The Experts below are selected from a list of 1608 Experts worldwide ranked by ideXlab platform
Robert J Alpern - One of the best experts on this subject based on the ideXlab platform.
-
treatment of severe metabolic alkalosis in a patient with congestive heart failure
American Journal of Kidney Diseases, 2013Co-Authors: Aldo J Peixoto, Robert J AlpernAbstract:Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased Urine Acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment.
-
acid base and electrolyte teaching case treatment of severe metabolic alkalosis in a patient with congestive heart failure
2013Co-Authors: Aldo J Peixoto, Robert J AlpernAbstract:Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased Urine Acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment. Am J Kidney Dis. 61(5):822-827. Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc. This is a US Government Work. There are no restrictions on its use. INDEX WORDS: Metabolic alkalosis; treatment; congestive heart failure. Note from Feature Editor Jeffrey A. Kraut, MD: This article is part of a series of invited case discussions highlighting either the diagnosis or treatment of acid-base and electrolyte disorders. The present case discussion is the second of 2 articles discussing metabolic alkalosis. In this article, Drs Peixoto and Alpern present their approach to the treatment of metabolic alkalosis; in the first teaching case, Gennari et al 1 describe a physiologic-based approach to its diagnosis and evaluation.
Jung Sang Lee - One of the best experts on this subject based on the ideXlab platform.
-
Evaluation of Urine Acidification by Urine anion gap and Urine osmolal gap in chronic metabolic acidosis
American Journal of Kidney Diseases, 1996Co-Authors: Gheun-ho Kim, Jin Suk Han, Yon Su Kim, Kwon Wook Joo, Suhnggwon Kim, Jung Sang LeeAbstract:Abstract To investigate the clinical significance of Urine anion gap and Urine osmolal gap as indirect markers of Urine Acidification in chronic metabolic acidosis, we evaluated Urine ammonium (NH 4 + ), net acid excretion (NAE), Urine anion gap (Na + + K + − Cl − ), and Urine osmolal gap (Urine osmolality − [2(Na + + K + ) + urea]) in 24 patients with chronic renal failure (CRF), eight patients with classic distal renal tubular acidosis (dRTA), and eight NH 4 Cl-loaded normal controls (NCs). Urine NH 4 + excretion was lower ( P P P P 4 + ( r = −0.70, P r = −0.83, P 4 + ( r = 0.69, P r = 0.71, P 4 + .
Aldo J Peixoto - One of the best experts on this subject based on the ideXlab platform.
-
treatment of severe metabolic alkalosis in a patient with congestive heart failure
American Journal of Kidney Diseases, 2013Co-Authors: Aldo J Peixoto, Robert J AlpernAbstract:Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased Urine Acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment.
-
acid base and electrolyte teaching case treatment of severe metabolic alkalosis in a patient with congestive heart failure
2013Co-Authors: Aldo J Peixoto, Robert J AlpernAbstract:Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased Urine Acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment. Am J Kidney Dis. 61(5):822-827. Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc. This is a US Government Work. There are no restrictions on its use. INDEX WORDS: Metabolic alkalosis; treatment; congestive heart failure. Note from Feature Editor Jeffrey A. Kraut, MD: This article is part of a series of invited case discussions highlighting either the diagnosis or treatment of acid-base and electrolyte disorders. The present case discussion is the second of 2 articles discussing metabolic alkalosis. In this article, Drs Peixoto and Alpern present their approach to the treatment of metabolic alkalosis; in the first teaching case, Gennari et al 1 describe a physiologic-based approach to its diagnosis and evaluation.
Bryan M Tucker - One of the best experts on this subject based on the ideXlab platform.
-
metabolic acidosis or respiratory alkalosis evaluation of a low plasma bicarbonate using the Urine anion gap
American Journal of Kidney Diseases, 2017Co-Authors: Daniel Batlle, Jamie Chintheodorou, Bryan M TuckerAbstract:Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of Urine anion gap, as a surrogate marker of Urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of Urine acid-base indexes at bedside (Urine pH, Urine bicarbonate, and Urine anion gap) to evaluate Urine Acidification are discussed.
Orson W Moe - One of the best experts on this subject based on the ideXlab platform.
-
the diurnal variation in Urine Acidification differs between normal individuals and uric acid stone formers
Kidney International, 2012Co-Authors: Mary Ann Cameron, Naim M Maalouf, John R Poindexter, Beverley Adamshuet, Khashayar Sakhaee, Orson W MoeAbstract:Many biological functions follow circadian rhythms driven by internal and external cues that synchronize and coordinate organ physiology to diurnal changes in the environment and behavior. Urinary acid–base parameters follow diurnal patterns and it is thought these changes are due to periodic surges in gastric acid secretion. Abnormal Urine pH is a risk factor for specific types of nephrolithiasis and uric acid stones result from excessively low Urine pH. Here we placed 9 healthy volunteers and 10 uric acid stone formers on fixed metabolic diets to study the diurnal pattern of urinary Acidification. All showed clear diurnal trends in urinary Acidification, but none of the patterns were affected by inhibitors of the gastric proton pump. Uric acid stone formers had similar patterns of change throughout the day but their Urine pH was always lower compared to healthy volunteers. Uric acid stone formers excreted more acid (normalized to acid ingestion), with the excess excreted primarily as titratable acid rather than ammonium. Urine base excretion was also lower in uric acid stone formers (normalized to base ingestion), along with lower plasma bicarbonate concentrations during part of the day. Thus, increased net acid presentation to the kidney and the preferential use of buffers, other than ammonium, result in much higher concentrations of undissociated uric acid throughout the day and consequently an increased risk of uric acid stones.
