Glomerular injury and tubular injury would induce hyperphosphatemia, which in turn regulates PTH, FGF23, vitamin D, etc. In a podocyte-specific injury mice model manifesting strong proteinuria, serum Pi, serum FGF23 and intact PTH increased gradually, which might lead to secondary hyperparathyroidism and bone disease (6). This evidence concerns the gene PTH and hyperphosphatemia.