Progression of secondary hyperparathyroidism involves deregulation of genes related to DNA and RNA stability.

摘要: Progression of secondary hyperparathyroidism involves deregulation genes related to DNA and RNA stability. Background Renal in its late stages becomes autonomous, so excessive parathyroid hormone (PTH) secretion no longer responds physiologic stimuli or aggressive medical treatment. Methods To gain molecular understanding progression renal hyperparathyroidism, normal hyperplastic tissue with diffuse nodular growth were analyzed. The results also compared adenomas. analysis was performed by high-density oligonucleotide microarray bidirectional subtraction library. Results Analysis the arrays found 16 overexpressed 132 repressed nodules while library produced 34 40 genes. differentially expressed between samples included some stability repair ( TALDO1 , PRDX2 DDB1 XRCC1 POLB ), degradation OASL AUF1 protein synthesis processing PFDN5 HSPD1 NACA cell CDC25C GRPR tumorigenesis cycle VIL2 TPD52 ). Conclusion According function described for deregulated genes, when autonomous refractory treatment, may be increased integrity compromised. These two mechanisms, combined differentiation show complex pathway glands' evolution explain large amount cytogenetic aberrations hyperparathyroidism. Considering that altered expression hyperplasia lead irreversible consequences genomic cells, an adequate early management chronic kidney disease mandatory.