The Impact of Comorbid Post-Traumatic Stress Disorder and Sleep Disturbances on Sympathetic Nerve Activity in Individuals with Chronic Kidney Disease

BACKGROUND: Both chronic kidney disease (CKD) and post-traumatic stress disorder (PTSD) are associated with sympathetic nervous system (SNS) overactivity which contributes to increased cardiovascular risk. However, the impact of comorbid PTSD on SNS activation in CKD remains poorly understood. Importantly, disturbances in sleep are a major feature of PTSD that are linked to SNS overactivation. Similarly, CKD are also prone to a variety of sleep complaints such as decreased sleep efficiency (SE) which is associated with increased cardiovascular risk. PURPOSE: Determine if comorbid PTSD augments SNS activity in CKD and evaluate the relationship between SNS and sleep metrics. HYPOTHESIS: Individuals with PTSD+CKD will have greater SNS activity compared to individuals with CKD alone. Sleep quality and SE will be associated with SNS activity. METHODS: 30 individuals (n = 16 PTSD+CKD, 85% male, 60 ± 9 yrs., n = 14 CKD alone, 81% male, 62 ± 7 yrs.) with CKD stages III-IV were enrolled. Muscle sympathetic nerve activity (MSNA) was measured via microneurography during a 5–10-minute rest period. In a sub-set of participants (n = 7 PTSD+CKD, n = 5 CKD), sleep quality was measured via the Pittsburgh Sleep Quality Index (PSQI). Sleep efficiency (SE) was calculated from the PSQI. Independent t-tests were used to compare group means for systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), PSQI, SE, MSNA burst frequency (BF), and burst incidence (BI) at rest. Pearson correlations were performed to evaluate the relationship between PSQI, SE, MSNA-BF, and MSNA-BI. RESULTS: There was no significant difference in SBP, DBP, or HR between PTSD+CKD compared to CKD alone. There was no significant difference between PTSD+CKD versus CKD alone in MSNA-BF (45.32 ± 11.21 vs. 38.32 ± 9.23 burst/min, t (28) = -1.85, p = 0.075, Cohen’s d = 0.70). However, there was a significant difference between PTSD+CKD versus CKD alone in MSNA-BI (72.31 ± 15.58 vs. 59.67 ± 13.15 burst/100hb, t (28) = -2.38, p = 0.024, Cohen’s d = 0.90). There was a significant difference between PTSD+CKD versus CKD alone in PSQI (14.14 ± 3.34 vs. 5.00 ± 1.58 a.u., t (10) = 5.63, p < 0.001, Cohen’s d = 3.54). SE was not significantly different between PTSD+CKD versus CKD alone (67.21 ± 20.71 vs. 87.85 ± 7.93 %, t (10) = -2.10, p = 0.062, Cohen’s d = 1.33). PSQI was significantly related to MSNA-BI ( r (12) = 0.58, p = 0.047). SE was significantly correlated to both MSNA-BF ( r (12) = -0.70, p = 0.012) and MSNA-BI ( r (12) = -0.73, p = 0.007). CONCLUSION: Our findings suggest individuals with comorbid PTSD+CKD have elevated SNS activity at rest, as indicated by MSNA-BI, compared to those with CKD alone. The moderate effect size observed for MSNA-BF suggests a larger sample size may be needed to detect a significant difference. In a small sub-set of participants poor sleep quality and reduced SE was associated with augmented MSNA. These results suggest that comorbid PTSD may augment SNS overactivation in CKD and sleep disturbances should be further explored as a therapeutic target to improve SNS overactivation in individuals with PTSD+CKD. Funded by: NIH grants R01HL135183, R33AT010457 and R61AT10457. M.J. McGranahan is supported by the ATLANTIS grant from the NIDDK (TL1DK136047 and U2CDK129501). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.