| Background and purposeNephrotic syndrome(NS)is a systemic immune inflammatory disorder syndrome,thromboembolism is one of the serious complications,resulting in poor therapeutic effect and poor prognosis.Platelet overactivation is a risk factor for hypercoagulability and thromboembolism in patients with NS.It is reported that podoplanin(PDPN)is coupled with C-type lectin like receptor-2(CLEC-2)receptor on platelet surface,causing a series of cascade reactions,leading to platelet activation,formation of platelet aggregates and the promotion of thrombosis.At present,relevant studies have not revealed that platelet activation mediated by the interaction between PDPN and CLEC-2 plays a corresponding role in the pathophysiological process of thromboembolic complications in patients with NS.The purpose of this study is to explore whether the serum in patients with NS induces platelet aggregation and activation through PDPN in healthy people,and in order to clarify the role of PDPN/CLEC-2 in platelet activation and hypercoagulability in patients with NS.MethodsA total of 30 patients with primary nephrotic syndrome admitted to the Department of Nephrology of our hospital from May 2021 to January 2022 were selected as the experimental group.Meanwhile,30 healthy subjects from physical examination center were selected as healthy controls.The levels of platelet aggregation stimulated by serum in patients with NS,serum in patients with NS after adding CLEC-2 antagonist,serum in healthy people and PBS were analyzed by flow cytometry.SPSS 25.0 statistical software was used to analyze the correlation between the levels of platelet aggregation stimulated by serum in patients with NS and 24-hour urinary protein,serum albumin,D-dimer,fibrinogen and total blood cholesterol in patients with NS.Results(1)Compared with healthy controls,serum PDPN concentration in NS patients was significantly higher(P < 0.001),and serum platelet aggregation rate in NS patients was significantly higher(P < 0.0001).(2)Compared with NS patients,platelet aggregation rate in NS patients was significantly decreased after adding CLEC-2antagonist(P < 0.0001).(3)Compared with blank controls,platelet aggregation rate in NS patients was significantly increased after adding CLEC-2 antagonist(P < 0.0001).(4)Correlation analysis shows that: There was a negative correlation between the increase of platelet aggregation rate caused by serum in NS patients and the level of serum albumin(R =-0.362,P=0.049).There was a positive correlation between the increase of platelet aggregation rate caused by serum in NS patients and the 24-hour urine protein quantification(R =0.218,P=0.046).There was no significant correlation between the increase of platelet aggregation rate in NS patients after adding CLEC-2antagonist and the 24-hour urine protein level and serum albumin level.Conclusions(1)Serum in NS patients resulted in increased platelet aggregation rate.(2)The platelet aggregation rate of NS patients increased through PDPN,but decreased after the addition of CLEC-2 antagonist.(3)Platelet activation and aggregation in NS patients was related to platelet PDPN-CLEC-2 pathway.(4)Antagonistic PDPN/CLEC-2 pathway can reduce the correlation between platelet aggregation rate and serum albumin and 24-hour urine protein quantification in NS patients,and reduce the risk of thrombosis in NS patients. |
