Decreased phosphate reabsorption by volume expansion in the dog

Decreased phosphate reabsorption by volume expansion in the dog. The effect of volume expansion on tubular phosphate reabsorption (TRP) was studied in intact and acutely thyroparathyroidectomized (TPTX) dogs infused with a neutral phosphate solution. The infusion of a Ca++-containing balanced electrolyte solution increased CNa × 100/GFR from 0.23 to 6.87% and reduced TRP × 100/GFR from 6.2 to 3.6 mg/min in the intact dogs; in TPTX dogs these values changed from 0.35 to 7.02% and from 6.7 to 4.6 mg/min, respectively. Ultrafilterable Ca++ did not fall in either group. When Ca++ was omitted from the loading electrolyte solution ultrafilterable Ca++ fell significantly in both groups. In the intact dogs CNa × 100/GFR increased from 0.48 to 6.26% and TRP × 100/GFR fell from 4.5 to 2.8 mg/min; in TPTX dogs these values changed from 0.48 to 8.26% and from 6.5 to 4.1 mg/min. Thus volume loading appears to inhibit TRP regardless of the presence or absence of parathyroid hormone, and whether dilutional hypocalcemia was prevented or not. It is concluded that the previously reported blunting of the phosphaturic effect of volume expansion by acute parathyroidectomy or calcium infusion may have been due to a low serum phosphorus or filtered phosphate load relative to an increased threshold or tubular reabsorptive maximum or decreased splay

Medical Procedures Manual

ix. 230 hal.; ill.; 21.5 c

MEDICAL PROCEDURES MANUAL

xii,229 hlm ; 14 x 21,5 c

Hepatorenal syndrome: a historical appraisal of its origins and conceptual evolution

The hepatorenal syndrome (HRS), a progressive but potentially reversible deterioration of kidney function, constitutes a serious complication of hepatic decompensation. Coexistence of liver/kidney damage, mentioned in the dropsy literature, was highlighted by Richard Bright in 1827 and confirmed in 1840 by his contemporary nephrology pioneer Pierre Rayer. Cholemic nephrosis was described in 1861 by Friedrich Frerichs, and the renal tubular lesions of HRS by Austin Flint in 1863. The term “acute hepato-nephritis” was introduced in 1916 by Paul Merklen, and its chronic form was designated HRS by Marcel Dérot in 1930s. HRS then was applied to renal failure in biliary tract surgery and to cases of coexistent renal and hepatic failure of diverse etiology. The pathogenesis of HRS was elucidated during the 1950 studies of renal physiology. Notably, studies of salt retention in edema and its relation to regulating the circulating plasma volume by John Peters and subsequently Otto Gauer defined the concept of “effective blood volume” and the consequent elucidation of ascites formation in liver failure. Parallel studies of intrarenal hemodynamics demonstrated severe renal vasoconstriction and preferential cortical ischemia to account for the functional renal dysfunction of HRS. Dialysis and liver or combined liver-kidney transplantation transformed the fatal HRS of old into a treatable disorder by the 1970s. Elucidation of the pathogenetic mechanisms of renal injury and refinements in definition, classification, and diagnosis of HRS since then have allowed for earlier therapeutic intervention with combined i.v. albumin and vasoconstrictor therapy, enabling the continued improvement of patient outcomes