SEKUNDARNI HIPERPARATIREOIDIZAM I KARDIO-RENALNI SINDROM TIP 4: ETIOPATOGENEZA, KLINIČKI ZNAČAJ I LEČENJE
Abstract
Uvod. Kardio-renalni sindrom je patofiziološki poremećaj funkcije srca i bubrega, gde akutni ili hronični poremećaj funkcije jednog organa podstiče akutni ili hronični poremećaj funkcije drugog organa. U kardio-renalnom sindromu tip 4 (hronični reno-kardijalni sindrom) nedostatak vitamina D i sekundarni hiperparatireoidizam dovode do poremećaja funkcije srca i bubrega. Cilj. Rad je imao za cilj da analizira faktore rizika, patogenetske mehanizme razvoja sekundarnog hiperparatireoidizma, kliničke posledice i da ukaže na klinički značaj njegovog ranog otkrivanja i pravovremenog lečenja. Metod. Analizirani su stručni radovi i kliničke studije koje se bave etiopatogenezom, dijagnostikom i lečenjem sekundarnog hiperparatireoidizma. Rezultati. U hroničnoj bolesti bubrega (stadijum 2 i 3) uključuju se mehanizmi adaptacije, povećava se koncentracija FGF-23 i parathormona u serumu. Ovi hormoni povećavaju frakcionu ekskreciju fosfata na nivou bubrega, a parathormon oslobađa kalcijum iz koštanog tkiva i na taj način održavaju koncentraciju kalcijuma i fosfata u serumu u normalnom rasponu. Gubitak sposobnosti bubrega da stvara aktivni metablit vitamina D i izlučuje fosfat iz organizma značajno doprinosi razvoju i napredovanju kardio-renalnog sindroma tip 4. Glavne kliničke posledice sekundarnog hiperparatiroeidizma su koštana bolest ubrzanog prometa, vaskularne i valvularne kalcifikacije i razvoj bolesti srca. Savremeno lečenje uključuje primenu: vezača fosfata koji ne sadrže kalcijum, novih analoga vitamina D i primenu kalcimimetika. Zaključak. Rana dijagnostika i optimalna kontrola sekundarnog hiperparatireoidizma sprečavaju progresiju hronične bolesti bubrega, ravoj kardiovaskularnih bolesti, smanjuju stopu kardiovaskularnog morbiditeta i mortaliteta i popravljaju kvalitet života ovih bolesnika.
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