Reversal of hyperparathyroidism in response to dietary phosphorus restriction in the uremic dog

Kaplan, Michael A.; Canterbury, Janet M.; Bourgoignie, Jacques J.; Veliz, Gaston; Gavellas, George; Reiss, Eric; Bricker, Neal S.

doi:10.1038/ki.1979.6

Cited by 41 publications

(24 citation statements)

References 32 publications

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“…In confirming that restriction of dietary phosphorus can reverse the hyperparathyroidism of patients with moderate renal insufficiency (52), the observations made in the present study, like those made previously in the dog with experimental reduction ofrenal mass (27,(53)(54)(55), provide further support for the formulation that a normal dietary intake ofphosphorus can pathogenetically determine the hyperparathyroidism characteristic of chronic renal insufficiency (27,(53)(54)(55).…”

Section: Discussionsupporting

confidence: 74%

“…In dogs with experimental chronic renal insufficiency, Kaplan et al (55) Phosphorus is known to be an important determinant of the renal synthesis of 1,25-(OH)2D and thereby of its plasma concentration. In parathyroidectomized, vitamin D-deficient chicks and rats, the activity of 1-hydroxylase (33) and the apparent production of 1,25-(OH)2D (73) varies inversely with the serum concentration of phosphorus.…”

Section: Discussionmentioning

confidence: 99%

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Effect of dietary phosphorus on circulating concentrations of 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone in children with moderate renal insufficiency.

Portale¹,

Booth²,

Halloran³

et al. 1984

J. Clin. Invest.

337

165

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Abstract. The hyperparathyroidism characteristic of patients with moderate renal insufficiency could be caused by decreases in the plasma concentration of ionized calcium (Ca"+) evoked by: (a) recurring increases in the plasma concentration ofinorganic phosphorus that may be detectable only in the post-prandial period; (b) a reversible, phosphorus-mediated suppression of renal 25-hydroxyvitamin D-la-hydroxylase that decreases the plasma concentration of 1 ,25-dihydroxyvitamin D (1,25-(OH)2D) enough to decrease both gut absorption and bone resorption of Ca"+; (c) both of these. In a group of eight children with moderate renal insufficiency, mean glomerular filtration rate (GFR) 45±4 (SE) ml/min per 1.73 M2, ages 6-17 yr, we tested these hypotheses by determining the effect of short term (5 d) restriction and supplementation of dietary intake of phosphorus on the plasma concentration of 1,25-(OH)2D, the serum concentrations of immunoreactive parathyroid hormone (iPTH) and phosphorus, and the fractional renal excretion ofphosphorus (FEPi). When boxyl-terminal iPTH (C-iPTH) were greater, 59±9 vs.17±3 Aleq/ml, and unchanging; the serum concentration of intact-iPTH was also greater, 198+14 vs. 119±8 pg/ ml. The plasma concentration of 1,25-(OH)2D was lower than that of age-matched controls, 27±3 vs. 36±2 pg/ml (P < 0.01). When dietary phosphorus was restricted to 0.35 g/d, the plasma concentration of 1,25-(OH)2D increased by 60% to a mean value not different from that of normal controls, while serum concentrations of CiPTH and intact-iPTH decreased by 25%, the latter concentration to a mean value not different from that of controls. FEPi decreased from 31 to 9%. When dietary phosphorus was supplemented to 2.4 g/d, the plasma concentration of 1,25-(OH)2D decreased 32%, while those of C-iPTH and intact-iPTH increased by 131 and 45%, respectively; FEPi increased from 27 to 53%. Plasma concentrations of 25-hydroxyvitamin D remained normal and unchanged, and GFR did not change when dietary phosphorus was manipulated.The data demonstrate that in children with moderate renal insufficiency: (a) A normal dietary intake of phosphorus is attended by a decreased circulating concentration of 1,25-(OH)2D and an increased concentration of iPTH, but not by recurring increases in the serum concentration of phosphorus at any time of the day; (b) Dietary

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Effect of dietary phosphorus on circulating concentrations of 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone in children with moderate renal insufficiency.

Portale¹,

Booth²,

Halloran³

et al. 1984

J. Clin. Invest.

337

165

View full text Add to dashboard Cite

show abstract

“…If true, this thesis serves as a guide to management of progressive renal disease, as means may now be in hand to prevent or modify the formerly inevitable increase in PTH activity by medical [16] or nutritional [17,18] means. Because of these implications, further work is needed to enlarge the base for this interesting possibility.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic Disease in Uremia and Parathyroid Hormone Excess

Avram¹,

Iancu²

1982

Nephron

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To assess the coexistence of pancreatic alterations and elevation of parathyroid hormone (PTH) as contributors to morbidity, a study correlating evidence of histological pancreatitis with elevated PTH has been undertaken. A retrospective autopsy study of pancreatic histology in 21 patients who died during maintenance hemodialysis (MD) (group I) compared their level of serum PTH with a group of patients who died without historical or clinical evidence of renal insufficiency (group II). Each patient in this group had creatinine clearance of less than 5 ml/min and had been treated with hemodialysis from 4 to 120 months preceding death. There was a difference in the incidence of histological and PTH levels between groups I and II. A total of 15 out of 21 (71.4%) of group I patients had severe pancreatic disease. By contrast, none of the group II control patients had marked pancreatic disease (p < 0.01). Also a statistically different demarcation was present between groups I and II on the basis of PTH levels. Group I patients with pancreatic disease (n = 5) had a higher PTH level (567 ± 76 pg/ml) than those (n = 6) without diseased pancreata (218 ± 6.5 pg/ml). These data infer that a possible correlation between measured iPTH excess and histological alterations in pancreas may exist.

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“…Phosphate retention is a commonly encountered con sequence of chronic renal failure and has been impli cated in the development of secondary hyperparathy roidism and renal osteodystrophy [1][2][3][4][5][6][7], Its importance as a primary pathogenetic factor was first proposed in 1969 by Bricker et at. [ 1 ] who suggested that small recur rent increments in serum phosphate levels occurring in the course of progressive renal insufficiency initiate a series of events which ultimately result in secondary hyperparathyroidism and that this was an adaptive mechanism geared to maintaining plasma inorganic phosphate (P,) homeostasis.…”

mentioning

confidence: 99%