Renal Vasodilatation: Effect on Renal Handling of Phosphate

1971 ◽  
Vol 41 (2) ◽  
pp. 109-121 ◽  
Author(s):  
J. J. Ahumada ◽  
S. G. Massry

1. The combined effects of unilateral renal vasodilatation produced by acetylcholine or bradykinin and intravenous infusion of angiotensin on phosphate excretion and reabsorption were investigated in fourteen anaesthetized dogs. The influence of these manoeuvres on the excretion of sodium, calcium and magnesium was also evaluated. 2. Unilateral renal vasodilatation alone produced an increase in the excretion of phosphate, calcium, magnesium and sodium; and the infusion of angiotensin caused further augmentation of the excretory rates of these ions from the vasodilated kidney in most experiments. 3. The maximal tubular reabsorptive capacity (Tm) for phosphate was decreased by renal vasodilatation. 4. There was a close and significant correlation between the fraction of the filtered load of phosphate, calcium, and magnesium which was excreted and that of sodium. 5. The results indicate that renal vasodilatation with or without the infusion of angiotensin causes a decrease in the renal tubular reabsorption of phosphate, calcium, magnesium and sodium.

DICP ◽  
1989 ◽  
Vol 23 (12) ◽  
pp. 1013-1017 ◽  
Author(s):  
Gregory L. Kearns ◽  
Phillip L. Berry ◽  
Joseph A. Bocchini ◽  
Bettina C. Hilman ◽  
John T. Wilson

We evaluated the renal handling of beta2-microglobulin (β2-M) and creatinine in healthy outpatients (n = 6), normal children hospitalized for infections treated with antibiotics (not including an aminoglycoside) (n = 4); outpatients with cystic fibrosis (CF; n = 12), and hospitalized patients with CF (n = 6) who received a 10- to 14-day course of antibiotic treatment that included an aminoglycoside. The serum β2-M concentrations in the normal outpatients (2020.1 ± 276.6 μg/L) were significantly lower (p <0.05) than those observed for outpatients (2833.3 ± 202.6 μg/L) or patients with CF (2861.8 ± 340.5 μg/L. There were no significant differences found for creatinine clearance or fractional excretion of β2-M when subjects without CF were compared with those with the disease. Furthermore, no significant differences were observed in hospitalized patients with CF when creatinine clearance and fractional excretion of β2-M were compared between the initiation and conclusion of aminoglycoside treatment. Glomerular filtration and proximal tubular reabsorption of β2-M were not altered in patients with CF. These findings do not support a global defect in proximal renal tubular reabsorption as the underlying cause for altered aminoglycoside clearance in patients with CF.


1973 ◽  
Vol 44 (2) ◽  
pp. 99-111 ◽  
Author(s):  
Frances T. Lester ◽  
D. C. Cusworth

1. The renal handling of lysine was studied during the intravenous infusion of a lysine load given in such a way that the plasma lysine concentration was constantly increasing. Theoretical renal thresholds, and maximum rates of renal tubular reabsorption of lysine, have been determined in three normal adults, five homozygous cystinuric patients, and three persons, two ‘completely’ and the third ‘incompletely’ recessive, heterozygotes for cystinuria. All the cystinuric patients were found to have thresholds at less than 1 mg of lysine/100 ml of plasma; the thresholds of all three heterozygotes fell within the same range as those of the three normal persons, that is, at values only two to three times the fasting plasma lysine concentration. 2. Not only was the lysine load shown to greatly increase the excretion of cystine, arginine and ornithine in the normal and heterozygous persons, but it was also shown to increase the already high clearance of these three amino acids in three of the homozygous cystinuric patients. 3. It was shown that a water diuresis alone will not cause increased excretion of any amino acids except taurine.


2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.


1995 ◽  
Vol 14 (6) ◽  
pp. 494-499 ◽  
Author(s):  
CJ Lote ◽  
JA Wood ◽  
A. Thewles ◽  
M. Freeman

The known toxicity of aluminium, and the toxicity of agents (such as desferrioxamine) used to remove alumini um from the body, has prompted us to investigate whether there may be ways of enhancing aluminium excretion by exploiting the normal renal handling of aluminium. Aluminium (as sulphate or citrate) was administered intravenously to conscious rats at doses ranging from 25 μg (0.93 μmol) to 800 μg (29.6 μmol) aluminium, and alu minium excretion was monitored over the following 2 h. Measurements of the filterability of aluminium from the rat plasma, and the glomerular filtration rate (inulin clearance), enabled us to calculate the filtered load of alu minium, and hence determine aluminium reabsorption. At all doses of administered aluminium, that adminis tered as sulphate was excreted less effectively than that administered as citrate. This difference was attributable to the much greater filterability of aluminium administered as citrate. However, for any given filtered load, the excre tion of aluminium administered as citrate was not signifi cantly different (in either fractional or absolute terms) from the excretion of aluminium administered as sulphate. It seems likely that, following aluminium sulphate administration, the filtered aluminium may be an alumini um citrate form which is then reabsorbed in the same way as aluminium administered as citrate. It is thus apparent that aluminium removal from the body could be further enhanced if it were possible to pre vent the tubular reabsorption of the aluminium species which is so effectively filtered following aluminium citrate administration.


1965 ◽  
Vol 208 (6) ◽  
pp. 1165-1170 ◽  
Author(s):  
W. Joseph Rahill ◽  
Mackenzie Walser

Simultaneous clearances of inulin, calcium, and either Be7, Ba140, or Ra226, given by constant infusion, were measured in salt-depleted dogs or dogs undergoing mild saline, mannitol, or sulfate diuresis. Urine-to-plasma ratios of all three cations less than 0.5 were noted, suggesting that all can be actively reabsorbed. Clearances of barium and radium were correlated with calcium clearance, but the clearance of beryllium was unpredictable. Protein binding of beryllium was shown to be of the same order of magnitude as other alkaline earths when errors due to adsorption of Be7 onto containers were minimized. Protein binding of barium averaged 54%. The excreted-to-filtered ratio for barium was a constant power (.54) of the ratio for calcium. The data do not exclude the possibility that these cations are reabsorbed by a common transport mechanism with calcium.


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