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Biomedical subjects

K Olgaard

Publications and source records attributed to K Olgaard.

At least 127 records · Page 7Linked to original sources
PubMed1978

Inhibition of aldosterone response to surgery by saline administration.

The renin-angiotensin system, ACTH and hyperkalaemia are known to induce increased plasma levels of aldosterone. In order to assess the relative significance of these mechanisms during surgical stress, aldosterone, cortisol and electrolytes in plasma were measured in 12 otherwise healthy women during and after cholecystectomy. The patients received either isotonic sodium chloride or 5 per cent glucose in water during the experimental period of 22 h. The results showed that the pronounced increase of aldosterone and the concomitant decrease of sodium in plasma found in patients given glucose in water could almost be inhibited by the administration of saline. Cortisol and potassium concentrations were identical in the two groups of subjects. It is concluded that the aldosterone response to surgery is mainly mediated via the renin-angiotensin system. This response is probably due to a reduced sodium content or volume of extracellular fluid, since it could almost be inhibited by administration of sodium chloride. The rationale of saline restriction during and after surgery is questioned.

Adult↗
PubMed1978

Has vitamin D a direct renal effect on the tubular reabsorption of phosphate? A study in parathyroidectomized (PTX) and non-PTX man.

The effect of 1-alpha-hydroxycholecalciferol (1alpha-OH-D3) on the renal handling of phosphate and the immunoreactive parathyroid hormone in serum (i-PTH) has been studied in 10 patients with a wide range of glomerular filtration rate (GFR), maximal tubular reabsorption of phosphate (TmP) and i-PTH. The patients were treated with 2 microgram 1alpha-OH-D3 per day for approximately 80 days. Before and after this period of treatment, the TmP, i-PTH, 51Cr EDTA clearance, extracellular volume, standard bicarbonate, and serum calcium were measured in each patient. The TmP/GFR ratio was used as an index of the renal handling of phosphate. The index increased significantly (mean 26.5%, p less than 0.01) during the treatment, while i-PTH decreased significantly (mean 37.0%, p less than 0.01). A significant inverse correlation was demonstrated between the TmP/GFR index and i-PTH both before (r = -0.87; p less than 0.001) and after (r = -0.79; p less than 0.01) the administration of 1alpha-OH-D3, while none of the other factors investigated were correlated to the index. This may suggest that the stimulating effect of biologically active vitamin D on the tubular reabsorption of phosphate is mediated via the parallel suppression of PTH, but does not exclude that biologically active vitamin D exerts a direct effect on the human renal tubule. Therefore, the effect of 1alpha-OH-D3 was studied in 5 totally parathyroidectomized patients, in whom concomitant suppression of PTH would not occur. Estimation of TmP/GFR was performed 1) when the patients were vitamin D depleted and hypocalcemic, and 2) after 14-27 days of treatment with 1alpha-OH-D3 to obtain stable normocalcemia. In patients with absent parathyroid function, no increasing effect of 1alpha-OH-D3 on TmP/GFR could be demonstrated. It is therefore concluded 1) that 1alpha-OH-D3 exhibits no antiphosphaturic effect in the absence of PTH and 2) that the previously demonstrated antiphosphaturic effect of 1alpha-OH-D3 in man is mediated via a concomitant suppression of PTH.

Absorption↗
PubMed1978

Calcium-dependent aldosterone secretion in anephric and nonnephrectomized patients on regular hemodialysis.

The present study was undertaken to investigate the effect of a continuous calcium infusion on the plasma levels of aldosterone, renin activity, and cortisol in six anephric and four nonnephrectomized patients on regular hemodialysis. In both groups, a significant increase in whole blood ionized calcium (b-Ca2+) was demonstrated. A significant increase in plasma aldosterone (PAC) was noted in the nonnephrectomized patients, in whom the rise in PAC correlated with the increase in b-Ca2+. However, in the anephric patients only a smaller and insignificant increase in PAC was found. No significant changes were demonstrated in plasma cortisol or renin activity, nor in potassium or sodium concentrations in either group. It is concluded that ionized calcium influences the plasma levels of aldosterone in uremic patients on regular hemodialysis.

Adrenocorticotropic Hormone↗
PubMed1978

Cessation of bone loss in chronic renal failure by 1-alpha-hydroxyvitamin D3: a controlled trial.

The study was undertaken in patients with chronic renal failure (CRF patients) in order to evaluate 1) the degree and course of skeletal demineralisation and 2) the effect on the bone mineral content (BMC) of long-term treatment with 1alpha-hydroxyvitamin D3 (1alpha(OH)D3). BMC was measured on the radius by 241 Am-photonabsorptiometry and the results were corrected for age, sex and bone width. In a cross-sectional study BMC was measured in 191 normal subjects and in 88 renal patients. In a controlled longitudinal trial 22 CRF patients were treated for 25.6 months with 1alpha(OH)D3, while 22 CRF patients did not receive vitamin D supplements. In CRF patients an accelerated bone loss (approximately 3%/year) and a significantly reduced BMC (mean 87.2% of normal) was found. In the 1alpha(OH)D3 treated patients BMC increased on an average 0.9%/year. This was significantly different from the continued bone loss recorded in the non-treated control patients. The data indicate that 1) CRF patients develop reduced bone mass because of accelerated bone loss; 2) cessation of this bone loss may be achieved by long-term treatment with 1alpha(OH)D3.

Adult↗
PubMed1977

The maximal tubular reabsorption of phosphate in relation to serum parathyroid hormone.

The relation between the renal handling of phosphate and the serum concentration of immunoreactive parathyroid hormone (i-PTH) was investigated in 15 patients with a very wide range of i-PTH, glomerular filtration rate (GFR), maximal tubular reabsorption of phosphate (TmP) and TmP/GFR-ratio. The latter was used as an index of the renal handling of phosphate. Seven patients had well functioning kidney allografts (GFR 43.1-64.9 ml/min), while 8 had varying degrees of chronic nephropathy (GFR 2.3-26.7 ml/min). The TmP, i-PTH, 51Cr EDTA clearance, the extracellular volume and serum concentrations of calcium and standard bicarbonate were estimated. An inverse significant correlation was demonstrated between TmP/GFR and i-PTH (p less than 0.001), while none of the other investigated factors correlated thyroid hormone has a key role in the regulation of the tubular handling of phosphate in patients with impaired renal function.

Adult↗
PubMed1977

Aldosterone response to ACTH stimulation in anephric and non-nephrectomized patients on regular hemodialysis.

The effect of ACTH on plasma aldosterone concentration (PAC) and plasma cortisol concentration (PCC) has been investigated in 5 anephric and 6 non-nephrectomized patients on regular homodialysis. Basal PAC was significantly lower (p less than 0.01) in the anephric (mean 37.6 pg/ml) than in the nonnephrectomized group (mean 117.5 pg/ml), whereas basal PCC (18.6 and 16.5 mug/100 ml, respectively) did not differ significantly (p less than 0.05). Following administration of synthetic beta1-24 ACTH, the maximal percentage increase in PAC was significantly lower ( less than 0.001) in the anephric (105%) than in the nonnephrectomized group (286%). The rise in PCC, 118%, in both groups showed no significant difference (p less than 0.05). The higher basal level of PAC and the more pronounced response to ACTH in nonnephrectomized patients correlated with higher basal levels of plasma renin activity compared with the anephric group. An influence of the remaining renin-angiotensin system on the ability to react to an ACTH stimulation is therefore suggested.

Adrenocorticotropic Hormone↗
PubMed1977

Regulation of plasma aldosterone in anephric and non-nephrectomized patients during hemodialysis treatment.

The relationships between plasma aldosterone and changes in plasma potassium, plasma cortisol, plasma sodium, blood volume and body weight have been studied in 6 anephric and 11 non-nephrectomized patients on regular hemodialysis. In all patients, the plasma aldosterone concentration decreased during dialysis. In the anephric patients, a significant correlation (p less than 0.001) was demonstrated between the fall in plasma aldosterone and the fall in plasma potassium (total body potassium depletion). Measurements between consecutive hemodialyses, furthermore, showed a significant correlation (p less than 0.001) in anephric patients between total body potassium repletion (increasing plasma potassium) and the rise in plasma aldosterone. In contrast, the potassium and aldosterone changes did not correlate in the non-nephrectomized group. During dialysis, a decrease was found in all parameters, but no correlation was demonstrable in either group between the changes in plasma aldosterone and the fall in plasma cortisol, sodium, blood volume and body weight. The data in the anephric patients emphasize the important role of potassium in the regulation of aldosterone secretion.

Adolescent↗
PubMed1977

The effect of 1-alpha-hydroxycholecalciferol on the renal handling of phosphate in parathyroidectomized man.

In a previous investigation by our group it was suggested that the stimulating effect of 1-alpha-hydroxycholecalciferol (1-alpha-OH-D3) on the tubular reabsorption of phosphate is mediated via the parallel suppression of the parathyroid hormone (PTH). A direct effect of 1-alpha-OH-D3 on the renal tubule could however not be completely excluded. Therefore, the effect of 1-alpha-OH-D3 was studied in 5 totally parathyroidectomized patients, in whom concomitant suppression of PTH would not occur. TmP/GFR, i.e. the ratio between the maximal tubular reabsorption of phosphate (TmP) and the glomerular filtration rate (GFR), was used as an indicator of the renal handling of phosphate. Estimation of TmP/GFR was performed 1) when the patients were vitamin D depleted and hypocalcemic, and 2) after 14-27 days of treatment with 1-alpha-OH-D3 to obtain stable normocalcemia. In patients with absent parathyroid function, no effect of 1-alpha-OH-D3 on TmP/GFR could be demonstrated. It is therefore concluded that 1-alpha-OH-D3 exhbits no antiphosphaturic effect in the absence of PTH and that the previously demonstrated antiphosphaturic effect of 1-alpha-OH-D3 in man is mediated via a concomitant suppression of PTH.

Adult↗
PubMed1977

The adrenocortical response to angiotensin II infusion in anephric and non-nephrectomized patients on regular hemodialysis.

In the present study 8 anephric and 4 non-nephrectomized patients were stimulated with angiotensin II (A-II). In 5 of the anephric patients, an increased plasma aldosterone concentration (PAC) in response to ACTH stimulation had previously been demonstrated. After A-II stimulation, all 8 anephric patients responded with a significant rise in PAC although the increase was less pronounced than in 4 non-nephrectomized patients. In both groups of patients the increase in PAC was correlated to the increase in diastolic and systolic BP and to the A-II dose. Furthermore, in the non-nephrectomized patients, the plasma renin activity showed a significant decline, which was inversely correlated to the increase in PAC. When all 12 patients, regardless of the difference in remaining renin-angiotensin system, were considered as one population, the variable basal levels of PAC correlated significantly to the increase in PAC during A-II and ACTH stimulation. It is concluded that the adrenals of anephric man respond to A-II with an increase in PAC and that the reason for a lower response appears to be the lack of the renin-angiotensin system.

Adrenal Cortex↗
PubMed1977

Plasma aldosterone during extracellular fluid volume expansion in patients on regular haemodialysis.

The influence of extracellular fluid volume expansion on the plasma aldosterone concentration (PAC) was investigated in five anephric and six non-nephrectomized patients on regular haemodialysis, and compared to a control group of four anephric and four non-nephrectomized patients. Plasma-renin activity, cortisol, Na+, and K+ were measured together with the PAC during the investigation. In anephric patients the PAC remained constant during the control period as well as during extracellular fluid volume expansion by infusion of 350 mmol of 20% mannitol. In the non-nephrectomized patients PAC diminished after mannitol infusion. The decline in PAC was correlated with the basal levels of PAC and the plasma renin activity. It is concluded that 5% extracellular fluid volume expansion has no direct influence on the regulation of PAC in patients without the renal renin-angiotensin system and that the regulation of PAC in anephric patients in the present investigation is probably mediated by changes in potassium and ACTH.

Adult↗