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Journal of Histochemistry and Cytochemistry | 1955

THE HISTOCHEMICAL CHARACTERISTICS OF ABSORPTION DROPLETS IN THE NEPHRON

Jean Oliver; Werner Straus; Norman Kretchmer; Yin Chen Lee; H. W. Dickerman; Frances Cherot

If a protein of 70,000 niolecular weight or less is illtroduced into the blood stream either directly or by absorption from the peritoneal cavity, 5OIHC of it passes the glomerular membralle and, as has beell shown iii the case of egg white, appears immunologically unchallged ( I ) h1 the urine. If, like hemoglobin, it coIltaiuis a visible component, it. can be eeu within 15 millutes after ilhtravellotls ilijCCtiOll diffusely dispersed throughout. the cytoplasm of the cells of the mid portioni of the proximal convolutions (2). If excretion of it Colltilliles, as after intraperitoneal ilijection, minute accretions of colored material appear vhich by 18 hours grow to large droplets that distend the epithelial cells. There is a eoncomitant S\\’elliflg and dissolution of the mitochondrial rods. The droplets have the color of hemoglobin but, stained supravitally, they react positively to Janus GI’eell ill high dilution. With the passage of time the droplets disintegrate leavilig a residue of Fe pigment free ill the cytoplasm of the cells.


Annals of the New York Academy of Sciences | 1969

RENAL LESIONS AND DISTURBANCE OF RENAL FUNCTION IN RATS WITH MAGNESIUM DEFICIENCY

Robert Whang; Jean Oliver; Louis G. Welt; Muriel MacDowell

Magnesium (Mg) deprivation in the rat results in the following biochemical alterations: hypomagnesemia, hypercalcemia, and azotoemia,l-“ as well as a coexisting small but significant decrement in muscle potassium content.44 The renal morphologic counterpart of these biochemical abnormalities has in past investigations been described by the general term “nephrocalcinosis,” affecting various regions of the renal ti~sues.7-l~ Microdissection studies have been carried out to define more precisely the morphologic characteristics and location of the renal lesion induced by Mg depletion.12J3 Initially, microliths appear in the thin limb of Henle’s Loop sometime during the second week of depletion (FIGURE 1 ) . These laminated microliths react positively with para-aminosalicylic acid (PAS), von Kossa and alizarin stains, indicating the presence of calcium as well as organic matrix. With repeated formation and accretion of new microliths, the lumen of the tubule becomes filled and distended by this composite mass, an intranephronic calculus (FIGURE 2). The structural disturbances exerted by these intraluminal aggregates are manifested locally as well as more generally. First, the local effects are illustrated in FIGURE 3. Note that a microspherolith has lodged in the “hairpin” turn of this portion of the loop. Proximal to the microlith the lumen is filled with PAS positive, von Kossa and Alizarin negative, material. Throughout the entire length of the proximal convolution up to the glomerulus, the epithelium of this first portion of the nephron appeared normal; specifically there was no dilatation of the tubule or Bowman’s Space. Distal to the calculus, scattered debris from erosion of the epithelial wall lies within the tubular lumen and extends throughout the remainder of the thin ascending limb and into the thick ascending portion of Henle’s Loop. This cellular debris, staining deeply with iron hematoxylin, was in part negative to alizarin. A conglomerate of calcareous salts was noted in the large scattered masses of cellular debris which distended and compressed the tubular wall (FIGURE 4); there was no evidence of the periodic pattern of mineral deposition (Liesegang rings) that characterized the original calculus. With increase of this amorphous accumulation, not only is the normal contour of the tubule destroyed but neighboring broad ascending tubules are similarly affected through lateral compression exerted by the enlarging calcareous mass (FIGURE 5) . The terminal portion of the


Journal of Clinical Investigation | 1951

THE PATHOGENESIS OF ACUTE RENAL FAILURE ASSOCIATED WITH TRAUMATIC AND TOXIC INJURY. RENAL ISCHEMIA, NEPHROTOXIC DAMAGE AND THE ISCHEMURIC EPISODE

Jean Oliver; Muriel MacDowell; Ann Tracy


American Journal of Physiology | 1941

THE COLLECTION AND ANALYSIS OF FLUID FROM SINGLE NEPHRONS OF THE MAMMALIAN KIDNEY

Arthur M. Walker; Phyllis A. Bott; Jean Oliver; Muriel MacDowell


Journal of Experimental Medicine | 1954

Cellular mechanisms of protein metabolism in the nephron. I. The structural aspects of proteinuria; tubular absorption, droplet formation, and the disposal of proteins.

Jean Oliver; Muriel MacDowell; Yin Chen Lee


The American Journal of Medicine | 1953

Correlations of structure and function and mechanisms of recovery in acute tubular necrosis

Jean Oliver


The American Journal of Medicine | 1968

A study by micropuncture and microdissection of acute renal damage in rats

Thomas U.L. Biber; Margaret Mylle; Andrew D. Baines; Carl W. Gottschalk; Jean Oliver; Muriel MacDowell


Journal of Experimental Medicine | 1957

THE RENAL LESIONS OF ELECTROLYTE IMBALANCE I. THE STRUCTURAL ALTERATIONS IN POTASSIUM-DEPLETED RATS

Jean Oliver; Muriel MacDowell; Louis G. Welt; Malcolm A. Holliday; Walter Hollander; Robert W. Winters; T. F. Williams; W. E. Segar


Journal of Experimental Medicine | 1947

ON THE ORIGIN OF HEPARIN : AN EXAMINATION OF THE HEPARIN CONTENT AND THE SPECIFIC CYTOPLASMIC PARTICLES OF NEOPLASTIC MAST CELLS.

Jean Oliver; Frank Bloom; Carmen Mangieri


American Journal of Physiology | 1941

METHODS FOR THE COLLECTION OF FLUID FROM SINGLE GLOMERULI AND TUBULES OF THE MAMMALIAN KIDNEY

Arthur M. Walker; Jean Oliver

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Louis G. Welt

University of North Carolina at Chapel Hill

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Robert W. Winters

University of North Carolina at Chapel Hill

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Walter Hollander

United States Department of Veterans Affairs

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Arthur M. Walker

University of Pennsylvania

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Andrew D. Baines

University of North Carolina at Chapel Hill

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Carl W. Gottschalk

University of North Carolina at Chapel Hill

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