Hyperoncotic Albumin Infusion Research Articles

Postpartum acute renal failure: a multicenter study of risk factors in patients admitted to ICU.

BackgroundEven in developed countries, severe specific pregnancy complications may occur in the immediate postpartum period and require admission to the ICU. The characteristics and risk factors of acute renal failure (ARF) induced by these complications and their treatments are not well known.MethodsWe performed a retrospective multicenter study in three intensive care departments linked to level III maternity wards in the north of France. All patients admitted to ICU for postpartum complications over a 5-year period (2008 to 2012) were included. Clinical and biological data, delivery characteristics, type of complications, and treatments were compared by univariate and multivariate analyses according to the occurrence and severity of ARF.ResultsOne hundred eighty-two patients admitted to ICU for postpartum complications were included in the study. Sixty-eight patients (37%) developed an ARF: 49 with a low or medium severity and 19 with a severe ARF requiring renal replacement therapy. Hemolysis, elevated liver enzyme, and low platelet count (HELLP) syndrome on its own (p = 0.047) or combined with postpartum haemorrhage (p = 0.003), previous treatment by hyperoncotic albumin infusion (p = 0.001) and blockade of fibrinolysis by tranexamic acid (p = 0.03), was associated with secondary ARF. By multivariate analysis, the only independent factors were the association of HELLP syndrome with postpartum haemorrhage and the use of hyperoncotic albumin infusion.ConclusionsHELLP syndrome associated with postpartum haemorrhage induces a high risk of ARF in the complicated postpartum setting. A particular attention should be given to treatments that could worsen the kidney function in that situation.

Hyperoncotic colloids and acute kidney injury: a meta-analysis of randomized trials

IntroductionIt has been hypothesized that hyperoncotic colloids might contribute to acute kidney injury (AKI). However, the validity of this hypothesis remains unclear.MethodsA meta-analysis was conducted of randomized controlled trials evaluating AKI after infusion of hyperoncotic albumin and hydroxyethyl starch (HES) solutions. Mortality was a secondary endpoint. Eligible trials were sought by multiple methods, and the pooled odds ratios (OR) for AKI and death and 95% confidence intervals (CI) were computed under a random effects model.ResultsEleven randomized trials with a total of 1220 patients were included: 7 evaluating hyperoncotic albumin and 4 hyperoncotic HES. Clinical indications were ascites, surgery, sepsis and spontaneous bacterial peritonitis. Hyperoncotic albumin decreased the odds of AKI by 76% (OR, 0.24; CI, 0.12-0.48; P < 0.0001), while hyperoncotic HES increased those odds by 92% (OR, 1.92; CI, 1.31-2.81; P = 0.0008). Parallel effects on mortality were observed, with hyperoncotic albumin reducing the odds of death by 48% (OR, 0.52; CI, 0.28-0.95; P = 0.035) and hyperoncotic HES raising those odds by 41% (OR, 1.41; CI, 1.01-1.96; P = 0.043).ConclusionsThis meta-analysis does not support the hypothesis that hyperoncotic colloid solutions per se injure the kidney. Renal effects appear instead to be colloid-specific, with albumin displaying renoprotection and HES showing nephrotoxicity.

Changes in serum albumin concentration and volume expanding effects following a bolus of albumin 20% in septic patients

Patients with systemic sepsis develop a capillary leak syndrome, and serum -albumin concentration decreases. Hyperoncotic albumin infusion can be used for volume expansion in these patients, but the degree and duration of effect are not well described. We assessed volume expansion by albumin 20% infusion and compared the retention of infused albumin in septic patients and healthy controls. We gave albumin 20%, 200 ml as a rapid infusion to 70 patients with septic shock and 26 controls. Blood samples were taken before and 1, 5, 15, 30, 60, 120 and 240 min after the infusion for measurement of serum albumin concentration and haematocrit. Haemodilution and the percentage of administered albumin remaining intravascularly at each time were calculated. The mean proportion of the increase in albumin remaining at 4 h was 68.5 (sd 10)% in septic patients and 79 (5)% in controls (P<0.001). The albumin 20%, 200 ml caused a secondary fluid resorption and volume expansion maximal at 30 min, equivalent to a 430 ml infusion in septic patients and 500 ml in controls. After giving albumin, serum albumin concentrations decrease significantly faster in septic patients than in healthy controls.

Renal haemodynamics and sodium handling after hyperoncotic albumin infusion in sodium-restricted normal man.

The effect of plasma volume expansion with hyperoncotic albumin (HA) on renal haemodynamics and segmental tubular sodium (Na) handling was studied in eight water-loaded normal men. Clearance studies were performed before, during and after a 60-min infusion of 300 ml 20% HA. Sodium intake was restricted (20 mmol day-1) to mimic clinical conditions of relative hypovolaemia in which HA is often applied. Plasma volume rose by 740 +/- 160 ml after infusion and colloid oncotic pressure (COP) by 3.6 +/- 1.3 mm Hg. No natriuresis was induced. In fact, Na output fell from 43 +/- 29 to 28 +/- 25 mumol min-1 during infusion, returning to 41 +/- 36 mumol min-1 afterwards. Corresponding clearances of inulin were 121 +/- 19, 110 +/- 19 and 117 +/- 21 ml min-1 and of p-aminohippurate (CPAH) 602 +/- 87, 637 +/- 100 and 751 +/- 148 ml min-1. Fractional reabsorption of sodium in the proximal tubules (FPRNa), assessed from maximal free-water and lithium clearance, rose consistently during infusion but diverging patterns (further rise, no change or fall) were seen afterwards. Fractional distal reabsorption remained unchanged both during and after HA infusion. Changes in plasma volume and CPAH in the post-infusion period were correlated. These results indicate that, despite considerable plasma volume expansion, HA infusion does not enhance Na excretion in Na-restricted subjects. This is mainly due to elevation of plasma COP, which reduces glomerular filtration and enhances proximal reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of colloid volume expansion on glomerular barrier size–selectivity in humans

Colloid volume expansion magnifies proteinuria in subjects with the nephrotic syndrome. To elucidate this phenomenon, we performed differential solute clearances prior to and following infusion of hyperoncotic albumin in 21 nephrotic subjects and seven healthy controls. Urinary excretion rate and fractional clearance of albumin (radius = 36 A) and immunoglobulin G (radius = 55 A) increased significantly in nephrotic subjects. However, urinary albumin excretion rate was unchanged in controls. The fractional clearances of dextrans of broad size distribution (radii = 28 to 58 A) were markedly altered in both groups following albumin infusion. A heteroporous model which depicts the major portion of the glomerular capillary wall as an isoporous membrane (pore radius approximately 55 A) and the minor portion as a non-discriminatory shunt, revealed the latter to be much more prominent in nephrotic subjects than in controls, and to be enlarged further following albumin infusion. By contrast no increase in pore size of the non-shunt pathway occurred in either group. We infer that enhancement of a pre-existing defect of glomerular size-selectivity in nephrotic subjects accounts, in large part, for exaggerated proteinuria in the colloid volume-expanded state. Increases in glomerular perfusion rate and pressure associated with plasma hypervolemia may mediate this alteration in glomerular membrane-pore structure.

Effects of plasma volume expansion on renal salt handling in patients with the nephrotic syndrome.

In 10 patients with the nephrotic syndrome (NS) and edema persisting despite a NaCl-poor diet, the effect of a single infusion of hyperoncotic albumin (75 g) on NaCl excretion was studied. 6 patients had minimal lesions, and 2 patients were studied twice. On half of the occasions the glomerular filtration rate was reduced. Blood volume (BV), calculated from plasma volume and hematocrit, was slightly elevated before infusion, and increased to 136 and 120% of normal at 4 and 20 h after it, respectively. Plasma renin activity (PRA) and plasma aldosterone (PA) both decreased to suppressed levels at 20 h after infusion. Sodium excretion increased from 9.2 +/- 7.6 muEq/min before, to 3.10 +/- 22.4 (0-4 h) and 43.1 +/- 36.3 muEq/min (4-20 h) after infusion. In 6 of these patients clearance studies were done before and after the infusion, maximal free water clearance being used as marker for distal NaCl reabsorption. Proximal fractional NaCl reabsorption was elevated before (94.9 +/- 1.4%) and decreased after the infusion (92.8 +/- 1.7%). Distal fractional NaCl reabsorption was also elevated before (93.0 +/- 6.4%), but unaltered after infusion (93.0 +/- 5.6%). Thus, after marked expansion of BV and suppression of PRA and PA, sodium excretion remained low despite the present edema. The results indicate that in many patients with the NS, including minimal lesion NS, intravascular hypovolemia is not the sole cause of sodium retention.

Hemodynamic alterations in ischaemic acute renal failure.

It is concluded that the condition of 'acute renal failure' starts in the first minutes after restoration of the circulation, following the ischemic period. The aggregation of red blood cells in the renal medulla with the subsequent cessation of medullary blood flow represents an important factor causing both the reduced urinary concentrating ability and the depressed urinary potassium concentration. The persisting medullary ischemia leads to cellular swelling and eventually to cell necrosis, which in turn results in a mechanical obstruction of the tubular lumen in the region of the loops of Henle and the medullary collecting ducts. In contrast, the anuria which is evident weeks after the primary damage, seems to be caused by the release of vasoconstrictor principles, whose origin is unclear, but it seems not to be mediated via the renal nerves, since the same symptoms are found in transplanted kidneys. Therapeutic endeavors using heparin, saline expansion and mannitol to improve the rheological characteristics of the blood seems to be of limited value. Infusion of hyperoncotic albumin during the ischemic period, however, seems to be of some benefit, since glomerular filtration is better preserved. The addition of ATP and magnesium, glucose or adjustment of the acid base status with buffers has not been encouraging in the present models, in which glomerular filtration rate is reduced to only a few percent of control.

Effect of albumin infusion on renal glucose reabsorption in the rat.

Clearance and micropuncture techniques were employed to assess the relationship between renal glucose and sodium reabsorption in the rat. Late proximal tubular fluid was collected from surface nephrons before and at two intervals after the infusion of hyperoncotic albumin by a double recollection technique. Plasma glucose levels were maintained at 28-44 mM throughout. Proximal tubular reabsorptive rates for both glucose and sodium were elevated 20 min after the start of the hyperoncotic infusion. Continued infusion of the hyperoncotic albumin resulted in a natriuresis and a parallel fall in proximal glucose and sodium reabsorption. Changes in maximal glucose reabsorption rates for the whole kidney paralleled changes in glucose reabsorption in surface nephrons. The addition of calcium and magnesium to the hyperoncotic infusate diminished the natriuresis but did not alter the relationship between sodium and glucose reabsorption. These observations indicate a close relationship between proximal tubular glucose reabsorption and sodium reabsorption during hyperoncotic infusion.

Direct measurement of papillary collecting duct sodium transport in the rat. Evidence for heterogeneity of nephron function during Ringer loading.

It has been suggested that collecting duct sodium transport was inhibited by extracellular volume expansion. To directly evaluate this possibility, micropuncture of the papillary collecting duct of young rats was performed during hydropenia and Ringer loading. The possibility of heterogeneity of nephron function was evaluated during Ringer and hyperoncotic albumin loading by comparing the delivery of sodium to the end of the distal tubule of superficial nephrons with papillary base delivery. During hydropenia (n = 14), sodium delivery to the base averaged 0.95% of the filtered sodium load and reabsorption along the collecting duct was noted from base to tip in each collection pair averaging 0.80% of the filtered load. During Ringer loading, sodium delivery to the base was markedly greater than in hydropenia, 11.8 vs. 0.95% of the filtered load (P less than 0.001). Yet, sodium reabsorption was also much greater, 6 vs. 0.8% (P less than 0.001). In 13 paired collections, during Ringer loading, sodium delivery to the papillary base, 12.2% of the filtered load, was consistently greater than late distal tubular delivery from superficial nephrons. 8% (P less than 0.005). In contrast, reabsorption of sodium from late distal tubule to papillary base was found during albumin infusion, 6.2 vs. 3.1% (P less than 0.001). Therefore, these studies demonstrate that: (a) the delivery of sodium to and reabsorption along the papillary collecting duct were markedly greater during Ringer loading than in hydropenia; (b) the amount of sodium delivered to the papillary base was greater than the delivery to the end of the distal tubule of superficial nephrons during Ringer loading, suggesting that deeper nephrons deliver more sodium to the collecting duct in this setting; and (c) the difference in sodium excretion between Ringer loading and hyperoncotic albumin infusion is due to events occurring between the late distal tubule of superficial nephrons and the base of the papillary collecting duct.

On the role of the interstitial volume in the response of the rat to blood volume expansion.

Patterns of body fluid distribution and selected cardiovascular and renal responses were studied following vascular expansion in normal rats and in rats with altered interstitial fluid volume produced by dehydration, prehydration or hyperoncotic albumin infusion. In all four groups the patterns of the renal excretory response and the accompanying change in central venous pressure (CVP) were closely parallel and the disturbance in CVP was finally corrected in the presence of a considerable residual vascular expansion. During the diuresis and saluresis following iso-oncotic vascular expansion in prehydrated and dehydrated rats, both groups removed fluid chiefly from the interstitium; this fluid removal was attributable mainly to urinary excretion in prehydrated rats but mainly to redistribution into the cellsin dehydrated rats. In the latter series, preferential renal excretion of sodium over water was observed. Hyperoncotic vascular expansion led to a peak renal excretory response only 70% of that following iso-oncotic expansion. The excreted volume was accounted for by a similar depletion of interstitial fluid after the iso-oncotic load. These findings are consistent with the hypothesis that the renal response to volume expansion regulates some parameter which is more closely related to the mean central venous pressure than to the vascular volume. This regulation was associated with incomplete correction of the vascular expansion and absolute decrease in interstitial fluid volume compared to the initial size of that compartment. This provides support for a functionally important influence of the interstitial volume on venous compliance.

Effect of hemodilution on the distribution of renal blood flow.

We evaluated the effects of hemodilution, expansion of intravascular volume, and expansion of interstitial volume on the distribution of cortical renal blood flow, utilizing the microsphere technique. Hemodilution without volume expansion (saline exchange) produced an increase in fractional blood flow in zone 1 (outermost zone) of the cortex from 34 plus or minus 1% to 43 plus or minus 2% and a decrease in fractional blood flow in zone 4 (innermost zone) from 16 plus or minus 2% to 13 plus or minus 2%. Hemodilution without volume expansion or a decrease in plasma protein concentration (isoncotic exchange) produced a similar redistribution in blood flow in zone 1 from 34 plus or minus 2% to 41 plus or minus 2% and in zone 4 from 14 plus or minus 2% to 10 plus or minus 1%. Hemodilution with intravascular volume expansion (hyperoncotic albumin infusion) also produced a superficial shift; blood flow in zone 1 increased from 27 plus or minus 1% to 30 plus or minus 1% and that in zone 4 decreased from 19 plus or minus 2% to 15 plus or minus 1%. Previous studies have demonstrated a redistribution to the juxtamedullary area after saline expansion. Our data demonstrate that hemodilution causes flow to redistribute to the superficial rather than the deep cortex. This superficial shift appears to be secondary to decrease hematocrit rather than to dilution of plasma proteins or expansions of intravascular volume. The deep shift in cortical blood flow which occurs during saline loading is presumably a consequence of expansion of interstitial volume.

Proximal tubule reabsorption after hyperoncotic albumin infusion. Role of parathyroid hormone and dissociation from plasma volume.

Preferential expansion of the plasma volume by infusion of salt-poor hyperoncotic albumin solution decreases sodium reabsorption by the proximal tubule. The present micropuncture studies test the thesis that albumin infusion depresses proximal reabsorption by an effect unrelated to expansion of the plasma volume, perhaps due to an effect of parathyroid hormone (PTH) on proximal sodium reabsorption. Infusion of salt-poor hyperoncotic albumin significantly decreased plasma ionized calcium, increased immunoreactive PTH (iPTH) in plasma, decreased sodium reabsorption by the proximal tubule, and increased phosphate clearance. In contrast, infusions of albumin, in which the ionized calcium was restored to normal plasma levels, had no significant effect on ionized calcium, iPTH, proximal reabsorption, or phosphate clearance in intact dogs. Similarly, in parathyroidectomized animals given a constant replacement infusion of PTH, albumin infusion had no significant effect on proximal reabsorption or phosphate clearance. Plasma volume was markedly expanded following albumin infusion in all groups of dogs. These findings (a) indicate that PTH plays a significant role in the decrease in sodium reabsorption by the renal proximal tubule after salt-poor hyperoncotic albumin infusion, and (b) dissociate preferential expansion of the plasma volume from decreases in sodium reabsorption by the proximal tubule.

Relationship between proximal sodium reabsorption and excretion of calcium, magnesium and phosphate

Relationship between proximal sodium reabsorption and excretion of calcium, magnesium and phosphate. The relationship between sodium reabsorption by the proximal tubule, measured by micropuncture techniques, and the urinary excretion of calcium, magnesium, and phosphate was determined following a number of experimental maneuvers known to increase sodium excretion. Following intravenous infusion of saline or Ringer's solution and the renal arterial infusions of acetylcholine and prostaglandin E 1 , proximal sodium reabsorption was significantly decreased while the fractional clearances of Na, Ca, Mg and PO 4 were significantly increased. Following the intravenous infusion of hyperoncotic albumin and the renal arterial infusion of parathyroid hormone, proximal sodium reabsorption was significantly decreased and the fractional clearances of Na and PO 4 were significantly increased. The fractional clearances of Ca and Mg were not increased following these infusions. Following the renal arterial infusion of bradykinin and prostaglandin E 2 , there was no significant change in proximal sodium reabsorption or in the fractional clearance of PO 4 while the fractional clearances of Na, Ca and Mg were significantly increased. It was concluded that changes in the fractional clearance of PO 4 are related to decreases in sodium reabsorption by the proximal tubule. Changes in the fractional clearances of Ca and Mg were not consistently associated with changes in proximal sodium reabsorption, suggesting that the excretion of these ions is primarily controlled by nephron segments distal to the proximal tubule.

A comparison of the segmental analysis of sodium reabsorption during Ringer's and hyperoncotic albumin infusion in the rat.

Studies were designed to compare the segmental analysis of sodium reabsorption along the nephron during volume expansion with either 10% body weight Ringer's or 0.6% body weight hyperoncotic albumin. Total kidney and nephron glomerular filtration rate increased similarly with both, but urinary sodium excretion (12.7 vs. 4.0 mueq/min, P < 0.001) and fractional sodium excretion (5.0 vs. 1.6%, P < 0.001) increased to a greater extent with Ringer's. Fractional reabsorption of sodium in the proximal tubule was diminished in both groups but to a significantly greater extent during Ringer's (P < 0.005). Absolute reabsorption was inhibited only in the Ringer's group. Delivery of filtrate out of the proximal tubule was greater in the Ringer's studies, 45 vs. 37 nl/min (P < 0.001). However, both fractional and absolute sodium delivery to the early and late distal tubule were not significantly different in the two groups. Fractional reabsorption in the collecting duct decreased from 96% in hydropenia to 31% during Ringer's but fell only slightly to 80% in the albumin studies. Absolute collecting duct reabsorption was also greater in the albumin studies, 0.55 vs. 0.21 neq/min (P < 0.001), which could totally account for the difference in urinary sodium excretion between the two groups. (22)Na recovery in the final urine after end distal microinjections was 71% during Ringer's infusion and 34% during albumin (P < 0.001). From these data we conclude that: (a) Ringer's solution has a greater inhibitory effect on proximal tubular sodium reabsorption, and (b) in spite of this effect, differences in mucosal to serosal collecting duct sodium transport are primarily responsible for the greater natriuresis during Ringer's infusion.

Effect of volume expansion on sodium excretion in the presence and absence of increased delivery from superficial proximal tubules.

The role of the proximal tubule in the natriuresis after volume expansion was investigated by evaluating sodium excretion both in the presence and absence of increased delivery from the proximal tubule. Proximal delivery was calculated from fractional reabsorption in superficial proximal tubules determined by micropuncture and glomerular filtration rate of the micropunctured kidney. Infusion of Ringer's solution in six dogs increased delivery from the proximal tubule 4.7+/-1 ml/min (P < 0.01) and increased fractional sodium excretion 3.6+/-1.1% (P < 0.025). Infusion of hyperoncotic albumin into the renal artery during sustained volume expansion decreased delivery from the proximal tubule 6.5+/-0.9 ml/min (P < 0.01). Although proximal delivery was restored to below control levels, fractional sodium excretion was significantly increased 2.5+/-0.5% (P < 0.01) as compared with the hydropenic control period. Fractional phosphate excretion was increased 15.5+/-3.7% (P < 0.01) after Ringer's infusion and was decreased 10.5+/-1.6% (P < 0.005) after intrarenal albumin infusion, suggesting that changes in superficial nephron reabsorption were paralleled by changes in reabsorption in deeper nephrons. Similar results were found in six additional dogs in which other factors known to affect phosphate reabsorption were controlled; however, these studies cannot completely eliminate a role for deep nephrons in the natriuresis after intrarenal albumin infusion. Since 70% of the natriuresis after volume expansion was present without increased delivery from superficial proximal tubules, it is likely that increased delivery from the proximal tubule contributes a relatively minor fraction to the natriuresis of volume expansion.

Nephron function during volume expansion in the rat

ARTICLESNephron function during volume expansion in the ratM Davidman, E Alexander, R Lalone, and N LevinskyM Davidman, E Alexander, R Lalone, and N LevinskyPublished Online:01 Jul 1972https://doi.org/10.1152/ajplegacy.1972.223.1.188MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByRenal haemodynamics and sodium handling after hyperoncotic albumin infusion in sodium-restricted normal manEuropean Journal of Clinical Investigation, Vol. 17, No. 5Distal blockade in experimental glomerulonephritis: The rôle of the diluting segment in sodium retention26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 93, No. 4Site and magnitude of the tubular inhibitory effect of expanding the extracellular volume in dogsActa Physiologica Scandinavica, Vol. 122, No. 3DEMONSTRATION OF PROXIMAL TUBULAR ?-ADRENOCEPTORS IN VIVOClinical and Experimental Pharmacology and Physiology, Vol. 11, No. 4Colloids Vs. Crystalloids—A Continuing Controversy30 August 2016 | Drug Intelligence & Clinical Pharmacy, Vol. 18, No. 3Factors influencing renal sodium reabsorption in volume expansion20 June 2005The pathology of marginal renal function21 June 2005Effects of sodium orthovanadate on whole kidney and single nephron functionKidney International, Vol. 18, No. 3Natriuretic factor in rats acutely expanded by Ringer's versus albumin solutionKidney International, Vol. 18, No. 1Renal micropuncture study of normotensive and Milan hypertensive rats before and after development of hypertensionKidney International, Vol. 13, No. 6Changes in interstitial pressure during acute interstitial volume depletion in normally hydrated ratsPflügers Archiv European Journal of Physiology, Vol. 369, No. 3Resuscitation of the Injured Patient: The Three Phases of TreatmentSurgical Clinics of North America, Vol. 57, No. 1The Renal Response to Acute Injury and SepsisSurgical Clinics of North America, Vol. 56, No. 4The Effect on Total Renal and Tubular Function and Plasma Renin of a Moderate Isotonic Saline Load in Rats Anesthetized with Amytal and InactinActa Physiologica Scandinavica, Vol. 94, No. 4Renal function and diuretic therapy in infants and children. Part IThe Journal of Pediatrics, Vol. 86, No. 4Resetting of tubulo-glomerular feedback sensitivity by dietary salt intakePfl�gers Archiv European Journal of Physiology, Vol. 346, No. 4Natriuretic HormonesNatriuretic and sodium transport inhibitory activity in plasma of volume-expanded dogsKidney International, Vol. 5, No. 1The acutely reduced kidneyKidney International, Vol. 3, No. 6 More from this issue > Volume 223Issue 1July 1972Pages 188-193 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.223.1.188PubMed5039062History Published online 1 July 1972 Published in print 1 July 1972 Metrics

Evaluation of interrelationship between calcium and sodium excretion by canine kidney

The effect of intravenous infusion of hyperoncotic albumin on calcium excretion was evaluated, and compared with that of intravenous saline. Albumin increased sodium excretion but had no effect on calcium excretion. Given in amounts ranging from 10 ml./Kg. to 100 ml./Kg., saline increased calcium excretion at all doses tested. Because albumin inhibits sodium reabsorption in the proximal nephron, and saline exerts its effect in both proximal and distal areas, the results indicate that calcium and sodium excretion parallel one another only when distal tubular sodium reabsorption is inhibited.

Interrelationship of physical factors affecting sodium reabsorption in the dog.

ARTICLESInterrelationship of physical factors affecting sodium reabsorption in the dogTM Daugharty, LJ Belleau, JA Martino, and LE EarleyTM Daugharty, LJ Belleau, JA Martino, and LE EarleyPublished Online:01 Dec 1968https://doi.org/10.1152/ajplegacy.1968.215.6.1442MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffects of prostaglandin E1 on renal hemodynamicsJournal of Anesthesia, Vol. 8, No. 2Renal haemodynamics and sodium handling after hyperoncotic albumin infusion in sodium-restricted normal manEuropean Journal of Clinical Investigation, Vol. 17, No. 5Postnatal development of renal function during the first year of lifePediatric Nephrology, Vol. 1, No. 3Modulation of the natriuretic response to atrial natriuretic peptide by alterations in peritubular Starling forces in the rat.Circulation Research, Vol. 59, No. 6Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat.Hypertension, Vol. 6, No. 6_pt_1Die Pathogenese des kardialen ÖdemsEffect of short-term bile duct ligation on peripheral blood steroids urinary PGE2 and the rate of sodium excretion in male rabbitsGeneral Pharmacology: The Vascular System, Vol. 15, No. 5The role of the kidney in sodium homeostasis during maturationKidney International, Vol. 21, No. 4Role of the Kidney in the Pathogenesis of Primary HypertensionRegulation of sodium balance in hypertension.Hypertension, Vol. 2, No. 4Dopamine-induced diuresis in the cat without changes in renal hemodynamicsNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 312, No. 1Escape from the sodium-retaining effects of mineralocorticoidsKidney International, Vol. 17, No. 3Effects of Positive End-Expiratory Pressure on Renal FunctionActa Anaesthesiologica Scandinavica, Vol. 22, No. 5Renal Hemodynamic Factors and the Regulation of Sodium ExcretionChapter 7. DiureticsChanges in interstitial pressure during acute interstitial volume depletion in normally hydrated ratsPflügers Archiv European Journal of Physiology, Vol. 369, No. 3Effects of PGD2 on canine renal functionNature, Vol. 267, No. 5612The effect of an acute increase in renal perfusion pressure on sodium transport in the rat kidney.Circulation Research, Vol. 39, No. 5Excretion of Sodium and Water by Kidneys in situ and by Transplanted Kidneys Following Isotonic, Hypotonic, Iso-Oncotic and Hyperoncotic Intravenous Infusions in Sodium-Loaded and Sodium-Deprived Dogs26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 84, No. 5Role of physical and neuroendocrine factors in proximal electrolyte reabsorptionMetabolism, Vol. 23, No. 8The control of sodium excretion following saline infusion in dogsPfl�gers Archiv European Journal of Physiology, Vol. 350, No. 4Symposium on Paediatric Anaesthesia and Intensive Care: Renal Physiology in Children14 January 2019 | Anaesthesia and Intensive Care, Vol. 1, No. 6Electrolyte content and ultrastructure of the kidney in hamsters with heart failureExperimental and Molecular Pathology, Vol. 19, No. 2Driving Forces over the Peritubular Capillary Membrane in the Rat Kidney during Antidiuresis and Saline ExpansionActa Physiologica Scandinavica, Vol. 89, No. 1Renal vasodilation and uncoupling of blood flow and filtration rate autoregulationKidney International, Vol. 4, No. 1On the mechanism of the phosphaturia of extracellular fluid volume expansion in the dogKidney International, Vol. 3, No. 4The mechanisms of fast renal compensationPfl�gers Archiv European Journal of Physiology, Vol. 341, No. 3The tissue effects of mineralocorticoidsThe American Journal of Medicine, Vol. 53, No. 5The influence of uremia on fractional sodium reabsorption by the proximal tubule of ratsKidney International, Vol. 2, No. 2Renal effects of prostaglandin A1 in patients with essential hypertensionKidney International, Vol. 1, No. 4Is There a Natriuretic Hormone?Physiological Properties of a Natriuretic Humoral Substance Occurring in Human Urine and PlasmaEffect of plasma albumin on sodium reabsorption in patients with nephrotic syndromeKidney International, Vol. 1, No. 1Tubular Reabsorption of Sodium Ion: Influence of Factors Other Than Aldosterone and Glomerular Filtration RateNew England Journal of Medicine, Vol. 285, No. 22Renal Physiology: Impact of Recent Developments on Clinical NephrologyPediatric Clinics of North America, Vol. 18, No. 2Further Studies of a Natriuretic Substance Occurring in Human Urine and PlasmaCirculation Research, Vol. 28, No. 5_suppl_2Sodium MetabolismNew England Journal of Medicine, Vol. 281, No. 2 More from this issue > Volume 215Issue 6December 1968Pages 1442-1447 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.6.1442PubMed4301937History Published online 1 December 1968 Published in print 1 December 1968 Metrics

Inhibition of sodium transport by Henle's loop after intravenous saline infusion.

Abstract The effects of saline and hyperoncotic albumin infusion given to dogs during a stable water diuresis were compared. Both inhibited proximal tubule-sodium reabsorption and caused an increase in free water clearance. Only saline caused a rise in the concentration of sodium in the urine. This finding strongly suggests that the saline infusion resulted in inhibition of sodium reabsorption by the loop of Henle. As previously noted, the U Na V rose only slightly after albumin and quite markedly following the saline infusion. These data are interpreted as indicating that more than sodium reabsorption by the proximal tubule (Factor III) is operative in the renal response to a saline infusion.

EFFECT OF RENAL ARTERIAL INFUSION OF ALBUMIN ON SALINE DIURESIS IN THE DOG.

It has been suggested that the protein concentration of peritubular plasma may be an important determinant of sodium and water reabsorption by the renal tubule (1,2 −3). The effect of protein on excretion of water and electrolyte has been the subject of several investigations (4,5,6,7). Infusions of hyperoncotic albumin reduce excretion of sodium in normal man(4,5,7). In the dog, infusion of hyperoncotic albumin may not result in increased excretion of sodium(6)) whereas the infusion of iso-oncotic “plasma-like” solutions is associated with a natriuresis similar to that resulting from the infusion of equal volumes of saline(8). Since the excretion of sodium must be the difference between total filtered load and net tubular reabsorption, changes in filtration rate could mask changes in tubular reabsorption when plasma volume is expanded during the infusion of solutions containing protein. Thus, an increase in filtration rate associated with infusions of protein solutions may result in a natriuresis which could be independent of any effect that plasma protein concentration may have on tubular reabsorption. Despite the demonstration by micropuncture that active reabsorption by the proximal tubule of Necturus is not grossly influenced by the transtubular gradient of oncotic pressure (9), the possibility cannot be excluded that overall net tubular reabsorption by the mammalian kidney is in some way affected by the protein concentration of peritubular plasma. Even though the osmotic gradient for water produced by the protein concentration gradient between tubular lumen and capillary is too small to account for a major fraction of tubular reabsorption(9), changes in protein concentration could conceivably influence net reabsorption indirectly through such mechanisms as a change in interstitial volume or a redistribution of blood within the kidney. The present studies were designed to determine whether increasing the protein concentration of renal arterial blood during the natriuresis of saline loading results in any major change in sodium excretion.