scholarly journals Clinical syndromes associated with disorders of renal tubular chloride transport: Excess and deficiency of a circulating factor?

1984 ◽  
Vol 14 (4) ◽  
pp. 387-400 ◽  
Author(s):  
P.L. Padfield ◽  
R.J. Grekin ◽  
M.G. Nicholls
1978 ◽  
Vol 14 (5) ◽  
pp. 414-427 ◽  
Author(s):  
Robert G. Luke ◽  
Fred S. Wright ◽  
Nicole Fowler ◽  
Michael Kashgarian ◽  
Gerhard H. Giebisch

1965 ◽  
Vol 209 (3) ◽  
pp. 655-658 ◽  
Author(s):  
Michael Kashgarian ◽  
Yves Warren ◽  
Howard Levitin

The electrical potential difference and the concentration of chloride in tubular fluid and plasma were measured in stopped-flow microperfusion of the proximal tubule of rats breathing either air or 12% CO2 in air. Perfusion with 10% PVP completely stopped net transtubular fluid movement. Chloride was not in electrochemical equilibrium under these conditions and hypercapnea increased the concentration of chloride in tubular fluid relative to that in plasma. This suggests that the net reabsorption of chloride must overcome a force which moves chloride into the tubular lumen. An anion pump is postulated which secretes chloride into the tubular lumen and is linked to acidification of proximal tubular fluid.


1985 ◽  
Vol 248 (2) ◽  
pp. F206-F211 ◽  
Author(s):  
M. W. Roy ◽  
C. E. Ott ◽  
W. J. Welch ◽  
J. H. Downs ◽  
T. A. Kotchen

Plasma volume expansion alters renal tubular sodium chloride transport and renal nerve activity. The purpose of this study was to determine the mechanism(s) for inhibition of renin secretion by acute volume expansion with albumin in the anesthetized dog. In dogs with a single intact kidney, albumin infusion decreased renin release by 86% and significantly increased renal blood flow, glomerular filtration rate, and sodium excretion. Albumin volume expansion inhibited renin secretion to a lesser extent in dogs with denervated filtering kidneys and in dogs with innervated nonfiltering kidneys. In dogs with denervated nonfiltering kidneys, albumin infusion did not change renin secretion. Comparable volume expansion was produced in all groups. Thus, inhibition of renin release by acute plasma volume expansion is dependent on both a renal tubular mechanism and the integrity of the renal nerves. Partial inhibition of renin release was observed with interruption of either one of the mechanisms, whereas interruption of both mechanisms totally abolished the effect of acute plasma volume expansion on renin secretion.


PEDIATRICS ◽  
1967 ◽  
Vol 39 (2) ◽  
pp. 316-317
Author(s):  
FRANCIS X. FELLERS

Professor Woolf has attempted to put together in this book a diverse group of 20 clinical syndromes which have in common some change in concentration of substances normally present in the urine. Each of these abnormalities is then identified, according to the compound present, as a specific renal dysfunction. This classification, convenient for historical description, was derived from a review of some 387 references from the English, French, and American literature. Very clear accounts are presented of cystinuria, galactosemia, Wilson's disease, hepatorenal syndrome, and renal hypoelectrolytemia (Bartter's syndrome).


Author(s):  
Jared Grantham ◽  
Larry Welling

In the course of urine formation in mammalian kidneys over 90% of the glomerular filtrate moves from the tubular lumen into the peritubular capillaries by both active and passive transport mechanisms. In all of the morphologically distinct segments of the renal tubule, e.g. proximal tubule, loop of Henle and distal nephron, the tubular absorbate passes through a basement membrane which rests against the basilar surface of the epithelial cells. The basement membrane is in a strategic location to affect the geometry of the tubules and to influence the movement of tubular absorbate into the renal interstitium. In the present studies we have determined directly some of the mechanical and permeability characteristics of tubular basement membranes.


1952 ◽  
Vol 36 (4) ◽  
pp. 911-920 ◽  
Author(s):  
Julius Bauer
Keyword(s):  

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