Alterations In Hormonal Responses Research Articles

Growth in children on renal replacement therapy: a shrinking problem?

Growth failure has been almost inextricably linked with chronic kidney disease (CKD) and end-stage renal disease (ESRD) since initial reports of renal dwarfism dating back to the turn of the twentieth century. Growth failure in CKD has been associated with both increased morbidity and mortality. Growth failure in the setting of kidney disease is multifactorial and is related to poor nutritional status as well as comorbidities, such as anemia, bone and mineral disorders, and alterations in hormonal responses, as well as to aspects of treatment such as steroid exposure. In this issue of Pediatric Nephrology, Franke et al. report on the gains made in growth and maturation in pediatric patients with ESRD in recent decades, particularly in Germany. Through advances in the care of CKD and ESRD over recent decades, the prevalence of growth failure appears to be decreasing. These findings, along with a recent report demonstrating decreases in mortality in childhood ESRD in the United States Renal Data System (USRDS), suggest overall improvements in the outcomes of care, perhaps reflecting improvements in the quality of care for children with kidney disease worldwide.

Growth Retardation in Children with Kidney Disease

Growth failure is almost inextricably linked with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Growth failure in CKD has been associated with both increased morbidity and mortality. Growth failure in the setting of kidney disease is multifactorial and is related to poor nutritional status as well as comorbidities, such as anemia, bone and mineral disorders, and alterations in hormonal responses, as well as to aspects of treatment such as steroid exposure. This review covers updated management of growth failure in these children including adequate nutrition, treatment of metabolic alterations, and early administration of recombinant human growth hormone (GH).

Resistance exercise‐induced hormonal response under the influence of delayed onset muscle soreness in men and boys

It was hypothesized that exercise-induced muscle damage (EIMD)-related alterations in hormonal responses could be observed if a second exercise bout is performed soon after an identical unaccustomed bout leading to delayed onset muscle soreness (DOMS). Eight men (31 ± 7 years) and eight boys (14 ± 0 years) performed two exercise bouts (E1 and E2, with 48 h rest in between) consisting of three sets of bilateral knee extensions until exhaustion with 40% load. No differences between the groups or bouts were observed in the number of repetitions performed and maximal isometric force decline, or between groups in serum creatine kinase activity and DOMS. Decreased peak epinephrine (EPI) (-38%), growth hormone (GH) (-45%) and cortisol (COR) (-31%) concentrations were found in E2 in men (P<0.05). In men, the peak GH concentration was also lower in E2 and COR was higher in both bouts than in boys. No changes in norepinephrine and testosterone responses were found in either group. The results suggest that in men, the responses of EPI, GH and COR are attenuated when the second bout is performed under the influence of DOMS. In boys, the lack of this attenuation may not be explained by less severe EIMD.

Gap Junctional Intercellular Communication Contributes to Hormonal Responsiveness in Osteoblastic Networks

To evaluate whether intercellular coupling via connexin43 gap junction channels modulates hormonal responsiveness of cells in contact, we have created osteoblastic cell lines deficient in connexin43. Osteoblastic ROS 17/2.8 cells were transfected with a plasmid containing an antisense cDNA construct to rat connexin43. Control transfection did not alter cell-to-cell coupling nor connexin43 mRNA or protein expression relative to nontransfected ROS 17/2.8 cells. In contrast, stable transfection with an antisense connexin43 cDNA resulted in two clones, RCx4 and RCx16, which displayed significant decreases in connexin43 mRNA and protein expression and were dramatically deficient in cell-to-cell coupling. Phenotypically, all transfectants retained osteoblastic characteristics. However, cells rendered connexin43-deficient through antisense transfection displayed a dramatic attenuation in the cAMP response to parathyroid hormone. Alterations in hormonal responses were not due to changes in parathyroid hormone receptor number or binding kinetics nor to alterations in adenylyl cyclase activity. These results indicate that gap junctions may be required for mediating hormonal signals. Furthermore, these experiments support a regulatory role for connexin43-mediated intercellular communication in the modulation of hormonal responses within elaborately networked bone cells.