Mechanisms of autonomic nervous system dysfunction in uremia

Autonomic dysfunction in hemodialysis patients is one of the components of uremic neuropathy. In this prospective study, we investigated the effect of renal transplantation on uremic autonomic dysfunction with long-term time-domain and frequency-domain heart rate variability. Fourteen hemodialysis patients (10 male, 4 female; mean age 33 ± 11 (range 16–50) years) were examined before and at the early after transplantation period (mean 4.6 ± 1.5 (range 3–7.5) months). The mean time spent on hemodialysis was 16.7 ± 15.6 (range 6–65) months. In time-domain analysis, significant increases in all parameters except pNN50 (SD, SDANN, SDNN, rMSSD) were observed after renal transplantation (p < 0.01). In frequency-domain analysis, low-frequency (LF) (0.04–0.15 Hz) and high-frequency (HF) (0.15–0.40 Hz) spectral power were found to be significantly increased after renal transplantation (4.54 ± 1.04 vs. 12.58 ± 8.69 for LF (p = 0.005), 2.80 ± 1.0 vs. 6.50 ± 3.55 for HF (p = 0.005)), but the LF/HF ratio was not different from a pretransplant period (1.71 ± 0.349 vs. 1.85 ± 0.49, p = 0.26). It was concluded that autonomic dysfunction in hemodialysis patients is reversible and renal transplantation reverses the sympathetic and parasympathetic autonomic dysfunction simultaneously and at a relatively early stage.

Section: Discussionmentioning

confidence: 99%

Improvement of Uremic Autonomic Dysfunction after Renal Transplantation: A Heart Rate Variability Study

Yildiz¹,

Sever²,

Demirel

et al. 1998

“…Early studies [1, 2, 3]suggested cardiac autonomic nervous system abnormalities in chronic renal failure (CRF). Patients with CRF frequently have complications such as hypertension, myocardial hypertrophy, decreased left ventricular contractility, or dialysis-induced hypotension which may be associated with cardiac autonomic nervous system abnormalities [1, 4, 5, 6].…”

Section: Introductionmentioning

confidence: 99%

Cardiac Autonomic Neuropathy in Patients with Chronic Renal Failure on Hemodialysis

Kurata¹,

Uehara²,

Sugi³

et al. 2000

To characterize uremic cardiac autonomic neuropathy, we measured plasma catecholamines, analyzed the 24-hour heart rate variability (HRV), and acquired serial images with ¹²³I-metaiodobenzylguanidine (MIBG) in 44 patients with chronic renal failure on hemodialysis and in 14 controls. Time-domain measures were calculated using the Marquette HRV program. MIBG clearance rates from the heart and lung were evaluated on planar images, and the regional MIBG uptake in the left ventricular myocardium was evaluated with single-photon emission computed tomography. Compared with controls, plasma dopamine and norepinephrine levels were elevated (p < 0.001 and p = 0.03, respectively), and all the time-domain measures of HRV were reduced in the patients (p < 0.001). The MIBG clearance rate from the heart was higher (p < 0.001), that from the lung was lower (p < 0.001), and the myocardial MIBG distribution was more heterogeneous in patients than in controls (total uptake score p ≤ 0.03). These variables were similar between 26 patients without and 18 patients with hypertension. Uremic cardiac autonomic neuropathy may be characterized by high plasma levels of dopamine and norepinephrine, reduced HRV, and abnormal MIBG kinetics in the heart with heterogeneous myocardial MIBG distribution, suggesting cardiac sympathetic overactivity and parasympathetic deterioration. In addition, abnormal MIBG kinetics in the lung may imply pulmonary sympathetic nervous dysfunction and/or endothelial dysfunction in uremic patients.

“…In conclusion: patients on maintenance hemodialysis exhibit numerous alterations in the activity of the sympathetic nervous system [1, 2, 3]including hyporesponsiveness of α- and β-adrenoceptors [4, 7, 22, 23]. The present results show that for β-adrenoceptor hyporesponsiveness – at least partly – the presence of inhibitory substance(s) in uremic plasma could be responsible; the mechanism leading to α-adrenoceptor hyporesponsiveness remains to be elucidated.…”

Section: Discussionmentioning

confidence: 85%

“…Autonomic dysfunction is frequently observed in patients on chronic hemodialysis treatment [1, 2, 3]. This is accompanied by many cardiovascular disturbances including hyporesponsiveness of adrenergic receptors.…”

Section: Introductionmentioning

confidence: 99%

Effects of Uremic Plasma on α- and β-Adrenoceptor Subtypes

Ferchland

Rettkowski²,

Pönicke³

et al. 1998

Responsiveness of adrenergic receptors is decreased in patients on maintenance hemodialysis. In this study we investigated whether uremic plasma might affect adrenergic receptors. For this purpose we determined the effects of uremic plasma obtained from 10 patients on hemodialysis treatment (mean age 61 ± 3 years, dialysis frequency 3 × 4 h/week, duration of treatment 3 ± 1 years) before and at the end of the 4-hour dialysis treatment on binding of radioligands to β₁- and β₂- as well as α₁- and α₂-adrenoceptors. Plasma from 6 healthy volunteers served as control; the plasmas were studied in three dilutions: undiluted, 1:1 (v/v) and 1:4 (v/v) with saline diluted. Plasma from healthy control did not significantly affect the number of β₁- and β₂- or α₁- and α₂-adrenoceptors. On the other hand, uremic plasma significantly decreased the number of β₁- and β₂-adrenoceptors; this inhibitory effect was also observed when plasma obtained at the end of the 4-hour dialysis treatment was investigated. On the other hand, uremic plasma did not significantly decrease the number of α₁- and α₂-adrenoceptors. We conclude that in patients on maintenance hemodialysis, the presence of inhibitory substance(s) in uremic plasma could be – at least partly – responsible for the β-adrenoceptor hyporesponsiveness; the mechanism leading ot α-adrenoceptor hyporesponsiveness, however, remains to be elucidated.