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LETTER TO THE EDITOR SODIUM RETENTION AND EDEMA Dear Sirs: Witte and Witte [1] recently provided a most useful review of lymphatic involvement in the causation of edema. They suggested that "many investigators of salt and water balance over the past century had underestimated or overlooked a fundamental physiologic truth, namely that sodium does not in itself initiate edema/ effusion. Instead sodium retention is an aggravator, albeit the sine qua non of progressive expansion of the interstitial fluid compartment," which is absolutely true. But among these investigators they include Micheli [2], which is not correct: "if we prefer the 'overfill' to the 'underfill' concept of oedema formation, renal dysfunction , arising from hepatic disease or other causes of oedema, is regarded as the main drive, i.e. expansion of interstitial fluid is a natural result of excessive sodium retention. The more traditional view is that renal sodium retention is a homeostatic response protecting plasma volume when factors in the capillary beds favour an increased outflow into interstitial fluid. Whichever is correct, it remains true that a large compartment cannot be expanded at the expense of a small compartment unless the latter is continuously replenished. The kidney, therefore, is always the 'enabling' cause of oedema." [3]. While [2] discusses edema in depth, it was primarily , as the title suggested, an evaluation of the usefulness of the concept of "effective blood volume" in understanding either the regulation or disturbances of body sodium . My conclusion, which seems to be shared by [1] is that it "obfuscates rather than clarifies, inhibits rather than stimulates original ideas . . .". Witte and Witte [1] point out that traditional Starling approach to edema is not specifically concerned with sodium although it is implicitly, because it involves "a shift in the partition of extracellular fluid, the constituency of which is primarily water, along with sodium". This dangerously under-represents the role of sodium in extracellular fluid; it is not simply a passenger on the tide. The majority of body water is intracellular; the factor which enables the vital minority to remain in ECF, including plasma, is the distinctive preponderance of sodium in ECF, kept there by its extrusion from cells by Na-KATP ase. Sodium, therefore, is the 'osmotic skeleton ' of ECF; it dictates ECF volume [3]. But sodium loading per se does not cause edema, nor does excessive aldosterone secretion [1, 3]. The central conundrum of sodium regulation is our inability to explain how ECF volume is regulated [2, 3] and, in particular, the impediment to progress imposed by preoccupation with the minority component, plasma. Hence my specific interest in interstitial fluid and its dysregulation in edema [2]. My conclusion [3] was that we might "be forced to accept that . . . the most urgent areas of inquiry turned Perspectives in Biology and Medicine, 41, 3 ¦ Spring 1998 461 out to be the sensory mechanisms monitoring bone sodium or interstitial volume, rather than those fine tuning renal sodium excretions"—entirely consistent with [I]. Clarification will not, however, result from the replacement of "effective blood volume" by concepts—such as "optimal urine output", "optimal intravascular volume " or the ability of the kidneys to "see enough cortical flow for sufficient glomerular filtration" [1]—which are equally comfortable and unverifiable. The question remains: where are the receptors, what are the set-points and how is the information integrated? [3]. So far as ANP is concerned [1] "it is important to reiterate that, while ANP is an appropriate response to volume expansion, it not only corrects the increased cardiac pre-load by increasing sodium excretion, but also by increasing the transfer of fluid from plasma to interstitial fluid—thus worsening edema" [3]. This precisely illustrates the trade offbetween a physiological response and a pathophysiological consequence; neither can be understood in isolation. REFERENCES 1.Witte, CL. and Witte, M.H. On the causation of edema: a lymphological perspective . Persp. Biol. Med. 41:86-97, 1997. 2.Michell, A.R. Effective blood volume: an effective concept or a modern myth? Persp. Biol. Med. 39:471-490, 1996. 3.Michell, A.R. The Clinical Biology of Sodium. Oxford: Elsevier Science, 1995. 1-27, 179-234, 281-294. Alastair Michell 462 Letter to the Editor ...

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Additional Information

ISSN
1529-8795
Print ISSN
0031-5982
Pages
pp. 461-462
Launched on MUSE
2015-01-07
Open Access
No
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