The level of transforming growth factor beta as a possible predictor of cyclophosphamide response in children with steroid-resistant nephrotic syndrome
Background:Steroid-resistant nephrotic syndrome (SRNS) is a burden in the country due to the progressive severity of chronic kidney disease (CKD). Calcineurin inhibitors (CNIs) or monoclonal antibodies are currently recommended for the treatment of this disease. In developing countries, steroid and cyclophosphamide (CPA) are available drugs used during the treatment. This study aims to provide a non-invasive modality that can be used to predict the response of SRNS children to CPA therapy. Subsequently, the proteinuria duration was shortened to reduce the risk of glomerular damage.
Method:A prospective-cohort-study was conducted at Hasan Sadikin General Hospital Bandung, Indonesia. A total of 88 SRNS children, aged 1 to 18 were accessed for serum TGF-ß level before receiving CPA therapy for six months, and clinical signs were observed. Furthermore, after six months of CPA treatment, the subjects were divided into CPA responder and non-responder based on the present of proteinuria, then the data were analyzed using multiple logistic regression to adjust age and gender.
Results:There was a statistically significant relationship between TGF-β and the risk of non-response to CPA therapy, after accounting for age, gender, baseline GFR, baseline ureum, and baseline urinary protein, the adjusted-OR was 1.051 (95% CI 1.007, 1.097, p = 0.022).
Conclusion:The high level of serum TGF-β obtained prior to CPA administration are reliable data for estimating adverse results on CPA therapy. Based on these results, a high baseline TGF-β level correlates with the poor response of CPA therapy.
Albumin-creatinin ratio, correlation, cyclophosphamide, steroid-resistant nephrotic syndrome, TGF-ß
Widiasta, Ahmedz; Wahyudi, Kurnia; Sribudiani, Yunia; and Rachmadi, Dedi
"The level of transforming growth factor beta as a possible predictor of cyclophosphamide response in children with steroid-resistant nephrotic syndrome,"
BioMedicine: Vol. 11
, Article 10.
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