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Edematous States

  • Jules B. Puschett
  • N. Kevin Krane

Abstract

Whatever the etiology of the edematous state, if one excludes from consideration “local” conditions such as thrombophlebitis, the final common pathway by which edema occurs involves stimuli that cause the kidney to become more sodium avid than is appropriate for the particular clinical circumstance. Quite often, the stimulus is provided by ineffective renal plasma flow, which signals the kidney that body volume is under threat—whereas, in reality, in situations such as severe congestive heart failure and advanced liver disease, for example, total body sodium and volume are, of course, elevated. Therefore, as is the case in all of medicine, any therapeutic measures must first involve attempts to determine the underlying pathophysiology. Efforts should be undertaken to reverse the pathogenetic sequence if at all possible. When this is not feasible, then symptomatic therapy must be instituted that is directed at reducing sodium intake and increasing sodium excretion. For the latter purpose, diuretics are utilized. All such agents have in common an ability to interfere with sodium transport from the tubular lumen in one or more segments of the nephron.

Keywords

Congestive Heart Failure Nephrotic Syndrome Atrial Natriuretic Peptide Sodium Excretion Loop Diuretic 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • Jules B. Puschett
    • 1
  • N. Kevin Krane
    • 2
  1. 1.Department of MedicineTulane University Medical CenterNew OrleansUSA
  2. 2.Clinical Nephrology Section of NephrologyTulane University Medical CenterNew OrleansUSA

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