Comparison of estimated renal net acid excretion from dietary intake and body size with urine pH

2003 ◽  
Vol 103 (8) ◽  
pp. 1001-1007 ◽  
Author(s):  
Dominique S. Michaud ◽  
Richard P. Troiano ◽  
Amy F. Subar ◽  
Shirley Runswick ◽  
Sheila Bingham ◽  
...  
Keyword(s):  
Body Size ◽  
Dietary Intake ◽  
Acid Excretion ◽  
Urine Ph ◽  
Renal Net Acid Excretion ◽  
Net Acid Excretion

On the mechanism of growth hormone-induced stimulation of renal acidification in humans: effect of dietary NaCl

2000 ◽  
Vol 99 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Sigrid JEHLE ◽  
Henry N. HULTER ◽  
Reto KRAPF
Keyword(s):  
Growth Hormone ◽  
Human Subjects ◽  
Collecting Duct ◽  
Acid Excretion ◽  
Urine Ph ◽  
Gh Treatment ◽  
Renal Net Acid Excretion ◽  
First Time ◽  
Stimulation Of ◽  
Net Acid Excretion

Sustained administration of growth hormone (GH) to human subjects with NH4Cl-induced chronic metabolic acidosis (CMA) results in a large (4.5±0.5 mmol/l) increase in the plasma HCO3- concentration, as mediated by a large increase in renal net acid excretion. The renal mechanism(s) responsible for the potent stimulation of renal hydrogen ion secretion by GH remain to be elucidated. Accordingly, we have assessed the Na+ dependence of prolonged GH-stimulated renal acidification in four normal NaCl-restricted subjects (Na+ intake 0.3 mmol⋅kg-1⋅day-1) during CMA (4.2 mmol of NH4Cl⋅kg-1⋅day-1 for 7 days), CMA plus GH (0.1 unit/kg every 12 h for 5 days) and then CMA plus GH plus NaCl (1.7 mmol⋅kg-1⋅day-1 for 6 days). During CMA, urine Na+ excretion averaged 22.4±4.1 mmol/24 h. In response to GH administration, urinary net acid excretion was essentially unchanged, and the accumulated increment over 5 days of GH treatment was not different from zero (14±12 mmol; not significant). The plasma HCO3- concentration increased only slightly, from 14.2±0.8 to 15.0±1.1 mmol/l (P < 0.05). Despite the constraint on net acid excretion imposed by NaCl restriction, renal ammonia production increased, as suggested by increases in urine pH from 5.58±0.05 to 5.82±0.04 (P < 0.005) and unchanged NH4+ excretion (202±17 to 211±19 mmol/24 h; not significant). In response to dietary NaCl, urine pH decreased to 5.27±0.1 (P < 0.001) and a large increment in net acid excretion accumulated (233±20 mmol; P < 0.05), in association with an increase in plasma HCO3- to 18.7±1.3 mmol/l (P < 0.001), a plasma HCO3- value similar to that reported previously in salt-replete, NH4Cl-fed subjects. These results demonstrate for the first time in any species that the acid excretory effect of GH administration is critically dependent on the availability of a surfeit of Na+ for tubular reabsorption. GH and/or insulin-like growth factor-1 affect renal acid excretion proximally (by stimulation of NH3 production) and by a Na+-transport-dependent mechanism in the collecting duct (voltage-driven acidification) in humans. The present results indicate that an isolated increase in renal NH3 production is insufficient to obligate an increase in net acid excretion.

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.

Effects of glucocorticoid steroids on renal and systemic acid-base metabolism

1980 ◽  
Vol 239 (1) ◽  
pp. F30-F43 ◽  
Author(s):  
H. N. Hulter ◽  
J. H. Licht ◽  
E. L. Bonner ◽  
R. D. Glynn ◽  
A. Sebastian
Keyword(s):  
Steady State ◽  
Acid Production ◽  
Chronic Administration ◽  
Acid Excretion ◽  
Acid Base ◽  
Unmeasured Anion ◽  
Urine Ph ◽  
Group I ◽  
Potassium Clearance ◽  
Net Acid Excretion

Clinical states of hyperglucocorticoidism are associated with renal metabolic alkalosis, yet the systemic and renal acid-base response to chronic administration of glucocorticoid steroids (dexamethasone, triamcinolone) possessing little or no mineralocorticoid activity has not been investigated. In balance studies studies in dogs administration of triamcinolone (Tcn), 1.0 mg. kg-1. day-1 for 6–9 days (group I, n = 5), resulted in a persistent reduction in urine pH and increase in net acid excretion (NAE), and in the excretion of urinary unmeasured anions (C+NH4,Na;K minus A-Cl,HCO3,Pi), which were identified as organic anions and sulfate. A significant degree of metabolic acidosis occurred initially (delta [HCO3-]p, -3.4 meq/liter, P less than 0.05, day 1). As Tcn administration was continued, the cumulative increment in net acid excreted exceeded the cumulative increment in urinary unmeasured anion excreted and [HCO-3]p returned to pre-Tcn control values and remained stable thereafter. In the steady state of Tcn administration plasma potassium concentration and renal potassium clearance were not significantly different from pre-Tcn control, in contrast to the findings of hypokalemia and increased renal potassium clearance during chronic administration of deoxycorticosterone (DOC). Triamcinolone did not result in antinatriuresis or antichloruresis. Chronic administration of a 10–fold smaller dose of Tcn (0.1 mg . kg-1 . day-1) in an additional group (group III) also resulted in a persisting reduction in urine pH and an increase in net acid excretion that exceeded unmeasured anion excretion and resulted in a small increase in steady-state plasma bicarbonate concentration. These results suggest that chronic administration of potent glucocorticoid steroids results in 1) a persisting increase in endogenous acid production, and 2) stimulation of renal hydrogen ion secretion that was of greater degree than accounted for by the increment in endogenous acid production and that was not accompanied by renal mineralocorticoid effects on sodium and potassium transport.

Estimated Net Acid Excretion Inversely Correlates With Urine pH in Vegans, Lacto-Ovo Vegetarians, and Omnivores

2008 ◽  
Vol 18 (5) ◽  
pp. 456-465 ◽  
Author(s):  
Lynne M. Ausman ◽  
Lauren M. Oliver ◽  
Barry R. Goldin ◽  
Margo N. Woods ◽  
Sherwood L. Gorbach ◽  
...  
Keyword(s):  
Acid Excretion ◽  
Urine Ph ◽  
Net Acid Excretion

scholarly journals Net Acid Excretion and Urinary Organic Anions in Idiopathic Uric Acid Nephrolithiasis

2019 ◽  
Vol 14 (3) ◽  
pp. 411-420 ◽  
Author(s):  
I. Alexandru Bobulescu ◽  
Sun K. Park ◽  
L.H. Richie Xu ◽  
Francisco Blanco ◽  
John Poindexter ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Uric Acid ◽  
Organic Acids ◽  
Body Mass ◽  
Organic Anions ◽  
Acid Excretion ◽  
Urine Ph ◽  
Control Subjects ◽  
Uric Acid Nephrolithiasis ◽  
Net Acid Excretion

Background and objectivesIdiopathic uric acid nephrolithiasis, which is closely associated with obesity and the metabolic syndrome, is increasing in prevalence. Unduly acidic urine pH, the quintessential pathophysiologic feature of this disease, is in part explained by inadequate excretion of the principal urinary buffer ammonium. The role of net acid excretion in the pathogenesis of uric acid nephrolithiasis is incompletely understood.Design, setting, participants, & measurementsWe compared acid-base parameters of patients with idiopathic uric acid nephrolithiasis with matched control subjects under controlled diets in an inpatient metabolic unit. Measurements included fasting blood and 24-hour urine chemistries and 24-hour urine metabolomic analysis. Comparisons between groups included analysis of covariance models controlling for urine pH or body mass index.ResultsSubjects with idiopathic uric acid nephrolithiasis had lower urine pH (5.5 versus 5.9; P<0.001) and higher net acid excretion (60 versus 43 mEq/24 h; P<0.001), with the excess H+ carried by nonammonium buffers. In all subjects, there was a positive relationship of net acid excretion with higher body mass index in spite of strictly controlled equivalent dietary acid intake. This relationship was most evident among control subjects (r=0.36; P=0.03). It was attenuated in patients with idiopathic uric acid nephrolithiasis whose net acid excretion remained fixedly high and ammonium excretion remained low relative to net acid excretion, resulting in low urine pH over a wide body mass index range. Urinary metabolomics was performed to attempt to identify excess organic acids presented to the kidney in idiopathic uric acid nephrolithiasis. Among the tricarboxylic acid cycle intermediates and amino acid and lipid metabolites analyzed, 26 organic anions with acid dissociation constants values in the range of urine pH showed greater protonation. However, protons carried by the identified organic acids did not entirely account for the higher titratable acidity seen in idiopathic uric acid nephrolithiasis.ConclusionsHigher acid load to the kidney, resulting in higher urinary net acid excretion, is an important factor in the pathogenesis of idiopathic uric acid nephrolithiasis.

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