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Biomedical subjects

P Rødbro

Publications and source records attributed to P Rødbro.

63 records · Page 4Linked to original sources
PubMed1979

Microvascular permeability to albumin and glomerular filtration rate in diabetic and normal children.

In order to examine the permeability of microvessels in diabetic children, the glomerular filtration rate, urinary excretion rates of albumin and beta 2-microglobulin, intravascular mass of albumin, and transcapillary escape rate of albumin were studied in 26 diabetic children without clinical signs of microangiopathy (age: 7-14 years; duration of disease: 3-14 years). Similar measurements were made in 28 healthy school children (age: 8-14 years). Mean glomerular filtration rate in the diabetic children was higher than in the normal children (138 versus 109 ml/min per 1.73 m2, p less than 0.01). Urinary excretion rates of albumin and beta 2-microglobulin did not differ in diabetics. Mean intravascular albumin mass in the diabetic girls (1.64 g/kg body weight) was lower (p less than 0.01) than in the diabetic boys (1.89 g/kg body weight) and also lower (p less than 0.02) than in the normal girls (1.94 g/kg body weight). Mean transcapillary escape rate of albumin in the twenty diabetics with duration of diabetes less than 10 years (7.14%/h) was lower (p less than 0.01) than that in normal children (8.90%/h); the escape rate showed a positive correlation with duration of diabetes (r=0.47; p less than 0.02). Thus glomerular filtration rate in diabetic children is elevated to the same extent as in adult short-term juvenile diabetics while the permeability of the glomerular membrane to macromolecules is normal. Interpretation of the results on intravascular albumin mass and transcapillary escape rate of albumin requires further investigation.

Adolescent↗
PubMed1979

Effect of puberty on rates of bone growth and mineralisation: with observations in male delayed puberty.

The bone mineral content (BMC) and body height were measured in 301 normal children and adolescents aged 7--20 years, and in 8 boys with constitutional delayed puberty aged 14--17 years. Serum testosterone was measured in the last group as well as in a subpopulation of the normal children and adolescents. The growth spurt, which coincided with a steep increase of serum testosterone in boys, indicated a great change in skeletal growth and mineralisation in both sexes. After the growth spurt, linear growth slowed down considerably while bone mineralisation rose steeply. When low levels of serum testosterone were maintained, as in delayed puberty, these combined changes of skeletal growth and mineralisation did not occur. It is suggested that gonadal hormones are the true initiators of the short-lived growth spurt as well as of prolonged acceleration of bone mineralisation.

Adolescent↗
PubMed1978

Deterioration of renal function during treatment of chronic renal failure with 1,25-dihydroxycholecalciferol.

A controlled study of the effects of the potent vitamin-D metabolite, 1, 25-dihydroxycholecalciferol (1,25[OH]2D3), and vitamin D3 was done in 18 non-dialysed patients with chronic renal failure (C.R.F.). Patients with a creatinine clearance below 35 ml/min and mild renal osteodystrophy were selected. After 6 months' observation of the spontaneous course the patients were randomly allocated to 6 months' oral treatment with either 1, 25 (OH)2D3 or vitamin D3 in initial daily doses of 1microgram and 4000 I.U., respectively, combined with 0.5 g calcium. 1,25(OH)2D3 quickly corrected hypocalcaemia, reduced serum-alkaline-phosphatases and serum-immunoreactive-parathyroid-hormone, and more than doubled the urinary excretion rate of calcium. D3 had similar, but less pronounced effects. 7 out of 8 patients on 1,25(OH)2D3, developed hypercalcaemia which necessitated a reduction in dosage. None of the patients on D3 treatment developed hypercalcaemia. The percentage fall in creatinine clearance was greater during treatment than before treatment in all patients on 1, 25 (OH)2D3 (P less than 0.01) and in 7 of 9 patients on vitamin D3 treatment (though the group change here was not significant). Deterioration of renal function is a major limitation of the clinical use of 1, 25(OH)2D3 and D3 in non-dialysed patients with C.R.F. In fact, the decrased formation of 1, 25(OH)2D3 seen in C.R.F. might protect renal function at the expense of abnormalities in mineral metabolism.

Administration, Oral↗
PubMed1978

Bone mineral loss during maintenance hemodialysis.

With the aim of investigating bone mineral loss during maintenance hemodialysis (MDH), bone mineral content (BMC) was measured by means of two-dimensional scanning photon absorptiometry in 47 chronic renal failure patients on MDH: 13 females (age range 22-50 years, mean dialysis duration 189 days) and 34 males (age range 23-69 years, mean dialysis duration 449 days). Measurements were carried out in most patients three times at an interval of 6 months. Initial mean BMC values were for both sexes significantly lower than normal, but did not correlate to duration of MHD. The longitudinal measurements demonstrated a highly significant decrease in BMC with time: the mean BMC values after 6 and 12 months, respectively, were for females 95.8 and 93.4% and for males 97.3 and 94.4% of the initial values with no significant differences between sexes. The fall in BMC did not correlate to duration of MHD, initial BMC value, or age. In some of the patients a substantial loss of BMC was observed, and it is suggested that these patients in particular may develop server bone disease. A BMC method with high precision is mandatory for selection of such patients.

Absorption↗
PubMedDate not supplied

Long-term bone loss in insulin-dependent diabetic patients with microvascular complications.

Insulin-dependent diabetic patients have an approximately 10% decreased bone mineral content (BMC) when they are studied a few years after clinical onset of diabetes. After that time, patients without diabetic microvascular complications have no, or only very little, further bone loss. The aim of the present study was to investigate if any substantial long-term bone loss occurs in diabetic patients with microvascular complications. We studied 19 insulin-dependent diabetic patients with neither physiologic nor pathologic conditions known to interfere with bone metabolism, other than diabetes. BMC was determined twice, with an interval of 11 years. At initial examination, no patient had diabetic microangiopathy, but at final examination 7 patients had developed diabetic microvascular complications while 12 patients had not. As compared with gender- and age-matched controls, both subgroups had significantly decreased BMC at the initial examination. During the study period, the patients with complications showed further bone loss, whereas the subgroup without complications had unchanged decreased BMC. At final examination, BMC was significantly lower in patients with microvascular complications than in patients without them. The biochemistry of bone metabolism showed a significantly increased fasting urinary excretion of calcium and hydroxyproline in patients with complications, but not in the group without complications, and there was a negative correlation between plasma BGP (osteocalcin) and hemoglobin A1C for all patients. These findings indicate that, in addition to a decreased BMC (before or shortly after clinical onset of diabetes), patients who develop microvascular complications also develop ongoing bone loss. This loss may be caused by an increased bone resorption, but decreased bone formation during periods of poor diabetic control may be involved as well.

Adult↗