ORIGINAL ARTICLE |
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Year : 2020 | Volume
: 3
| Issue : 1 | Page : 4-9 |
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Endothelial dysfunction in children with frequently relapsing and steroid-resistant nephrotic syndrome
Anuja Bhatia1, Abhijeet Saha2, Bobbity Deepthi2, Parul Goyal3, Ashish Datt Upadhyay4, Nand Kishore Dubey1
1 Department of Pediatrics, Division of Pediatric Nephrology, Postgraduate Institute of Medical Education and Research and Associated Dr. Ram Manohar Lohia Hospital, New Delhi, India 2 Division of Pediatric Nephrology, Department of Pediatrics, Lady Hardinge Medical College and Kalawati Saran Children Hospital, New Delhi, India 3 Department of Biochemistry, Postgraduate Institute of Medical Education and Research and Associated Dr Ram Manohar Lohia Hospital, New Delhi, India 4 Department of Biostatistics, All India Institute of Medical Sciences, New Delhi, India
Correspondence Address:
Abhijeet Saha Department of Pediatrics, Division of Pediatric Nephrology, Lady Hardinge Medical College and Kalawati Saran Children Hospital, New Delhi - 110001 India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/AJPN.AJPN_28_19
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Background: Impaired endothelial function is a precursor of the atherosclerotic process leading to cardiovascular adverse events. This study evaluated endothelial dysfunction using endothelial markers in children with steroid-resistant NS (SRNS) and frequently relapsing or steroid-dependent NS (FRNS/SDNS). Methods: This was a cross-sectional study with short-term follow up. Thirty-five patients with nephrotic syndrome (NS), aged 1–18 years, including 19 with frequent relapses or steroid-dependent NS (FRNS/SDNS) and 16 with steroid resistant NS (SRNS), and 19 age- and gender-matched controls, were enrolled for the study. Soluble thrombomodulin (sTM), plasminogen activator inhibitor 1 (PAI-1), and von Willebrand factor (vWF) levels were measured in patients with FRNS/SDNS in relapse and after 6 months of steroid-induced remission, at diagnosis in SRNS, and in controls. Results: Levels of vWF, PAI-1, and sTM were significantly higher than controls in patients with active NS (FRNS/SDNS in relapse or SRNS; P < 0.0001). Patients with FRNS/SDNS had significantly elevated vWF levels, compared to controls, even after 6 months of corticosteroid therapy. Levels of vWF were significantly higher for patients with recently diagnosed SRNS than relapse of FRNS/SDNS (P < 0.0001). Conclusion: Children with FRNS/SDNS and SRNS have significant endothelial dysfunction in all stages of disease in varying severity. It is unclear whether persistently elevated biomarkers of endothelial dysfunction contribute to future atherosclerotic events in patients with NS.
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