Abstract Background Chronic kidney disease (CKD) is a major global health concern with a multifactorial pathogenesis. Emerging evidence suggests that the gut microbiota and its metabolic products contribute to CKD development. However, robust evidence supporting metabolites as causal mediators in this pathway remains limited. We aimed to investigate causal relationships and mediating effects linking gut microbiota, circulating metabolites, and CKD. Methods Two-sample Mendelian randomization (MR) analyses were conducted using summary statistics from large-scale genome-wide association studies (GWAS) on gut microbiota, plasma metabolites, and CKD-related outcomes. Independent single-nucleotide polymorphisms strongly associated with each exposure were selected as instrumental variables. The inverse-variance weighted method served as the primary analysis, complemented by four additional MR approaches. Heterogeneity and pleiotropy were assessed using Cochran’s Q test, the MR-Egger intercept, and MR-PRESSO. Mediation analysis quantified the proportion of microbiota–CKD effects mediated by specific metabolites. Results MR analyses identified causal associations among multiple gut microbial pathways, circulating metabolites, and CKD-related traits. Mediation analysis revealed that argininate partially mediated the effect of the microbial pathway PWY-6629 on the urinary albumin-to-creatinine ratio (UACR), accounting for 22% of the total effect. A one–standard-deviation increase in genetically predicted PWY-6629 activity was associated with a 1.3% increase in UACR, mediated through a 7.9% reduction in argininate levels. Conversely, higher genetically predicted argininate levels were associated with a 3.7% reduction in UACR. Conclusion This study provides genetic evidence that gut microbiota influence CKD risk partially through circulating metabolites, highlighting the gut microbiota–metabolite–CKD axis as a potential therapeutic target.

Fibrosis is a hallmark and common outcome of progressive chronic kidney disease (CKD). Noninvasive and accurate diagnosis of kidney fibrosis remains unavailable in clinics, limiting effective patient management. Here, we report the development of fibrogenesis sensing reporters (FSRs) for sensitive in vivo near-infrared fluorescence imaging and ex vivo translational urinalysis of kidney fibrosis. FSR achieves enhanced diagnostic accuracy by engaging two crucial, concurrently up-regulated biomarkers in fibrotic kidneys: lysyl oxidase-derived allysine (LysAld) and transglutaminase 2 (TG2). Engineered to be intrinsically nonfluorescent with excellent renal clearance, injected FSRs preferentially target kidneys through covalent binding to LysAld and are robustly cleaved by TG2, which is elevated in the fibrotic kidney, to unquench a renal-clearable fluorophore, enabling fluorescence "turn-on" for sensitive fibrosis detection by both kidney imaging and urine assays. Leveraging the high specificity of urinary TG2, FSR-based urinalysis distinguished kidney fibrosis from nonfibrotic acute kidney injury and was not confounded by extrarenal fibrosis (such as pulmonary and hepatic), providing diagnostic insights unattainable with routine kidney function tests. In a clinical cohort (n = 35), FSR-based urinalysis discriminated patients with CKD from healthy controls with 84% sensitivity and 94% specificity and provided discrimination between histological mild versus severe fibrosis. In contrast, traditional clinical metrics such as the estimated glomerular filtration rate, serum creatinine, and blood urea nitrogen were not able to classify mild versus severe fibrosis cases. This noninvasive activatable reporter holds translational potential for early identification of renal fibrosis and patient stratification of CKD to improve clinical management and patient outcome.

Objective:Multiple organ dysfunction syndrome (MODS) is a life-threatening complication of wasp stings. This study aimed to identify factors associated with MODS and develop a quantitative risk prediction model. Methods:A retrospective cohort study included 324 wasp sting patients (January 2018-December 2023), divided into MODS (n = 90) and non-MODS (n = 234) groups. General characteristics, imaging findings, and laboratory parameters were compared. Composite indicators with clinical interpretability were incorporated into binary logistic regression to identify risk factors. A nomogram-based prediction model was established and evaluated using ROC curves, calibration curves, and decision curves. Results:Significant differences were observed between groups in age, time from sting to admission, pleural effusion, RALE score, PLT, LYM, MO, FIB, ALB, MPV/PLT, P-LCR, FAR, FPR, CLR, SHR, NLR, PLR, PNR, SIRI, and SII (all P < 0.05). After excluding collinear variables (VIF > 5), binary logistic regression identified age, time to admission, pleural effusion, RALE score, MPV/PLT, and SIRI as independent risk factors (OR > 1, all P < 0.05). A nomogram prediction model was developed. ROC analysis showed an AUC of 0.828 (95% CI: 0.776-0.880). At the optimal cutoff of 0.368, sensitivity was 66.7%, specificity 87.9%, PPV 68.9%, and NPV 86.8%. Calibration curves showed good agreement, and decision curves demonstrated high net clinical benefit. Conclusion:MODS occurrence after wasp stings may be associated with RALE score, MPV/PLT, and SIRI levels, while the roles of age, time to admission, and pleural effusion require further validation. The nomogram model provides a useful reference for clinical MODS risk assessment but lacks external validation, requiring confirmation in future large-scale, multicenter, prospective studies.

Lipid disorder is an independent risk factor of diabetic kidney disease (DKD). Excess accumulation of lipid in podocytes can cause cell dysfunction and cell death. Chaperone-mediated autophagy (CMA) serves as a critical role in regulating lipid metabolism. However, the exact role of CMA in the podocytes of DKD with dyslipidemia is still uncertain. Herein, we aimed to explore the role of CMA in hyperlipidemia-induced lipid accumulation and apoptosis in podocytes. In the present study, we showed that palmitic acid (PA) treatment induced the activation of CMA, increased lipid accumulation and apoptosis in podocytes. We further found that blocking CMA with inhibitor VER155008 or LAMP-2 A siRNA significantly upregulated PA-induced increased expression of PLIN2, exacerbated PA-induced lipid accumulation and apoptosis, whereas promoting CMA with Torin1 downregulated the expression of PLIN2, ameliorated lipid accumulation and apoptosis in PA-induced podocytes. Moreover, we also observed the activation of CMA and increased lipid accumulation in the kidney tissue of DKD mice. Taken together, these results suggest that CMA plays a protective role in PA-induced podocytes apoptosis and that the potential protective mechanism of CMA is involved in reducing cellular lipid accumulation through mediating the degradation of PLIN2.

Inflammation is a key driver of diabetic kidney disease (DKD) progression, with the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome representing a promising therapeutic target. Soluble epoxide hydrolase (sEH), an enzyme that inactivates renoprotective epoxyeicosatrienoic acids into less active diols, has been implicated in renal pathophysiology. This study investigated the role of sEH in renal tubular NLRP3 inflammasome activation and its underlying mechanisms in DKD. We observed upregulated sEH expression in high glucose (HG)-stimulated human proximal tubular epithelial (HK-2) cells and diabetic kidneys. Pharmacological inhibition of sEH attenuated diabetes-induced mitochondrial damage, mitochondrial reactive oxygen species (mtROS) production, NLRP3 inflammasome activation, and renal dysfunction both in vivo and in vitro. Furthermore, sEH inhibition restored autophagy flux and enhanced PINK1/Parkin mediated-mitophagy. Activation of mitophagy by the autophagy inducer rapamycin (Rapa) alleviated HG-induced mitochondrial impairment, mtROS overproduction, and NLRP3 inflammasome activation in HK-2 cells, suggesting that the anti-inflammatory effect of sEH inhibition is mediated through mitophagy regulation. Further mechanistic studies indicated that sEH inhibition promotes mitophagy, thereby improving mitochondrial function, reducing mtROS generation, and subsequently suppressing mtROS-dependent NLRP3 inflammasome activation in DKD. In conclusion, our findings establish a novel link between sEH and NLRP3 inflammasome activation in DKD pathogenesis, highlighting sEH inhibition as a promising therapeutic strategy for DKD treatment.

Diabetic kidney disease (DKD) remains the leading cause of end-stage renal disease, yet many patients progress despite optimal glycemic control, a paradox termed metabolic memory that lacks a unifying mechanism. We hypothesize that hyperglycemia and associated metabolic stressors induce trained immunity, a persistent state of metabolic and epigenetic reprogramming in innate immune cells and their bone marrow progenitors, which drives autonomous disease progression. Transient metabolic insults lock macrophages into a hyper-responsive, pro-inflammatory state via a self-reinforcing axis involving mTOR-HIF-1 alpha-driven glycolysis, accumulation of tricarboxylic acid cycle metabolites (succinate, fumarate), and sustained activating histone marks (H3K4me3, H3K27ac) at inflammatory loci. Critically, reprogramming extends to hematopoietic stem and progenitor cells, ensuring continuous output of trained myeloid cells that perpetuate renal inflammation and fibrosis independently of the original trigger. If validated, this hypothesis reframes DKD as a state of maladaptive immune memory and shifts therapeutic strategy from strict metabolic control toward targeted resetting of the innate immune system, potentially via epigenetic modulators or metabolic inhibitors.

Background Asprosin, a recently discovered adipokine, is a glucotropic hormone involved in the pathogenesis of diabetes and closely associated with diabetic kidney disease (DKD). Renal tubular epithelial cell injury is one of the important pathological characteristics of DKD. However, the precise molecular mechanism remains unclear. In this study, we aimed to investigate the role of Asprosin in proximal tubular epithelial cells injury in DKD. Methods The plasma Asprosin level was measured using ELISA in both healthy people and patients with DKD. Immunohistochemistry was employed to detect the level of Asprosin in renal biopsy tissues from DKD patients as well as normal renal tissues adjacent to cancer resected by surgery. Western Blot and q-PCR were utilized to determine the level of Asprosin in DKD mouse kidney tissues. HK-2 cells were exposed to high glucose conditions to simulate injury in renal tubular epithelial cells seen in DKD patients. Following intervention with Asprosin, we analyzed the expression of HK-2 gene, autophagic flux and apoptosis. Results The expression level of Asprosin was found to be higher in kidney tissues and plasma from DKD patients compared to the control group. In addition, the kidney tissues of DKD mice and HK-2 cells treated with high glucose exhibited elevated levels of Asprosin expression. Furthermore, intervention with Asprosin in HK-2 cells resulted in insufficient autophagy and increased apoptosis. These findings suggest that Asprosin exacerbates disturbance in autophagy and induces apoptosis in HK-2 cells under the high glucose conditions. Importantly, our results indicate that Asprosin promotes the apoptosis of HK-2 cells by inhibiting autophagy. Conclusions Our findings collectively demonstrate that elevated glucose levels can induce the upregulation of Asprosin in both kidney tissue and plasma. Furthermore, Asprosin has the ability to enhance apoptosis in HK-2 cells by inhibiting autophagy, exacerbate autophagy dysregulation and apoptosis caused by high glucose, as well as promote injury in renal tubular epithelial cells.

Nephrotic syndrome(NS) can be classified into steroid-sensitive nephrotic syndrome (SSNS) and steroid-resistant nephrotic syndrome (SRNS). Rifampicin is potentially leading to treatment resistance in NS. Here we report a case of SRNS secondary to rifampicin-induced drug interactions during antituberculosis therapy.

Renal fibrosis (RF) is a prevalent clinical symptom of numerous chronic kidney illnesses and a significant pathological alteration in end-stage renal disease resulting from various mechanisms, such as abnormally activated signaling pathways, microRNAs, aging, autophagy disorders, and fibrotic ecological niches, all of which contribute to RF development. Inhibiting, blocking, or delaying the aforementioned mechanisms may yield novel approaches for treating RF. This article explores advancements in the comprehension of the mechanisms and therapeutic approaches for RF.

Chronic kidney disease-associated pruritus (CKD-aP) is a common and burdensome dermatologic condition in which patients can experience various symptoms. This study aimed to summarize and describe the patient-reported outcomes (PROs) and patient-reported outcome measures (PROMs) used in CKD-aP studies over the past 5 years. A total of 99 studies were identified, which included 5 different PROs and 40 different PROMs. The most frequently evaluated PRO was pruritus (n = 99), followed by health-related quality of life (HRQoL) (n = 31), sleep disturbances (n = 12), psychiatric symptoms (n = 7), and other skin symptoms (n = 5). Among the 40 different PROMs, 19 were generic, 18 were skin-specific, and 3 were CKD-specific. The most commonly used PROMs in the PROs of pruritus, HRQoL, sleeping, and psychiatric symptoms were the visual analog scale (n = 47), dermatological life quality index (n = 8), Pittsburgh sleep quality index (n = 7), and Beck depression inventory (n = 3), respectively. The PROs and PROMs are common and effective tools for evaluating CKD-aP, but more high-quality studies and guidelines are needed to reach a clear consensus on their application.

Dyslipidemia is the most prevalent independent risk factor for patients with chronic kidney disease (CKD). Lipid-induced NLRP3 inflammasome activation in kidney-resident cells exacerbates renal injury by causing sterile inflammation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that modulates the cellular redox balance; however, the exact role of Nrf2 signaling and its regulation of the NLRP3 inflammasome in hyperlipidemia-induced kidney injury are poorly understood. In this study, we demonstrated that activation of the mtROS-NLRP3 inflammasome pathway is a critical contributor to renal tubular epithelial cell (RTEC) apoptosis under hyperlipidemia. In addition, the Nrf2/ARE signaling pathway is activated in renal tubular epithelial cells under hyperlipidemia conditions both in vivo and in vitro, and Nrf2 silencing accelerated palmitic acid (PA)-induced mtROS production, mitochondrial injury, and NLRP3 inflammasome activation. However, the activation of Nrf2 with tBHQ ameliorated mtROS production, mitochondrial injury, NLRP3 inflammasome activation, and cell apoptosis in PA-induced HK-2 cells and in the kidneys of HFD-induced obese rats. Furthermore, mechanistic studies showed that the potential mechanism of Nrf2-induced NLRP3 inflammasome inhibition involved reducing mtROS generation. Taken together, our results demonstrate that the Nrf2/ARE signaling pathway attenuates hyperlipidemia-induced renal injury through its antioxidative and anti-inflammatory effects through the downregulation of mtROS-mediated NLRP3 inflammasome activation.

Asprosin, a recently discovered adipokine, is a glucotropic hormone involved in the pathogenesis of diabetes and closely associated with diabetic kidney disease (DKD). Renal tubular epithelial cell injury is one of the important pathological characteristic of DKD. However, the precise molecular mechanism remains unclear. In this study, we validated the role of Asprosin in proximal tubular epithelial cells injury in DKD. The expression level of Asprosin was found to be higher in kidney tissues and plasma of DKD patients than in the healthy group. Additionally, the kidney tissues of DKD mouse and HK-2 cells treated with high glucose showed elevated Asprosin expression. Moreover, Asprosin intervention in HK-2 cells led to insufficient autophagy and increased apoptosis. These findings suggest that Asprosin exacerbates autophagy disturbance and induces apoptosis in HK-2 cells under high glucose conditions, and our further studies verified that Asprosin promotes HK-2 cell apoptosis by inhibiting autophagy. Thus, our findings demonstrate for the first time that elevated glucose levels can upregulate Asprosin in both kidney tissue and plasma. Moreover, Asprosin can enhance apoptosis in HK-2 cells by inhibiting autophagy, aggravate autophagy dysregulation and apoptosis caused by high glucose, and promote injury in renal tubular epithelial cells.

Purpose:To evaluate the association of the systemic immune-inflammatory index (SII) and systemic inflammatory response index (SIRI) with the clinical and pathological features and progression of diabetic kidney disease (DKD).Patients and Methods:We analyzed 303 patients with type 2 diabetes mellitus (T2DM), classifying them into distinct groups: T2DM, early DKD (EDKD), and clinical DKD (Cli-DKD). Variations in SII and SIRI levels across these groups and their association with renal function were assessed. Logistic regression analysis was used to identify independent risk factors for DKD. Additionally, in 43 patients with biopsy-confirmed DKD, we analyzed the relationship between SII, SIRI, and pathological changes. Kaplan-Meier survival analysis and the Cox proportional hazards model were used to assess the influence of SII and SIRI levels on outcomes in patients with DKD.Results:SII and SIRI were significantly higher in the Cli-DKD group than in the T2DM and EDKD groups, and were positively correlated with the urinary albumin-creatinine ratio and negatively correlated with estimated glomerular filtration rate. Notably, SIRI was identified as an independent risk factor for DKD development. Additionally, a lower SII score was associated with a higher cumulative survival rate.Conclusion:This study demonstrates an association between SII, SIRI, and renal function in patients with T2DM. A high SIRI was an independent risk factor for DKD, while an elevated SII was associated with an increased risk of kidney disease progression in biopsy-confirmed DKD cases. Our findings underscore the potential implications of utilizing SII and SIRI as cost-effective and readily available inflammatory indicators for monitoring DKD in primary care settings.

BACKGROUND AND AIMS:Chronic kidney disease (CKD) causes low quality of life and alarming morbidity and mortality. The crucial to retard CKD progression is to diagnose early for timely treatment. IgA nephropathy (IgAN) is a typical CKD and the most common glomerulonephritis. Both CKD and IgAN lack accurate and sensitive blood biomarkers for early diagnosis. Here we report the potential of plasma biomarkers for early diagnosis of CKD and IgAN. MATERIALS AND METHODS:Plasma levels of metabolites derived from tryptophan were quantified with an LC-MS/MS-based metabolomics for two cohorts. Based on the predictive probability of each metabolite, multivariate models including logistic regression and random forest were used to establish the early diagnostic biomarkers for CKD and IgAN. RESULTS:The plasma melatonin diagnosed early CKD (stages Ⅰ-Ⅱ) with an accuracy exceeding 95%, and a panel of melatonin and tryptophan achieved a remarkable 100% accuracy in diagnosing early CKD. Furthermore, indole-3-lactic acid had an excellent ability to distinguish IgAN among CKD patients. Based on the CKD screening and IgAN diagnosis primarily contributed by melatonin and indole-3-lactic acid, early IgAN could be diagnosed with an accuracy of over 85%. CONCLUSIONS:This study provides promising plasma biomarkers for early diagnosis of CKD and IgAN.

Background:Lipid metabolism disorders lead to lipotoxicity. The hyperlipidemia-induced early stage of renal injury mainly manifests as podocyte damage. CD36 mediates fatty acid uptake and the subsequent accumulation of toxic lipid metabolites, resulting in podocyte lipotoxicity. Methods:Male Sprague-Dawley rats were divided into two groups: the normal control group and the high-fat diet group (HFD). Podocytes were cultured and treated with palmitic acid (PA) and sulfo-N-succinimidyl oleate (SSO). Protein expression was measured by immunofluorescence and western blot analysis. Boron-dipyrromethene staining and Oil Red O staining was used to analyze fatty acid accumulation. Results:Podocyte foot process (FP) effacement and marked proteinuria occurred in the HFD group. CD36 protein expression was upregulated in the HFD group and in PA-treated podocytes. PA-treated podocytes showed increased fatty acid accumulation, reactive oxygen species (ROS) production, and actin cytoskeleton rearrangement. However, pretreatment with the CD36 inhibitor SSO decreased lipid accumulation and ROS production and alleviated actin cytoskeleton rearrangement in podocytes. The antioxidant N-acetylcysteine suppressed PA-induced podocyte FP effacement and ROS generation. Conclusions:CD36 participated in fatty acid-induced FP effacement in podocytes via oxidative stress, and CD36 inhibitors may be helpful for early treatment of kidney injury.

Lysosomal dysfunction and impaired autophagic flux are involved in the pathogenesis of lipotoxicity in the kidney. Here, we investigated the role of transcription factor EB (TFEB), a master regulator of autophagylysosomal pathway, in palmitic acid induced renal tubular epithelial cells injury. We examined lipid accumulation, autophagic flux, expression of Ps211-TFEB, and nuclear translocation of TFEB in HK-2 cells overloaded with palmitic acid (PA). By utilizing immunohistochemistry, we detected TFEB expression in renal biopsy tissues from patients with diabetic nephropathy and normal renal tissue adjacent to surgically removed renal carcinoma (controls), as well as kidney tissues from rat fed with high-fat diet (HFD) and low-fat diet (LFD). We found significant lipid accumulation, increased apoptosis, accompanied with elevated Ps211-TFEB, decreased nuclear TFEB, reduced lysosome biogenesis and insufficient autophagy in HK-2 cells treated with PA. Kidney tissues from patients with diabetic nephropathy had lower nuclear and total levels of TFEB than that in control kidney tissues. Level of renal nuclear TFEB in HFD rats was also lower than that in LFD rats. Exogenous overexpression of TFEB increased the nuclear TFEB level in HK-2 cells treated with PA, promoted lysosomal biogenesis, improved autophagic flux, reduced lipid accumulation and apoptosis. Our results collectively indicate that PA is a strong inducer for TFEB phosphorylation modification at ser211 accompanied with lower nuclear translocation of TFEB. Impairment of TFEB-mediated lysosomal biogenesis and function by palmitic acid may lead to insufficient autophagy and promote HK-2 cells injury.

Objective·To further clarify the mechanism of podocyte damage by studying the expression of cartilage oligomeric matrix protein(COMP)in glomerular podocytes and its relationship with podocyte autophagy under high glucose environment.Methods·The gene expression dataset GSE104948 was downloaded from the GENE EXPRESSION OMNIBUS(GEO)database,and differentially expressed genes(DEGs)were obtained via GEO2R.The molecular functions and signaling pathways related to differential genes were summarized.The most correlated key genes(hub genes)were acquired by Weighted Gene Co-Expression Network Analysis(WGCNA)and the protein-protein interaction network(PPI)of DEGs was constructed with STRING database.The enrichment analysis was performed again.Conditionally immortalized mouse podocyte cells were cultured in vitro.After being fully differentiated,they were stimulated with high glucose,and the expressions of COMP,mammalian target of rapamycin(mTOR),microtubule-associated protein 1 light chain3(LC3)and other proteins in podocytes were detected by Western blotting.The shRNA constructed by lentiviral vector was further used to infect podocytes to inhibit the expression of COMP,and the stable cell strains were screened by puromycin.The expression of COMP,mTOR,and LC3 of stable strains were detected by Western blotting,in order to observe the effect of COMP on autophagy.Results·A total of 362 DEGs were filtered for subsequent analysis.Among these DEGs,284 genes were up-regulated and 78 genes were down-regulated.The results of Gene Onotology(GO)term analysis showed that DEGs in diabetic nephropathy(DN)were mainly enriched in cell surface receptor signaling pathway,receptor binding,etc.The main enriched Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways included phosphatidylinositol 3-kinase(PI3K)/protein kinase B(PKB/AKT)signaling pathway,extracellular matrix(ECM)-receptor interaction,etc.Sixty-four hub genes were refined through the intersection of WGCNA and PPI hub genes,and the hub genes with significantly increased or decreased expression were sifted.The hub genes were annotated with KEGG again,and it was found that most of the hub genes were enriched in"ECM-receptor interaction"and"PI3K/AKT signaling pathway".The PI3K/AKT/mTOR signaling pathway is a classic autophagy pathway,and COMP was absolutely overexpressed(logFC>2)in the 64 hub genes,suggesting that it may affect autophagy through this pathway.Western blotting showed that compared with the mannitol control group and the low glucose group,the expression of COMP in podocytes was significantly increased under high glucose stimulation.Compared with the control group,the expression of LC3-Ⅱ in the high glucose group was significantly decreased,indicating that the autophagy initiation of podocytes was inhibited under the high glucose environment.Compared with the negative control,the expression of LC3-Ⅱ in renal podocytes of mice with knockdown of COMP was significantly increased,and the mTOR decreased with the decrease of the expression of COMP,indicating that inhibiting COMP contributed to the recovery of autophagy in podocytes.Conclusion·COMP is highly expressed in DN patients and highly enriched in ECM receptor and PI3K/AKT signaling pathway.Autophagy in mouse renal podocytes is inhibited under high glucose conditions,and the high expression of COMP induced by high glucose may be a key factor in autophagy inhibition.Inhibiting COMP helps to restore autophagy in mouse renal podocytes.

A mounting body of evidence suggests that the endoplasmic reticulum stress and the unfolded protein response are involved in the underlying mechanisms responsible for vascular diseases. Inositol-requiring protein 1α (IRE1α), the most ancient branch among the UPR-related signaling pathways, can possess both serine/threonine kinase and endoribonuclease (RNase) activity and can perform physiological and pathological functions. The IRE1α-signaling pathway plays a critical role in the pathology of various vascular diseases. In this review, we provide a general overview of the physiological function of IRE1α and its pathophysiological role in vascular diseases.

慢性肾脏病(CKD)起病隐匿,患病率高、知晓率低、诊治率低,为中国重大慢性疾病之一.立足社区的CKD早期筛查、分层管理有利于疾病的及时诊治、延缓进展、降低终末期肾病发生率.基于循证医学证据,结合中国国情,由多学科联合推进模式下CKD及其并发症管理项目联盟组织全国多学科专家讨论,针对初诊医生和基层医疗机构,提出了基于个体筛查模式的中国成人CKD及并发症早期筛查临床路径的专家建议.