Nephritic Edema

Yesterday I mentioned Ludwig Eichna. One of his great contributions to medical pathophysiology was the delineation between congestive heart failure and a congestive state. He built on the ideas of John Peters an Yale. Peters observed that while all measurable fluid compartments in patients with CHF were expanded their kidneys acted as if volume were contracted. He then propounded the concept of effective arterial blood volume (EABV). Patients with CHF have a contracted EABV which explains their salt and water retention.

The concept of EABV was disseminated by Peters great student Donald Seldin of Southwestern Medical School in Dallas and in turn by Seldin’s many students who exerted (and still do) a great influence over modern nephrology.

The article below examines the difference between CHF and a congested state using acute salt retaining glomerulonephritis as an example of the latter. Physicians often have trouble making this distinction though once the concept of EABV is firmly grasped it’s not difficult.

Nepritic edema

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2 Responses to Nephritic Edema

  1. Cioran says:

    Very good review.
    It seems that the Trans Assoc Am Physicians journal is not longer issued. You have a reference (No. 3) from Eichna (1954), from that journal and I was curious about current editions from it.

    Please answer me this question: How did Peters measured the EABV? which animal model and under which circumstances he discovered a low EABV in CHF?

  2. The Transactions of the AAP ceased publication many years ago, though the AAP is still active. The AAP was founded by William Osler and colleagues towards the end of the 19th century. It continues as a super exclusive club that almost nobody has heard of.

    Peters did not measure effective arterial blood volume (EABV); he invented it. He reasoned that a normal kidney in a patient with congestive heart failure (CHF) will relentlessly retain salt to the point where it kills the patient. Normal kidneys retain salt when volume is contracted. But all the measurable volume compartments in patients with CHF are expanded – blood volume, interstitial volume, extracellular volume. So Peters said that the volume compartment that was contracted was EABV. It’s essentially the degree of arterial filling or organ perfusion. Its contraction is discerned by history and other markers or poor organ perfusion such as low urinary Na concentration, high renin, high aldosterone, high vasopressin, etc. All the markers for a low EABV are presented in the paper under the features of CHF. EABV is expanded in patients with renal disease when the disease causes primary salt retention. The example I used in the paper is a patient with salt retaining acute glomerulonephritis.

    A lot of investigators failed to make the distinction between EABV and other volume compartments and accordingly got into trouble. The problem of cirrhotic edema is a good example of this failure to understand EABV on the part of some investigators who tried to argue that volume was expanded early in the course of this disease.

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