The session highlights the long-term skeletal effects of kidney disease

“Our goal as a pediatrician is to optimize health development as patients move into adulthood,” said Mary B. Leonard, professor and chairman of the Department of Pediatrics, Stanford University School of Medicine. .. According to Leonard, there may be certain periods between the growth and development of a child in which the skeleton and vascular system are uniquely vulnerable to the effects of CKD.

Peak bone mass is a lifelong determinant of skeletal health and can serve as a marker of the effects of certain conditions on the skeleton. On the other hand, sex hormones play an important role in bone structure. For example, having a boy with high peak bone mass does not mean that he is dense, but that he is actually big, Leonard explained.

According to one study, healthy children had significantly higher parathyroid hormone (PTH) levels and 125 significantly higher during the period of fastest growth and bone development. [vitamin] Although it is in the normal range, it is D level. This is independent of calcium intake and reflects a response to increased calcium needs during bone development, Leonard said.

In another study, researchers followed children who started renal replacement therapy before the age of 14. More than 250 adults were included in the study, and participants eventually reported a serious musculoskeletal morbidity. In adulthood, 37% reported clinical bone disease, 26% reported malformations, 13% reported sterile osteonecrosis, and 7% developed severe disability bone disease. Overall, clinical bone disease was more pronounced in people with long periods of renal replacement therapy, those who started renal replacement therapy early in history, and those with a history of severe hyperparathyroidism.

Yet another study showed that low glomerular filtration rate and high PTH were associated with fractures in children with CKD. The study also showed “a very strong signal of phosphorus adsorbents with a 63% reduction in fracture rate,” regardless of phosphorus levels or fibroblast growth factor 23 levels. About 20% of children used binders at any time during the study, and most of these binders contained calcium.

“Our hypothesis is that these are observational data and we cannot infer the cause and effect, but they are suggestions that potentially speak to the calcium demand of the growing skeleton,” Leonard said.

Abnormal mineral metabolism, muscle loss, lack of physical activity, inflammation, and delayed maturation are all potential threats to long-term bone quality from childhood CKD. Limited data also suggest that even after kidney transplantation, the loss of periosteal diastolic dysfunction during growth is irreversible, despite recovery of muscle mass and improved metabolic parameters.

Prospective clinical trials need to be conducted to identify strategies for promoting bone structure growth and optimizing bone mineralization. “We need to know how to do this without exacerbating vascular calcification, which can vary depending on the stage of growth and development,” Leonard concludes.

Apart from the long-term effects of CKD on the skeleton, Michelle Denberg, MD, a doctor in charge of nephrology and a cancer survival program at the Philadelphia Children’s Hospital, has found that glomerular disease is skeletal throughout an individual’s life. We reviewed the impact. course.

“Because 90% of peak bone mass is established by age 18, threats to bone development in childhood and adolescence can have significant lifelong implications,” said Denberg. Related factors that affect bone structure and metabolism. “

Changes in vitamin D homeostasis, varying degrees of systemic inflammation, and exposure to toxic drugs can all contribute to the bone health of this population.

In particular, “Glucocorticoid treatment is frequently used in patients with carriers, and the disease is the most common cause of secondary osteoporosis,” explained Denberg. Other drugs, such as calcineurin inhibitors such as cyclosporine and tacrolimus, “have been shown to induce dose- and duration-dependent bone loss by increasing osteoclast formation.”

Even in remission, studies have shown that vitamin D deficiency is very prevalent among people with glomerular disease. However, supplements can protect people with normal and impaired kidney function.

In the future, mechanistic studies that leverage advances in high-resolution bone imaging and bone biopsy techniques may help better characterize mineral and bone disorders among people with glomerular disease. Hmm. Studies also need to investigate the effects of inflammation and immunodysregulation on bone health, as well as the effects of concomitant drug exposure and interventions to reduce skeletal morbidity in this population.