scholarly journals Postprandial adjustments in renal phosphate excretion do not involve a gut-derived phosphaturic factor

2017 ◽  
Vol 102 (4) ◽  
pp. 462-474 ◽  
Author(s):  
Grace J. Lee ◽  
Lina Mossa-Al Hashimi ◽  
Edward S. Debnam ◽  
Robert J. Unwin ◽  
Joanne Marks
1978 ◽  
Vol 14 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Michael A. Kaplan ◽  
Janet M. Canterbury ◽  
George Gavellas ◽  
David Jaffe ◽  
Jacques J. Bourgoignie ◽  
...  

1985 ◽  
Vol 248 (2) ◽  
pp. F175-F182
Author(s):  
E. Kraus ◽  
G. Briefel ◽  
L. Cheng ◽  
B. Sacktor ◽  
D. Spector

As progressive renal failure develops, phosphate excretion per functioning nephron increases, thus preserving homeostasis. To test whether dietary phosphate supply might contribute to the regulation of renal phosphate excretion in the uremic setting, groups of male Sprague-Dawley rats that were either parathyroidectomized (PTX) or sham PTX (S-PTX) and either five-sixths nephrectomized (Nx) or sham Nx (S-Nx) were studied following a 4-wk dietary regimen consisting of 0.1 or 0.7% phosphate. For Nx rats fed the 0.7% phosphate diet the fractional excretion of phosphate (FEPi) was enhanced (47 +/- 6 vs. 21 +/- 3%) and the maximum tubular reabsorption of phosphate per milliliter GFR (TmPi/GFR) was suppressed (1.65 +/- 0.19 vs. 2.33 +/- 0.19 mumol/ml). FEPi was unchanged by PTX in these Nx animals (42 +/- 6 vs. 47 +/- 6%). TmPi/GFR remained suppressed in PTX, NX animals when compared with S-Nx, PTX controls (3.38 +/- 0.33 vs. 5.07 +/- 0.41 mumol/ml). For rats fed the 0.1% phosphate diet Nx did not affect TmPi/GFR in either S-PTX (5.40 +/- 0.43 vs. 4.97 +/- 0.34 mumol/ml) or PTX (7.03 +/- 0.23 vs. 6.98 +/- 0.21 mumol/ml) animals. For both S-Nx and Nx animals the effects of PTX and dietary phosphate restriction on TmPi/GFR were independent and additive. In all groups of animals, tubular reabsorption of phosphate per milliliter GFR (TRPi/GFR) dropped acutely with continued infusion of phosphate once TmPi/GFR was achieved. Thus, a resetting of TRPi/GFR occurs among Nx rats in response to both chronic dietary phosphate deprivation and acute intravenous phosphate loading.(ABSTRACT TRUNCATED AT 250 WORDS)


1977 ◽  
Vol 232 (2) ◽  
pp. F105-F110 ◽  
Author(s):  
J. A. Haas ◽  
M. V. Larson ◽  
G. R. Marchand ◽  
F. C. Lang ◽  
R. F. Greger ◽  
...  

The first objective of this study was to examine the effects of furosemide on renal phosphate excretion in the presence and absence of a constant level of parathyroid hormone (PTH) while extracellular fluid volume was held constant. In the absence of PTH, furosemide did not significantly increase fractional phosphate excretion (FEP%, 4.2 +/- 2.7 to 6.2 +/- 1.9%; five dogs). In the presence of PTH, furosemide increased FEP% from 23.4 +/- 3.7 to 33.8 +/- 6.0% (P less .025; five dogs). Thus, the phosphaturia induced by furosemide was dependent on the presence of PTH. The second objective was to evaluate the hypothesis that furosemide exerts its phosphaturic effect through carbonic anhydrase inhibition, and therefore we tested for additivity of the phosphaturic effect of furosemide, and acetazolamide. In the presence of a constant level of PTH, acetazolamide increased FEP % from 24.5 +/- 1.8% to 40.7 +/- 5.1% P less than .025, five dogs. The subsequent administration of furosemide did not further increase FEP%, delta 3.3 +/- 8.9%; NS. Thus, the phosphaturic effect of furosemide was not additive to that of acetazolamide, indicating that acetazolamide and furosemide may share similar mechanisms for inhibiting phosphate reabsorption.


1967 ◽  
Vol 56 (1) ◽  
pp. 85-92 ◽  
Author(s):  
F. Camanni ◽  
O. Losana ◽  
F. Massara ◽  
G. M. Molinatti

ABSTRACT Renal phosphate excretion was measured in 23 cases of Cushing's syndrome using the phosphate excretion index (PEI) described by Nordin & Fraser (1960). The majority of the patients had an increased PEI associated with a tendency towards hypophosphoraemia. Regression of the syndrome due to intrasellar implantation of 90Y or to removal of an adrenal neoplasm led to prompt correction of both the PEI and the phosphoraemia. In patients with adrenal insufficiency the PEI values fell below the lower limit of the normal.


1996 ◽  
Vol 213 (2) ◽  
pp. 193-195 ◽  
Author(s):  
M. Onsgard-Meyer ◽  
A. L. McCoy ◽  
F. G. Knox

1998 ◽  
Vol 45 (1-10) ◽  
pp. 145-153 ◽  
Author(s):  
I. Widiyono ◽  
K. Huber ◽  
K. Failing ◽  
G. Breves

Physiology ◽  
1997 ◽  
Vol 12 (5) ◽  
pp. 211-214
Author(s):  
R Kumar

Some tumors elaborate a phospaturic factor, "phosphatonin," that is unlike known peptide or sterol hormones. The same, or a similar, factor may exist in hypophosphatemic mice and humans with X-linked hypophosphatemic rickets. Such a factor may play a role in the control of phosphate homeostasis in normal physiological states.


1983 ◽  
Vol 244 (3) ◽  
pp. F265-F269 ◽  
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox

Dietary phosphate intake is now recognized to be a primary regulator of renal phosphate excretion. However, the nephron sites involved in the adaptation to changes in dietary phosphate are unclear. We tested the hypothesis that deep and superficial nephrons respond differently to changes in dietary phosphate by comparing fractional phosphate delivery (FDP%) from proximal tubules of both nephron populations. Because phosphate reabsorption is not detectable in the ascending loop of Henle, FDP% to the superficial early distal tubule and papillary loop of Henle reflect delivery from superficial and deep nephron proximal tubules, respectively. Micropuncture experiments were performed in 17 acutely TPTX rats fed either a low (0.07%) or a high (1.8%) phosphate diet for 4 days prior to the experiment. In low phosphate diet, fractional phosphate excretion was 0.93 +/- 0.26%. FDP% was 7.5 +/- 0.5 and 9.1 +/- 2.2% from superficial and deep nephron proximal tubules, respectively (P greater than 0.05). In high phosphate diet, fractional phosphate excretion was 29.6 +/- 5.0%. FDP% was significantly greater from superficial proximal tubules, 33.9 +/- 4.6%, compared with that from deep nephron proximal tubules, 14.0 +/- 2.7% (P less than 0.05). We conclude that significant adaptation of phosphate reabsorption in response to changes in dietary phosphate intake occurs in the superficial but not in the deep nephron proximal tubule in acutely TPTX volume-expanded rats. In addition, the presence of distal phosphate reabsorption was not evident in high phosphate diet but must occur in low phosphate diet.


2016 ◽  
Vol 6 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Shuhei Watanabe ◽  
Keiji Kono ◽  
Hideki Fujii ◽  
Kentaro Nakai ◽  
Shunsuke Goto ◽  
...  

We encountered 2 cases of hypophosphatemia due to Legionella pneumonia. Both cases showed increased urinary phosphate excretion and renal tubular dysfunction, which ameliorated with recovery from Legionella pneumonia. Serum fibroblast growth factor-23 level was suppressed, whereas serum 1,25(OH)2 vitamin D and parathyroid hormone levels were normal. Delayed elevation of serum 1,25(OH)2 vitamin D levels was observed with improvement in renal tubular function. These findings suggested hypophosphatemia might be mediated by renal tubular dysfunction.


Sign in / Sign up

Export Citation Format

Share Document