-)7.5%).

Conclusion: HNP is by far the most prevalent presumed cause of CKD in this African population. Cardiovascular risk and disease differ markedly across CKD etiological categories.

Hyperphosphataemia represents a significant challenge in the management of chronic kidney disease, exerting a pronounced influence on the pathogenesis of cardiovascular complications and mineral bone disorders. Traditional approaches to address hyperphosphataemia involve implementing dietary phosphate restrictions, administering phosphate binders, and, in cases of end-stage renal disease, resorting to dialysis. Unfortunately, these interventions frequently prove inadequate in maintaining phosphate levels within recommended ranges. Additionally, commonly employed pharmacological agents are not immune to eliciting adverse events, thereby limiting their prescription and therapeutic adherence. There is a growing focus on exploring novel therapeutic strategies in this context. The current discussion centres on tenapanor, a pharmacological agent predominantly acting as a selective inhibitor of sodium/hydrogen exchanger isoform 3 (NHE3). Its mechanism of action involves modulating tight junctions, resulting in reduced sodium absorption and intestinal paracellular permeability to phosphate. Furthermore, tenapanor downregulates sodium-dependent phosphate 2b transport protein (NaPi2b) expression, thereby impeding active transcellular phosphate transport. Clinical trials have elucidated the efficacy and safety profile of tenapanor. This evidence hints at a potential paradigm shift in the management of hyperphosphataemia. However, the burgeoning optimism surrounding tenapanor warrants tempered enthusiasm, as further research remains indispensable. The imperative lies in meticulously delineating its efficacy and safety contours within the crucible of clinical practice. In this review, we synthesize the intricate interplay between hyperphosphataemia and Chronic Kidney Disease-Mineral Bone Disorder, and we discuss the existing pharmacological interventions for hyperphosphataemia and explore emerging treatment paradigms that offer novel perspectives in managing elevated phosphate levels in CKD patients.

Background: We assessed the anti-SARS-CoV-2 spike antibody response to four doses of BNT162b2 mRNA COVID-19 vaccine in Japanese hemodialysis patients and determined factors associated with the anti-SARS-CoV-2 spike antibody titer after the fourth dose.

Methods: Fifty-one patients were enrolled in this single-center, prospective, longitudinal study. Change in anti-SARS-CoV-2 spike antibody titers between after the second and fourth doses were evaluated. Multiple linear regression analysis was used to identify factors associated with the anti-SARS-CoV-2 spike antibody titer after the fourth dose.

Results: The anti-SARS-CoV-2 spike antibody titer was higher 4 weeks after the fourth dose compared with 4 weeks after the third dose (30,000 [interquartile range (IQR), 14,000-56,000] vs 18,000 [IQR, 11,000-32,500] AU/mL, p<0.001) and 4 weeks after the second dose (vs 2896 [IQR, 1110-4358] AU/mL, p<0.001). Hypoxia-inducible factor prolyl hydroxylase inhibitor use (standard coefficient [β]=0.217, p=0.011), and the log-anti-SARS-CoV-2 spike antibody titer 1 week before the fourth dose (β=0.810, p<0.001) were correlated with the log-anti-SARS-CoV-2 spike antibody titer 4 weeks after the fourth dose, whereas only the log-anti-SARS-CoV-2 spike antibody titer 1 week before the fourth dose (β=0.677, p<0.001) was correlated with the log-anti-SARS-CoV-2 spike antibody titer 12 weeks after the fourth dose.

Conclusion: Hypoxia-inducible factor prolyl hydroxylase inhibitor use and the anti-SARS-CoV-2 spike antibody titer before the fourth dose were associated with the anti-SARS-CoV-2 spike antibody titer after the fourth dose in Japanese hemodialysis patients.

Background: Acute kidney injury (AKI) is a frequent complication in critical patients, leading to a worse prognosis. Although its consequences are worse among critical patients, AKI is also associated with less favorable outcomes in non-critical patients. Therefore, understanding the magnitude of the problem in these patients is crucial, yet there is a scarcity of evidence in non-critical settings, especially in resource limited countries. Hence, the study aimed at determining the incidence and predictors of hospital acquired acute kidney injury (HAAKI) in non-critical medical patients who were admitted at a large tertiary hospital in Ethiopia.

Methods: A retrospective chart review study was conducted from September 25, 2022 to January 20, 2023 among 232 hospitalized non-critical medical patients admitted to St. Paul's Hospital Millennium Medical College between January 2020 and January 2022. The incidence of HAAKI was estimated using incidence density per total person day (PD) observation of the study participants. To identify predictors of HAAKI, a log binomial regression model was fitted at a p value of ≤0.05. The magnitude of association was measured using adjusted relative risk (ARR) with its 95% CI.

Results: During the median follow-up duration of 11 days (IQR, 6-19 days), the incidence of HAAKI was estimated to be 6.0 per 100 PD (95% CI = 5.5 to 7.2). Significant predictors of HAAKI were found to be having type 2 diabetes mellitus (ARR = 2.36, 95% CI = 1.03, 5.39, p-value=0.042), and taking vancomycin (ARR = 3.04, 95% CI = 1.38, 6.72, p-value=0.006) and proton pump inhibitors (ARR = 3.80, 95% CI = 1.34,10.82, p-value=0.012).

Conclusion: HAAKI is a common complication in hospitalized non-critical medical patients, and is associated with a common medical condition and commonly prescribed medications. Therefore, it is important to remain vigilant in the prevention and timely identification of these cases and to establish a system of rational prescribing habits.

Introduction: AKI is a frequent complication in sepsis patients and is estimated to occur in almost half of patients with severe sepsis. However, there is currently no effective therapy for AKI in sepsis. Therefore, the therapeutic approach is focused on prevention. Based on this, there is an opportunity to examine a panel of biomarker models for predicting AKI.

Material and methods: This prospective cohort study analysed the differences in Cystatin C, Beta-2 Microglobulin, and NGAL levels in sepsis patients with AKI and sepsis patients without AKI. The biomarker modelling of AKI prediction was done using machine learning, namely Orange Data Mining. In this study, 130 samples were analysed by machine learning. The parameters used to obtain the biomarker panel were 23 laboratory examination parameters.

Results: This study used SVM and the Naïve Bayes model of machine learning. The SVM model's sensitivity, specificity, NPV, and PPV were 50%, 94.4%, 71.4%, and 87.5%, respectively. For the Naïve Bayes model, the sensitivity, specificity, NPV, and PPV were 83.3%, 77.8%, 87.5%, and 71.4%, respectively.

Discussion: This study's SVM machine learning model has higher AUC and specificity but lower sensitivity. The Naïve Bayes model had better sensitivity; it can be used to predict AKI in sepsis patients.

Conclusion: The Naïve Bayes machine learning model in this study is useful for predicting AKI in sepsis patients.

Advances in the treatment of kidney failure with chronic dialysis have stagnated over the past three decades, with over 50% of patients still managed by conventional in-hospital haemodialysis. In parallel, the demands of chronic dialysis medical care have changed and evolved due to a growing population that has higher frailty and multimorbidity. Thus, the gap between the needs of kidney failure patients and the healthcare capability to provide effective overall management has widened. To address this problem, healthcare policy has increasingly aligned towards a human-centred approach. The paradigm shift of human-centred approach places patients at the forefront of decision-making processes, ensuring that specific needs are understood and prioritised. Integration of human-centred approaches with patient care has been shown to improve satisfaction and quality of life. The aim of this narrative is to evaluate the current clinical challenges for managing kidney failure for dialysis providers; summarise current experiences and unmet needs of chronic dialysis patients; and finally emphasise how human-centred care has advanced chronic dialysis care. Specific incremental advances include implementation of renal supportive care; home-assisted dialysis; hybrid dialysis; refinements to dialysis methods; whereas emerging advances include portable and wearable dialysis devices and the potential for the integration of artificial intelligence in clinical practice.

Glomeruli can be damaged in several conditions after kidney transplantation, with a potential impact on the graft function and survival. Primary glomerulonephritis, a group of glomerular immunological damage that results in variable histological patterns and clinical phenotypes, can occur in kidney transplant recipients as a recurrent or de novo condition. Specific immunologic conditions associated with kidney transplantation, such as acute rejection episodes, can act as an additional trigger after transplantation, impacting the incidence of these glomerulopathies. The post-transplant GN recurrence ranges from 3% to 15%, varying according to the GN subtype and post-transplant time, mainly occurring after 3-5 years of kidney transplantation. Advances in the knowledge of glomerulonephritis pathophysiology have provided new approaches to pre-transplant risk evaluation and post-transplant monitoring. Glomeruli can be affected by several systemic viral infections, such as human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B virus (HBV), severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), cytomegalovirus (CMV), and BK virus. The diagnosis of these infections, as well as the identification of possible complications associated with them, are important to minimize the negative impacts of these conditions on kidney transplant recipients' outcomes.

Background: Cardiovascular disease (CVD) is the primary cause of mortality in chronic kidney disease (CKD) patients, with metabolic disorders exacerbating this risk. Compared with body mass index, waist circumference (WC) has been proposed as a more effective indicator of abnormal visceral fat. However, the associations among CKD, abnormal WC, and CVD remain understudied.

Material and methods: A cross-sectional study in Taiwan (July 2006 to May 2016) involved 10,342 participants undergoing self-paid health checkups at a single medical center. Physical examinations and blood samples were taken to assess metabolic parameters, and renal function was evaluated using the Chronic Kidney Disease Epidemiology Collaboration formula. Coronary artery calcification (CAC) scores were determined through coronary 256-slice multidetector computed tomography angiography, with a CAC score of >0 Agatston unit (AU) and ≥ 400 AU denoting positive CAC and severe CAC, respectively.

Results: Sex-based comparisons were conducted between individuals with CKD and those without CKD. In the CKD group, both sexes exhibited significantly elevated levels for systolic blood pressure, serum fasting blood glucose (FBG), and hemoglobin A1c (HbA1c) as well as reduced serum high-density lipoprotein cholesterol. Examination of the associations of abnormal WC revealed that for both sexes, individuals with abdominal obesity (AO) were significantly older and had higher systolic/diastolic blood pressure, serum FBG, HbA1c, and lipid profiles compared with those without AO. Multiple logistic regression analysis revealed that CKD patients exhibited a more pronounced association with severe CAC scores compared with AO patients (odds ratios [ORs]: 2.7 and 1.4, respectively). Furthermore, the combined effects of AO and CKD (AO[+]/CKD[+]) resulted in increased risks of positive CAC (OR: 2.4, 95% confidence interval [CI]: 1.6-3.5) and severe CAC (OR: 4.4, 95% CI: 1.4-14.2).

Conclusion: Abdominal obesity significantly raised the odds of CAC and was associated to a 4.4-fold increased risk of severe CAC in CKD patients.

Background: Mounting evidence suggests that mitochondrial dysfunction contributes to lupus nephritis (LN) pathogenesis. Mitochondrial pyruvate carrier 1 (MPC1) and mitochondrial pyruvate carrier 2 (MPC2) mediating pyruvate transport from the cytoplasm to the mitochondrial matrix, determines the cell survival and cellular energy supply. Here, we aimed to investigate the association of mitochondrial pyruvate carrier expression with the clinical and histological features in LN.

Methods: Patients with biopsy-proven proliferative LN (class III and class IV, n=18) and membranous LN (class V, n=18) were included. Expression of MPC1 and MPC2 were examined by immunohistochemistry. MPC protein levels in the two groups were evaluated by the Student's t-test. Correlation analysis between MPC levels and clinicopathological features was performed by Spearman's rank correlation.

Results: Both MPC1 and MPC2 were exclusively expressed in renal tubules of enrolled LN. Significantly lower MPC1 and MPC2 were observed in patients with proliferative LN compared to membranous LN. In addition, the MPC1 and MPC2 were negatively correlated with SLEDAI-2K score, renal function, and renal pathology activity index.

Conclusion: Both MPC1 and MPC2 were localized in renal tubules, and decreased MPC content was more pronounced in proliferative LN than membranous LN. MPC levels were significantly correlated with renal functions and renal pathology activity.