Childhood renal osteodystrophy

Chronic renal insufficiency is characterized by profound alterations in the orderly metabolic sequences which normally guarantee cellular integrity and metabolic homeostasis. Hormonal imbalances which contribute to these acquired defects include abnormal growth hormone secretory patterns, elevations in plasma aldosterone and glucagon, decreases in testosterone and thyroid hormone, and defective biological degradation of Cortisol, insulin, and parathyroid hormone. These findings are often coupled with blunted end-organ responsivity to hormonal stimulation, e.g., insulin, and contribute to the disturbances in carbohydrate and lipid metabolism and to defective synthesis and catabolism of structural and enzymatic proteins. The normal kidney functions as a biological filter by regulating the excretion of a variety of substances, normally generated by either biological synthetic or degradative reactions. These products can function as metabolic “toxins” when retained by the body in sufficient quantities.The kidney also occupies a pivotal role in the regulation of calcium, inorganic phosphate, parathyroid hormone, calcitonin, and vitamin D metabolism. Adults and children with progressive loss of renal parenchyma sustain derangements in mineral and bone metabolism with resultant osteodystrophy. Children experience abnormalities in growth and remodeling of bone as well. These changes may progress to a renal osteodystrophy characterized by growth retardation and bone pain. Hyperparathyroidism and deficiency in biological activation of vitamin D are the basic pathophysiologic mechanisms involved. The requirement of vitamin D or its biologically more active forms is increased. In this review, normal bone development is described as a basis for interpreting the pathophysiology of renal osteodystrophy in children. Because renal osteodystrophy is often termed “renal rickets” and the processes of osteodystrophy and rickets differ, the evolution of the histological changes of each are contrasted. Some of the ways renal osteodystrophy affects growth are explained by the evolution of these processes.The unique features of childhood renal osteodystrophy relate to distinctions between the effects uremia has on the fully grown skeleton and growing bone. Understanding the development of bone is important to the understanding of bone disease and growth retardation which occurs in children with uremia