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

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.

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.

Bone Mineral Changes in Acute Metabolic Acidosis due to Acute Gastroenteritis

2004 ◽  
Vol 75 (5) ◽  
pp. 380-383 ◽  
Author(s):  
Dincer Yildizdas ◽  
A. Kemal Topaloglu ◽  
Neslihan O. Mungan ◽  
Bilgin Yuksel ◽  
Guler Ozer
Keyword(s):  
Metabolic Acidosis ◽  
Bone Mineral ◽  
Acute Gastroenteritis ◽  
Acute Metabolic Acidosis ◽  
Mineral Changes

scholarly journals Acute metabolic acidosis in a GLUT2-deficient patient with Fanconi-Bickel syndrome: new pathophysiology insights

2014 ◽  
Vol 29 (suppl 4) ◽  
pp. iv113-iv116 ◽  
Author(s):  
F. Mihout ◽  
O. Devuyst ◽  
A. Bensman ◽  
I. Brocheriou ◽  
C. Ridel ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Deficient Patient ◽  
Acute Metabolic Acidosis

scholarly journals The infusion rate dependent influence of acute metabolic acidosis on pulmonary vascular resistance in broilers

1998 ◽  
Vol 77 (2) ◽  
pp. 309-321 ◽  
Author(s):  
R.F. Wideman ◽  
Y Kochera Kirby ◽  
M.F. Forman ◽  
N Marson ◽  
R.W. McNew ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Infusion Rate ◽  
Rate Dependent ◽  
Acute Metabolic Acidosis
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