Kidney & blood pressure research最新文献

Introduction: Regular physical activity is beneficial for health but is often reduced in patients receiving maintenance hemodialysis treatment. Irisin is a muscle-secreted hormone that reportedly improves metabolism and slows down the progression of some chronic diseases. In this study, we aimed to investigate the relationship between physical activity capacity and serum irisin levels in hemodialysis patients.

Methods: Our study included 252 patients undergoing hemodialysis at Xuanwu Hospital Capital Medical University. Enzyme-linked immunosorbent assay was used to measure blood irisin levels. Body composition was analyzed by bioelectrical impedance analysis. The International Physical Activity Questionnaire (IPAQ) was used to score physical activity ability.

Results: Bivariate correlation analysis showed a positive correlation between IPAQ scores and ln irisin (the natural logarithm of irisin; r = 0.326, p < 0.001). Independent determinants of IPAQ scores were ln irisin, age, fasting glucose, and carbon dioxide combining power.

Conclusion: Our findings provide the first clinical evidence that serum irisin levels are positively correlated with physical activity capacity in hemodialysis patients.

Introduction: Serum platelet-activating factor (PAF) was proven to be associated with gestational hypertension. However, the predictive value of serum PAF at early pregnancy for the occurrence and outcomes of hypertensive disorders complicating pregnancy (HDCP) remained unclear.

Methods: The demographic and clinical characteristics of patients were compared among the different subgroups. The serum PAF level was determined using an enzyme-linked immunosorbent assay. The predictive value of serum PAF for the occurrence and outcomes of HDCP was evaluated using receiver operating characteristic curve analysis. The correlation of serum PAF with blood pressure was assessed using Spearman analysis.

Results: Both systolic blood pressure and diastolic blood pressure were significantly higher in HDCP patients, as well as the serum levels of TNF-α and IL-1β at diagnosis/enrollment, while serum levels of IL-10 showed the opposite trend. Serum PAF levels were significantly higher in patients with HDCP compared to normal pregnant women. Furthermore, serum PAF levels were higher in HDCP patients with mild preeclampsia compared to those with gestational hypertension and even more elevated in HDCP patients with severe preeclampsia at the early pregnancy stage and at diagnosis. In HDCP patients, increased serum PAF levels at early pregnancy and at diagnosis were associated with poor outcomes. Additionally, serum PAF levels could predict the occurrence of HDCP and poor outcomes.

Conclusion: Serum PAF from HDCP patients at both the early pregnancy and diagnosis stages could effectively predict the occurrence and outcome of HDCP.

Introduction: Gout, characterized by hyperuricemia and urate crystal deposition, is associated with systemic inflammatory complications, including kidney injury. This study aimed to investigate the role of serum nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome and associated cytokines (IL-1β and IL-18) in gout-related kidney injury (GRI).

Methods: A total of 279 gout patients (96 with renal injury and 183 without renal injury) and 100 healthy controls were included. Serum NLRP3, IL-1β, and IL-18 were measured and compared using an enzyme-linked immunosorbent assay. Receiver operating characteristic (ROC) analysis was carried out to evaluate the diagnostic values of individual or combinational biomarkers. Spearman's correlation analysis was employed to analyze correlations between NLRP3, IL-1β, and IL-18 and renal function indicators or serum uric acid.

Results: Serum levels of NLRP3, IL-1β, and IL-18 were significantly higher in gout patients compared to healthy controls (p < 0.001, gout group with kidney injury [GKI]: n = 96, gout group without kidney injury [GNKI]: n = 183, controls: n = 100), with elevated levels observed in GKI patients compared to GNKI (p < 0.001). Correlations between these markers were confirmed among all gout patients (n = 279), including serum NLRP3 with IL-1β (r = 0.34, p < 0.001) and NLRP3 with IL-18 (r = 0.47, p < 0.001). ROC analysis revealed that the combined model of NLRP3, IL-1β, and IL-18 showed improved diagnostic accuracy for GRI, with an AUC of 0.85 (95% CI: 0.81-0.89, p < 0.001). In GKI patients (n = 96), serum NLRP3, IL-1β, and IL-18 were inversely correlated with eGFR (NLRP3: r = -0.43, p < 0.01). Additionally, serum IL-18 positively correlated with serum uric acid levels (r = 0.27, p = 0.009).

Conclusion: These findings highlight the potential of serum NLRP3, IL-1β, and IL-18 as diagnostic markers and therapeutic targets in GRI, providing insights into early intervention and improved clinical outcomes in gout patients with renal complications.

Introduction: Serum Nostrin was recently identified as novel predictor of important clinical outcomes in acute kidney injury (AKI) and has also emerged as a predictor of recovery of kidney function (ROKF) in AKI patients. ROKF is a critical factor for the transition of AKI into chronic kidney disease (CKD). Therefore the aim of the present study was to evaluate serum Nostrin levels in CKD patients.

Methods: Blood samples were collected from CKD patients before and after dialysis, and serum Nostrin levels were determined using ELISAs.

Results: Serum Nostrin levels were previously shown to be significantly increased in AKI patients in comparison with healthy controls. In CKD patients, the levels of serum Nostrin were further increased without significant differences of Nostrin concentrations before and after dialysis.

Conclusion: The further elevation of serum Nostrin concentrations in CKD in comparison with AKI indicates a significant impairment of Nostrin turnover and supports the possible suitability of Nostrin as potential diagnostic value in both AKI and CKD.

Introduction: Although previous studies have investigated the impact of perirenal fat on chronic kidney disease (CKD), there are yet no systematic reviews and meta-analyses to investigate the association between perirenal fat and CKD.

Methods: We searched six English electronic databases including PubMed, Scopus, Web of Science, Ovid, Embase, and the Cochrane Library to select clinical studies that reported the relationship between perirenal fat and CKD, and the search period ranged from the establishment of the database to September 10, 2024. Two researchers independently screened the studies and ultimately compared the literature. Stata (version 16 SE; College Station, TX, USA) software was used for statistical analysis.

Results: A total of eight articles that included 2,576 patients were included in this meta-analysis. The results showed a significant association between perirenal fat and CKD (95% CI: 0.48-0.65, p = 0.00), and no heterogeneity was detected between these two groups (I2 = 31.06%, p = 0.18). Subgroup analysis revealed that whether it is diabetic nephropathy, nephropathy caused by abnormal cardiac function, or primary CKD, perirenal fat is closely related to them.

Conclusion: The results of this systematic review and meta-analysis showed that perirenal fat thickness is closely related to CKD. Clinicians should pay attention to relevant indicators when diagnosing and treating patients with CKD.

Introduction: Previous studies have found a relative risk of 1.6-2 for renal function deterioration with serum uric acid level increment. However, the association between the baseline urinary uric acid (UUA) level and renal function decline remains unclear, and we aimed to assess this association.

Methods: In this retrospective cohort-controlled study, we included patients who met the following inclusion criteria: age >18 years, the presence of at least one UUA level in their electronic medical records (EMR), and two eGFR values. The exclusion criteria were chronic dialysis treatment before the baseline eGFR or any history of kidney transplantation. The EMR of the patients have been retrospectively screened between December 31, 2001, and January 31, 2022. The study group consisted of patients with UUA levels of ≥750 mg/day. In the control group, we included patients whose every UUA level was <750 mg/day. The primary endpoint was a composite of eGFR decline of ≥50%, eGFR <15 mL/min, dialysis initiation, or death. Secondary endpoints were as follows: eGFR decline of ≥50%, the latest eGFR <15 mL/min, or death. The endpoints were compared between the groups by Cox proportional hazards model analysis.

Results: We included 480 patients in the study group and 2,998 in the control group. The primary endpoint was observed in 30.95% and 16.25% of participants in the control and study groups, respectively; however, after it was compared between the two groups using the Cox model, there was no significant difference (HR: 1.20, 95% CI: 0.96-1.51, p = 0.11). Similarly, no significant differences in the rates of secondary endpoints between the two groups were observed, except the difference between the eGFR declines >50% which was significant, as was observed by the Cox model (HR: 2.22, 95% CI: 1.47-3.37, p < 0.001).

Conclusion: There was no significant difference in the rate of the composite endpoint between the study and control groups. Kidney function deterioration (as measured by eGFR decline of ≥50%) was significantly higher among patients with baseline hyperuricosuria (UUA ≥750 mg/day) than in those with normal uricosuria, as was observed by the Cox model. Further prospective studies are needed to clarify the role of uricosuria in renal function deterioration.

Introduction: Limited studies have explored the link between sleep duration and chronic kidney disease (CKD). However, the longitudinal alteration of sleep duration over time, known as sleep duration trajectories, has not been well explored. This gap results in an unclear understanding of the relationship between sleep duration trajectories and the risk of developing CKD, which is addressed in this study.

Methods: Based on longitudinal data from the China Health and Retirement Longitudinal Study (2011, 2013, and 2015 waves), a group-based trajectory model was used to identify distinct patterns of sleep duration. A Cox proportional hazards model was employed to assess the hazard ratios associated with each trajectory in relation to CKD onset (2018 and 2020 waves). Additionally, interaction analysis was conducted to examine potential individual-level modifiers of the relationship between sleep duration trajectories and CKD onset. Three different sensitivity analyses were performed to ensure the robustness of the findings.

Results: A total of 11,059 individuals were included in this survey with three distinct sleep duration trajectories identified: Group 1 (mean sleep duration: 3.56 ± 1.32), Group 2 (mean sleep duration: 5.83 ± 1.36), and Group 3 (mean sleep duration: 7.70 ± 1.17). Group 1 showed the highest risk of developing CKD, with an incidence of 10.54 cases per 1,000 person-years (95% confidence interval 8.77-12.68). Relative to group 1, group 3 was significantly associated with a reduced risk of CKD (hazard ratio 0.55, 95% confidence interval 0.44-0.70). A notable decrease in CKD risk was observed across all subgroups, and no significant interaction effects were found between covariates and the association between sleep duration trajectory and CKD.

Conclusion: Among middle-aged and elderly adults, persistent long sleep duration was associated with a lower risk of CKD. Maintaining adequate and stable sleep duration may be beneficial for CKD risk management in this population. However, further evidence is required to inform definitive public health recommendations.

Objectives: Depression and cognitive decline are common and frequently co-occur among older adults with hypertension, but their symptom-level relationships are poorly understood. This study explored interrelationship between depressive symptoms and cognitive function as well as their associations with quality of life (QoL) in a national hypertension sample from China.

Methods: Depression, cognitive function, and global QoL were assessed utilizing Chinese versions of the 10-item Center for Epidemiological Studies Short Depression Scale (CESD-10), Mini-Mental State Examination, and World Health Organization Quality of Life-brief version (WHOQOL-BREF), respectively. We identified central symptoms and bridge symptoms based on centrality strength and bridge strength indexes, while symptoms having links to QoL were analyzed via flow network analysis.

Results: The study included 4,683 older adults. The prevalence of depression (CESD-10 total score ≥10) and cognitive impairment (MMSE total score <24) were 28.5% (95% CI = 27.2-29.8%) and 19.9% (95% CI = 18.8-21.1%), respectively. "Feeling blue/depressed" (CESD3) and "language" (Lan) were emerged as the most influential symptoms within the network model. "Naming" and "Language" were identified as most important bridge symptoms. Finally, "sleep disturbances" (CESD10) and "hopelessness" (CESD5) exhibited the strongest negative association with QoL.

Conclusions: Targeting central and bridge symptoms (e.g., depressed emotions, language, and naming ability) may provide pathways for addressing both depression and cognitive decline among older adults with hypertension. Moreover, improving sleep quality and alleviating hopelessness could help increase QoL in this population.

Introduction: Atheroembolic kidney disease (AEKD) is an under-recognized cause of kidney failure, secondary to the obstruction of the renal artery and/or its branches due to the rupture of an unstable atherosclerotic plaque in patients treated with surgical and invasive cardiovascular procedures. The embolization of cholesterol crystals in the renal artery activates the complement and triggers an inflammatory reaction. Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy caused by the hyperactivation of the alternative complement pathway, leading to a prothrombotic and proinflammatory state on the endothelial surface. AEKD and aHUS could share the involvement of the complement in their pathophysiological mechanism and the former could lead to the latter.

Case presentation: A 72-year-old man was referred to our clinic because of a rapid worsening of renal function after 9 months from an endovascular aortic repair (EVAR). After 4 months from the intervention, his renal function worsened, he developed hypereosinophilia and skin lesions; the renal ultrasound showed increased resistance indexes, strongly suggestive of atheroembolic kidney disease. Successively, we observed thrombocytopenia, anemia, increased LDH, low plasmatic haptoglobin, schistocytes in blood smear, and normal ADAMTS13. We promptly diagnosed an atypical hemolytic uremic syndrome and started ravulizumab.

Conclusion: To our knowledge, this is the first case of aHUS secondary to a subacute AEKD. Further studies are necessary to fill the gap in the knowledge of the precise mechanism leading to aHUS secondary to AEKD and to confirm that they are two sides of the same coin.

Introduction: Milan hypertensive strain (MHS) of rat represents as one of the ideal rat models to study the genetic form of hypertension associated with aberrant renal salt reabsorption. In contrast to Milan normotensive strain (MNS), MHS rats possess missense mutations in three adducin genes and develop hypertension at 3 months old due to upregulation of sodium-chloride cotransporter (NCC). At prehypertensive stage (23-25 days old), MHS rats show enhanced protein abundance of Na+-K+-2Cl- cotransporter (NKCC2) but retain blood pressure comparable to MNS probably through enhanced GFR and reduced NCC and α-subunit of epithelial sodium channel (ENaC) expressed in distal convoluted tubule (DCT) and collecting duct (CD).

Methods: In the present study, mRNA and protein expressions of ion transporters in thick ascending limb of Henle's loop (TAL) of young MHS rats were investigated.

Results: Protein abundance of core-glycosylated form of renal outer medullary potassium (ROMK) channel in inner stripe of outer medulla (ISOM) is remarkably increased in MHS rats at prehypertensive stage. Furthermore, basolaterally expressed Na+-K+-ATPase and Barttin were upregulated.

Discussion/conclusion: These results may indicate that in TAL of MHS rats at this age, both total NKCC2 and core-glycosylated ROMK are upregulated in tandem potentially to balance the luminal potassium concentration. On the basolateral side, upregulation of Na+-K+-ATPase and CLC-Ka/b may energize the excretion of sodium and chloride out from the cells. These data may suggest the interplay of apical and basolateral ion transporters in TAL for the modulation of TAL function in favor of enhancing the transepithelial sodium reabsorption, although this seems compensated by NCC and ENaC expressed at the downstream nephron segments in young MHS rats.