Secondary hyperparathyroidism and cardiorenal syndrome type IV: Etiopathogenesis, clinical significance and treatment

Labudović, Tatjana; Nedeljković, Branislava; Petrović, Dejan; Poskurica, Mileta

doi:10.5937/mckg48-4232

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Medicinski časopis

2014, vol. 48, br. 2, str. 76-84

Sekundarni hiperparatireoidizam i kardiorenalni sindrom tip 4 - etiopatogeneza, klinički značaj i lečenje

Labudović Tatjana^a, Nedeljković Branislava^b, Petrović Dejan^a

, Poskurica Mileta^a

^aKlinički centar Kragujevac, Klinika za urologiju, nefrologiju i dijalizu, Srbija + Univerzitet u Kragujevcu, Fakultet medicinskih nauka, Srbija
^bKlinički centar Kragujevac, Klinika za urologiju, nefrologiju i dijalizu, Srbija

e-adresa: tanjalab@gmail.com

Projekat:

Analiza strukture troškova i uticaja na zdravstveni budžet Republike Srbije epidemiološki najmasovnijih i/ili najskupljih oboljenja i procena odnosa troškovi / efektivnost / korisnost medicinskih intervencija (MPNTR - 175014)

Ključne reči: hiperparatireoidizam; sekundarni; kardiorenalni sindrom; terapija

Sažetak

Kardiorenalni 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 kardiorenalnom sindromu tip 4 (hronični renokardijalni sindrom) nedostatak vitamina D i sekundarni hiperparatireoidizam dovode do poremećaja funkcije srca i bubrega. Rad je imao za cilj da analizira faktore rizika, patogenetske mehanizme razvoja sekundarnog hiperparatireoidizma i kliničke posledice i da ukaže na klinički značaj njegovog ranog otkrivanja i pravovremenog lečenja. Analizirani su stručni radovi i kliničke studije koje se bave etiopatogenezom, dijagnostikom i lečenjem sekundarnog hiperparatireoidizma. Kod hronične 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 tako 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 kardiorenalnog sindroma tip 4. Glavne kliničke posledice sekundarnog hiperparatiroeidizma jesu koštana bolest ubrzanog prometa, vaskularne i valvularne kalcifikacije i razvoj bolesti srca. Savremeno lečenje uključuje primenu vezivača fosfata koji ne sadrže kalcijum, novih analoga vitamina D i primenu kalcimimetika. Rana dijagnostika i optimalna kontrola sekundarnog hiperparatireoidizma sprečavaju progresiju hronične bolesti bubrega, razvoj kardiovaskularnih bolesti, smanjuju stopu kardiovaskularnog morbiditeta i mortaliteta i popravljaju kvalitet života ovih bolesnika.

Abstract

Cardiorenal syndrome is a psychophysical disorder of the functions of the heart and kidneys, where the acute or chronic disorder of the functioning of one organ causes the acute or chronic disorder of the functioning of the other organ. In the type 4 of the cardiorenal syndrome (chronic renocardial syndrome), the deficiency of the vitamin D and the secondary hyperparathyroidism cause a disorder of the functioning of the heart and kidneys. The goal of this work is to analyze the risk factors, pathogenetic mechanisms of the development of the secondary hyperparathyroidism and to point out the clinical importance of its early detection and timely treatment. Works written by experts have been examined, as well as the clinical studies researching etiopathogenesis, diagnostics and treatment of secondary hyperparathyroidism. In the chronic kidney disease (stadiums 2 and 3), adaptation mechanisms are activated, while the concentration of FGF-23 and the concentration of parathyroid in the serum both increase. These hormones increase the fractional excretion of the phosphates within the kidney, while parathyroid releases the calcium from the bone tissue, therefore maintaining the concentration of calcium and phosphates in the serum within the normal range. The kidneys' loss of ability to create active vitamin D metabolites and excrete phosphate out of the organism significantly contributes to the development and progress of type 4 cardiorenal syndrome. The main clinical consequences of the secondary hyperparathyroidism are the high turnover bone disease, vascular and valvular calcification and the development of heart diseases. Modern treatment includes the use of phosphate binders that not contain calcium, new vitamin D metabolites and the use of calcimimetics. The early diagnosis and optimal control of secondary hyperparathyroidism prevent the progress of the chronic kidney disease and the development of cardiovascular diseases, reduce the rate of cardiovascular morbidity and mortality and improve the patients' quality of life.

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O članku

jezik rada: srpski
vrsta rada: pregledni članak
DOI: 10.5937/mckg48-4232
objavljen u SCIndeksu: 10.10.2014.

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