Iso-Oncotic Volume Expansion in the Nephrotic Syndrome

1993 ◽  
Vol 84 (6) ◽  
pp. 627-632 ◽  
Author(s):  
Ton J. Rabelink ◽  
Joost A. Bijlsma ◽  
Hein A. Koomans
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Plasma Volume Expansion ◽  
Humoral Factors

1. In previous studies we found that albumin infusions caused only a modest natriuresis in the nephrotic syndrome, suggesting that hypovolaemia played no part in the sodium retention of these patients. However, this finding was inconclusive, since the hyperoncocity of the infused albumin probably opposed sodium excretion. 2. In the present study, we examined the effect of sustained (68 h) plasma volume expansion (+18%), by means of iso-oncotic albumin infusions, on renal function, blood pressure, humoral factors and sodium balance. 3. Plasma atrial natriuretic peptide levels increased almost threefold and renin-angiotensin system activity was suppressed. Glomerular filtration rate remained unchanged, whereas estimated renal plasma flow increased, resulting in a further decrease in filtration fraction. 4. The increase in plasma volume expansion was accompanied by a modest increase in sodium excretion, which, however, was less than the amount of sodium daily infused with the albumin solutions and consumed with the diet, so that net sodium was retained. 5. This observation supports the concept that an intrinsic renal defect causes the sodium retention in the nephrotic syndrome, and argues against the therapeutic use of albumin infusions.

scholarly journals The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone system

2016 ◽  
Vol 311 (6) ◽  
pp. F1125-F1134 ◽  
Author(s):  
Crystal A. West ◽  
Jennifer M. Sasser ◽  
Chris Baylis
Keyword(s):  
Blood Pressure ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Critical Role ◽  
Maternal Blood ◽  
Sodium Retention ◽  
Plasma Volume Expansion ◽  
Salt Wasting ◽  
Vascular Responsiveness

Pregnancy is characterized by avid renal sodium retention and plasma volume expansion in the presence of decreased blood pressure. Decreased maternal blood pressure is a consequence of reduced systemic vascular tone, which results from an increased production of vasodilators [nitric oxide (NO), prostaglandins, and relaxin] and decreased vascular responsiveness to the potent vasoconstrictor (angiotensin II). The kidneys participate in this vasodilatory response, resulting in marked increases in renal plasma flow and glomerular filtration rate (GFR) during pregnancy. In women, sodium retention drives plasma volume expansion (∼40%) and is necessary for perfusion of the growing uterus and fetus. For there to be avid sodium retention in the presence of the potent natriuretic influences of increased NO and elevated GFR, there must be modifications of the tubules to prevent salt wasting. The purpose of this review is to summarize these adaptations.

Sodium retention and salt appetite following deoxycorticosterone in hamsters

1983 ◽  
Vol 244 (1) ◽  
pp. R78-R83
Author(s):  
D. A. Fitts ◽  
O. O. Yang ◽  
E. S. Corp ◽  
J. B. Simpson
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Body Weight Gain ◽  
Sodium Balance ◽  
Salt Appetite ◽  
Sodium Retention ◽  
Plasma Volume Expansion ◽  
Sodium Metabolism

Previous research suggests that hamsters 1) fail to retain sodium after mineralocorticoid injections, 2) retain sodium after adrenalectomy equal to controls, and 3) do not develop salt appetite after mineralocorticoid or adrenalectomy. The present studies demonstrate sodium retention, body weight gain, hypernatremia, plasma volume expansion, and reduced fecal sodium excretion after daily injections of deoxycorticosterone acetate (DOCA). Salt appetite appeared after the 3rd and 4th days. Adrenalectomy caused reductions of sodium balance, plasma volume, and food intake, which were reversed by DOCA administration. Mineralocorticoids therefore represent one control of sodium metabolism in hamsters.

Collecting Duct Na+/K+-ATPase Activity Is Correlated with Urinary Sodium Excretion in Rat Nephrotic Syndromes

2000 ◽  
Vol 11 (4) ◽  
pp. 604-615 ◽  
Author(s):  
GEORGES DESCHÊNES ◽  
ALAIN DOUCET
Keyword(s):  
Nephrotic Syndrome ◽  
Atpase Activity ◽  
Sodium Excretion ◽  
Collecting Duct ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Brattleboro Rats ◽  
Sodium Retention ◽  
Puromycin Aminonucleoside ◽  
Stimulation Of

Abstract. In puromycin aminonucleoside (PAN)-treated nephrotic rats, sodium retention is associated with increased Na+/K+-ATPase activity in the cortical collecting ducts (CCD). This study was undertaken to determine whether stimulation of Na+/K+-ATPase in the CCD is a feature of other experimental nephrotic syndromes, whether it might be responsible for renal sodium retention, and whether it is mediated by increased plasma vasopressin levels or activation of calcineurin. For this purpose, the time courses of urinary excretion of sodium and protein, sodium balance, ascites, and Na+/K+-ATPase activities in microdissected CCD were studied in rats with PAN or adriamycin nephrosis or HgCl2nephropathy. The role of vasopressin and calcineurin in PAN nephrosis were evaluated by measuring these parameters in Brattleboro rats and in rats treated with cyclosporin or tacrolimus. Despite different patterns of changes in urinary sodium and protein excretion in the three nephrotic syndrome models, there was a linear relationship between CCD Na+/K+-ATPase activities and sodium excretion in all three cases. The results also indicated that there was no correlation between proteinuria and sodium retention, but ascites was present only when proteinuria was associated with marked reduction of sodium excretion. Finally, the lack of vasopressin in Brattleboro rats or the inhibition of calcineurin by administration of either cyclosporin or tacrolimus did not prevent development of the nephrotic syndrome in PAN-treated rats or stimulation of CCD Na+/K+-ATPase. It is concluded that stimulation of Na+/K+-ATPase in the CCD of nephrotic rats might be responsible for sodium retention and that this phenomenon is independent of proteinuria and vasopressin and calcineurin activities.

Glucose and bicarbonate reabsorption in edematous dogs

1976 ◽  
Vol 231 (3) ◽  
pp. 749-753 ◽  
Author(s):  
JA Arruda ◽  
C Westenfelder ◽  
R Lockwood ◽  
NA Kurtzman
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Sodium Retention ◽  
Aortocaval Fistula ◽  
Bicarbonate Reabsorption ◽  
Glucose Reabsorption ◽  
Clearance Studies ◽  
Expansion Volume

Glucose and bicarbonate reabsorption were studied in dogs made edematour by aortocaval fistula (A-V dogs) and in sham-operated dogs. Following construction of the A-V fistula, there was a significant increase in body weight; glomerular filtration rate, renal plasma flow, hematocrit, and sodium excretion decreased significantly. Bicarbonate reabosorption was significantly higher in A-V than in sham dogs both during control and volume expansion. Volume expansion depressed bicarbonate reabsorption significantly in both groups. Glucose reabsorption fell following volume expansion in both groups; glucose reabsorption was significantly higher in A-V dogs than in sham dogs during control and volume expansion. Volume expansion led to a minimal increase in sodium excretion in A-V dogs when compared to the increase in the sham dogs. These data demonsttate that chronic sodium retention is associated with enhanced reabsorption of glucose and bicarbonate. The site in the neophron responsible for the increase in reabsorption of these substances cannot be determined with certainty based on these clearance studies although it is possible that proximal reabsorption may be enhanced in this model.

scholarly journals Effects of sildenafil on maternal hemodynamics and fetal growth in normal rat pregnancy

2010 ◽  
Vol 298 (2) ◽  
pp. R433-R438 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Chris Baylis
Keyword(s):  
Blood Pressure ◽  
Fetal Growth ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Pde5 Inhibitor ◽  
Maternal Plasma ◽  
Sodium Retention ◽  
Maternal Weight ◽  
Plasma Volume Expansion ◽  
Normal Rat

It has been suggested that the phosphodiesterase-5 (PDE5) inhibitor sildenafil may be useful in the treatment of hypertension during pregnancy. However, we have reported a selective increase in renal inner medullary PDE5 that participates in the sodium retention of pregnancy. Therefore, the purpose of this study was to determine whether oral sildenafil treatment impairs maternal plasma volume expansion and/or fetal growth during rat pregnancy. Rats received sildenafil (10 mg·kg−1·day−1, 50 mg·kg−1·day−1, or 90 mg·kg−1·day−1) or vehicle on days 4–20 of pregnancy. On days 14–19, rats were housed in metabolic cages for collection of urine and measurement of food and water intake. Terminal hemodynamic and fetal measurements were taken on day 20. None of the sildenafil doses lowered blood pressure, and although all doses increased plasma cGMP concentrations, only the highest dose increased aortic and inner medullary cGMP content. Sildenafil had no effect on maternal weight gain; however, the highest dose decreased both plasma volume and renal sodium retention. The pup number and size were similar among the groups. Therefore, these studies suggest that low doses of systemic sildenafil may be safe during pregnancy in the rat, but higher doses may interfere with the physiological sodium retention and volume expansion of pregnancy. The effects of systemic sildenafil on blood pressure and sodium retention during hypertension in human pregnancy remain to be examined.

Effects of Plasma Volume Expansion on Renal Salt Handling in Patients with the Nephrotic Syndrome

1984 ◽  
Vol 4 (4) ◽  
pp. 227-234 ◽  
Author(s):  
Hendrik A. Koomans ◽  
Anton B. Geers ◽  
Anton H.v.d. Meiracker ◽  
Jan C. Roos ◽  
Peter Boer ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Plasma Volume Expansion

Plasma volume expansion is necessary for edema formation in the rate with Heymann nephritis

1985 ◽  
Vol 248 (2) ◽  
pp. F247-F253
Author(s):  
G. A. Kaysen ◽  
T. T. Paukert ◽  
D. J. Menke ◽  
W. G. Couser ◽  
M. H. Humphreys
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Initial Period ◽  
Control Period ◽  
Plasma Renin ◽  
Volume Depletion ◽  
Plasma Volume Expansion ◽  
Edema Formation ◽  
Heymann Nephritis

Edema formation in nephrotic syndrome has been attributed to intravascular volume depletion resulting from leakage of plasma water into the interstitial space and activating secondary renal sodium retention. However, clinical studies indicate that edematous patients with nephrotic syndrome may have normal or expanded plasma volumes. We evaluated the relationship between plasma volume and edema formation in control rats and rats with chronic renal failure (CRF) produced by 7/8 nephrectomy. In each group, plasma volume and 22Na space were measured during the control period and after induction of hypoalbuminemia from passive Heymann nephritis. Rats with CRF had expanded plasma volume during the initial period (4.23 +/- 0.46 vs. 3.32 +/- 0.68 ml/100 g body wt) that became significantly more expanded (to 5.44 +/- 1.16 ml/100 g body wt) when they became nephrotic as 22Na space also increased. Plasma volume and 22Na space did not change in the sham-operated rats when nephrosis was produced. Plasma renin activity was lower in the CRF rats during the control period than in the sham-operated rats and fell significantly during the nephrotic period when edema developed. Nonnephrotic rats had a plasma colloid osmotic pressure (COP) of 17.8 +/- 4.3 mmHg compared with 8.5 +/- 2.9 mmHg when nephrotic. Despite this large difference in COP, both nephrotic and nonnephrotic rats exhibited the same relationship between plasma volume and extravascular sodium space, a measure of edema formation. Hypoproteinemia is not sufficient for edema formation in the rat with passive Heymann nephritis; concomitant plasma volume expansion resulting from CRF is a necessary additional component.

Hormonal and renal response to plasma volume expansion in the primate Macaca mulatta

1983 ◽  
Vol 244 (2) ◽  
pp. H201-H205
Author(s):  
G. E. Billman ◽  
M. J. Keyl ◽  
D. T. Dickey ◽  
D. C. Kem ◽  
L. C. Keil ◽  
...  
Keyword(s):  
Rhesus Monkey ◽  
Blood Volume ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
The Body ◽  
Plasma Volume Expansion ◽  
Renal Response

The purpose of this study was to investigate the hormonal and renal response to plasma volume expansion in the ketamine-anesthetized rhesus monkey. The blood volume was determined in nine animals and found to be 6% of the body weight. Six monkeys received isoncotic isotonic fluid amounting to 25% of the blood volume. Plasma volume expansion led to significant decrease in the plasma concentrations of antidiuretic hormone (46.7%) and aldosterone (78.4%) as well as plasma renin activity (50.0%). The mean arterial pressure, plasma osmolality, and plasma concentrations of Na+ and K+ were unaffected by plasma volume expansion. However, renal plasma flow, glomerular filtration rate, the excretion of Na+ and K+, and urine flow increased. It was concluded that, in the ketamine-anesthetized rhesus monkey, circulating hormones contribute to blood volume homeostasis presumably through a neural mechanism similar to that observed in dogs and humans.

Natriuretic Response to Preferential Plasma Volume Expansion in Normal Unanaesthetized Dogs

1971 ◽  
Vol 40 (1) ◽  
pp. 73-79 ◽  
Author(s):  
J. A. Reyburn ◽  
J. P. Gilmore
Keyword(s):  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urine Flow ◽  
Saline Infusion ◽  
Potassium Excretion ◽  
Plasma Volume Expansion ◽  
Volume Increase

1. The natriuretic response of normally hydrated unanaesthetized dogs to preferential plasma volume expansion was studied, comparing the response to infusion of hyperoncotic dextran in isotonic saline with that to infusion of an identical volume of isotonic saline. 2. Significant increases in urine flow, sodium excretion, sodium filtration and potassium excretion were observed with each type of infusion. 3. The changes with each type of infusion were not significantly different however, even though plasma volume increased significantly following dextran saline infusion. 4. The natriuretic response of normal dogs to preferential plasma volume expansion appears to be commensurate with the saline load infused rather than the induced plasma volume increase.

Role of endogenous endothelin on renal functions in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F34-F38
Author(s):  
K. Yamada ◽  
S. Yoshida
Keyword(s):  
Sodium Excretion ◽  
Salt Intake ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Sodium Balance ◽  
High Salt Intake ◽  
Fractional Excretion Of Sodium

This study was conducted to determine the involvement of endogenous endothelin (ET), a novel potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system by inhibiting ET action via infusion of a specific ET antiserum at a time of altered sodium balance. Infusion of 1:50 diluted ET antiserum, which completely inhibited renal vasoconstriction by the exogenously administered ET (0.25 to 1.0 nmol/kg), caused an increase in urinary sodium excretion and fractional excretion of sodium and a decrease in plasma renin concentration without significant changes in blood pressure, heart rate, glomerular filtration rate, renal plasma flow, and urine volume compared with the values with nonimmune serum in conscious rats fed a low-salt diet. A time control study showed no significant changes in all parameters. These results suggest that the state of low- compared to high-salt intake causes a relatively stronger activity of endogenous ET, and that the endogenous ET contributes to the adaptative modulations of sodium excretion via renal tubular action and renin release in association with the changed state of sodium balance.

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