Vagus-sparing gastric fundectomy in the rat: development of osteopenia, relationship to urinary phosphate and net acid excretion, serum gastrin and vitamin D

2001 ◽  
Vol 200 (1) ◽  
pp. 1-16 ◽  
Author(s):  
P. O. Schwille ◽  
H. Gepp ◽  
M. Koch ◽  
R. G. Erben ◽  
G. Rümenapf ◽  
...  
Keyword(s):  
Vitamin D ◽  
Serum Gastrin ◽  
Acid Excretion ◽  
Rat Development ◽  
Net Acid Excretion

Net Endogenous Acid Excretion and Kidney Allograft Outcomes

2021 ◽  
pp. CJN.00780121
Author(s):  
Stanley Yeung ◽  
Antonio Gomes-Neto ◽  
Maryse Osté ◽  
Else van den Berg ◽  
Jenny Kootstra-Ros ◽  
...  
Keyword(s):  
Kidney Transplant ◽  
Graft Failure ◽  
Plasma Creatinine ◽  
Transplant Recipients ◽  
Acid Excretion ◽  
Kidney Transplant Recipients ◽  
Dietary Acid Load ◽  
Dietary Acid ◽  
Acid Load ◽  
Net Acid Excretion

Background and objectives: High dietary acid load may accelerate kidney function decline. We prospectively investigated whether dietary acid load is associated with graft outcomes in kidney transplant recipients and whether venous bicarbonate (HCO3−) mediates this association. Design, setting, participants and measurements: We used data from 642 kidney transplant recipients with a functioning graft ≥1 year after transplantation. Net endogenous acid production (NEAP) was estimated using food frequency questionnaires (FFQ) and, alternatively, 24-hour urinary urea and potassium excretion to estimate NEAPUrine. We defined composite kidney endpoint as doubling of plasma creatinine or graft failure. Multivariable Cox regression analyses, adjusted for potential confounders, were used to study the associations of dietary acid load with kidney endpoint. We evaluated potential mediation effects of venous HCO3− , urinary HCO3− excretion, urinary ammonium (NH4+) excretion, titratable acid excretion, and net acid excretion on the association between NEAP and kidney endpoint. Results: Median NEAPFFQ and NEAPUrine were 40 (Interquartile range [IQR] 35-45) and 54 (IQR 44-66) mEq/day, respectively. During a median follow-up time of 5.3 (IQR 4.1-6.0) years, 121 (19%) participants reached kidney endpoint. After multivariable adjustment, NEAPFFQ and NEAPUrine (per SD higher) were independently associated with higher risk for kidney endpoint (hazard ratio [HR] 1.33; 95% confidence interval [CI] 1.12-1.57, P=0.001 and HR 95%CI, 1.44 [1.24-1.69], P<0.001 resp.). Baseline venous HCO3− mediated 20% of the association between NEAPFFQ and kidney endpoint. Baseline venous HCO3−, urinary NH4+ excretion and net acid excretion mediated 25%, -14% and -18% resp. of the association between NEAPUrine and kidney endpoint. Conclusion: Higher dietary acid load was associated with a higher risk of doubling of plasma creatinine or graft failure, and this association was partly mediated by venous HCO3−, urinary NH4+ and net acid excretion.

scholarly journals Ca2+-driven intestinal HCO3− secretion and CaCO3 precipitation in the European flounder in vivo: influences on acid-base regulation and blood gas transport

2010 ◽  
Vol 298 (4) ◽  
pp. R870-R876 ◽  
Author(s):  
Christopher A. Cooper ◽  
Jonathan M. Whittamore ◽  
Rod W. Wilson
Keyword(s):  
Teleost Fish ◽  
Gas Transport ◽  
Driving Forces ◽  
Marine Teleost ◽  
Acid Excretion ◽  
Acid Base ◽  
Marine Teleost Fish ◽  
Net Acid Excretion

Marine teleost fish continuously ingest seawater to prevent dehydration and their intestines absorb fluid by mechanisms linked to three separate driving forces: 1) cotransport of NaCl from the gut fluid; 2) bicarbonate (HCO3−) secretion and Cl− absorption via Cl−/HCO3− exchange fueled by metabolic CO2; and 3) alkaline precipitation of Ca2+ as insoluble CaCO3, which aids H2O absorption). The latter two processes involve high rates of epithelial HCO3− secretion stimulated by intestinal Ca2+ and can drive a major portion of water absorption. At higher salinities and ambient Ca2+ concentrations the osmoregulatory role of intestinal HCO3− secretion is amplified, but this has repercussions for other physiological processes, in particular, respiratory gas transport (as it is fueled by metabolic CO2) and acid-base regulation (as intestinal cells must export H+ into the blood to balance apical HCO3− secretion). The flounder intestine was perfused in vivo with salines containing 10, 40, or 90 mM Ca2+. Increasing the luminal Ca2+ concentration caused a large elevation in intestinal HCO3− production and excretion. Additionally, blood pH decreased (−0.13 pH units) and plasma partial pressure of CO2 (Pco2) levels were elevated (+1.16 mmHg) at the highest Ca perfusate level after 3 days of perfusion. Increasing the perfusate [Ca2+] also produced proportional increases in net acid excretion via the gills. When the net intestinal flux of all ions across the intestine was calculated, there was a greater absorption of anions than cations. This missing cation flux was assumed to be protons, which vary with an almost 1:1 relationship with net acid excretion via the gill. This study illustrates the intimate link between intestinal HCO3− production and osmoregulation with acid-base balance and respiratory gas exchange and the specific controlling role of ingested Ca2+ independent of any other ion or overall osmolality in marine teleost fish.

Role of organic anions in renal response to dietary acid and base loads

1989 ◽  
Vol 257 (2) ◽  
pp. F170-F176 ◽  
Author(s):  
J. C. Brown ◽  
R. K. Packer ◽  
M. A. Knepper
Keyword(s):  
Organic Anion ◽  
Organic Anions ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Response ◽  
Base Balance ◽  
Net Acid Excretion

Bicarbonate is formed when organic anions are oxidized systemically. Therefore, changes in organic anion excretion can affect systemic acid-base balance. To assess the role of organic anions in urinary acid-base excretion, we measured urinary excretion in control rats, NaHCO3-loaded rats, and NH4Cl-loaded rats. Total organic anions were measured by the titration method of Van Slyke. As expected, NaHCO3 loading increased urine pH and decreased net acid excretion (NH4+ + titratable acid - HCO3-), whereas NH4Cl loading had the opposite effect. Organic anion excretion was increased in response to NaHCO3 loading and decreased in response to NH4Cl loading. We quantified the overall effect of organic ion plus inorganic buffer ion excretion on acid-base balance. The amounts of organic anions excreted by all animals in this study were greater than the amounts of NH4+, HCO3-, or titratable acidity excreted. In addition, in response to acid and alkali loading, changes in urinary organic anion excretion were 40-50% as large as changes in net acid excretion. We conclude that, in rats, regulation of organic anion excretion can contribute importantly to the overall renal response to acid-base disturbances.

scholarly journals Dietary acid increases blood and renal cortical acid content in rats

1998 ◽  
Vol 274 (1) ◽  
pp. F97-F103 ◽  
Author(s):  
Donald E. Wesson
Keyword(s):  
Acid Content ◽  
Base Excess ◽  
Renal Cortex ◽  
T Test ◽  
Acid Excretion ◽  
Dietary Acid ◽  
Paired T Test ◽  
Net Acid Excretion

We examined whether dietary acid that increases net acid excretion (NAE) without measurably decreasing plasma pH or total CO2(tCO2) causes net acid retention. Control rats drinking distilled H2O were compared with those drinking 40 mM (NH4)2SO4, 40 mM Na2SO4, or drinking Na2SO4and given aldosterone (Na2SO4+ Aldo) to increase NAE without dietary acid. Systemic plasma tCO2 increased in Na2SO4+ Aldo animals, but systemic and stellate vessel plasma tCO2 and pH were not different from control among remaining groups. NAE increased in (NH4)2SO4and Na2SO4+ Aldo but not in Na2SO4animals. Blood base excess (BBE) decreased compared with its respective baseline in (NH4)2SO4(−0.44 ± 0.06 vs. 0.66 ± 0.04 μmol/ml; P < 0.01, paired t-test), increased in Na2SO4+ Aldo (0.79 ± 0.05 vs. 0.61 ± 0.03 μmol/ml; P < 0.04, paired t-test), but was unchanged in Na2SO4animals. Renal cortical H+ content assessed by microdialysis of the renal cortex in situ increased in (NH4)2SO4, decreased in Na2SO4+ Aldo, but was unchanged in Na2SO4animals. The data show that dietary acid sufficient to increase NAE without decreasing plasma tCO2 or pH nevertheless decreases BBE and increases renal cortical acid content, consistent with net acid retention.

Effects of Chloride Restriction and Depletion on Acid-Base Balance and Chloride Conservation in the Rat

1970 ◽  
Vol 38 (3) ◽  
pp. 385-396 ◽  
Author(s):  
R. G. Luke ◽  
Y. Warren ◽  
M. Kashgarian ◽  
H. Levitin
Keyword(s):  
Proximal Tubule ◽  
Respiratory Acidosis ◽  
Dietary Sodium ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Plasma Bicarbonate ◽  
Chloride Depletion ◽  
Plasma Chloride ◽  
Urinary Acid ◽  
Net Acid Excretion

1. In the rat dietary chloride restriction has been shown to cause an elevation of the plasma bicarbonate and urinary net acid excretion, provided dietary sodium is available. Likewise the degree of elevation of plasma bicarbonate during chloride depletion, produced by prior exposure to 8% CO2 for 24 hr, was dependent on whether sodium (as the neutral phosphate) was or was not being ingested. 2. Correction of the hypochloraemia and the elevated plasma bicarbonate following exposure to CO2 and subsequent recovery on a low chloride diet is more complete in the rat than the dog. Evidence is presented that the plasma chloride rises in the rat because of the movement of chloride out of intracellular sites, and that chloride depletion and/or the associated metabolic alkalosis elevates endogenous acid production. 3. Chloride depleted rats were re-exposed to 8% CO2 in air. Renal chloride conservation remained intact. The hypochloraemia and rise in plasma bicarbonate in response to CO2 were not dependent on chloruresis although urinary acid excretion and the rise in serum bicarbonate were inhibited when the plasma chloride did not fall. 4. Consideration of these experiments with the related micropuncture experiments of Warren et al. (1970) suggests that: (a) the intimate relationship between hypochloraemia and the elevation of plasma bicarbonate in respiratory acidosis is related to reciprocal changes in proximal tubular absorption of chloride and bicarbonate; (b) chloride depletion can increase bicarbonate absorption in the proximal tubule and urinary net acid excretion; (c) a rise in TF/P Cl in the proximal tubule does not necessarily correlate with changes in external chloride balance; (d) the distal chloride conserving mechanism is unaffected by rates of sodium or phosphate excretion, exposure to carbon dioxide, or increases in the rate of tubular bicarbonate absorption.

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