Monitoring the growth dynamics of somatic traits based on a semi-longitudinal study.

Possibilities of conducting longitudinal human growth studies are very limited, since it is necessary to monitor the probands for a long time. Another problem can be a loss of data currency, and the small size of the final sample. The solution can be a follow-up semi-longitudinal observation. This research is drawn up as a short longitudinal monitoring of 1925 children (990 boys, 935 girls), aged 6-15 years, at 20 elementary schools in four regions of the Czech Republic, which has been conducted at the same time. Data of repeatedly examined probands of a wide age range were acquired in a short time period. With the help of a linear regression model with mixed effect, the growth velocity curves of 12 somatic traits have been obtained. The timing, intensity and duration of separate growth spurts have been observed, as well as the mutual location of both points of growth velocity, local maxima and minima, and points of the maximal acceleration and deceleration. The results demonstrate that the velocity of characters with variable growth dynamics (skin-fold thicknesses, circumferences of limbs) - contrary to characters with regular growth velocity - have a higher number of partial growth spurts and an opposite course. In the period of separate growth velocity, peaks of somatic characters with regular growth dynamics reach points of partial local minima. In comparison to previous longitudinal studies of body height growth dynamics, the shift of both the beginning and the peak of boys' and girls' pubertal spurt, to a lower age can be found.

Decreased urinary kallikrein with hyperglycemia in patients with short-term insulin-dependent diabetes mellitus.

The aim of the study was to evaluate the role of urinary kallikrein in the regulation of renal hemodynamics and sodium handling in insulin-dependent diabetes mellitus (IDDM), and to test the effect of acutely induced hyperglycemia. Urinary kallikrein excretion was evaluated (1) under basal conditions and after stimulation with i.v. furosemide (0.5 mg x kg(-1)), (2) during glycemic clamp-induced eu- and hyperglycemia (5 and 12 mmol/L) and, (3) during time-controlled euglycemia in 21 short-term IDDM patients without microalbuminuria and in 18 weight-, age- and gender-matched healthy controls. Sodium excretion and renal hemodynamics using the clearances of inulin and para-amino-hippuric acid were measured during examinations in both groups. The baseline urinary kallikrein excretion during clamp-induced euglycemia was comparable in diabetic and control subjects (10.89+/-5.98 versus 10.38+/-3.73 mUE x min(-1)), whereas it was decreased in the baseline for furosemide (5.77+/-3.22 versus 10.9+/-3.7 mUE x min(-1); p < 0.01) and even after furosemide administration (12.0+/-1.6 versus 21.3+/-2.0 mUE x min(-1); p < 0.01) while the patients were hyperglycemic. During intravenous dextrose-induced hyperglycemia, the urinary kallikrein excretion significantly declined in diabetic patients (10.89+/-5.98 versus 5.45+/-0.88 mUE x min(-1); p < 0.01), whereas it did not change in controls (10.38+/-3.73 versus 12.55+/-5.47 mUE x min(-1)). A decrease in the fractional excretion of sodium and an attenuated rise in natriuresis after furosemide administration have been found in diabetic compared to control subjects. There were no significant relationships between kallikrein excretion and (1) renal hemodynamics, which was comparable in both groups, or (2) plasma renin activity, plasma and urine aldosterone and cortisol. We conclude that short-term IDDM without renal hemodynamic alterations is associated with decreased basal and furosemide-stimulated kallikrein excretion, which is directly related to the blood glucose level. The decreased activity of the renal kallikrein-kinin system might be involved in the increased tendency to sodium retention in diabetic patients.

[Renal hemodynamics and its regulation in recently diagnosed type 1 diabetes mellitus (insulin-dependent diabetes mellitus). The effect of hyperglycemia]. / Renální hemodynamika a její regulace u nove zjistených diabetiku 1. typu (inzulin-dependentní diabetes mellitus). Vliv akutní hyperglykémie.

BACKGROUND: The changes in renal haemodynamics are considered to be one of the pathophysiological mechanisms of the development of diabetic nephropathy. The aim of the study was to evaluate the renal haemodynamics and its regulation in insulin-dependent diabetes mellitus (IDDM) during glycemic clamp-induced eu- and hyperglycaemia (5 and 12 mmol/l), and to test the hormonal vasoactive systems after stimulation with furosemide. METHODS AND RESULTS: Renal haemodynamics using the clearances of inulin and paraaminophippuric acid during eu-hyperglycaemic clamp and furosemide test were performed in 21 short-term IDDM patients without microalbuminuria (DM) and in 18 weight-, age- and sex-matched healthy controls (K). The glomerular filtration rate and effective renal plasma flow were comparable in IDDM and C and were not affected by hyperglycaemia. Compared to C diabetics had lowered fractional excretion of sodium (1.41 +/- 0.68 vs 2.23 +/- 0.67%; p < 0.01), which did not change during hyperglycaemia, and lowered furosemide stimulated natriuresis (1242 +/- 339 vs 1606 +/- 340 mumol/min; p < 0.01). Hyperglycaemia resulted in comparable fall in fractional excretion of potassium in both groups (p < 0.001). Decreased basal (5.77 +/- 3.22 vs 10.9 +/- 3.7 mEU/min; p < 0.05) and furosemide-stimulated (12.0 +/- 1.6 vs 21.3 +/- 2.0 mEU/min; p < 0.01) urinary kallikrein has been found in diabetic compared to control subjects. During clamp-induced euglycaemia, kallikrein excretion was comparable in diabetic and control subjects (10.89 +/- 5.98 vs 10.38 +/- 3.73 mEU/min) and significantly declined during intravenous dextrose-induced hyperglycaemia in diabetics (p < 0.01), while it did not change in controls. There were no differences and no changes in plasma renin activity, plasma and urine aldosterone and cortisol in IDDM and C. CONCLUSIONS: The short-term IDDM without renal haemodynamic alterations is associated with the tendency to sodium retention and decreased basal and furosemide-stimulated kallikrein excretion, which is directly related to the blood glucose level. Acutely-induced hyperglycaemia decreases fractional excretion of potassium, which cannot be explained by the changes of evaluated hormonal systems.