The value of shoe size for prediction of the timing of the pubertal growth spurt.

Background: Knowing the timing of the pubertal growth spurt of the spine, represented by sitting height, is essential for the prognosis and therapy of adolescent idiopathic scoliosis. There are several indicators that reflect growth or remaining growth of the patient. For example, distal body parts have their growth spurt earlier in adolescence, and therefore the growth of the foot can be an early indicator for the growth spurt of sitting height. Shoe size is a good alternative for foot length, since patients can remember when they bought new shoes and what size these shoes were. Therefore the clinician already has access to some longitudinal data at the first visit of the patient to the outpatient clinic.The aim of this study was to describe the increase in shoe size during adolescence and to determine whether the timing of the peak increase could be an early indicator for the timing of the peak growth velocity of sitting height.Methods: Data concerning shoe sizes of girls and boys were acquired from two large shoe shops from 1991 to 2008. The longitudinal series of 242 girls and 104 boys were analysed for the age of the peak increase in shoe size, as well as the age of cessation of foot growth based on shoe size.Results: The average peak increase in shoe size occurred at 10.4 years (SD 1.1) in girls and 11.5 years (SD 1.5) in boys. This was on average 1.3 years earlier than the average peak growth velocity of sitting height in girls, and 2.5 years earlier in boys. The increase in shoe size diminishes when the average peak growth velocity of sitting height takes place at respectively 12.0 (SD 0.8) years in girls, and 13.7 (SD 1.0) years in boys.Conclusions: Present data suggest that the course of the shoe size of children visiting the outpatient clinic can be a useful first tool for predicting the timing of the pubertal growth spurt of sitting height, as a representative for spinal length.This claim needs verification by direct comparison of individual shoe size and sitting height data and than a step forward can be made in clinical decision making regarding adolescent idiopathic scoliosis. © 2011 Busscher et al; licensee BioMed Central Ltd

Prognostic value of the short-term antiproteinuric response to ACE inhibition for prediction of GFR decline in patients with nondiabetic renal disease

In chronic renal disease, the severity of proteinuria is associated with the rate of renal function loss. Proteinuria, therefore, was postulated to play a role in the final common pathway of chronic renal function loss. If so, reduction of proteinuria would improve long-term renal outcome. Improvement of long-term renal function outcome has been obtained in several intervention trials; in these studies, regimens providing better renoprotection were associated with more effective reduction of poteinuria than control regimens. As the reduction of proteinuria is mostly associated with a fall in blood pressure, however, it is difficult to delineate the respective roles of the lowering of blood pressure and of proteinuria. Interestingly, the initial reduction of proteinuria (but not of blood pressure) by antihypertensive treatment appears to predict long-term renal outcome in man as well as in experimental renal disease. This suggests that an intervention strategy aimed not only at the normalization of blood pressure, but also specifically at elimination of proteinuria, might be able to improve longterm renal outcome in proteinuric patients. If so, this would provide further evidence in support of the hypothesis that proteinuria is causally involved in the progression of long-term renal function loss

ACE inhibition preserves heparan sulfate proteoglycans in the glomerular basement membrane of rats with established adriamycin nephropathy.

Item does not contain fulltextThe gradual onset of the antiproteinuric effects of ACE inhibition suggests that structural effects on the glomerular basement membrane (GBM) may be involved in their renoprotective action. To test this hypothesis, we studied the effects of lisinopril (5 mg/kg/24 h) on proteinuria, focal glomerulosclerosis (FGS) and glomerular heparan sulfate (HS) proteoglycan (HSPG) GBM staining in rats with established Adriamycin nephrosis. Treatment was started 6 weeks after disease induction. As expected, lisinopril reduced blood pressure, proteinuria and the FGS score. In control rats, Adriamycin nephrosis was associated with significantly impaired GBM staining for both HSPG core protein (assessed from BL-31 staining) and HS staining (assessed from JM-403 staining) 12 weeks after disease induction. In rats treated with lisinopril (5 mg/kg/24 h) GBM staining was significantly better preserved for HS as well as for HSPG core protein. These data suggest that structural effects on the GBM, improving glomerular permselectivity, may be involved in the renoprotective effects of ACE inhibition in proteinuria-induced renal damage