BACKGROUND Posterior urethral valves (PUVs) are one of the leading causes of pediatric chronic kidney disease (CKD). Growth impairment is prevalent in pediatric CKD, and children with PUVs are at… Click to show full abstract
BACKGROUND Posterior urethral valves (PUVs) are one of the leading causes of pediatric chronic kidney disease (CKD). Growth impairment is prevalent in pediatric CKD, and children with PUVs are at high risk for growth retardation. OBJECTIVE The objective of this study was to describe growth profiles in PUVs and to identify risk factors for stunting, defined as age-specific height standard deviation score (SDS) below -2. PATIENTS AND METHODS Medical records of 65 patients with PUVs and a minimum follow-up of two years were retrospectively reviewed. Chronic kidney disease stage 1-3 was considered mild CKD, whereas CKD stage 4-5 was considered advanced CKD. Age-specific height, weight, and body mass index (BMI) SDS were determined. Seven potential risk factors for stunting, namely timing of diagnosis, renal dysplasia, timing of surgery, requirement of urinary diversion, nadir serum creatinine after surgery, recurrent febrile urinary tract infection (UTI), and severity of CKD, were analyzed. RESULTS Median age at diagnosis, at surgery, and at last follow-up was 0.51, 0.75, and 7.53 years, respectively. All patients underwent valve ablation, and 33.8% required urinary diversion. Median nadir serum creatinine after surgery was 0.40 mg/dL and was higher in patients who underwent urinary diversion (P < 0.001). Growth profiles by CKD stage are displayed in Fig. 1. Median height SDS was -0.40 and was lower in patients with advanced CKD (P = 0.03). Stunting was diagnosed in 15.4%. Advanced CKD was an independent risk factor for stunting, with the odds ratio of 12.7. Urinary diversion and nadir creatinine more than 0.80 mg/dL were weakly associated with stunting but not significant. Timing of diagnosis and surgery, unilateral renal dysplasia, and recurrent febrile UTI were not associated with stunting. Median SDS of weight and BMI was -0.64 and -0.19, respectively. Patients who were thin, of normal weight, overweight, and obese comprised 26.2%, 58.5%, 10.8%, and 4.6%, respectively. There was no significant difference of SDS of weight and BMI across CKD stages (Fig. 1). DISCUSSION Deterioration in height began early in the course of disease and was worsening in relation to the decline of renal function. The impact of timing of diagnosis or surgery on height was controversial. Patients who underwent urinary diversion had high nadir creatinine and were likely to have severe PUVs. Although patients with severe baseline renal dysfunction may require urinary diversion, nadir serum creatinine and urinary diversion are not associated with stunting. Delaying progression of CKD could maximize linear growth potential in PUVs. A substantial proportion of patients were overweight or obese. Sufficient caloric intakes may be maintained in patients with PUVs.
               
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