Prasad G V Ramesh, Yan Andrew T, Nash Michelle M, Kim S Joseph, Wald Ron, Wald Rachel, Lok Charmaine, Gunaratnam Lakshman, Karur Gauri R, Kirpalani Anish, Connelly Philip W
Division of Nephrology, St. Michael's Hospital, University of Toronto, ON, Canada.
Division of Cardiology, St. Michael's Hospital, University of Toronto, ON, Canada.
Can J Kidney Health Dis. 2018 Nov 9;5:2054358118809974. doi: 10.1177/2054358118809974. eCollection 2018.
Cardiac magnetic resonance (CMR) imaging accurately and precisely measures left ventricular (LV) mass and function. Identifying mechanisms by which LV mass change and functional improvement occur in some end-stage kidney disease (ESKD) patients may help to appropriately target kidney transplant (KT) recipients for further investigation and intervention. The concentration of serum adiponectin, a cardiovascular biomarker, increases in cardiac failure, its production being enhanced by B-type natriuretic peptide (BNP), and both serum adiponectin and BNP concentrations decline posttransplantation.
We tested the hypothesis that kidney transplantation alters LV characteristics that relate to serum adiponectin concentrations.
Prospective and observational cohort study.
The study was performed at 3 adult kidney transplant and dialysis centers in Ontario, Canada.
A total of 82 KT candidate subjects were recruited (39 to the KT group and 43 to the dialysis group). Predialysis patients were excluded.
Subjects underwent CMR with a 1.5-tesla whole-body magnetic resonance scanner using a phased-array cardiac coil and retrospective vectorographic gating. LV mass, LV ejection fraction (LVEF), LV end-systolic volume (LVESV), and LV end-diastolic volume (LVEDV) were measured by CMR pre-KT and again 12 months post-KT (N = 39), or 12 months later if still receiving dialysis (N = 43). LV mass, LVESV, and LVEDV were indexed for height (m) to calculate left ventricular mass index (LVMI), left ventricular end-systolic volume index (LVESVI), and left ventricular end-diastolic volume index (LVEDVI), respectively. Serum total adiponectin and N-terminal proBNP (NT-proBNP) concentrations were measured at baseline, 3 months, and 12 months.
We performed a prospective 1:1 observational study comparing KT candidates with ESKD either receiving a living donor organ (KT group) or waiting for a deceased donor organ (dialysis group).
Left ventricular mass index change was -1.98 ± 5.5 and -0.36 ± 5.7 g/m for KT versus dialysis subjects ( = .44). Left ventricular mass change was associated with systolic blood pressure (SBP) ( = .0008) and average LV mass ( = .0001). Left ventricular ejection fraction did not improve (2.9 ± 6.6 vs 0.7 ± 4.9 %, = .09), while LVESVI and LVEDVI decreased more post-KT than with continued dialysis (-3.36 ± 5.6 vs -0.22 ± 4.4 mL/m, < .01 and -4.9 ± 8.5 vs -0.3 ± 9.2 mL/m, = .02). Both adiponectin (-7.1 ± 11.3 vs -0.11 ± 7.9 µg/mL, < .0001) and NT-proBNP (-3811 ± 8130 vs 1665 ± 20013 pg/mL, < .0001) declined post-KT. Post-KT adiponectin correlated with NT-proBNP ( = .001), but not estimated glomerular filtration rate (eGFR) ( = .13). Change in adiponectin did not correlate with change in LVEF in the KT group (Spearman ρ = 0.16, = .31) or dialysis group (Spearman ρ = 0.19, = .21).
Few biomarkers of cardiac function were measured to fully contextualize their role during changing kidney function. Limited intrapatient biomarker sampling and CMR measurements precluded constructing dose-response curves of biomarkers to LV mass and function. The CMR timing in relation to dialysis was not standardized.
The LVESVI and LVEDVI but not LVMI or LVEF improve post-KT. LVMI and LVEF change is independent of renal function and adiponectin. As adiponectin correlates with NT-proBNP post-KT, improved renal function through KT restores the normal heart-endocrine axis.
心脏磁共振成像(CMR)能够准确且精确地测量左心室(LV)质量和功能。确定某些终末期肾病(ESKD)患者左心室质量变化和功能改善的机制,可能有助于为肾移植(KT)受者确定合适的进一步研究和干预目标。血清脂联素是一种心血管生物标志物,其浓度在心力衰竭时升高,B型利钠肽(BNP)可增强其产生,并且移植后血清脂联素和BNP浓度均下降。
我们检验了肾移植会改变与血清脂联素浓度相关的左心室特征这一假设。
前瞻性观察队列研究。
该研究在加拿大安大略省的3个成人肾移植和透析中心进行。
共招募了82名KT候选受试者(39名进入KT组,43名进入透析组)。排除透析前患者。
受试者使用相控阵心脏线圈和回顾性矢量门控技术,通过1.5特斯拉全身磁共振扫描仪进行CMR检查。在KT前及KT后12个月(N = 39)测量LV质量、左心室射血分数(LVEF)、左心室收缩末期容积(LVESV)和左心室舒张末期容积(LVEDV),如果仍在接受透析,则在12个月后再次测量(N = 43)。LV质量、LVESV和LVEDV根据身高(米)进行指数化,分别计算左心室质量指数(LVMI)、左心室收缩末期容积指数(LVESVI)和左心室舒张末期容积指数(LVEDVI)。在基线、3个月和12个月时测量血清总脂联素和N末端脑钠肽前体(NT-proBNP)浓度。
我们进行了一项前瞻性1:1观察性研究,比较接受活体供体器官的ESKD KT候选者(KT组)和等待尸体供体器官的患者(透析组)。
KT组与透析组的左心室质量指数变化分别为-1.98±5.5和-0.36±5.7 g/m(P = 0.44)。左心室质量变化与收缩压(SBP)(P = 0.0008)和平均LV质量(P = 0.0001)相关。左心室射血分数没有改善(2.9±6.6对0.7±4.9%,P = 0.09),而KT后LVESVI和LVEDVI的下降幅度比继续透析时更大(-3.36±5.6对-0.22±4.4 mL/m,P < 0.01和-4.9±8.5对-0.3±9.2 mL/m,P = 0.02)。KT后脂联素(-7.1±11.3对-0.11±7.9 µg/mL,P < 0.0001)和NT-proBNP(-3811±8130对1665±20013 pg/mL,P < 0.0001)均下降。KT后脂联素与NT-proBNP相关(P = 0.001),但与估计肾小球滤过率(eGFR)无关(P = 0.13)。KT组中脂联素的变化与LVEF的变化无关(Spearman ρ = 0.16,P = 0.31),透析组中也是如此(Spearman ρ = 0.19,P = 0.21)。
测量的心脏功能生物标志物较少,无法全面了解其在肾功能变化过程中的作用。患者体内生物标志物采样和CMR测量有限,无法构建生物标志物与LV质量和功能的剂量反应曲线。CMR与透析的时间关系未标准化。
KT后LVESVI和LVEDVI改善,但LVMI或LVEF未改善。LVMI和LVEF的变化与肾功能和脂联素无关。由于KT后脂联素与NT-proBNP相关,通过KT改善肾功能可恢复正常的心内分泌轴。