Abstract
Background and AimsCompensatory renal hypertrophy following unilateral nephrectomy (UNX) occurs in the remaining kidney. However, the long-term cardiac adaptive process to UNX remains poorly defined in humans. Our goal was to characterize myocardial structure and function in living kidney donors (LKDs), approximately 12 years after UNX.Methods and ResultsCardiac function and structure in 15 Italian LKDs, at least 5 years after UNX (median time from donation = 8.4 years) was investigated and compared to those of age and sex matched U.S. citizens healthy controls (n = 15). Standard and speckle tracking echocardiography (STE) was performed in both LKDs and controls. Plasma angiotensin II, aldosterone, atrial natriuretic peptide (ANP), N terminus pro B-type natriuretic peptide (NT-proBNP), cyclic guanylyl monophosphate (cGMP), and amino-terminal peptide of procollagen III (PIIINP) were also collected. Median follow-up was 11.9 years. In LKDs, LV geometry and function by STE were similar to controls, wall thickness and volumes were within normal limits also by CMR. In LKDs, CMR was negative for myocardial fibrosis, but apical rotation and LV torsion obtained by STE were impaired as compared to controls (21.4 ± 7.8 vs 32.7 ± 8.9 degrees, p = 0.04). Serum creatinine and PIIINP levels were increased [1.1 (0.9–1.3) mg/dL, and 5.8 (5.4–7.6)] μg/L, respectively), while urinary cGMP was reduced [270 (250–355) vs 581 (437–698) pmol/mL] in LKDs. No LKD developed cardiovascular or renal events during follow-up.ConclusionsLong-term kidney donors have no apparent structural myocardial abnormalities as assessed by contrast enhanced CMR. However, myocardial deformation of the apical segments, as well as apical rotation, and LV torsion are reduced. The concomitant increase in circulating PIIINP level is suggestive of fibrosis. Further studies, focused on US and EU patients are warranted to evaluate whether these early functional modifications will progress to a more compromised cardiac function and structure at a later time.
Highlights
Kidney transplantation as optimal treatment and standard care for patients with end-stage renal disease (ESRD) confers a survival benefit and is cost effective compared to hemodialysis [1]
In living kidney donors (LKDs), left ventricular (LV) geometry and function by STE were similar to controls, wall thickness and volumes were within normal limits by cardiac magnetic resonance (CMR)
In LKDs, CMR was negative for myocardial fibrosis, but apical rotation and LV torsion obtained by STE were impaired as compared to controls (21.4 ± 7.8 vs 32.7 ± 8.9 degrees, p = 0.04)
Summary
Kidney transplantation as optimal treatment and standard care for patients with end-stage renal disease (ESRD) confers a survival benefit and is cost effective compared to hemodialysis [1]. It is known that living kidney donation causes functional adaptation and hypertrophy of the remaining kidney (a process named compensatory hyperfiltration). A recent report in a model of mild renal insufficiency produced by unilateral nephrectomy (UNX) suggests that removal of a single kidney induces pathologic myocardial accumulation of extracellular matrix components [6], a fibrotic process that has been increasingly implicated as a major cause of cardiovascular morbidity and mortality in humans. Compensatory renal hypertrophy following unilateral nephrectomy (UNX) occurs in the remaining kidney. The long-term cardiac adaptive process to UNX remains poorly defined in humans. Our goal was to characterize myocardial structure and function in living kidney donors (LKDs), approximately 12 years after UNX
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