The effects of diet and stool composition on the net external acid balance of normal subjects.

233

149

Antacids used to decrease phosphorus absorption in patients with renal failure may be toxic. To find more efficient or less toxic binders, a three-part study was conducted. First, theoretical calculations showed that phosphorus binding occurs in the following order of avidity: Al3+ > H+ > Ca2+ > Mg2+. In the presence of acid (as in the stomach), aluminum can therefore bind phosphorus better than calcium or magnesium. Second, in vitro studies showed that the time required to reach equilibrium varied from 10 min to 3 wk among different compounds, depending upon solubility in acid and neutral solutions. Third, the relative order of effectiveness of binders in vivo was accurately predicted from theoretical and in vitro results; specifically, calcium acetate and aluminum carbonate gel were superior to calcium carbonate or calcium citrate in inhibiting dietary phosphorus absorption in normal subjects. We concluded that: (a) inhibition of phosphorus absorption by binders involves a complex interplay between chemical reactions and ion transport processes in the stomach and small intestine; (b) theoretical and in vitro studies can identify potentially better in vivo phosphorus binders; and (c) calcium acetate, not previously used for medical purposes, is approximately as efficient as aluminum carbonate gel and more efficient as a phosphorus binder than other currently used calcium salts.

Section: Resultsmentioning

confidence: 98%

Reduction of dietary phosphorus absorption by phosphorus binders. A theoretical, in vitro, and in vivo study.

Sheikh¹,

Maguire²,

Emmett³

et al. 1989

233

149

“…In addition, when changes in urine pH were related to changes in net acid excretion, as shown in Fig. 2 (19). The lack of equivalent suppression of acid excretion during the recovery period in three of four studies, as well as the pattern of urinary chloride and cation losses, favors the latter alternatives.…”

Section: Electrolytementioning

confidence: 88%

Renal Adaptation to a High Potassium Intake

Tannen¹,

Wedell²,

Moore³

1973

A B S T R A C T The influence on urinary acidification of prolonged ingestion of a high potassium diet was explored in normal men and dogs. In men, the response to acute ingestion of ammonium chloride was assessed in a paired fashion after 5 days of ingesting a formula diet of normal or high potassium content; whereas in animals chronically ingesting a small amount of hydrochloric acid, the response to an increase in daily potassiunm intake was assessed. Urine pH was lower in the potassium-loaded state with both these models, and the effect persisted in the dog studies as long as a high potassium intake was continued. The decrease in urine pH could not be accounted for by changes in plasma acid-base status, net acid excretion, rate of urine flow, urine ionic strength, or fixed buffer excretion, i.e., phosphate, creatinine, or organic acids. Studies of men with administration of exogenous aldosterone and studies of adrenalectomized dogs with constant, maintenance steroid replacement indicated that the decrease in urine pH does not result from altered aldosterone secretion.In the human studies the largest decreases in urine pH were associated with a concomitant diminution in both ammonium and net acid excretion, suggesting a primary decrease of ammonia diffusion into the urine. These events during potassium loading, which are the mirror image of changes during potassium depletion, suggest that the relation between potassium, urine acidification, and ammonia metabolism may play an important role. in the maintenance of hydrogen ion and possibly potassium homeostasis during alterations in potassium intake.Preliminary reports appeared in the Abstracts of the American Society of Nephrology, 1971. 5: 80. and CliGu. Res. 1972. 20: 612, 613. Dr. Tannen is an Established Investigator of The American Heart Association.Received for publication 13 June 1972 and in revised formt 12 February 1973. INTRODUCTIONThe acute administration of a potassium load results in an alkaline diuresis, presumably the result of an interaction between renal handling of potassium and hydrogen ion. It has been speculated that these ions are secreted in a competitive fashion (1) and that the mechanism involves a decrease in renal tubular cellhydrogen ion content (2, 3).On the other hand, urinary acidification after the chronic ingestion of a high potassium intake has received little attention. This seemed particularly cogent in light of recent studies of urinary acidification during potassium depletion that suggested an interaction between potassium regulation and renal ammonia production (4). The possibility that this mechanism might also play a role in the adaptive response to potassium loading was of interest, especially since the process leading to enhanced renal potassium excretion during chronic ingestion of a high potassium intake is currently undefined (3,(5)(6)(7). Therefore, urinary acidification was explored during chronic potassium loading in normal men and dogs. In contrast to acute administration, chronic potassium loading resulted ...

“…We evaluated the responses to induced metabolic acidosis by comparing the observed changes in net renal acid excretion from control values to the changes in net fixed acid production, including diet and stool unmeasured anion, as before (4).…”

Section: Discussionmentioning

confidence: 99%

“…The subjects received one multiple vitamin capsule containing 1,000 USP U of vitamin D daily. Techniques of collection of blood, urine, and stool specimens, analytical methods, and calculations of endogenous production of fixed acid and renal acid excretion and acid balance have been described previously (4). Acid and mineral balances during ammonium chloride loading and recovery periods are presented as changes from the balances observed during control periods.…”

Section: Methodsmentioning

confidence: 99%

The effects of chronic acid loads in normal man: further evidence for the participation of bone mineral in the defense against chronic metabolic acidosis.

Lemann¹,

Litzow²,

Ej³

1966

Self Cite

541

238

Acute acid loads have been shown to titrate extra-and intracellular buffers (1, 2). The state of titration of these buffers is reflected by the level of serum bicarbonate. With sustained acid loading, serum bicarbonate ultimately stabilizes at some reduced level despite continuing acid retention, indicating that an additional buffer system is titrated. It has been suggested that such additional quantities of buffer could arise from the slow dissolution of bone mineral during chronic metabolic acidosis (3).The present metabolic balance studies were carried out to study further the relationship between acid retention and calcium balance during chronic ammonium chloride acidosis. MethodsWe carried out five metabolic balance studies in healthy men, who were hospitalized in the