Differences in associated factors between aortic and mitral valve calcification in hemodialysis

Abstract

Increased prevalence of aortic and mitral valve calcification has been reported in patients on hemodialysis, but it remains unknown whether aortic and mitral valve calcification arise from similar pathogenesis. We detected heart valve calcification using two-dimensional echocardiography, and we related valve calcification to various clinical parameters in patients treated with hemodialysis three times a week for more than 1 year. In 112 patients (77 men and 35 women, age 67±10 years, duration on hemodialysis 95 ± 67 months), aortic and mitral valve calcification were observed in 84 (75.0%) and 58 (51.7%) patients, respectively. Aortic valve calcification was associated with increased age, higher serum calcium, lower serum albumin, lower total cholesterol and higher high-sensitivity C-reactive protein. Multivariate analysis showed that increased age and higher serum calcium were independently associated with aortic valve calcification. Conversely, mitral valve calcification was associated with increased age, higher high-sensitivity C-reactive protein and higher serum b 2 -microglobulin, but not with higher serum calcium. In multivariate analysis, increased age and higher serum b 2 -microglobulin were independently associated with mitral valve calcification. Serum b 2 -microglobulin was associated with longer duration on hemodialysis, malnutrition inflammation (lower serum albumin and higher high-sensitivity C-reactive protein) and dyslipidemia. Considering the results in previous studies showing that the distribution of b 2 -microglobulin amyloid deposition was consistent with that of tissue calcification in patients on hemodialysis, b 2 -microglobulin may have pathogenic roles in valve calcification.

Malnutrition–inflammation complex syndrome: link between end-stage renal disease, atherosclerosis and valvular calcification

“…Despite the different correlations between b2-microglobulin and mitral and aortic calcification demonstrated by Ikee et al, 9 there is still clear evidence of a pro-inflammatory pathophysiology of valvular calcium deposits in hemodialysis subjects, such as the strong association between hs-CRP and aortic and mitral calcification. According to the presented results, carotid intima-media thickness was significantly associated with AVC but not MVC, suggesting that AVC may be more closely associated with systemic atherosclerosis compared with MVC.…”

“…The paper presented by Ikee et al 9 addresses an interesting and important issue in the pathophysiology of heart VC in a hemodialysis patient with ESRD. Their group used a novel cardiovascular risk factor, b2-microglobulin, to investigate the associated factors of aortic and mitral VC.…”

“…Low serum albumin and high serum CRP are two main features observed in dialysis patients. 9 Epidemiological studies have consistently shown a strong association between clinical outcome and measures of both malnutrition and inflammation in dialysis subjects. These two conditions tend to occur concurrently and to coexist in patients with ESRD.…”

Calcification of Heart and Vessels in Chronic Kidney Disease: Problems of Etiology and Pathogenesis

“…По-відомлень щодо зв'язку кардіоваскулярної кальцифікації та процесів запалення у до-ступній літературі багато [22,30,[40][41][42], проте більшість даних є фрагментарні, розріз-нені [22,42], розглядаються в контексті МІА-синдрому [41] і стосуються, за виключенням окремих праць [40,43], діаліззалежної ХХН. Погляди науковців щодо ролі порушень ліпід-ного обміну в реалізації механізмів судинної/ клапанної кальцифікації при ХХН неодноз-начні [3,22,42,44], а вивчення маркерів ОС як чинника прогресування атеросклеротич-ного пошкодження і кальцифікації [1,19] проводилось головним чином у пацієнтів на ГД [45,46].…”

“…Зростаючий інтерес науковців до проблеми патогенезу кальцифікації серцево-судинної системи при ХХН призвів до появи цілої низки праць [26,41,54,55] щодо можливої уча-сті у цих процесах уремічних токсинів, їх зв'язку з ОС і запаленням, ендотеліальною дисфункцією (ЕД), кардіоваскулярною і загальною смертністю. Встановлено, що токсинасоційовані ефекти пов'язані головним чином із пошкодженням наступних типів клітин -лейкоцитів, ендотеліальних клітин, гладеньком'язових клітин і тромбоцитів [54].…”