Research Article
II. RENAL THRESHOLD FOR HEMOGLOBIN IN DOGS UNINFLUENCED BY MERCURY POISONING
William H. Havill, John A. Lichty, Gordon B. Taylor, George H. Whipple
Published:
October 31, 2019
DOI:
License:
Copyright © Copyright, 1932, by The Rockefeller Institute for Medical Research New York
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
Abstract
The minimal or depression renal threshold for dog hemoglobin is not modified by moderate doses of mercuric chloride. This type of renal injury involves the epithelium of the convoluted tubules but the glomeruli escape. We are unable to explain our findings if we assume that the tubular epithelium takes an active part in the passage of dog hemoglobin from the blood into the urine. The evidence points toward the glomerular tuft as responsible for the passage of the hemoglobin from the blood plasma into the tubules. The glomerular tuft establishes the true hemoglobin threshold under these conditions. If the convoluted tubules are normal, we note that hemoglobin is taken into the epithelium and this explains the high initial renal threshold. With repeated hemoglobin injections this tubular epithelium becomes stuffed with hemoglobin pigment fractions and can absorb no more, which explains the minimal or depression threshold. Further injury of this tubular epithelium with mercury causes no change in this minimal renal threshold, unless we produce actual tubular obstruction.