Purpose: Hypophosphatemia due to secondary hyperparathyroidism is common but usually resolves in the first 6 months post kidney transplant (Tx). We sought to investigate point prevalence and determinants of prolonged and late onset hypophosphatemia in children after kidney Tx.

Methods: Records of 70 children (age 2-21) were reviewed at 6, 12, 18, 24, and 36 month time points post-Tx for serum phosphorus, 25hydroxy and 1,25 dihydroxy Vitamin D, PTH, urine phosphorus and creatinine, and BMI. Renal tubular reabsorption of phosphate (TMP/GFR) was calculated in those with prolonged hypophosphatemia (defined as those with low phosphorus levels or requiring supplementation at majority of time points ≥ 6 months).

Results: Study population included 40 male and 30 female children 14±4.5 yrs old; of these, 8 were severely obese (BMI Z score ≥ 2). Of 70 children, 25.4%, 26.1%, 22%, 22.5%, and 21.9% were hypophosphatemic at 6,12,18, 24, and 36 months, respectively. In the 8 severely obese patients > 6 months post-Tx, 87.5% were hypophosphatemic vs only 27.1% of non-obese children (p=0.0007). Mean serum phosphorus (during time period 12-36 months post-Tx) of obese was lower (2.6±0.25) than non-obese (3.8±0.09), p=0.0001. TMP/GFR was assessed in 12 children with prolonged hypophosphatemia (serum phosphorus 2.3±0.5; mean duration of hypophosphatemia 22.8±8.8 months). All had low TMP/GFR (mean 1.7±0.5, range 0.81-2.38 mg/dL, whereas normal TMP/GFR is 2.8-4.4 mg/dL) with normal PTH and 1,25 dihydroxy vitamin D levels. 11 of 12 had normal 25hydroxy vitamin D; phosphorus level corrected with repletion of vitamin D in 1 vitamin D deficient child. There were 6 additional children with normal phosphorus levels during the first 2 years who became hypophosphatemic during the third year post-Tx; this late onset hypophosphatemia corresponded with high dose steroid treatment for acute rejection (AR) in 5, and pyelonephritis in 1.

Conclusion: After 6 months post-Tx, hypophosphatemia is observed in a subset of children, and appears more common in severely obese than non-obese children. Steroid treatment for AR may contribute to late-onset hypophosphatemia. Prolonged hypophosphatemia was associated with low renal tubular reabsorption, but not explained by traditional risk factors (PTH, 25hydroxy and 1,25 dihydroxy Vitamin D), suggesting involvement of more novel factors. Emerging roles of phosphatonins, including FGF-23, in obesity and post-transplant hypophosphatemia require further investigation.

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