Background. Obesity is associated with hypertension and glomerular hyperfiltration. A major mechanism responsible for the obesity-associated hypertension is renal salt retention. An increased glomerular filtration fraction (FF) is expected to raise postglomerular oncotic pressure and to increase proximal tubular sodium reabsorption. The aim of the present study was to verify whether obesity-associated hyperfiltration leads to increased postglomerularoncoticpressureandincreasedproximalsodium reabsorption. Methods. Twelve obese subjects (BMI >36) and 19 lean subjectsparticipatedinthestudy.Theyunderwentmeasurement of glomerular filtration rate (GFR), renal plasma flow (RPF) and fractional excretion of lithium (FE Li). Results. GFR, RPF and FF were 61%, 28% and 29% higher, respectively, in the obese than in the control group (P <0.00001 for GFR,P <0.005 for RPF andP <0.00005 for FF). Half of the obese group had increased FF with increasedGFR,whiletheotherhalfhadnormalFFwithhighnormal or increased GFR. Postglomerular oncotic pressure was 13% higher (P <0.03) and FE Li was 33% lower (P <0.005) in the obese group with high FF than in the leangroup.PostglomerularoncoticpressureandFELiwere normal in the obese group with normal FF. Conclusions. These results suggest that glomerular hyperfiltration may lead to increased proximal tubular sodium reabsorption in the obese.

Obesity-induced glomerular hyperfiltration: its involvement in the pathogenesis of tubular sodium reabsorption.

We recently showed that vitamin D receptor (VDR) inactivation results in deregulated stimulation of the renin-angiotensin system (RAS). To address further the relation between RAS activation and the abnormalities in electrolyte and volume homeostasis, we studied the effect of the ANG II type I receptor antagonist losartan and the angiotensin-converting enzyme inhibitor captopril on VDR-null mice. Treatment with losartan or captopril normalized the water intake and urine excretion of VDR-null mice. However, the increase in salt excretion in VDR-null mice was not affected by either drug, suggesting that this abnormality is independent of the RAS. Northern blot and immunohistochemical analyses revealed that both drugs caused a drastic stimulation of renin expression in wild-type and VDR-null mice, but renin expression remained much higher in the treated VDR-null mice than in the treated wild-type mice, suggesting that the ANG II feedback mechanism remains intact in the mutant mice. These data firmly established a causative relation between RAS overstimulation and the abnormal volume homeostasis in VDR-null mice and demonstrated that vitamin D repression of renin expression is independent of the ANG II feedback regulation in vivo.

Effect of ANG II type I receptor antagonist and ACE inhibitor on vitamin D receptor-null mice

Publisher Summary This chapter discusses the kidney function in calcium and phosphate metabolism. Production of urine is the most conspicuous expression of kidney function but not the most significant always. The amount of phosphate excreted per day is equal to the amount of phosphate adsorbed from the diet. The average diet contains about 1500 mg phosphate per day, and the average 24-hour renal excretion of phosphate is about 600 mg. Variations in intake and urinary output are closely related. The most common cause of a low phosphate excretion rate is a phosphate-poor diet—such as low protein or low calcium diets—or administration of aluminum hydroxyde gels, which bind phosphate in the gut. Phosphate reabsorption is decreased in primary and secondary hyperparathyroidism and increased in hypoparathyroidism. A chronic high phosphate intake produces a steady state with reduced tubular reabsorption of phosphate, reduced calcium excretion, normocalcemia or slight hypocalcemia, increased immunoreactive parathyroid hormone serum level, and parathyroid hyperplasia. Chronic renal failure with decreased glomerular filtration rate is associated with bone disease.

Kidney Function in Calcium and Phosphate Metabolism

Parathyroid hormone and calcitonin regulation of renal function

Recent advances in calcium metabolism: I. Mechanisms of calcium homeostasis

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.

/pdf/proximal-tubule-reabsorption-after-hyperoncotic-albumin-57jil49k15.pdf

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

A B S T R A C T 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 This work was presented in part at the Fall meetings

/pdf/role-of-parathyroid-hormone-and-dissociation-from-plasma-3gjlykh9a6.pdf

Role of parathyroid hormone and dissociation from plasma volume

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.

/pdf/effect-of-volume-expansion-on-sodium-excretion-in-the-291o0pufz7.pdf

Effect of Volume Expansion on Sodium Excretion in the Presence and Absence of Increased Delivery from Superficial Proximal Tubules

Hydrostatic pressures in proximal tubules and peritubule capillaries in the dog

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

Role of parathyroid hormone and dissociation from plasma volume

Effect of Volume Expansion on Sodium Excretion in the Presence and Absence of Increased Delivery from Superficial Proximal Tubules

Hydrostatic pressures in proximal tubules and peritubule capillaries in the dog