[Pathogenesis of polyglobulia after kidney transplantation].
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Alleles↗
Biomedical subjects
A Bar
Publications and source records attributed to A Bar.
Renal clearance of endogenous erythropoietin in patients with proteinuria.
Recent data indicated the importance of urinary losses of erythropoietin (Epo) in the pathogenesis of anaemia in patients with nephrotic syndrome. In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. We found that patients with SNP were characterized by lower plasma levels of Epo than healthy subjects but no differences were found in urinary excretion of Epo, endogenous Epo clearance and its fractional excretion (FEEpo). There were no differences between groups in FE beta 2m and FENa and plasma aldosterone levels but plasma renin activity was higher in patients with SNP than in the controls. No relationships were found between Epo levels and activity of the RAAS and sodium metabolism, respectively. Our data suggest that lower levels of plasma Epo in patients with SNP and normal renal excretory function are not due to urinary losses of Epo but rather to the decreased production/degradation ratio.
Adult↗
Erythropoietin concentration in cyst fluid in patients with simple renal cysts.
High erythropoietin (EPO) levels in cyst fluid and blood plasma in patients with autosomal dominant polycystic kidney disease (ADPKD) have been reported. In the present study we assessed EPO levels and the biochemical composition of cyst fluid obtained from 50 simple renal cysts. Basing on cyst fluid/plasma sodium ratio 38 cysts were classified as cysts of proximal origin, and 12 as cysts of undetermined origin. EPO concentrations in cyst fluid obtained from proximal cysts were significantly higher than in fluid from cysts of undetermined origin (472.9 +/- 116.2 vs. 112.1 +/- 33.3 mU/ml, p < 0.05). Patients with proximal cysts had significantly higher plasma EPO levels (31.8 +/- 3.5 mU/ml) than healthy subjects (17.3 +/- 1.96 mU/ml, p < 0.005). We conclude that: (1) simple renal cysts of distal origin seem to be rare; (2) the presence of high EPO level in cyst fluid suggests its proximal origin; (3) estimation of cyst fluid EPO levels seems to be of similar pathogenetic value as the assessment of the cyst fluid/plasma sodium ratio.
Adult↗
[Concentrations of B2-microglobulin and Tamm-Horsfall protein in cyst fluid and urinary excretion of these proteins in patients with simple renal cysts].
The existing classifications of simple renal cysts are based on cyst fluid sodium concentration or cyst fluid/plasma sodium ratio. The present study aimed to assess: 1) the usefulness of cyst fluid concentrations of beta-2-microglobulin (beta-2-MG) as a marker of proximal tubules function and Tamm-Horsfall protein (THP) as a marker of distal tubules function to define the origin of renal cysts (proximal or distal); and 2) the function of proximal and distal tubules in patients with simple renal cysts. 31 patients with simple renal cysts and 10 healthy subjects were examined. Basing on the cyst fluid/plasma sodium ratio, 25 cysts were classified as of proximal origin and 6 as of undetermined origin. In all patients cyst fluid and plasma concentrations of beta-2-MG, erythropoietin, sodium, potassium and total protein were assessed. Urinary excretion of beta-2-MG and THP was also estimated and fractional excretion of beta-2-MG was calculated. The concentration of beta-2-MG in fluid obtained from cysts of proximal origin were significantly higher than in fluid from cysts of undetermined origin (2.26 +/- 0.36 vs. 0.65 +/- 0.13 mg/l, p = 0.0004). Concentrations of THP (6.85 +/- 1.21 vs. 3.14 +/- 1.06 micrograms/ml, p < 0.05), erythropoietin (500.6 +/- 176.8 vs. 42.0 +/- 17.7 mU/ml, p < 0.05) and potassium (4.39 +/- 0.07 vs. 3.13 +/- 0.44 mmol/l, p < 0.05) were also higher in fluid from proximal cysts than in fluid from cysts of undetermined origin.(ABSTRACT TRUNCATED AT 250 WORDS)
Adjuvants, Immunologic↗
Interaction between calcium and 1,25-dihydroxyvitamin D3 in the regulation of preproparathyroid hormone and vitamin D receptor messenger ribonucleic acid in avian parathyroids.
Regulation of prepro-PTH and vitamin D receptor (VDR) mRNAs in the parathyroid glands was studied in chickens in vivo. The birds were raised to 21 days of age on a vitamin D-deficient diet with 1% calcium and 0.65% phosphorous. At the end of this period, the chicks exhibited marked hypocalcemia and enlarged parathyroid glands. In three separate trials, the birds were repleted for 6 days with vitamin D and different dietary calcium and phosphate concentrations, with 2 micrograms/kg 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and different dietary calcium concentrations (0.5%, 1.0%, or 1.8%), or with 2 or 10 micrograms/kg 1,25-(OH)2D3 and 0.6% or 1.9% calcium or were kept vitamin D3 deficient and fed 0.5%, 1.0%, or 1.8% dietary calcium. Vitamin D treatment when combined with a high level of dietary calcium resulted in an increase in plasma calcium from 6 mg/dl to greater than 10 mg/dl, a decrease in PTH mRNA of 65%, and a 6- to 8-fold increase in VDR mRNA. In another experiment in which no vitamin D source was given and the diets contained increasing levels of dietary calcium, plasma calcium increased significantly (5.5 vs. 7 mg/dl), while PTH mRNA decreased by 40% and VDR mRNA increased by 60%. Neither parathyroid gland weight nor total RNA was significantly affected. When chicks were repleted with 1,25-(OH)2D3, the increase in plasma calcium and VDR mRNA and the decrease in PTH mRNA were considerably more pronounced than those in the absence of the vitamin D source. Furthermore, in the presence of the hormone, parathyroid weight and total RNA decreased significantly with increasing concentrations of dietary calcium. When the chicks were repleted, respectively, with the two levels of 1,25-(OH)2D3, a marked positive interaction was evident between the hormone and dietary calcium in affecting levels of PTH and VDR mRNA. These results suggest that both 1,25-(OH)2D3 and calcium participate in the regulation of PTH and VDR gene transcription in the avian parathyroid gland. Whereas the action of 1,25-(OH)2D3 requires a minimal level of dietary calcium, calcium affects PTH and VDR gene transcription even in the absence of any vitamin D source.
Animals↗
Relationships between calbindin (Mr 28,000) and calcium transport by the eggshell gland.
1. Eggshell density (mg/cm2) and eggshell gland calbindin decreased in the aged hens. 2. Aged hens which laid eggs with a low shell weight and shell density had significantly lower intestinal and eggshell gland calbindin as compared with those which laid eggs with a high shell weight and shell density. 3. Significant correlations were found in aged hens between duodenal or eggshell calbindin and shell weight or shell density. 4. The results suggest that: (a) aged hens forming light shells absorbed calcium with a lower efficiency than those forming heavy shells or than young hens; (b) the decline in shell density in the aged hens is caused by a physiological calcium deficiency or by a defect in the hens' ability to alter calbindin synthesis in response to calcium needs; (c) in the aged hens, the deposition of calcium into the eggshell is dependent on, or at least associated with, eggshell gland calbindin.
Aging↗
Regulation of calbindin mRNA and calbindin turnover in intestine and shell gland of the chicken.
A synthetic oligonucleotide was used as a probe for measurement of calbindin mRNA in the shell gland and intestine of chickens. The half time of calbindin mRNA in the duodenum and shell gland was estimated at 2 and 3.6 h and that of calbindin at 13.9 and 32.6 h, respectively. The formation rates of calbindin mRNA were 0.37 and 0.17 pmol.h-1.g-1 and the rate of calbindin formation was 0.099 and 0.031 microgram.pmol mRNA-1.h-1 in the duodenum and shell gland, respectively. In the shell gland, calbindin mRNA and calbindin appeared at the time of sexual maturation during calcification of the first egg shell. Calbindin mRNA fluctuated markedly during the daily egg cycle, in close temporal association with egg shell calcification. When Ca2+ deposition was eliminated by expulsion of the ovum, the rise in calbindin mRNA was prevented. An indirect suppression of Ca2+ deposition by administration of the carbonic anhydrase inhibitor acetazolamide also resulted in a decrease in calbindin mRNA. The results are consistent with a possible role of Ca2+ flux in the regulation of calbindin mRNA appearance in the shell gland of chickens.
Animals↗
Modulation of quail intestinal and egg shell gland calbindin (Mr 28,000) gene expression by vitamin D3, 1,25-dihydroxyvitamin D3 and egg laying.
The effects of vitamin D3 sources, egg production and egg cycle on the genomic expression of calbindin (Mr 28,000) in the intestine and egg shell gland (ESG) of quail were characterized by Northern blot and solution hybridization, using synthetic oligonucleotide probe. In vitamin D3- or 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3)-fed quail, onset of egg production induced duodenal and ESG calbindin mRNA and calbindin synthesis. Duodenal calbindin mRNA was slightly higher during the period of shell calcification as compared with the period during which shells were not formed (ESG inactivity). ESG calbindin mRNA was markedly higher during the period of shell calcification than of ESG inactivity. Increasing dietary intake of [3H]1 alpha-hydroxyvitamin D3 increased the duodenal, but not ESG, content of 1,25-(OH)2D3 and calbindin. Duodenal calbindin and its mRNA were absent in vitamin D-deficient quail and were not affected by egg laying. ESG calbindin in the vitamin D-deficient quail was not affected by egg laying, but calbindin mRNA increased in the vitamin D-deficient birds during shell calcification. The results suggest that: (a) intestinal calbindin mRNA and calbindin are induced and/or regulated, either directly or indirectly, by 1,25-(OH)2D3; (b) intestinal calbindin and its mRNA are further induced at the onset of egg laying by an additional stimulator besides 1,25-(OH)2D3; (c) 1,25-(OH)2D3 is required for the expression of the latter stimulator; (d) ESG calbindin mRNA and calbindin are induced in egg-laying birds by a stimulator associated with the egg cycle; and (e) the induction of ESG calbindin mRNA does not need vitamin D metabolites, but 1,25-(OH)2D3 is required for the translation of the mRNA.
Animals↗
Modulation of chick intestinal and renal calbindin gene expression by dietary vitamin D3, 1,25-dihydroxyvitamin D3, calcium and phosphorus.
Synthetic oligonucleotide probes complementary to chick calbindin-28 kDa-mRNA were used to study the latter's regulation and relationship to calbindin in the chick. The effects of vitamin D3 sources and dietary alteration on the genomic expression were characterized by Northern blot and solution hybridization. Intestinal calbindin and its mRNA were almost absent in vitamin D-deficient chicks and were not affected by dietary alteration. Renal calbindin and its mRNA were lower in the vitamin D-deficient than in vitamin D3- or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-fed chicks. In the same animal, renal calbindin mRNA and calbindin were higher than intestinal. In vitamin D3-fed chicks, dietary calcium (Ca) or phosphorus (P) restriction induced, and high dietary Ca inhibited, intestinal calbindin and its mRNA synthesis. In the same chicks, dietary P restriction induced renal calbindin mRNA and calbindin synthesis. In 1,25-(OH)2D3-fed chicks, dietary P restriction induced and high dietary Ca inhibited the synthesis of intestinal and renal calbindin. The results suggest that: (a) most of the changes in renal and intestinal calbindin could be attributed to the changes in the mRNA; (b) the adaptation to dietary Ca and P alterations requires vitamin D metabolites; (c) high dietary Ca affects intestinal and renal calbindin-mRNA and calbindin via mechanisms independent of kidney 1-hydroxylase; and (d) plasma Ca and renal calbindin or its mRNA tend to change together in vitamin D-deficient or vitamin D3-fed, but not in 1,25(OH)2D3-fed chicks.
Animals↗
Differential regulation of calbindin-D28K mRNA in the intestine and eggshell gland of the laying hen.
The effect of shell calcification and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on calbindin-D28K (previously known as vitamin D-dependent calcium-binding protein) and calbindin mRNA was investigated in the intestine and eggshell gland (ESG) of juvenile female chicks, laying hens and non-laying female birds with active gonads. Increasing amounts of 1,25-(OH)2D3 were fed to laying hens and juvenile birds treated with oestradiol to develop the ESG. The intestinal concentration of calbindin was increased 30-fold by 1,25-(OH)2D3 in chicks treated with oestradiol and fed a vitamin D-deficient diet. In these same animals, 1,25-(OH)2D3 had no effect on the formation of calbindin mRNA or calbindin in the ESG even though fully viable 1,25-(OH)2D3 receptors are present in this tissue. In laying birds fed adequate amounts of vitamin D3, intestinal, but not ESG, calbindin was increased by the addition of 1,25-(OH)2D3 to the diet. At the onset of egg production the concentrations of calbindin and calbindin mRNA were increased in the intestine and ESG. This increase occurred within the period of calcification of the first egg, through a process unaffected by vitamin D. Calcification of the first egg increased the concentration of calbindin in the ESG by eight- to tenfold, although the concentration of calbindin mRNA was increased by only two- to threefold. These results suggest that the induction of calbindin synthesis by 1,25-(OH)2D3 or by the egg calcification process is associated with an increase in the concentration of calbindin mRNA in the ESG and intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Water-immersion-induced alterations of atrial natriuretic peptide, plasma renin activity, aldosterone and vasopressin in diabetic patients.
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Adult↗
[Current theories on the role of vitamin D in physiology and pathology. Therapeutic implications].
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Humans↗
[Insulin-like growth factors].
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Adipose Tissue↗
Egg shell quality and cholecalciferol metabolism in aged laying hens.
Calcium-binding protein D28K (calbindin) synthesis, vitamin D metabolism and shell quality were investigated in young and aged laying hens fed diets containing either cholecalciferol (CC) or its 1-hydroxylated derivatives. Duodenal calbindin concentration was similar in the young and in the aged laying hens. Exogenous 1-hydroxylated CC derivatives increased duodenal calbindin concentration, regardless of age. Shell weight and shell density (mg/cm2) were significantly lower (P less than 0.01) in the aged than in the young hens. Egg shell weight and density tended to decrease along the clutch. The rate of decline was higher in aged than in young hens. Feeding aged hens a diet containing 5 micrograms 1,25-dihydroxycholecalciferol [1,25(OH)2CC] or 1 alpha-hydroxycholecalciferol per kilogram improved shell quality, slowed down the progressive reduction in shell quality during the clutch and increased culling and mortality. The results indicate a) that the capacity for expression of 1,25(OH)2D3 in the intestine is not altered by age and b) that prolonged feeding of 1-hydroxylated derivatives of vitamin D3 improves shell quality in aged laying hens and increases culling and mortality.
25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
Use of 1 alpha-hydroxyvitamin D3 in prevention of bovine parturient paresis. 8. Maternal and neonatal plasma calcium, parathyroid hormone, and vitamin D metabolites concentrations.
Thirteen Israeli Friesian cows (3.71 average calvings) in the second or later lactation, fed a daily diet containing 90 g of Ca and 50 g of P, were injected once intramuscularly with 700 micrograms 1 alpha-hydroxy-vitamin D3 in order to investigate its placental transfer and its subsequent metabolism in the neonate. The injection of the vitamin 96 to 24 h before calving slightly increased plasma Ca at parturition, whereas uninjected controls displayed a prominent hypo-calcemia. On the 10th and 20th d after calving, difference in the plasma Ca concentration of the two groups was not significant. At parturition, plasma parathyroid hormone concentration was significantly higher and plasma 1,25-dihydroxyvitamin D lower in the control than in the treated cows. At parturition the plasma concentrations of Ca, parathyroid hormone, hydroxyproline, and 24,25-hydroxyvitamin D were higher in the calves than in their dams. Plasma concentrations of 25-hydroxyvitamin D were markedly higher and 1,25-hydroxyvitamin D was slightly higher in cows than in their offsprings.
Animals↗
[The significance of the injection site for the hypercalcemic effect of 1-alpha-hydroxyvitamin D3 in dairy cows].
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Animals↗
Efficacy of 1 alpha hydroxyvitamin D3 in the prevention of bovine parturient paresis.
One hundred and seventeen Israeli-Friesian cows from herds with a milk fever incidence of more than 15 per cent were injected intramuscularly with either 350 micrograms 1 alpha hydroxyvitamin D3 (1 alpha OHD3) in propylene glycol or with the vehicle alone, close to calving. If parturition had not occurred within 72 hours a second injection was administered; parturition was induced two days after the second injection if necessary. There were 10 cases of milk fever among 57 control cows as opposed to two cases among the 60 animals treated with 1 alpha OHD3. In an attempt to prolong the effect of the drug, Israeli-Friesian cows were injected intramuscularly with 350 micrograms 1 alpha OHD3 in either 10 ml propylene glycol or arachis oil. 1 alpha OHD3 in arachis oil did not prolong the effect of the drug. 1 alpha OHD3 in propylene glycol increased plasma calcium concentrations more rapidly than when the drug was administered in oil. Additional cows of the same breed and age were injected intramuscularly with 350 micrograms 1 alpha OHD3 in propylene glycol. Five of the animals received a second dose four days, and five received a second dose five days after the first injection. Five animals served as uninjected controls. The plasma calcium levels of the injected cows were significantly higher (P less than 0.01) than those of the controls from the second until the 14th day after the first injection. Based on these results 451 Israeli-Friesian cows from herds with a milk fever incidence of more than 15 per cent were injected intramuscularly with 1 alpha OHD3 close to calving.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Vitamin D metabolism and calbindin (calcium-binding protein) in aged laying hens.
Calbindin (calcium-binding protein) concentration, vitamin D metabolism and shell quality were investigated in young (7- to 9-mo-old) and aged (19- to 21-mo-old) laying hens consuming normal or low levels of calcium (Ca). Although egg weight and percent of cracked eggs were higher and egg production and shell density (mg/cm2) were lower (significantly, P less than 0.01) in aged hens, shell weight, plasma Ca and duodenal and egg shell gland calbindin were similar to those of young hens. Dietary Ca restriction reduced shell weight, shell density and structural bone and plasma Ca in both the young and aged birds. The production of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and its concentration in the plasma were higher in hens fed low dietary levels of Ca than in hens fed normal Ca levels only in the younger hens. However, a slightly higher production of 1,25(OH)2D3 and concentration of duodenal calbindin were also observed in severely Ca-restricted (1.4% Ca for 19 d) aged hens than in the younger hens. The results suggest that the aged hen loses its ability to adapt to changes in Ca intake or needs through mechanisms involving modulation of vitamin D metabolism.
25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗