LAUSR

In North America, children younger than 20 years of age account for less than 2% of the total chronic kidney disease (CKD) patient population; however, the prevalence of pediatric CKD within the population has increased by 32% since 1990 as pediatric CKD care improved [1, 2]. Approximately 50% of all pediatric CKD diagnoses are due to congenital, non-glomerular anomalies [3] and half of CKD patients with the congenital disease will need a kidney transplantation in their lifetime [2]. Cognitive deficits are known to emerge in parallel to CKD progression. Cross-sectional and metaanalytic data demonstrate that in contrast to advanced CKD, early-stage CKD patients have relatively intact IQ although with a general leftward skew of the distribution toward lower scores [4–6]. Furthermore, up to 35% of children with early CKD manifest impairment on measures of executive function (EF) [7]. More pervasive neurocognitive deficits have been well described in the pediatric CKD 5 population (e.g., dialysis, transplant, and/or post-transplant patients). There is greater variability in full-scale intelligence quotient (IQ) [8–11] with notable IQ deficits in advanced CKD/ kidney failure, accompanied by poorer performance on neurocognitive assessment of EF, memory, attention, and academic achievement [10]. Furthermore, EF deficits are more pronounced with lower kidney function (e.g., disease progression) [4, 5, 7], longer duration of kidney disease [4, 12, 13], metabolic acidosis [14, 15], and hypertension [16]. These observations point to a potential relationship between pediatric CKD and abnormal neurodevelopment. Magnetic resonance imaging (MRI) provides a valuable tool for assessing the neurobiological mechanism of the observed cognitive deficits in pediatric CKD.