Effect of divalent cation ionophore (A 23187) on renal handling of phosphorus

Effect of divalent cation ionophore (A 23187) on renal handling of phosphorus. To evaluate the effect of an increase in intracellular calcium on renal handling of phosphorus, calcium ionophore, which facilitates passive entry of calcium into cytosol, was given i.v. to four groups of rats: group 1, animals with intact parathyroid glands; group 2, parathyroidectomized (PTX) rats; group 3, PTX animals receiving i.v. parathyroid hormone (PTH); and group 4, PTX animals pretreated with i.v. ionophore, then given i.v. PTH. During the administration of ionophore in group 1, serum calcium (Sca) decreased from 8.7 ± 0.2 (mean ±SEM) to 7.5 ± 0.2mg/100 ml (P < 0.001), fractional excretion of phosphorus (CP/CIn) decreased from 0.110 ± 0.020 to 0.019 ± 0.006 (P < 0.001), and urinary cyclic 3′, 5′-adenosine monophosphate (UcAMP) decreased from 131 ± 23 to 46 ± 16 pmoles/min (P < 0.0125). In group 2, during the administration of ionophore, Sca decreased from 6.5 ± 0.2 to 5.7 ± 0.2mg/100 ml (P < 0.001), but neither CP/CIn nor UcAMP were altered. In group 2, during the administration of ionophore, CP/Cm decreased from 0.43 ± 0.05 to 0.19 ± 0.04 (P < 0.005), UcAMP decreased from 254 ± 20 to 159 ± 11 (P < 0.001). In group 4, during combined i.v. administration of ionophore and PTH, CP/CIn was reduced from 0.19 ± 0.009 to 0.044 ± 0.012 (P < 0.005), and serum calcium was reduced from 6.5 ± 0.3 to 5.1 ± 0.3mg/100 ml (P < 0.01). These findings indicate that i.v. ionophore suppresses urinary excretion of phosphorus, only in the presence of either endogenous or exogenous PTH. The associated decrease in UcAMP suggests that this effect could be mediated through inhibition of PTH-dependent formation of cAMP, possibly resulting from the ionophore-induced increase in intracellular calcium in renal tubular cells.Effet d'un ionophore des cations divalents (A 23187) sur le comportement renal vis a vis du phosphate. Afin d'évaluer l'effet de l'augmentation du calcium intracellulaire sur le comportement rénal vis à vis du phosphore, on a donné à quatre groupes de rats un ionophore de calcium qui facilite l'entrée passive de ce cation dans le cytosol. Le groupe 1 est composé d'animaux dont les parathyroïdes sont intactes, le groupe 2 d'animaux parathyroïdectomisés (PTX), le groupe 3 d'animaux PTX recevant de l'hormone parathyroïdienne (PTH) par voie intra-veineuse et le groupe 4 d'animaux pré-traités par l'ionophore qui reçoivent de la PTH. Au cours de l'administration de l'ionophore au groupe 1, le calcium séreique (SCa) diminue de 8,7 ± 0,2 (m ±SEM) à 7,5 ± 0,2mg/100 ml (P < 0,001), l'excrétion fractionnelle du phosphore (CP/CIn) diminue de 0,110 ± 0,020 à 0,019 ± 0,006 (P < 0,001) et l'AMP cyclique urinaire (UcAMP) diminue de 131 ± 23 à 46 ± 16 pmoles/min (P < 0,0125).Dans le groupe 2, au cours de l'administration de l'ionophore, Sca diminue de 6,5 ± 0,2 a 5,7 ± 0,2 mg/100 ml (P < 0,001), mais ni CP/CIn ni UcAMP ne sont modifiés. Dans le groupe 3, au cours de l'administration de l'ionophore, CP/CIn diminue de 254 ± 20 à 159 ± 11 (P < 0,001). Dans le groupe 4, au cours de l'administration combinée d'ionophore et de PTH, CP/CIn diminue de 0,19 ± 0,009 à 0,004 ± 0,012 (P < 0,005) et Sca de 6,5 ± 0,3 à 5,1 ± 0,3 mg/100 ml (P < 0,01). Ces constatations indiquent que l'ionophore ne diminue l'excrétion urinaire de phosphate qu'en présence de PTH endogène ou exogène. La baisse associée de UcAMP suggère que cet effet peut avoir pour médiateur l'inhibition de la formation d'AMP cyclique dépendante de la PTH, conséquence de l'augmentation du calcium intracellulaire dans les cellules tubulaires rénales, induite par l'ionophore

Variations in Arterial Blood Pressure after Kidney Transplantation

The course of hypertension within the first 2 months after kidney transplantation was correlated with renal function, plasma renin activity (PRA), and the daily maintenance dose of prednisone in 18 homograft recipients. During acute rejection blood pressure (BP) closely correlated with PRA. Patients with normal homograft function showed an increase in BP early after transplantation which in most returned to normal 3-8 weeks later. In the latter group no correlation could be found between the level of BP and PRA, however the BP correlated closely with the dose of prednisone. These observations suggest that during acute rejection the increase in BP may at least partly be mediated by a renal pressor mechanism, whereas with normal renal function the high dose of glucocorticoids may play an important role in the development of hypertension.</jats:p

Recovery from Hepatorenal Syndrome after Orthotopic Liver Transplantation

Three patients with progressive renal failure and advanced hepatic insufficiency due to cirrhosis of the liver underwent orthotopic liver transplantation. All three patients had immediate improvement in hepatic function and within two weeks after liver replacement regained nearly normal kidney function. However, the renal recovery was delayed in each case, and its course was not uniform. Plasma renin activity was high, and renin substrate was low before transplantation in one case in which these measurements were obtained; both returned to normal soon after liver replacement. (N Engl J Med 289:1155–1159, 1973). © 1973, Massachusetts Medical Society. All rights reserved

Halothane hepatitis with renal failure treated with hemodialysis and exchange transfusion

A 38-year-old white female, hepatitis B antigen negative, developed fluminating hepatic failure associated with oliguria and severe azotemia after two halothane anesthesia and without exposure to other hepatotoxic drugs or blood transfusions. She was treated with multiple hemodialysis and exchange blood transfusion. The combined treatment corrected the uremic abnormalities and improved her level of consciousness. The liver and kidney function gradually improved, and she made a complete recovery, the first recorded with hepatic and renal failure under these post-anesthetic conditions. Further evaluation of this combined treatment used for this patient is warranted. © 1974 The Japan Surgical Society