Unchanged expression of the sodium-dependent phosphate cotransporter NaPi-IIa despite diurnal changes in renal phosphate excretion

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)

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Phosphate homeostasis and the renal-gastrointestinal axis

AJP Renal Physiology ◽

10.1152/ajprenal.00508.2009 ◽

2010 ◽

Vol 299 (2) ◽

pp. F285-F296 ◽

Cited By ~ 131

Author(s):

Joanne Marks ◽

Edward S. Debnam ◽

Robert J. Unwin

Keyword(s):

Small Intestine ◽

Phosphate Transport ◽

Phosphate Absorption ◽

Renal Phosphate Reabsorption ◽

Sodium Dependent ◽

Dietary Phosphate ◽

Intestinal Phosphate Absorption ◽

End Stage ◽

And Control ◽

Renal Phosphate Excretion

Transport of phosphate across intestinal and renal epithelia is essential for normal phosphate balance, yet we know less about the mechanisms and regulation of intestinal phosphate absorption than we do about phosphate handling by the kidney. Recent studies have provided strong evidence that the sodium-phosphate cotransporter NaPi-IIb is responsible for sodium-dependent phosphate absorption by the small intestine, and it might be that this protein can link changes in dietary phosphate to altered renal phosphate excretion to maintain phosphate balance. Evidence is also emerging that specific regions of the small intestine adapt differently to acute or chronic changes in dietary phosphate load and that phosphatonins inhibit both renal and intestinal phosphate transport. This review summarizes our current understanding of the mechanisms and control of intestinal phosphate absorption and how it may be related to renal phosphate reabsorption; it also considers the ways in which the gut could be targeted to prevent, or limit, hyperphosphatemia in chronic and end-stage renal failure.

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Phosphaturic effect of furosemide: role of PTH and carbonic anhydrase

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.2.f105 ◽

1977 ◽

Vol 232 (2) ◽

pp. F105-F110 ◽

Cited By ~ 1

Author(s):

J. A. Haas ◽

M. V. Larson ◽

G. R. Marchand ◽

F. C. Lang ◽

R. F. Greger ◽

...

Keyword(s):

Parathyroid Hormone ◽

Carbonic Anhydrase ◽

Extracellular Fluid ◽

Constant Level ◽

Extracellular Fluid Volume ◽

Phosphate Excretion ◽

Carbonic Anhydrase Inhibition ◽

Renal Phosphate Excretion ◽

Subsequent Administration

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.

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INCREASED RENAL PHOSPHATE EXCRETION IN CUSHING'S SYNDROME

Acta Endocrinologica ◽

10.1530/acta.0.0560085 ◽

1967 ◽

Vol 56 (1) ◽

pp. 85-92 ◽

Cited By ~ 6

Author(s):

F. Camanni ◽

O. Losana ◽

F. Massara ◽

G. M. Molinatti

Keyword(s):

Adrenal Insufficiency ◽

Lower Limit ◽

Cushing’S Syndrome ◽

Cushing's Syndrome ◽

Adrenal Neoplasm ◽

Phosphate Excretion ◽

Renal Phosphate Excretion

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.

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Effect of Bromotetramisole on Renal Phosphate Excretion

Experimental Biology and Medicine ◽

10.3181/00379727-213-44050 ◽

1996 ◽

Vol 213 (2) ◽

pp. 193-195 ◽

Cited By ~ 1

Author(s):

M. Onsgard-Meyer ◽

A. L. McCoy ◽

F. G. Knox

Keyword(s):

Phosphate Excretion ◽

Renal Phosphate Excretion

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Renal Phosphate Excretion in Goats

Journal of Veterinary Medicine Series A ◽

10.1111/j.1439-0442.1998.tb00810.x ◽

1998 ◽

Vol 45 (1-10) ◽

pp. 145-153 ◽

Cited By ~ 11

Author(s):

I. Widiyono ◽

K. Huber ◽

K. Failing ◽

G. Breves

Keyword(s):

Phosphate Excretion ◽

Renal Phosphate Excretion

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New Concepts Concerning the Regulation of Renal Phosphate Excretion

Physiology ◽

10.1152/physiologyonline.1997.12.5.211 ◽

1997 ◽

Vol 12 (5) ◽

pp. 211-214

Author(s):

R Kumar

Keyword(s):

Hypophosphatemic Rickets ◽

Phosphate Homeostasis ◽

Phosphate Excretion ◽

New Concepts ◽

Similar Factor ◽

Renal Phosphate Excretion

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.

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