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Tissue-type plasminogen activator activity in HIV-associated HUS
M N Peraldi1, C Maslo, J Berrou
1Service de Néphrologie A, Hôpital Tenon, Paris, France.
Summary
HIV-associated hemolytic uremic syndrome (HUS) involves high tissue-type plasminogen activator (t-PA) activity, not decreased fibrinolysis. Cytomegalovirus infection is also a risk factor for HUS in these patients.
Area of Science:
- Nephrology
- Infectious Diseases
- Hematology
Background:
- Hemolytic uremic syndrome (HUS) in children is linked to high plasminogen activator inhibitor type 1 (PAI-1), potentially causing persistent renal thrombi.
- The pathophysiology of HUS in HIV-infected patients is not well understood.
- This study investigates plasma fibrinolytic activity in HIV-associated HUS.
Purpose of the Study:
- To investigate plasma fibrinolytic activity in HIV-infected patients with HUS.
- To compare tissue type plasminogen activator (t-PA) and PAI-1 levels in HIV+/HUS+ patients versus HIV+/HUS- patients.
Main Methods:
- Measured plasma t-PA and PAI-1 activities in 18 HIV-infected patients with biopsy-proven HUS (HIV+/HUS+).
- Compared these levels with 48 HIV-infected patients without HUS (HIV+/HUS-).
Main Results:
- Patients with HUS had higher creatinine, lower platelets, and increased cytomegalovirus (CMV) infection incidence (72% vs 25%).
- Plasma PAI-1 activity was similar between groups.
- t-PA activity was significantly higher in HUS cases (11.5 vs 4.5 U/ml, P=0.001). CMV infection was linked to increased t-PA.
- Multivariate analysis identified high t-PA (RR=9.21) and CMV infection (RR=3.36) as risk factors for HUS.
Conclusions:
- HIV-infected patients with HUS exhibit high plasma t-PA activity.
- Unlike non-HIV-associated HUS, PAI-1 plasma activity is not significantly increased.
- In HIV infection, HUS is not caused by decreased fibrinolytic activity.