RESUMO
In the original publication, the second author's affiliation was incorrectly published as "Department of Physiology, RAK College of Medical Sciences, Ras Al Khaimah, UAE". The correct affiliation should read as "Visiting Academic, Basic Medical Sciences Department, College of Medicine, University of Sharjah (UAE)".
RESUMO
BACKGROUND: The literature notes high prevalence of cognitive function (CF) impairment among hemodialysis patients. Renal transplantation by reversing metabolic factors should improve cognitive function; however, results in post-transplant patients are inconsistent. Lack of longitudinal studies, variable and small patient population, variable renal function and post-transplantation period and use of non-specific tests make results difficult to interpret. We looked at CF in stable hemodialysis patients just prior to live renal transplantation and approximately 3 months subsequently using well-validated electrophysiological study of P300 cognitive potential obtained by auditory oddball paradigm using multiple scalp electrodes. METHODS: Ten healthy age- and gender-matched controls (group 1) and 20 end-stage kidney disease (ESKD) male patients on maintenance hemodialysis with no other comorbidities that affect CF were studied before (group 2) and 3 months after successful transplantation (group 3). RESULTS: ESKD population had mean age of 29.7 ± 7.5 years, with mean dialysis vintage and post-transplant period being 10.3 ± 6.9 and 3.2 ± 0.4 months, respectively. Mean P300 latencies in groups 1, 2 and 3 were 319 ± 33.6, 348.6 ± 27.8 and 316.4 ± 33.4 ms, respectively (P < 0.001 group 1 vs 2 and group 2 vs 3; group 1 vs 3 NS). Mean P300 amplitude in groups 1, 2 and 3 was 27.9 ± 12.8, 13.4 ± 8.6 and 14.6 ± 9.4 µV, respectively (P < 0.001 group 1 vs 2 and group 1 vs 3; group 2 vs 3 NS). P300 latencies correlated negatively with hemoglobin and serum albumin. CONCLUSIONS: ESKD patients have impaired CF as documented by prolonged P300 latencies. There was normalization of P300 latencies post-transplantation indicating role of uremic toxins in CF impairment.