FGFR1 and chronic kidney disease: In contrast to these mineral metabolism parameters, the same genetic deletions significantly suppressed plasma PTHconcentrations in the CKD groups: Fgfr1–3flox/flox (3264.7 ± 1654.5 pg/mL, n = 10) vs Fgfr1–3flox/flox;PTH-Cre (1290.9 ± 312.2 pg/mL, n = 10), P < 0.001; αKlothoflox/flox (2452.4 ± 425.9 pg/mL, n = 9) vs αKlothoflox/flox;PTH-Cre (1357.3 ± 675.4 pg/mL, n = 11), P < 0.001; Fgfr1–4flox/flox (2226.8 ± 801.8 pg/mL, n = 8) vsFgfr1–4flox/flox;PTH-Cre (1144.3 ± 388.3 pg/mL, n = 8), P < 0.001, even though the suppressed levels were higher than those in the non-CKD groups.