Clinical research Cyclosporine A – treated nephrotic children show impaired vasodilatation but no autonomic neuropathy Aneta Czupryniak1, Anna Kałużyńska1, Anna Półtorak-Krawczyk1, Bartosz Ostrowski2, Bogusław Więcek2, Marcin Tkaczyk1 1Division of Nephrology, Polish Mother’s Memorial Hospital Research Institute of Lodz, Poland 2Institute of Electronics, Technical University of Lodz, Poland Submitted: 14 April 2009 Accepted: 22 February 2010 Arch Med Sci 2010; 6, 4: 573-577 DOI: 10.5114/aoms.2010.14470 Copyright © 2010 Termedia & Banach A b s t r a c t Introduction: The aim of the study was to determine the effect of long-term cyclosporine A (CsA) treatment in children with idiopathic nephrotic syndrome on autonomic nerve function and peripheral blood flow assessed with thermography. Material and methods: The study group consisted of 19 nephrotic children treated with cyclosporine A compared to 16 healthy children. The assessment of blood flow was made based on the results of thermographic measurements during the cold stress test by an infrared radiation registering camera. Ewing’s battery of non-invasive tests was used to assess autonomic function. Results: The study showed diminished temperature increase after the cooling test in children with nephrotic syndrome treated with CsA. Sympathetic activity test results were comparable to healthy children. Conclusions: It may be hypothesized that cyclosporine A administered even in low doses induces small vessel dysfunction measured by the thermographic method. This effect seems to be independent of sympathetic nervous system involvement, which was absent in cyclosporine A treated nephrotic children. Key words: cyclosporine A, autonomic function, vasodilatation, thermography, children, nephrotic syndrome. Introduction Cyclosporine A (CsA) is used routinely in the immunosuppressive regimen in children with both steroid-dependent and steroid-resistant nephrotic syndrome (SD-NS and SR-NS) [1-3]. However, its use is limited by adverse reactions, which include acute and chronic nephrotoxicity and hypertension [4, 5]. Mechanisms by which CsA treatment leads to nephrotoxicity and hypertension are poorly understood. It has been shown that acute dose- dependent CsA nephrotoxicity results from functional vasoconstriction of the afferent pre-glomerular arterioles followed by a decrease in renal blood flow [6]. Prolonged vasoconstriction causing chronic ischaemia may contribute to chronic CsA-dependent tubulointerstitial changes [4, 5, 7, 8]. The concept of CsA inducing hypertension through impairment of vascular regulatory mechanisms is still under debate. Acute CsA-dependent impairment of peripheral blood flow presenting as Raynaud’s phenomenon (RP) has recently been described by Arinsoy et al. and Sharma et al. [9, 10]. Raynaud’s phenomenon is a symptom of Corresponding author: Marcin Tkaczyk, MD PhD Division of Nephrology Department of Paediatrics and Immunology Polish Mother’s Memorial Hospital Research Institute 281/289 Rzgowska St. 93-338 Lodz, Poland Phone: +48 42 271 21 40 Fax: +48 42 271 10 91 E-mail: mtkaczyk@uni.lodz.pl