# Elevated Indoxyl Sulfate Levels Correlate with Increased Aortic Stiffness in Patients Undergoing Kidney Transplantation

## TL;DR

High levels of indoxyl sulfate in kidney transplant patients are linked to increased aortic stiffness, a risk factor for cardiovascular issues.

## Contribution

This study identifies indoxyl sulfate as an independent determinant of aortic stiffness in kidney transplant recipients.

## Key findings

- 27.7% of kidney transplant recipients had aortic stiffness (cfPWV > 10 m/s).
- Patients with aortic stiffness had higher indoxyl sulfate levels and other cardiovascular risk factors.
- Indoxyl sulfate remained independently associated with aortic stiffness after adjusting for other factors.

## Abstract

Although kidney transplantation (KT) restores renal function, residual uremic toxins, such as indoxyl sulfate (IS), may persist and contribute to vascular remodeling and aging. Aortic stiffness, reflected by carotid–femoral pulse wave velocity (cfPWV), is a strong predictor of cardiovascular events. This study enrolled KT recipients to examine the association of circulating IS with aortic stiffness. Using the SphygmoCor system, we assessed aortic stiffness, which was defined as cfPWV > 10 m/s. Serum IS concentrations were measured by liquid chromatography–tandem mass spectrometry. Of 94 KT recipients, 26 (27.7%) met the criteria for aortic stiffness. Compared with patients without aortic stiffness, those with aortic stiffness were older (p = 0.017) and had significantly higher systolic blood pressure (p = 0.011) and fasting glucose levels (p = 0.002), a higher prevalence of diabetes (p = 0.043), and higher IS levels (p = 0.002). According to multivariable logistic regression, serum IS remained independently associated with aortic stiffness (p = 0.017). According to stepwise linear regression, log-transformed IS further showed a positive correlation with cfPWV (p = 0.016). Serum IS remained an independent determinant of aortic stiffness in KT recipients, highlighting the burden of residual uremic toxins as a contributor to post-transplant vascular aging.