scholarly journals Prompt Rise in Urinary Ammonium Excretion Suffices To Mitigate Metabolic Acidosis in an Experimental Animal Model of Severe Normovolemic Hemodilution

2017 ◽  
pp. 615-620 ◽  
Author(s):  
J. K. TELOH ◽  
I. N. WAACK ◽  
H. DE GROOT
Keyword(s):  
Metabolic Acidosis ◽  
Absolute Amount ◽  
Ammonium Excretion ◽  
Acid Excretion ◽  
Urinary Ph ◽  
Normovolemic Hemodilution ◽  
Proton Excretion ◽  
Acute Metabolic Acidosis ◽  
Experimental Group ◽  
Hasselbalch Equation

Recently, we have established a model of severe stepwise normovolemic hemodilution to a hematocrit of 10 % in rats employing three different colloidal volume replacement solutions (Voluven, Volulyte and Gelafundin) that are routinely used in clinical practice at present. We did not see severe dilutional acidosis as to be expected, but a decline in urinary pH. We here looked on further mechanisms of renal acid excretion during normovolemic hemodilution. Bicarbonate, which had been removed during normovolemic hemodilution, was calculated with the help of the Henderson-Hasselbalch equation. The urinary amount of ammonium as well as phosphate was determined in residual probes. The absolute amount of free protons in urine was obtained from the pH of the respective samples. The amount of protons generated during normovolemic hemodilution was approximately 0.6 mmol. During experimental time (5.5 h), distinct urinary ammonium excretion occurred (Voluven 0.52 mmol, Volulyte 0.39 mmol and Gelafundin 0.77 mmol). Proton excretion via the phosphate buffer constituted 0.04 mmol in every experimental group. Excretion of free protons was in the range of 10-6 mmol. The present data prove that the prompt rise in urinary ammonium excretion is also valid for acute metabolic acidosis originating from severe normovolemic hemodilution.

Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis

1983 ◽  
Vol 61 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Marc Goldstein ◽  
Bobby Stinebaugh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Renal Medulla ◽  
Hydrogen Ion ◽  
Ammonium Excretion ◽  
Urine Ph ◽  
Ion Secretion ◽  
Medullary Collecting Duct ◽  
Acute Metabolic Acidosis

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary [Formula: see text]. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, [Formula: see text], and the urine minus blood [Formula: see text] difference (U-B [Formula: see text]) were lower during acute hypercapnia. In these experiments, the urine [Formula: see text] was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B [Formula: see text] was 5 ± 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary [Formula: see text] can modify this relationship.

Handling of ammonium by the renal proximal tubule during acute metabolic acidosis

1983 ◽  
Vol 245 (6) ◽  
pp. F680-F686 ◽  
Author(s):  
E. Simon ◽  
D. Martin ◽  
J. Buerkert
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Acid Excretion ◽  
Total Acid ◽  
Urine Ph ◽  
Acid Infusion ◽  
Acute Metabolic Acidosis ◽  
Fluid Collections ◽  
Tubule Fluid

The present studies were designed to assess the handling of ammonium (NH+4) by the proximal tubule during acute metabolic acidosis (AMA). After tubule fluid collections were obtained with micropuncture techniques and in situ pH was determined near the end of the proximal tubule, 0.2 N HCl was infused intravenously at 17 microliter X min-1 X 100 g body wt-1. Thirty to sixty minutes later, samples were obtained and pH measurements were made near the previous micropuncture sites. During AMA, urine pH fell and total acid excretion doubled due to an increase in NH+4 excretion from 581 +/- 63 to 1,153 +/- 61 nmol X min-1 X g kidney wt-1 (P less than 0.001). Acid excretion did not change in time controls. Tubule fluid NH+4 rose from 2.17 +/- 0.15 to 3.45 +/- 0.24 mM during acid infusion (P less than 0.001) and its delivery to the end of the proximal tubule nearly doubled (67.8 +/- 6.3 vs. 33.9 +/- 2.9 pmol X min X g kidney wt-1 before acid infusion, P less than 0.001). This increase in delivery during AMA was due to enhanced ammonia (NH3) entry into the proximal tubule. In situ pH determined near the end of the proximal tubule averaged 6.94 +/- 0.04 before acid infusion and did not change afterwards (6.87 +/- 0.05). These data are consistent with the hypothesis that in AMA the increase in NH+4 excretion is due primarily to an increase in the cortical production of NH3.

scholarly journals ACUTE METABOLIC ACIDOSIS: EFFECTS ON ARGININE IN VASOPRESSIN(AVP) RELEASE IN FETAL SHEEP

1984 ◽  
Vol 18 ◽  
pp. 137A-137A
Author(s):  
Daniel J Faucher ◽  
Tom Lowe ◽  
About Laptook ◽  
John C Porter ◽  
Charles R Rosenfeld
Keyword(s):  
Metabolic Acidosis ◽  
Fetal Sheep ◽  
Acute Metabolic Acidosis

scholarly journals Regulation of AE1 anion exchanger and H + -ATPase in rat cortex by acute metabolic acidosis and alkalosis

1997 ◽  
Vol 51 (1) ◽  
pp. 125-137 ◽  
Author(s):  
Ivan Sabolić ◽  
Dennis Brown ◽  
Stephen L. Gluck ◽  
Seth L. Alper
Keyword(s):  
Metabolic Acidosis ◽  
Anion Exchanger ◽  
Rat Cortex ◽  
Acute Metabolic Acidosis

scholarly journals Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Sodium Bicarbonate ◽  
Negative Impact ◽  
Qtc Interval ◽  
Bicarbonate Therapy ◽  
Proximal Tubular ◽  
Acute Metabolic Acidosis ◽  
Renal Proximal Tubular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Renal acid excretion in the domestic fowl

1983 ◽  
Vol 104 (1) ◽  
pp. 51-58
Author(s):  
S. Long ◽  
E. Skadhauge
Keyword(s):  
Uric Acid ◽  
Control Diet ◽  
Venous Blood ◽  
Ammonium Phosphate ◽  
Poultry Feed ◽  
Ammonium Excretion ◽  
Acid Excretion ◽  
Total Acid ◽  
Excretion Rates ◽  
Protein Rich

1. In order to assess the role of uricotelism in net renal acid excretion, blood and ureteral urine samples were collected from five hens fed a commercial poultry feed (Diet A) and five hens fed a protein-rich, Na-poor feed (Diet B). All samples were analysed for pH, PCO2, ammonium, phosphate, uric acid and urates (UA + U) and inulin. 2. On Diet A, average pH in venous blood was 7.42, while urinary pH (pHu) ranged from 4.74 to 7.25. At average pHu (6.10), uric acid accounted for 52% of total acid excreted, H2PO4 for 20% and NH4 for 28%. Net acid excretion in ureteral urine was 345 muequiv h-1 kg body weight-1, or 5–10 times that observed in ureotelic vertebrates (amphibians and mammals). 3. The relative contributions of these urinary buffers to net renal acid excretion changed with pHu. Significant negative correlations exist between pHu and both total phosphate and ammonium excretion rates (P less than 0.001). Excretion rates of (UA + U) showed a positive correlation (P less than 0.05) with pHu. 4. Feeding on Diet B revealed the homeostatic power of the avian kidney. Blood pH and PCO2 were not changed relative to values in hens fed the control diet while striking increases in excretion rates of all urinary buffers (except HCO3) were observed. Average pHu fell to 5.12, and the average net renal acid excretion rate doubled.

Free Circulating Magnesium and Renal Magnesium Handling during Acute Metabolic Acidosis in Humans

1998 ◽  
Vol 18 (3) ◽  
pp. 233-236 ◽  
Author(s):  
Daniel Blumberg ◽  
Alessandro Bonetti ◽  
Vincenzo Jacomella ◽  
Stellario Capillo ◽  
Anita C. Truttmann ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Acute Metabolic Acidosis

Effect of Acute Metabolic Acidosis on Plasma Phosphorus Concentration

1980 ◽  
pp. 263-279
Author(s):  
James R. Oster ◽  
Guido O. Perez ◽  
Albert Castro ◽  
Carlos A. Vaamonde
Keyword(s):  
Metabolic Acidosis ◽  
Phosphorus Concentration ◽  
Acute Metabolic Acidosis ◽  
Plasma Phosphorus

scholarly journals Combined Supplementation with Glycine and Tryptophan Reduces Purine-Induced Serum Uric Acid Elevation by Accelerating Urinary Uric Acid Excretion: A Randomized, Single-Blind, Placebo-Controlled, Crossover Study

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2562
Author(s):  
Oshima ◽  
Shiiya ◽  
Nakamura
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Water Solubility ◽  
Elevated Serum ◽  
Acid Excretion ◽  
Japanese Adult ◽  
Urinary Ph ◽  
Uric Acid Excretion ◽  
Combined Supplementation ◽  
Single Blind

The authors previously confirmed the serum uric acid-lowering effects of the combination of glycine and tryptophan in subjects with mild hyperuricemia. This study examined whether combined supplementation with glycine and tryptophan suppressed the elevation in serum uric acid levels caused by purine ingestion and accelerated urinary uric acid excretion in subjects with lower urate excretion using a randomized, single-blind, placebo-controlled, crossover clinical trial design. Healthy Japanese adult males with lower urate excretion ingested water containing purines in addition to dextrin (placebo), tryptophan, glycine, or a glycine and tryptophan mixture. The combined supplementation with glycine and tryptophan significantly reduced the elevated serum uric acid levels after purine ingestion. Glycine alone and in combination with tryptophan significantly increased urinary uric acid excretion and urate clearance compared with the effects of the placebo. Urinary pH increased by the ingestion of the mixture. These results suggested that the improved water solubility of uric acid due to increased urinary pH contributed to the increase of urinary uric acid excretion.

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