Fisiopatologia do hiperparatireoidismo secundário renal em cães - revisão de literatura
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Data
2022-01-19
Autores
Morethson, Juliette Garcia
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
O hiperparatireoidismo secundário renal (HPTr) é uma afecção multifatorial que ocorre frequentemente em pacientes doentes renais crônicos. A redução nas taxas de filtração glomerular e perda progressiva dos néfrons levam a hiperfosfatemia, aumento de FGF-23 e redução na síntese de vitamina D. Esses estímulos persistentes ocasionam a hiperplasia da glândula paratireoide, havendo aumento na produção do paratormônio, um dos principais responsáveis pela homeostase de cálcio e fósforo no organismo. As repercussões do HPTr são sistêmicas e incluem alterações ósseas e minerais relacionadas ao DRC havendo, entre outras consequências, a mineralização de tecidos moles e osteodistrofia fibrosa. Essa revisão tem como foco descrever a fisiopatologia do Hiperparatireoidismo Secundário Renal, bem como suas consequências nos cães acometidos.
Renal Secondary Hyperparathyroidism (rSHPT) is a multifactorial affliction that frequently occurs in chronic kidney disease patients. The reduction of glomerular filtration rates and progressive loss of nephrons leads to hyperphosphatemia, increase in FGF-23 and reduction of the synthesis of vitamin D. These persistent stimuli cause parathyroid gland hyperplasia, with increased parathormone production, one of the main responsibles for calcium and phosphorus homeostasis in the organism. The repercussions of rSHPT are systemic and include bone and mineral alterations related to CKD with, amongst other consequences, the mineralization of soft tissues and fibrous osteodystrophy. This review focuses on describing the physiopathology of Renal Secondary Hyperparathyroidism, as well as understanding its consequences in afflicted dogs.
Renal Secondary Hyperparathyroidism (rSHPT) is a multifactorial affliction that frequently occurs in chronic kidney disease patients. The reduction of glomerular filtration rates and progressive loss of nephrons leads to hyperphosphatemia, increase in FGF-23 and reduction of the synthesis of vitamin D. These persistent stimuli cause parathyroid gland hyperplasia, with increased parathormone production, one of the main responsibles for calcium and phosphorus homeostasis in the organism. The repercussions of rSHPT are systemic and include bone and mineral alterations related to CKD with, amongst other consequences, the mineralization of soft tissues and fibrous osteodystrophy. This review focuses on describing the physiopathology of Renal Secondary Hyperparathyroidism, as well as understanding its consequences in afflicted dogs.
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Palavras-chave
DRC, FGF-23, PTH, Calcitriol, CKD