Abstract

Objective To investigate the changes of serum lipoprotein(a) [Lp(a)] and plasminogen activator inhibitor-1 (PAI-1) in primary nephrotic syndrome (PNS). Methods 60 PNS cases whose renal pathological types were identified and 57 healthy physical examination people as normal controls (NC) were selected. Automatic biochemical analyzer detected the levels of serum Lp(a) and blood lipids. Enzyme-linked immunosorbent (Elisa) method tested the concentration of serum PAI-1. The nonparametric Spearman rank coefficient test was used to analyze correlations between variables. Results Compared with the NC group, Lp(a) and PAI-1 were significantly higher in PNS group (P<0.05). Lp(a), PAI-1 and lipids were found negatively related with albumin in PNS group. Lp(a) was positively correlated with PAI-1 in PNS patients, and the Spearman rank coefficient was 0.381 (P=0.003) Binary logistic regression analysis results showed that Lp(a) and PAI-1 were two risk factors in group PNS. Conclusions Lp(a) and PAI-1 concentrations are increased obviously in PNS patients, and Lp(a) was positively correlated with PAI-1 in PNS patients. They could be two risk factors of PNS patients.

Highlights

  • Clinical diagnosis and treatments found that the damages of kidney endothelial cells, micro vascular thrombosis and blood coagulation fibrinolytic system changes are closely associated with the occurrence and development of kidney disease [1, 2]

  • There was no significant difference of gender, age, body mass index (BMI) of the two groups

  • Urea nitrogen level was significantly higher in primary nephrotic syndrome (PNS) than normal controls (NC), but no significant change of creatinine level was noted between PNS and NC

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Summary

Results

We found that Lp(a) and lipids levels including triglycerides, total cholesterol and low density lipoprotein cholesterol were significantly higher in PNS than in the controls. We found that PAI-1 levels are much more higer in PNS than NC group, which showed that patients with primary nephrotic syndrome has serious fibrinolytic system disorder. PAI-1 is synthesized in the liver and by endothelial cells, and its synthesis is regulated by several physiologic mediators, including endotoxin, interleukin-1 and lipids [19], and PAI-1 gene plays an important part in PAI-1 concentration [20] These factors within PNS patients need to be further studies. Impact of the 4G/5G polymorphism in the plasminogen activator inhibitor-1 gene on primary nephrotic syndrome.

Introduction
Materials and methods
Detection methods
Statistical analysis
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