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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, 2013
    Co-Authors: Aldo J Peixoto, Robert J Alpern
    Abstract:

    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
    2013
    Co-Authors: Aldo J Peixoto, Robert J Alpern
    Abstract:

    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.

  • clinical syndromes of Metabolic Alkalosis
    Seldin and Giebisch's The Kidney (Fifth Edition)#R##N#Physiology & Pathophysiology 1-2, 2013
    Co-Authors: Orson W. Moe, Robert J Alpern, Donald W Seldin
    Abstract:

    Homeostatic control of acid–base parameters within discreet limits is vital to all living organisms. Acid–base disturbances are conditions that reflect abnormal underlying physiologic processes that can stem from a broad range of etiologies. In humans with a filtration-reabsorption nephron design, more than 4000 mEq of HCO 3 − is filtered daily at the glomerulus and virtually all of it is reabsorbed by the tubules.Two points are noteworthy. Since HCO 3 − absorption is an active process, in defense of elevated plasma [HCO 3 − ], the renal tubule simply has to do less work and bicarbonaturia invariably ensues. Given the relative magnitudes of filtered and reabsorbed versus excreted HCO 3 − , bicarbonaturia can be massive, which translates to rapid correction of excess extracellular fluid HCO 3 − . Within such context, one wonders why Metabolic Alkalosis would even be encountered. In contrast to Metabolic acidosis, where the pathophysiology reflects increased acid production, reduced acid excretion, or both, the maintenance of Metabolic Alkalosis is a quintessential renal disease of altered HCO 3 − absorption.Alkalosis is the condition in which there is an excess of base in total body fluids. By contrast, alkalemia refers to a state of decreased H + activity in the plasma (reduced plasma pH). Alkalosis can exist without alkalemia because Alkalosis might be part of a mixed acid–base disturbance. Conversely, alkalemia can be present without total body Alkalosis. The adjective Metabolic denotes that the disturbance is caused by a primary gain of base (e.g., HCO 3 − ) or loss of H + from the body.

Chris M Wood - One of the best experts on this subject based on the ideXlab platform.

Sandra Sabatini - One of the best experts on this subject based on the ideXlab platform.

  • Metabolic Alkalosis bedside and bench
    Seminars in Nephrology, 2006
    Co-Authors: Melvin E Laski, Sandra Sabatini
    Abstract:

    Although significant contributions to the understanding of Metabolic Alkalosis have been made recently, much of our knowledge rests on data from clearance studies performed in humans and animals many years ago. This article reviews the contributions of these studies, as well as more recent work relating to the control of renal acid-base transport by mineralocorticoid hormones, angiotensin, endothelin, nitric oxide, and pottasium balance. Finally, clinical aspects of Metabolic Alkalosis are considered.

  • effect of furosemide induced hypokalemic Metabolic Alkalosis on renal transport enzymes
    Kidney International, 1993
    Co-Authors: Somchai Eiamong, Neil A Kurtzman, Sandra Sabatini
    Abstract:

    Effect of furosemide-induced hypokalemic Metabolic Alkalosis on renal transport enzymes. Hypokalemic Metabolic Alkalosis is one of the most common complications of chronic furosemide administration. In this study we examined acid-base composition and ATPase enzyme activities in medullary thick ascending limb of Henle's loop (MTAL) and collecting tubule (CCT and MCT) after seven days of chronic furosemide therapy. All of the studies were conducted in adrenal intact (AI) rats or in adrenalectomized (ADX) glucocorticoid replete rats replaced with a physiological dose of aldosterone (Aldo). Furosemide (F) was administered to each rat by mini-osmotic pump. In the AI + F group, plasma Aldo was high and obvious Metabolic Alkalosis occurred (HCO 3 - = 37 ± 2 mEq/liter vs. 22 ± 2 mEq/liter in controls, P 3 - = 28 ± 2 mEq/liter, P

Patrick J Walsh - One of the best experts on this subject based on the ideXlab platform.

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, 2013
    Co-Authors: Aldo J Peixoto, Robert J Alpern
    Abstract:

    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
    2013
    Co-Authors: Aldo J Peixoto, Robert J Alpern
    Abstract:

    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.