Abstract
Hepatitis C virus (HCV) infection in kidney transplant recipients (KTRs) can be successfully treated with direct antiviral agents (DAA). The aim of our study was to analyze different measures of vascular function during and after the DAA treatment. As we have observed the improvement of blood pressure (BP) control in some individuals, we have conducted an analysis of potential explanatory mechanisms behind this finding. Twenty-eight adult KTRs were prospectively evaluated before and 15 months after start of DAA therapy. Attended office BP (OBP), augmentation index (AIx), pulse wave velocity (PWV), flow-mediated dilation (FMD), liver stiffness measurement (LSM), and liver steatosis assessment (controlled attenuation parameter (CAP)) were measured. In half of the patients, improvement of OBP control (decline of systolic BP by at least 20 mmHg or reduction of the number of antihypertensive drugs used) and parallel central aortic pressure parameters, including AIx, was observed. There was a significant decrease in CAP mean values (241 ± 54 vs. 209 ± 30 dB/m, p < 0.05) only in patients with OBP control improvement. Half of our KTRs cohort after successful HCV eradication noted clinically important improvement of both OBP control and central aortic pressure parameters, including AIx. The concomitant decrease of liver steatosis was observed only in the subgroup of patients with improvement of blood pressure control.
Highlights
Arterial hypertension is highly prevalent in kidney transplant recipients (KTRs) as a consequence of common pretransplant hypertension and as an additional effect of immunosuppressive medications [1,2]
The other 32 patients were treated with the direct antiviral agents (DAA) anti-Hepatitis C virus (HCV) protocol, including 8 with a 6-month regimen and 24 patients with a 3-month regimen based on sofosbuvir
We demonstrated the clinically important improvement of blood pressure control, defined as the decline of attended office systolic pressure by at least 20 mmHg without pharmacotherapeutic changes or the reduction of antihypertensive treatment due to the BP decline, in half of our cohort of HCV-infected stable kidney transplant recipients after successful HCV eradication with sofosbuvir-based DAA therapy
Summary
Arterial hypertension is highly prevalent in kidney transplant recipients (KTRs) as a consequence of common pretransplant hypertension and as an additional effect of immunosuppressive medications [1,2]. Higher BP values were associated with reduced graft and patient survival [5]. Cardiovascular disease is the primary cause of mortality among kidney transplant recipients, mostly due to long-term consequences of chronic kidney disease (CKD) [6]. CKD-related systemic inflammation, calcium-phosphate abnormalities, and oxidative stress promote endothelial dysfunction, vascular calcification, and accelerated atherosclerosis in addition to the traditional risk factors [7,8]. Vascular injury caused by the uremic milieu results in an increased arterial stiffness and reduced flow-mediated dilation (FMD) [9,10]
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