PMID- 3543637
OWN - NLM
STAT- MEDLINE
DCOM- 19870312
LR  - 20041117
IS  - 0378-0392 (Print)
IS  - 0378-0392 (Linking)
VI  - 12
IP  - 5-6
DP  - 1986
TI  - Reduced phosphate reabsorption unrelated to parathyroid hormone after renal 
      transplantation: implications for the pathogenesis of hyperparathyroidism in 
      chronic renal failure.
PG  - 356-62
AB  - We measured nephrogenous cyclic adenosine monophosphate (NcAMP) excretion, an in 
      vivo bioassay for endogenous parathyroid hormone (PTH) secretion, and renal 
      phosphate threshold (TmP/GFR) in 33 renal allograft recipients with stable renal 
      function (creatinine clearance greater than or equal to 60 ml/min/1.73 m2 body 
      surface area, 6 months or more post-transplant) and in 9 kidney donors. Sixteen 
      patients had normal parathyroid function, 8 had hypercalcemic hyperparathyroidism 
      and 9 had normocalcemic hyperparathyroidism; the latter were apparently resistant 
      to the hypercalcemic actions of endogenous PTH, but the cause for this was not 
      apparent. In all four subject groups, TmP/GFR was significantly and similarly 
      lower (by 0.8-1.0 mg/dl) than predicted by multiple regression on age, sex, 
      corrected plasma calcium and NcAMP (determined in 306 subjects spanning a wide 
      range of parathyroid function) indicating a major PTH-independent mechanism for 
      reducing phosphate reabsorption in the presence of a single kidney. In all four 
      groups the contribution of this mechanism to the observed depression of TmP/GFR 
      was substantially greater than the contribution of increased PTH secretion. In 
      all groups, but more so in the recipients than in the donors, fasting urinary 
      phosphate excretion/GFR was increased, so that fasting plasma phosphate, although 
      reduced, did not accurately reflect the severity of the defect in phosphate 
      reabsorption. We conclude that the dominant mechanism for the adaptive decrease 
      in renal tubular phosphate transport in response to nephron reduction does not 
      require the participation of PTH and is manifest in the presence of fasting 
      hypophosphatemia.
FAU - Parfitt, A M
AU  - Parfitt AM
FAU - Kleerekoper, M
AU  - Kleerekoper M
FAU - Cruz, C
AU  - Cruz C
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Miner Electrolyte Metab
JT  - Mineral and electrolyte metabolism
JID - 7802196
RN  - 0 (Parathyroid Hormone)
RN  - 0 (Phosphates)
SB  - IM
MH  - Absorption
MH  - Adult
MH  - Female
MH  - Humans
MH  - Hyperparathyroidism/*etiology
MH  - Kidney Failure, Chronic/*complications/therapy
MH  - *Kidney Transplantation
MH  - Male
MH  - Middle Aged
MH  - Parathyroid Hormone/*metabolism
MH  - Phosphates/*metabolism
MH  - Transplantation, Homologous
EDAT- 1986/01/01 00:00
MHDA- 1986/01/01 00:01
CRDT- 1986/01/01 00:00
PHST- 1986/01/01 00:00 [pubmed]
PHST- 1986/01/01 00:01 [medline]
PHST- 1986/01/01 00:00 [entrez]
PST - ppublish
SO  - Miner Electrolyte Metab. 1986;12(5-6):356-62.