scholarly journals Topiramate and severe metabolic acidosis: case report

2005 ◽  
Vol 63 (2b) ◽  
pp. 532-534 ◽  
Author(s):  
Jayme E. Burmeister ◽  
Rafael R. Pereira ◽  
Elisa M. Hartke ◽  
Michele Kreuz
Keyword(s):  
Case Report ◽  
Metabolic Acidosis ◽  
Distal Tubule ◽  
Careful Attention ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Carbonic Anhydrase Inhibition ◽  
Acid Base Status ◽  
Renal Tubular

Topiramate infrequently induces anion gap metabolic acidosis through carbonic anhydrase inhibition on the distal tubule of the nephron - a type 2 renal tubular acidosis. We report on a 40 years old woman previously healthy that developed significant asymptomatic metabolic acidosis during topiramate therapy at a dosage of 100mg/day for three months. Stopping medication was followed by normalization of the acid-base status within five weeks. This infrequent side effect appears unpredictable and should be given careful attention.

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Bicarbonate Reabsorption ◽  
Base Balance ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

Variation in cardiac output with acid-base changes in the anesthetized dog

1965 ◽  
Vol 20 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S. A. Allan Carson ◽  
Gordon E. Chorley ◽  
F. Norman Hamilton ◽  
Do Chil Lee ◽  
Lucien E. Morris
Keyword(s):  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Combined Effects ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Relationship Of ◽  
The Relationship

Studies were performed in dogs anesthetized with pentobarbital, 30 mg/kg, and ventilated mechanically during succinylcholine apnea in order to ascertain the variation in cardiac output under various acid-base conditions. The findings were: 1) metabolic acidosis decreases cardiac output; 2) increasing respiratory acidosis in the absence of severe metabolic acidosis causes increase in cardiac output; 3) increasing respiratory acidosis in the presence of severe metabolic acidosis causes depression of cardiac output. The effect on cardiac output of changing arterial pH at steady PaCOCO2 is shown quantitatively. The relationship of PaCOCO2 to “pH adjusted” cardiac output is determined. From these data a nomogram is presented from which the combined effects of arterial pH and PaCOCO2 on cardiac output can be estimated. cardiac output and anesthesia; acid-base status and cardiac output; pH and cardiac output; PaCOCO2 and cardiac output Submitted on June 29, 1964

scholarly journals Acid-base status of pregnant guineapigs during neuroleptanalgesia with diazepam and fentanyl-fluanisone

1983 ◽  
Vol 17 (2) ◽  
pp. 114-117 ◽  
Author(s):  
A. M. Carter
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Metabolic Acidosis ◽  
Late Pregnancy ◽  
Radioactive Microspheres ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Placental Blood ◽  
Acid Base Status ◽  
Placental Blood Flow

Neuroleptanalgesia was induced in late pregnancy in guineapigs with diazepam and fentanyl-fluanisone. Hypotension occurred, but the arterial acid-base status after 45-60 min was near normal. When repeated injections of fentanyl-fluanisone were given to maintain neuroleptanalgesia, the blood pressure fell further and severe metabolic acidosis developed. Placental blood flow determined with radioactive microspheres was much lower during maintained neuroleptanalgesia than in guineapigs anaesthetized with diazepam and pentobarbitone.

Effects of pH on potassium transport by renal distal tubule

1982 ◽  
Vol 242 (5) ◽  
pp. F544-F551 ◽  
Author(s):  
B. A. Stanton ◽  
G. Giebisch
Keyword(s):  
Metabolic Acidosis ◽  
Distal Tubule ◽  
Potassium Transport ◽  
Free Flow ◽  
Acid Base Balance ◽  
Acid Base ◽  
Solution Ph ◽  
Fluid Delivery ◽  
Urinary Potassium ◽  
Potassium Secretion

To determine the relative importance of plasma and luminal pH changes as factors regulating potassium secretion by rat distal tubule, superficial tubules were continuously microperfused in vivo. The effects of changes in plasma pH were examined by producing acute systemic metabolic acidosis or alkalosis and holding luminal flow rate, solute composition, and pH constant by microperfusion. Alternatively, the effect of luminal solution pH was evaluated by microperfusing tubules with solutions buffered to either pH 6.5 or 8.0 at constant systemic acid-base balance. Net transport of Na and K and the pH of the luminal fluid were measured. Results showed that metabolic acidosis inhibited and metabolic alkalosis stimulated potassium secretion. Increased luminal fluid pH, in contrast, did not stimulate potassium transport. In experiments in which metabolic acidosis produced a diuresis, urinary potassium excretion was enhanced compared with hydropenic controls. Free-flow micropuncture studies revealed that the rate of fluid delivery to the distal tubule was 45% greater during acidosis compared with control and that potassium secretion increased in both the distal and collecting tubule. Since the rate of fluid delivery is a potent stimulus of potassium secretion in the distal tubule, it is concluded that the stimulus of increased delivery of fluid, observed in free-flow conditions, masked the inhibitory effect of acidosis on potassium transport. Potassium transport by the distal tubule, during acid-base disorders, is regulated by plasma pH and the rate of delivery of fluid but is not stimulated by alkalinization of the luminal fluid.

Acute Butylglycol Intoxication: A Case Report

1989 ◽  
Vol 8 (3) ◽  
pp. 243-245 ◽  
Author(s):  
F.P. Gijsenbergh ◽  
M. Jenco ◽  
H. Veulemans ◽  
D. Groeseneken ◽  
R. Verberckmoes ◽  
...  
Keyword(s):  
Case Report ◽  
Metabolic Acidosis ◽  
Suicide Attempt ◽  
Rare Case ◽  
Severe Metabolic Acidosis ◽  
Forced Diuresis ◽  
Present On Admission

A rare case of butylglycol intoxication in a suicide attempt is reported. Coma and hypotension were present on admission and severe metabolic acidosis arose subsequently. Forced diuresis and haemodialysis led to an uneventful outcome.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Effects of acid-base disturbances on renal handling of magnesium in the dog

1986 ◽  
Vol 70 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
John H. Dirks
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Indirect Effect ◽  
Metabolic Alkalosis ◽  
Distal Tubule ◽  
Acid Base ◽  
Renal Handling ◽  
Chronic Metabolic Acidosis ◽  
Magnesium Transport

1. Clearance and micropuncture studies were performed in four groups of acutely thyropara-thyroidectomized animals to study the effects of alkalosis and acidosis on the renal handling of magnesium. 2. Our results indicate that chronic metabolic acidosis reduces, whereas acute metabolic alkalosis enhances, magnesium reabsorption. 3. The site within the nephron where absorption of magnesium increases or decreases during acid-base disturbances was beyond the late proximal tubule. 4. Tubular fluid bicarbonate was also measured in these experiments, and the results indicated that magnesium reabsorption in the distal tubule correlated to bicarbonate delivery. However, whether this was a direct or an indirect effect of bicarbonate on magnesium transport could not be delineated.

Pendrin in the mouse kidney is primarily regulated by Cl− excretion but also by systemic metabolic acidosis

2008 ◽  
Vol 295 (6) ◽  
pp. C1658-C1667 ◽  
Author(s):  
Patricia Hafner ◽  
Rosa Grimaldi ◽  
Paola Capuano ◽  
Giovambattista Capasso ◽  
Carsten A. Wagner
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Relative Number ◽  
High Protein ◽  
Acid Excretion ◽  
Acid Base ◽  
Urinary Acidification ◽  
Apical Side ◽  
Acid Base Status ◽  
Net Acid Excretion

The Cl−/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH4Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl− excretion and decreased upon Cl− loading. Hence, it is unclear if pendrin regulation during NH4Cl-induced acidosis is primarily due the Cl− load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl− load and examined the systemic acid-base status, urinary acidification, urinary Cl− excretion, and pendrin abundance in the kidney. NaCl or NH4Cl increased urinary Cl− excretion, whereas (NH4)2SO4, Na2SO4, and acetazolamide treatments decreased urinary Cl− excretion. NH4Cl, (NH4)2SO4, and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH4Cl, and (NH4)2SO4 loading and increased with the other treatments. (NH4)2SO4 and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl− excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl− excretion but not blood Cl−. However, metabolic acidosis caused by acetazolamide or (NH4)2SO4 loading prevented the increase or even reduced pendrin expression despite low urinary Cl− excretion, suggesting an independent regulation by acid-base status.

scholarly journals Potential Inaccuracies in Chloride Measurements in Patients with Severe Metabolic Acidosis

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Tetsuya Makiishi ◽  
Naomasa Nishimura ◽  
Keiko Yoshioka ◽  
Shinya Yamamoto ◽  
Ryuichi Mitsuhashi ◽  
...  
Keyword(s):  
Point Of Care ◽  
Blood Gas ◽  
Central Laboratory ◽  
Gas Analyzer ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Factors Associated ◽  
Acid Base Status ◽  
Blood Gas Analyzer ◽  
Laboratory Analyzer

Background. To address the cause(s) of the significant differences in chloride (Cl-) concentrations between point-of-care blood gas analyzers and central laboratory analyzers.Methods. Cl-concentrations measured simultaneously by a blood gas analyzer (ABL800 FLEX) and a central laboratory analyzer (Hitachi7600) were collected in patients with severe acidemia (pH<7.20) (n=32) and were examined for correlations between differences in Cl-and factors associated with the acid-base status. Cl-concentrations were measured with both analyzers for samples with different concentrations of lactate, inorganic phosphate, or bicarbonate (HCO3   −).Results. The differences in Cl-concentrations were correlated withHCO3   −concentrations (r=0.72,P<0.0001) and anion gap (r=0.69,P<0.0001). Only the addition ofHCO3   −proportionately increased Cl-levels measured by a Hitachi7600, but it did not affect those measured by an ABL800FLEX.Conclusion. Cl-measurements with some analyzers may be influenced byHCO3   −concentrations, which could result in the observed discrepancies.

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