Neurovascular coupling (NVC) reflects the coordination between brain activity and cerebral blood flow, while glymphatic function indicates the capacity to clear metabolic waste from the brain. However, differences in these two factors between patients on peritoneal dialysis (PD) and hemodialysis (HD), as well as their interrelationship, remain unclear. Functional magnetic resonance imaging, three-dimensional pseudo-continuous arterial spin labeling, and diffusion tensor imaging were prospectively performed in 56 patients on PD, 54 patients on HD, and 52 healthy controls (HC). The study calculated the amplitude of low frequency fluctuation-cerebral blood flow (ALFF-CBF) coupling coefficient and the diffusion tensor image analysis along the perivascular space (DTI-ALPS) index, which respectively represent the overall NVC level and the glymphatic function. Compared to HC, patients on PD and HD exhibited lower ALFF-CBF coupling coefficients and DTI-ALPS indices, but there were no significant differences between the PD and HD groups. Additionally, positive correlations were observed between ALFF-CBF coupling coefficients and DTI-ALPS indices across all three groups. he degrees of neurovascular decoupling and altered glymphatic function are comparable between patients on PD and HD. Importantly, neurovascular decoupling may be associated with altered glymphatic function in patients on dialysis. The degrees of neurovascular decoupling and altered glymphatic function are comparable between patients on PD and HD. Importantly, neurovascular decoupling may be associated with altered glymphatic function in patients on dialysis.

Glycated albumin (GA), a blood glucose monitoring biomarker, is impacted by variables such as albumin turnover and is not entirely relevant throughout diabetic kidney disease (DKD). There is insufficient data to routinely adjust GA measurements. We examined how albuminuria affected clinically measured GA (mGA) and adjusted GA (adjGA). We included 195 patients with DKD, 108 with non-macroalbuminuria and 87 with macroalbuminuria, and adjusted GA based on albumin, albuminuria, and body weight. Subgroups were divided to two groups according to albuminuria and serum albumin levels. The relationship between mGA, adjGA, and glucose was investigated. The optimum GA correction method based on albumin turnover metabolism was investigated: adjGA = mGA×[1+(8×K×UP) ÷ (11×V×SA)]. where K represents the standard metabolic days of albumin (15 days), UP is 24-hour urine protein excretion (g/24 h), V is plasma volume (calculated as 5% of body weight in liters), and SA is serum albumin concentration (g/L). In non-macroalbuminuria, mGA was 19.75% and adjGA was 22.32%, and in macroalbuminuria, mGA was 13.20% and adjGA was 22.45%, the mGA was substantially different across albuminuria categories (P < 0.001), but adjGA was not. HbA1c, 24-h urine protein(24hUP) and serum albumin (ALB) were influencing variables for mGA (P < 0.001), while 24hUP and ALB had no effect on adjGA (P > 0.05). The adjGA had stronger cor-relation with blood glucose than mGA, especially in the context of macroalbuminuria. Macroalbuminuria lowers mGA accuracy. In DKD patients with macroalbuminuria, adjusted GA is a novel indication of glucose monitoring.

IntroductionDiabetic kidney disease (DKD) progression is strongly associated with podocyte mitochondrial dysfunction. The clinically effective Chinese herbal Baoshentongluo formula (BSTL) has demonstrated significant proteinuria reduction in DKD patients. HPLC-ESI-MS analysis identified characteristic bioactive components in BSTL including astragalosides, rehmanniosides, and tanshinones. However, the molecular mechanisms through which BSTL maintains podocyte homeostasis remain incompletely understood. MethodsMouse podocyte clone-5 (MPC-5) cells and db/db mice were used. Db/db mice were randomized into db/db and db/db + BSTL (16.5 g/kg/d, intragastric administration for 12 weeks). A group of m/m mice served as the control. Renal function, urinary albumin-to-creatinine ratio (UACR), histopathological analysis, apoptotic, and mitophagy-related protein levels were evaluated. MPC-5 cells were exposed to high glucose (HG, 30 mM) and BSTL drug-containing serum (8%) for 24 h grouping as control, HG, HG + BSTL, and HG + siPINK1. Podocyte apoptosis, mitophagy levels, and expression of PTEN-induced putative kinase 1 (PINK1) and E3 ubiquitin ligase (Parkin) were assessed.ResultsIn db/db diabetic mice, oral administration of BSTL significantly lowered urinary albumin-to-creatinine ratio (P<0.05), improved glomerular filtration rate, and ameliorated renal histopathological changes, decreased LC3-II/LC3-I ratio, and downregulated expression of mitophagy-related proteins PINK1, Parkin, ATG5 and Beclin-1. Treatment with 8% BSTL-containing serum significantly attenuated HG-induced podocyte apoptosis (P<0.01) and suppressed excessive mitophagy, as evidenced by reduced TOM20/LC3 co-localization (P<0.01). Notably, BSTL treatment markedly reduced protein levels of both PINK1 and Parkin (P<0.01), key regulators of mitophagy initiation. Genetic silencing of PINK1 in podocytes phenocopied BSTL's protective effects, confirming the pathway specificity. DiscussionOur integrated in vitro and in vivo findings establish that BSTL protects against DKD progression by selectively inhibiting PINK1/Parkin-dependent mitophagy in podocytes to inhibit podocyte injury, which provides both mechanistic insights and therapeutic potential for clinical DKD management.

BackgroundQing-Re-Xiao-Zheng-Yi-Qi formula (QRXZYQF), based on the "Shen-Luo-Zheng-Jia" principles of traditional Chinese medicine, has been reported to reduce 24-hour urinary total protein in diabetic kidney disease (DKD) patients, slow disease progression, and improve podocyte injury. This study aims to explore the mechanisms of QRXZYQF in improving podocyte injury.MethodsDiabetes was induced in male C57BL/6J mice by intraperitoneal injection of streptozotocin (STZ). After 12 weeks of QRXZYQF, blood glucose, blood urea nitrogen, serum creatinine, microalbumin, and the urinary albumin-to-creatinine ratio (UACR) were monitored. Renal pathological changes were evaluated using hematoxylin and eosin (H&E), Masson, and periodic acid-Schiff (PAS) staining. RNA sequencing (RNA-Seq) was performed to identify differences in renal mRNA expression and enrichment pathways. The involvement of autophagy-lysosomal and NOD-like receptor pathways was examined by western blotting and immunofluorescence in renal tissues and cultured podocytes.ResultsFollowing 12 weeks of QRXZYQF, renal function improved and ECM accumulation and glomerulosclerosis were markedly reduced. Subsequently, RNA-Seq analysis showed that the autophagy-lysosomal and NOD-like receptor signaling pathways were the potential pathways involved in the mechanism of QRXZYQF. Moreover, QRXZYQF reduced the levels of NLRP3, apoptosis-associated speck-like protein (ASC), as well as Caspase-1 in vitro. Furthermore, we performed interventions using the lysosomal membrane-permeabilizing agent (L-leucyl-L-leucine-O-methylester) and found that QRXZYQF inhibits NLRP3 overexpression by protecting lysosomal membranes and preventing the leakage of Cathepsin B (CB) into the cytoplasm.ConclusionsQRXZYQF inhibits NLRP3-mediated podocyte pyroptosis by stabilizing lysosomal membranes, providing insights into its protective mechanism and potential therapeutic targets for DKD.

BACKGROUND:IgA nephropathy (IgAN) is a chronic immune-mediated progressive kidney disease. The Neutrophil-To-Lymphocyte Ratio (NLR) has emerged as a novel marker for systemic immune inflammation. This study aimed to explore the relationship between NLR and early renal function decline in patients with IgAN. METHODS:A real-world cross-sectional observational study was conducted on a cohort of 1073 patients diagnosed with IgAN. Patients were stratified into high and low NLR groups based on a predefined cut-off value. We examined the association between NLR levels and reduced renal function across these groups, defined as an estimated glomerular filtration rate (eGFR) of 60 mL/min·1.73 m2 or less, using receiver operating characteristic (ROC) curve analysis and Logistic regression models. RESULTS:Among the 1,073 patients evaluated, those with an eGFR ≤ 60 mL/min·1.73 m2 had significantly higher NLR levels compared to those with eGFR > 60 mL/min·1.73 m2 (Z = 9.598, p < 0.001). The area under the AUROC for NLR was 0.671 (p = 0.000, 95% CI: 0.638-0.703). The high NLR group showed significantly elevated levels of mean arterial pressure, 24-hour urinary protein and uric acid, along with lower hemoglobin, serum albumin, and eGFR (all p < 0.001). Multivariate logistic regression analysis revealed that high NLR was independently associated with reduced eGFR (≤ 60 mL/min·1.73 m2) (p = 0.009, OR = 2.110, 95% CI: 1.208-3.683). A nomogram was developed to identify IgAN patients with reduced eGFR (≤60 mL/min·1.73 m2). CONCLUSIONS:IgAN patients with higher NLR levels exhibited more severe clinical manifestations. A high NLR may be associated with an increased risk of eGFR ≤ 60 mL/min·1.73 m2 in patients with IgAN.

AimAdvanced glycation end products (AGEs) are pivotal mediators in diabetic kidney disease (DKD). However, their prognostic utility remains underexplored. This study introduced corrected lgAGEs [novel biomarker derived by adjusting logarithmically transformed AGEs (lgAGEs) levels based on serum albumin (ALB) levels] to enhance the prediction of adverse renal outcomes in patients with type 2 DKD (T2DKD).MethodsIn this prospective cohort study, 196 T2DKD patients were followed up longitudinally. Serum AGEs levels were log-transformed and adjusted for ALB to calculate corrected lgAGEs. Participants were stratified into the high- and low-level groups based on the median corrected lgAGEs. The association between corrected lgAGEs and renal outcomes was assessed using Cox proportional hazards models. Receiver operating characteristic (ROC) curve was utilized to evaluate the predictive performance of corrected lgAGEs alone and in combination with the urinary albumin-to-creatinine ratio (UACR).ResultsHigh level of corrected lgAGEs was independently associated with adverse renal outcomes [hazard ratio (HR), 3.252; 95% confidence interval (CI), 1.461–7.243; p = 0.003]. Kaplan-Meier analysis demonstrated that patients in the high-level group (12 months) exhibited significantly shorter median survival times compared with those in the low-level group (50 months). ROC analysis showed that UACR alone had an area under the curve (AUC) of 0.782 (95% CI, 0.705–0.858), with 82.8% sensitivity and 61.5% specificity. Corrected lgAGEs achieved an AUC of 0.725 (95% CI, 0.637–0.814), with 69.0% sensitivity and 76.9% specificity. Combining UACR and corrected lgAGEs improved the specificity to 75.6%, with an AUC of 0.764 (95% CI, 0.682–0.847), while maintaining a sensitivity of 70.7%.ConclusionCorrected lgAGEs are novel and independent biomarkers for predicting adverse renal outcomes in T2DKD. Combining UACR with corrected lgAGEs could enhance risk stratification by improving the specificity, highlighting its potential application in early identification of high-risk patients. These findings should be validated in broader populations in future research.

Acute kidney injury (AKI) represents a significant challenge to global public health problem and is associated with poor outcomes. There is still considerable debate about the effect of mean blood glucose (MBG) and coefficient of variation (CV) of blood glucose on the short-term mortality of AKI patients. This retrospective cohort study aimed to explore the association between glycemic variability and short-term mortality in patients with AKI. Data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database were analyzed, including 6,777 adult AKI patients. MBG and CV on the first day of ICU admission were calculated to represent the overall glycemic status and variability during the ICU stay in AKI patients. The primary outcome indicator was ICU 30-day mortality of AKI patients. Multivariate Cox regression analysis and smoothed curve fitting were used to assess the relationship between blood glucose levels and mortality. Eventually, the ICU 30-day mortality rate of AKI patients was 23.5%. The increased MBG and CV were significantly correlated with ICU 30-day mortality (hazards ratio (HR) = 1.20, 95% confidence interval (CI) 1.14–1.27; HR = 1.08, 95% CI 1.03–1.13). The smoothed curve fitting showed a U-shaped relationship between MBG on the first day of ICU admission and ICU 30-day mortality (inflection point = 111.3 mg/dl), while CV had a linear relationship with 30-day ICU mortality. Thus, we conclude that MBG and CV were significantly associated with short-term mortality in intensive care patients with AKI. Tighter glycemic control may be an effective measure to improve the prognosis of patients with AKI.

[This corrects the article DOI: 10.3389/fmed.2024.1344219.].

PurposeTo investigate the prevalence and characteristics of late gadolinium enhancement (LGE) by cardiac magnetic resonance (CMR) and its prognostic value in patients with Takayasu arteritis (TA).Materials and methodsSixty TA patients with a CMR examination were retrospectively included. All TA patients were divided into with LGE-positive and LGE-negative groups. Bi-ventricular function and location, distribution, and pattern of left ventricular (LV) LGE were evaluated in both LGE-positive and LGE-negative groups. Primary outcome was defined as a composite of cardiovascular death, hospitalization for heart failure, coronary artery revascularization, and stroke. Univariate and multivariate Cox proportional hazard regression analyses were used to evaluate the association between variables and primary outcomes.ResultsSixty consecutive TA patients were enrolled in this study. The mean age was 38.2 ± 13.8 years and 54 patients (54/60, 90.0%) were female. LGE-positive was observed in twenty-one (21/60, 35%) patients in the total patients with TA. LGE was predominantly distributed in the middle wall and subendocardial. The patchy and infarcted LGE patterns were the most common. Compared with the LGE-negative group, the LGE-positive group had reduced LV ejection fraction (P = 0.033), elevated LV end-diastolic volume index (P = 0.008), LV end-systolic volume index (P = 0.012), and LV mass (P = 0.008). During a median follow-up period of 1,892 days (interquartile range: 1,764–1,988 days), the primary outcomes occurred in thirteen patients. In the univariate analysis, LGE-positive (hazard ratio [HR] = 4.478, 95% confidence interval [CI]: 1.376–14.570; P = 0.013) were independently associated with the primary outcomes. However, LGE-positive did not retain its value as an independent predictor of primary outcomes in the multivariate analysis. Instead, LVMI (HR = 1.030, 95%CI: 1.013–1.048; P = 0.001) was the strongest independent predictor of primary outcomes in patients with TA. The Kaplan-Meier plot revealed that patients with LVMI ≥ 57.5 g/m2 have a worse prognosis.ConclusionLGE-positive detected by CMR was observed in 35% of total TA patients with different distributions and patterns. LGE is associated with adverse LV remodeling and worsen cardiac function. However, LVMI rather than LGE can provide independent prognostic information in patients with TA.

INTRODUCTION:Imbalances in blood potassium (K) homeostasis is a significant contributor to the emergence of severe complications, especially among critically ill patients. Hypokalemia and hyperkalemia are both associated with an increased risk of adverse events. However, it is not known about the impact of blood K levels on risk of intensive care units (ICU) mortality for Acute kidney injury (AKI) combined with sepsis patients. This study aimed to explore the relationship between admission blood K levels and ICU 30-day mortality in patients with AKI combined with sepsis. METHODS:We selected patients diagnosed with AKI and sepsis on their first ICU admission from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The first blood K levels within 24 hours of admission were categorized into three groups according to tertiles (T1 < 3.9 mmol/L, 3.9 ≤ T2 < 4.5 mmol/L, and T3 ≥ 4.5 mmol/L), with T2 serving as the reference. We examined the association between blood K levels and ICU 30-day mortality using accelerated failure time (AFT) models and survival analysis. RESULTS:A total of 8,242 ICU patients with AKI combined with sepsis were included. In multivariate AFT models, each 1 mmol/L increase in blood K levels was associated with a 13% increase in the risk of ICU 30-day mortality (p < 0.001, 95% confidence interval (CI): 1.06-1.20). Extended multivariable AFT models showed that, compared to the middle category, patients with high blood K levels (≥ 4.5 mmol/L) were associated with all-cause mortality (p = 0.002, adjusted hazard ratio (HR) = 1.22, 95% CI: 1.08-1.38), whereas those with low blood K levels (< 3.9 mmol/L) showed no significant difference (p = 0.385, adjusted HR = 1.06, 95% CI: 0.93-1.21). Kaplan-Meier curves indicated that patients with high blood K levels had higher mortality, and those with middle blood potassium levels (3.9 ≤ K < 4.5 mmol/L) had the lowest mortality. CONCLUSION:The admission baseline blood K levels were significantly associated with ICU 30-day mortality in intensive care patients suffering from AKI in conjunction with sepsis. Therefore, immediate and careful correction of blood potassium imbalances may prove to be a crucial approach in improving outcomes for these patients.

Objectives. Type 2 diabetic kidney disease (DKD), a chronic microvascular complication of diabetes, may exhibit a complex interrelation with coagulation function. This study is aimed at elucidating the association between coagulation function and DKD. Methods. This was a real-world observational study conducted in Beijing, involving 2,703 participants. All patients with diabetes were classified into two groups, viz., DKD and non-DKD groups. Effect magnitudes are denoted as odds ratios (OR) with a 95% confidence interval (CI). To mitigate potential bias in group comparisons, we employed propensity score matching (PSM). Results. After adjusting for variables such as age, gender, systolic blood pressure (SBP), hemoglobin A1c (HbA1c), triglyceride (TG), c-reactive protein (CRP), platelet (PLT), and serum albumin (sALB), it was discerned that fibrinogen (FIB) (OR, 95% CI, P: 1.565, 1.289-1.901, <0.001) and fibrinogen degradation products (FDP) (1.203, 1.077-1.344, 0.001) were significantly correlated with an increased risk of DKD. To facilitate clinical applications, a nomogram prediction model was established, demonstrating commendable accuracy for DKD prediction. Conclusions. Our findings suggest that elevated levels of FIB and FDP serve as potential risk indicators for DKD, and coagulation function may play an important role in the occurrence and development of DKD.

ObjectiveWe aimed to explore the association between serum complements and kidney function of diabetic kidney disease (DKD) in Chinese patients.MethodsThis is a retrospective study involving 2,441 participants. DKD was diagnosed according to the Kidney Disease: Improving Global Outcomes (KDIGO) categories. Participants were classified as stages G1-G5 by KDIGO glomerular filtration rate (GFR) categories. Effect sizes are expressed as odds ratio (OR) with 95% confidence interval (CI).ResultsAfter balancing age, gender, systolic blood pressure (SBP), hemoglobin A1c (HbA1C), serum triglyceride (TG), and urinary albumin-to-creatinine ratio (UACR) between the G2-G5 and control groups, per 0.1 g/L increment in serum complement C3 was significantly associated with a 27.8% reduced risk of DKD at G5 stage (OR, 95% CI, P: 0.722, 0.616-0.847, <0.001) relative to the G1 stage. Conversely, per 0.1 g/L increment in serum complement C4 was associated with an 83.0-177.6% increased risk of G2-G5 stage (P<0.001). Serum complement C1q was not statistically significant compared to controls at all stages prior to or after propensity score matching.ConclusionsOur results indicate that high concentrations of serum C4 were associated with the significantly elevated risk of kidney function deterioration across all stages, and reduced serum C3 levels with an increased risk of DKD stage G5.

Objectives: The study aimed to examine the association of three anemia-related biomarkers with the adequacy of peritoneal dialysis (PD) in patients with chronic kidney disease (CKD). Methods: This study included 127 PD patients. The total Kt/V urea (Kt/V) was calculated according to the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines. All patients were classified into two groups based on Kt/V, viz., adequate (Kt/V ≥1.7) and inadequate (Kt/V <1.7) groups. Effect sizes are expressed as odds ratios (ORs) and 95% confidence interval (CI). Results: After adjusting for age, gender, hypertension, diabetes, and PD duration, 20 g/L increment in hemoglobin (Hgb) was observed to significantly reduce the risk of inadequate PD by 19% (OR; 95% CI; P: 0.81; 0.70 to 0.95; 0.009), 5 g/L increment in the mean corpuscular hemoglobin concentration (MCHC) by 7% (0.93; 0.88 to 0.98; 0.009), and 5% increment in transferrin saturation (TS) by 23% (0.77; 0.64 to 0.94; 0.012). The gender-specific nomogram model was constructed by incorporating three significant anemia-related biomarkers and convenient influencing factors, and the prediction accuracy was good (concordance index (C-index): 0.686 for men and 0.825 for women). Conclusion: Our findings indicate that the deterioration of three anemia-related biomarkers (Hgb, MCHC, and TS) can precipitate the development of inadequate PD in Chinese patients with CKD.

Background Mitochondrial dysfunction is considered to be an important contributor in podocyte injury under diabetic conditions. The BaoShenTongLuo (BSTL) formula has been shown to reduce podocyte damage and postpone the progression of diabetic kidney disease (DKD). The potential mechanisms underlying the effects of BSTL, however, have yet to be elucidated. In this study, we aimed to investigate whether the effects of BSTL are related to the regulation of mitochondrial biogenesis via the adenosine monophosphate-activated protein kinase (AMPK) pathway. Methods High-Performance Liquid Chromatography Electrospray Ionization Mass Spectrometer (HPLC–ESI–MS) analysis was performed to investigate the characteristics of pure compounds in BSTL. db/db mice and mouse podocyte clone-5 (MPC5) cells were exposed to high glucose (HG) to induce DKD and podocyte damage. Body weight, random blood glucose, urinary albumin/creatinine ratio (UACR), indicators of renal function and renal histological lesions were measured. Markers of podocyte injury, mitochondrial morphology, mitochondrial deoxyribonucleic acid (mtDNA) content, mitochondrial respiratory chain complexes activities, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) levels were assessed. Protein expressions of AMPK, peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), transcription factor A (TFAM), mitochondrial fusion protein 2 (MFN2) and dynamin-related protein 1 (DRP1) were also detected. MPC5 cells were transfected with AMPKα small interfering RNA (AMPKα siRNA) to determine the underlying mechanisms of BSTL improvement of mitochondrial function under diabetic conditions. Results In vivo, treatment with BSTL reduced the UACR levels, reversed the histopathological changes in renal tissues, and alleviated the podocyte injury observed in db/db mice. After BSTL treatment, the decreased mtDNA content and mitochondrial respiratory chain complex I, III, and IV activities were significantly improved, and these effects were accompanied by maintenance of the protein expression of p-AMPKαT172, PGC-1α, TFAM and MFN2. The in vitro experiments also showed that BSTL reduced podocyte apoptosis, suppressed excessive cellular ROS production, and reversed the decreased in MMP that were observed under HG conditions. More importantly, the effects of BSTL in enhancing mitochondrial biogenesis and reducing podocyte apoptosis were inhibited in AMPKα siRNA-treated podocytes. Conclusion BSTL plays a crucial role in protecting against podocyte injury by regulating the AMPK-mediated mitochondrial biogenesis in DKD.

慢性肾脏病患病率高、治疗难度大,张炳厚认为肾为阴络,亦为血脏.CKD早期即存在肾络受损,肾虚为CKD瘀血之本,肾气虚则血液不行,肾阳虚则阴络不温,肾阴虚则火灼阴络.CKD瘀血的表现繁杂,可分为有形瘀血与无形瘀血,面色黧黑、水肿、视物模糊、肌肤甲错等为有形瘀血征象,血液高凝状态、微循环障碍则提示为无形瘀血.张炳厚认为,血瘀证在CKD中极为常见.瘀血可生热、痰、湿、水、浊毒、风等实邪,诸邪亦可促进瘀血产生,加速CKD进展,瘀血日久治疗难度愈大,预后愈差.因此治瘀之要在于补虚化瘀,生新血以祛瘀血;泄浊排毒,给瘀血以出路;以通为用,巧用藤类与虫蚁药以搜伏风、通结络;对于合并出血者应化瘀止血.在选用活血药时,应根据病情轻重分层论治,早期宜和血活血、中期宜破血逐瘀、晚期宜养血活血.

糖尿病肾病(DN)是导致终末期肾脏病的重要原因之一.代谢记忆学说背景下,晚期糖基化终末产物沉积于肾脏,导致疾病移时后发、迁延难愈与中医邪伏膜原理论相吻合.现基于邪伏膜原学说,提出DN 气阴不足、气化不利、痰瘀互结、邪伏膜原的病机.治疗方面,在透达膜原的基础上,重视三焦的畅通.从邪伏膜原角度论治DN,扩展了邪伏膜原学说的应用范畴,开拓了中医药治疗DN的新思路.

目的:探讨糖尿病肾脏病(DKD)患者发生终点事件的危险因素,分析补肾通络法的保护作用.方法:采用回顾性队列研究,收集2015年1月至2019年12月首都医科大学附属北京中医医院肾病科病房和专病门诊定期随访≥3个月,且基线估算肾小球滤过率(eGFR)为15～90 mL/(min·1.73 m2)的DKD患者资料.以进入慢性肾脏病5期、肾脏替代治疗或死亡为主要终点事件,以慢性肾脏病进展为次要终点.结果:共123例DKD患者完成随访,中位随访时间12个月(3～48)个月,81例(65.9％)进入终点事件.经多因素Cox分析显示,基eGFR低、心力衰竭和横纹肌溶解为终点事件发生的危险因素,使用补肾通络法为保护性因素.使用补肾通络法患者的终点事件发生率显著低于未使用患者(P<0.05),分别为61.1％与82.1％.补肾通络法患者的终点事件风险为0.530(95％CI 0.305～0.921,P<0.05).结论:基线eGFR低、心力衰竭和横纹肌溶解是DKD患者终点事件的危险因素,而补肾通络法能够降低DKD患者终点事件风险.

目的:探讨保肾通络方含药血清对于高糖培养下足细胞肾病蛋白(Nephrin)、结蛋白(Desmin)表达及细胞凋亡的影响.方法:细胞实验分为正常对照组、模型组和保肾通络方低、中、高剂量组.正常对照组足细胞予DMEM低糖培养基培养,模型组和保肾通络方不同剂量组予含有 30 mmol/L 葡萄糖的高糖培养基培养.保肾通络方不同剂量组足细胞在高糖培养基中分别加入保肾通络方含药血清低、中、高剂量进行干预,正常对照组及模型组加入等剂量空白血清.CCK-8 法检测足细胞的细胞活性,免疫荧光及 RT-PCR 检测足细胞 Nephrin、Desmin 蛋白及 mRNA表达水平,免疫荧光检测足细胞凋亡相关蛋白 Caspase-3 蛋白表达,Hochest33258 染色检测足细胞凋亡情况.结果:与正常对照组比较,模型组足细胞的细胞活性明显降低,Nephrin 蛋白表达明显下调,Desmin、Caspase-3 蛋白表达明显上调,足细胞凋亡细胞数目明显增加(均P＜0.05).与模型组比较,保肾通络方低、中、高剂量组足细胞的细胞活性明显升高,Nephrin蛋白表达明显上调,Desmin、Caspase-3 蛋白表达明显下调,足细胞凋亡数目明显减少(均P＜0.05).结论:保肾通络方可能通过上调足细胞 Nephrin蛋白表达,下调 Desmin蛋白表达,抑制足细胞凋亡,进而减轻足细胞损伤.

原发性膜性肾病是肾脏特异性的自身免疫性肾小球病.高彦彬教授认为本病属中医"络病"范畴,病性本虚标实,分为虚损期、虚衰期;主张以虚定型,以实定候.虚证分为脾肾气虚、肺脾气虚、脾肾阳虚、阴阳两虚、心肾阳虚证,实证分为湿热壅络、湿浊蕴络、风湿伏络、湿瘀滞络、毒瘀阻络.治疗上分期论治结合辨证论治,扶正祛邪,强调通络法贯穿始终.