Renal filtration and excretion of aluminium in the rat: dose-response relationships and effects of aluminium speciation

1995 ◽  
Vol 14 (6) ◽  
pp. 494-499 ◽  
Author(s):  
CJ Lote ◽  
JA Wood ◽  
A. Thewles ◽  
M. Freeman

The known toxicity of aluminium, and the toxicity of agents (such as desferrioxamine) used to remove alumini um from the body, has prompted us to investigate whether there may be ways of enhancing aluminium excretion by exploiting the normal renal handling of aluminium. Aluminium (as sulphate or citrate) was administered intravenously to conscious rats at doses ranging from 25 μg (0.93 μmol) to 800 μg (29.6 μmol) aluminium, and alu minium excretion was monitored over the following 2 h. Measurements of the filterability of aluminium from the rat plasma, and the glomerular filtration rate (inulin clearance), enabled us to calculate the filtered load of alu minium, and hence determine aluminium reabsorption. At all doses of administered aluminium, that adminis tered as sulphate was excreted less effectively than that administered as citrate. This difference was attributable to the much greater filterability of aluminium administered as citrate. However, for any given filtered load, the excre tion of aluminium administered as citrate was not signifi cantly different (in either fractional or absolute terms) from the excretion of aluminium administered as sulphate. It seems likely that, following aluminium sulphate administration, the filtered aluminium may be an alumini um citrate form which is then reabsorbed in the same way as aluminium administered as citrate. It is thus apparent that aluminium removal from the body could be further enhanced if it were possible to pre vent the tubular reabsorption of the aluminium species which is so effectively filtered following aluminium citrate administration.

1987 ◽  
Vol 114 (4) ◽  
pp. 503-508 ◽  
Author(s):  
I. Orden ◽  
J. Pie ◽  
M. G. Juste ◽  
J. A. Marsella ◽  
C. Blasco

Abstract. The aim of this work was to estimate the daily urinary excretion of free and conjugated thyroxine using a direct radioimmunoassay and enzyme hydrolysis. The renal clearance of free T4 was also determined. The mean urinary values of free and total T4 (mean ± 1 sd) in 112 euthyroid controls were 1353 ± 496 and 1855 ± 651 pmol/24 h, respectively. Urinary excretion of free hormone in 13 hyperthyroid patients was 5552 ± 4320 pmol/24 h and total T4 was 8122 ± 7219 pmol/24 h. Urinary free T4 excretion was 223 ± 223 pmol/24 h in hypothyroid patients and total T4 was 542 ± 490 pmol/24 h. These results indicate that daily urinary T4 excretion is a good indicator of thyroid function. The mean renal clearance of free T4 was 52 ± 19 ml/min (mean ± 1 sd) in euthyroid patients, 53.7 ± 12.3 ml/min in hyperthyroid patients, and 67.6 ± 13.1 ml/min in hypothyroid patients. We estimated the endogenous creatinine renal clearance as a control of the renal filtration rate. The data suggest that there is T4 filtration of unbound T4 and partial tubular reabsorption. Further experimental studies will be necessary to clarify the renal handling of thyroxine as well as the fate of reabsorbed T4.


1971 ◽  
Vol 41 (2) ◽  
pp. 109-121 ◽  
Author(s):  
J. J. Ahumada ◽  
S. G. Massry

1. The combined effects of unilateral renal vasodilatation produced by acetylcholine or bradykinin and intravenous infusion of angiotensin on phosphate excretion and reabsorption were investigated in fourteen anaesthetized dogs. The influence of these manoeuvres on the excretion of sodium, calcium and magnesium was also evaluated. 2. Unilateral renal vasodilatation alone produced an increase in the excretion of phosphate, calcium, magnesium and sodium; and the infusion of angiotensin caused further augmentation of the excretory rates of these ions from the vasodilated kidney in most experiments. 3. The maximal tubular reabsorptive capacity (Tm) for phosphate was decreased by renal vasodilatation. 4. There was a close and significant correlation between the fraction of the filtered load of phosphate, calcium, and magnesium which was excreted and that of sodium. 5. The results indicate that renal vasodilatation with or without the infusion of angiotensin causes a decrease in the renal tubular reabsorption of phosphate, calcium, magnesium and sodium.


1989 ◽  
Vol 256 (1) ◽  
pp. F29-F34
Author(s):  
A. J. van der Heijden ◽  
J. P. Guignard

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.


1986 ◽  
Vol 251 (2) ◽  
pp. F251-F256 ◽  
Author(s):  
V. Johnson ◽  
A. Spitzer

The isolated perfused kidney of the guinea pig has been used to assess the mechanism that accounts for the maintenance of the positive phosphate (Pi) balance during development. The kidneys obtained from mature guinea pigs (n = 25) had a glomerular filtration rate (GFR) of 0.48 +/- 0.04 ml/min (mean +/- SE), whereas those of the newborn (n = 20) had a GFR of 0.15 +/- 0.02 ml/min. These values compare favorably with those observed in intact animals. The fractional excretion of Na+ (FENa) was 3.8 +/- 0.7% in the mature kidneys and 4.7 +/- 0.7% in the newborn kidneys. The maximal tubular reabsorption of Pi (TmPi) by the newborn kidney was 24.3 +/- 2.8 micrograms/min. The filtered load at which the TmPi of the newborn was reached exceeds by 2.5-fold the filtered load of Pi encountered under physiological conditions. In the adult the TmPi was 53.9 +/- 2.6 micrograms/min. The filtered load at which the TmPi of the adult was reached is only slightly higher than the average normal filtered load of Pi. The TmPi/GFR was significantly higher (P less than 0.02) in the newborn (117.4 +/- 10.8 micrograms X min-1 X ml-1 GFR) compared with the adult (82.6 +/- 3.6 micrograms X min-1 X ml-1 GFR). Moreover, at any filtered load of Pi below Tm the newborn animals reabsorbed twofold more Pi per gram kidney weight than the adult (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


1964 ◽  
Vol 207 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Dorothea Hellman ◽  
H. Robert Baird ◽  
Frederic C. Bartter

In normal dogs, the maximal tubular reabsorption of phosphate (Tmp) on moderate phosphate (P) intake has been compared to that on high P intake. Oral P loading caused a reduction in glomerular filtration rate (GFR) in all the animals. A significant reduction in Tmp could be demonstrated in five of the six dogs while on sustained oral P loading. This decline in Tmp was significantly greater than could be accounted for by the regression of Tmp on GFR. A return toward normal values for TmP occurred following resumption of a normal diet. The reduction in Tmp during oral P loading suggests that a reduction in renal tubular reabsorption of phosphate (TRP) is one means whereby excess phosphate is eliminated from the body. This reduction in TRP may be related to an increased release of endogenous parathyroid hormone.


1981 ◽  
Vol 241 (6) ◽  
pp. F618-F624 ◽  
Author(s):  
C. Merlet-Benichou ◽  
M. Pegorier ◽  
M. Muffat-Joly ◽  
C. Augeron

Clearance experiments were carried out in fetal, young, and adult pigs undergoing salt loading. Kidney sections were histologically examined and the proximal tubular length, glomerular volume, and number of glomeruli were estimated. Between days 48 and 55 of gestation, the significant increase in glomerular filtration rate was proportionately higher than the concentration increase in water, total solutes, and sodium reabsorption. During this period, neither the proximal tubular length nor the glomerular volume of the juxtamedullary nephrons changed significantly. The main morphologic change took place in the superficial cortex, where new glomeruli attached to very short tubules differentiated. From day 55 to birth, the increase in water, total solutes, and sodium filtered loads was proportionately smaller than the concomitant increase in tubular reabsorption. During this phase, the major morphologic change was the significant lengthening of the proximal tubules of the juxtamedullary and superficial nephrons. These findings suggest that for water, sodium, and total solutes the maturation of superficial nephrons is accompanied by a phase of functional glomerular preponderance. Despite the differentiation of the superficial nephrons, renal handling of normally filtered glucose did not change significantly. Functional glomerulotubular coupling for water, sodium, and total solutes took place soon after birth.


1975 ◽  
Vol 229 (4) ◽  
pp. 901-906 ◽  
Author(s):  
MM Popovtzer ◽  
JB Robinette ◽  
KM McDonald ◽  
CK Kuruvila

The effect of hypercalcemia on renal handling of phosphorus was studied in parathyroidectomized rats during 1) extracellular volume expansion with normal saline (0.1 mg/100 g per min) and 2) parathyroid extract infusion (1 U/100 g per h). Hypercalcemia (serum calcium 12-15 mg/100 ml) blunted the phosphaturic response to volume expansion, both when serum calcium was raised acutely during volume expansion and when volume expansion was induced in rats with sustained hypercalcemia. These changes were not associated with significant variations in glomerular filtration rate and serum concentration of phosphorus. Hypercalcemia failed to alter the phosphaturic response and the increase in urinary cyclic AMP excretion following both continuous infusion and a single injection of parathyroid extract. These results are consistent with two components of tubular reabsorption of phosphorus. The first is suppressed by extracellular volume expansion and stimulated by hypercalcemia. The second is suppressed by parathyroid hormone and is not affected by hypercalcemia.


1990 ◽  
Vol 122 (4) ◽  
pp. 479-486 ◽  
Author(s):  
Atim B. Anwana ◽  
Hugh O. Garland

Abstract. Metabolic and renal clearance techniques were used to examine kidney function in conscious and anesthetised streptozotocin diabetic rats. All diabetics showed an enhanced calcium and magnesium excretion compared to controls. However, the renal handling of these ions in relation to other electrolytes varied with different experiments. In non-infused conscious rats, the excretion of all ions was higher in diabetics, but the increased output of Ca2+ and Mg2+ was far greater than that of other electrolytes. In infused anesthetised diabetics only the outputs of Ca2+ and Mg2+ were significantly raised. This resulted from a significant reduction in the tubular reabsorption of both ions (% Ca2+ reabsorption: Controls 97.0±0.5; Diabetics 86.1±2.1; p<0.001). Insulin treatment reversed these changes. Major differences therefore exist in the renal handling of Ca2+ and Mg2+ in control and diabetic kidneys. Such differences do not simply parallel changes in the handling of other ions, and thus represent specific Ca2+ and Mg2+ lesions. Anesthetised infused diabetic rats also showed a reduced glomerular filtration rate and urine output compared to controls. Such differences may relate to an altered fluid balance in the two groups, different responses to surgery and anesthesia, or the degree of hyperglycemia in diabetic animals.


2018 ◽  
Vol 54 (1) ◽  
pp. 29-36
Author(s):  
Nikola Musiała ◽  
Iga Hołyńska-Iwan ◽  
Dorota Olszewska-Słonina

Cortisol, also called “the” stress hormone is a glucocorticoid secreted by the adrenal cortex. This hormone plays a significant role in maintaining homeostasis, according to the body’s total stress. Cortisol interferes with many organs, affects glucose and fatty acids metabolism and neurotransmitter secretion. Predominantly, cortisol influences the carbohydrate metabolism, stimulating gluconeogenesis in the liver and inhibiting glucose utilization in peripheral tissues. As it is an element “fight or flight” it also stimulates central nervous system and enhances blood flow. To some extent cortisol influences also the renal handling of electrolytes, namely: increasing sodium resorption, and renal excretion of potassium, calcium and phosphates. Through its anti-inflammatory and immunosuppressive character this glucocorticoid modulates the immune system functioning. Cortisol has a circadian rhythm following ACTH (adrenocorticotropic hormone) secretion. Increased cortisol levels are observed physiologically during stress and pathologically in Cushing’s syndrome. Chronic hypercortisolism is harmful or the body, and its effects present an extremely wide spectrum, including insulin resistance, obesity, insomnia and even depression. Thus, laboratory diagnosis of cortisol level is important for the diagnosis, monitoring and evaluate the effectiveness of hypercortisolism treatment.


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