NDT Advance Access originally published online on December 7, 2005
Nephrology Dialysis Transplantation 2006 21(4):1089-1091; doi:10.1093/ndt/gfi321
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Regression of left ventricular hypertrophy after bilateral nephrectomy
Division of Nephrology and Hypertension, Allegheny General Hospital, West Penn Allegheny Health System, Pittsburgh, PA, USA
Correspondence and offprint requests to: Rita L. McGill MD, Division of Nephrology and Hypertension, 4th Floor, South Tower, 320 East North Avenue, Pittsburgh, PA 15212-4772, USA. Email: rmcgill{at}wpahs.org
Keywords: haemodialysis; hypertension; left ventricular hypertrophy; left ventricular mass index; magnetic resonance imaging; nephrectomy
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Introduction |
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Left ventricular hypertrophy (LVH) is common in hypertensive patients and predicts heart failure, arrhythmia, cerebrovascular complications and death. LVH is endemic in end-stage renal disease (ESRD). Risk factors for LVH in ESRD patients include hypertension, anaemia, secondary hyperparathyroidism and arteriovenous fistulae. LVH is a powerful predictor of cardiac morbidity and mortality in the ESRD population [1,2]. Regression of LVH has been reported in ESRD patients after blood pressure (BP) reduction with angiotensin converting enzyme inhibitors (ACE-Is), or angiotensin receptor antagonists (ARB) [3,4], and after erythropoietin therapy for anaemia.
We report a case in which dramatic regression in LVH was documented on magnetic resonance images (MRIs) of the heart performed before and after bilateral nephrectomy.
Cardiologists use measurements of left ventricular (LV) mass, relative wall thickness and mass–volume ratio to diagnose LVH. Data about LV mass and geometry in dialysis patients are based on echocardiography which is highly dependent upon operator skill, individual patient anatomy and mathematical assumptions. Changes in extracellular volume during and between dialysis treatments can also cause substantial variations in echocardiographic measurements. Cardiac MRI measures the heart independent of operator skill or patient habitus. MRI assessments of LV mass, relative wall thickness and mass–volume ratio rely on direct measurements rather than geometrical assumptions which have never been proven to apply to the ESRD ventricle [5].
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Case |
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A 54-year-old African-American male developed ESRD in 1983. Acquired cystic disease of both kidneys was noted in 1998. Bilateral nephrectomy was performed in April 2004 after development of gross haematuria. Cancer was found in both kidneys, without evidence for metastatic disease.
He had stable coronary artery disease and hypertension that was difficult to control. Despite antihypertensive medication, his predialysis systolic BPs averaged 170 mmHg in October 2003. Clinical and laboratory data are shown in Table 1. Cardiac MRI performed in October 2003 (MRI #1, Figure 1) showed an enlarged hypertrophic left ventricle (Table 2).
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His average pre-dialysis systolic BP fell precipitously over the month following bilateral nephrectomy, even as antihypertensive medication was reduced (Table 1). Without further changes in medication regimen his pre-dialysis systolic BP has declined to 130 mmHg 18 months after nephrectomy.
A second cardiac MRI performed in August 2004 (MRI #2, Figure 2) revealed substantial decreases in LV mass, LV mass index, LV mass–volume ratio and LV relative wall thickness, accompanied by an increase in LV ejection fraction (Table 2).
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Haemoglobin levels were significantly lower over the 2 months prior to MRI #2 than during the 2 months prior to MRI #1. Other laboratory and clinical parameters were unchanged (Table 1). His vascular access fistula functioned consistently.
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Discussion |
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Bilateral nephrectomy resulted in a 21% reduction of LV mass, 7% reduction of the LV mass–volume relationship and a 30% decline in the LV relative wall thickness, documented with MRI imaging of the heart. LV geometry in ESRD has not been extensively evaluated with MRI, despite the potential for more detailed and accurate depiction of cardiac anatomy. A single small study suggested that echocardiography may overestimate LV mass relative to cardiac MRI in dialysis patients, in the presence of LVH and ventricular dilation [6]. The effect of bilateral nephrectomy upon the MRI appearance of an ESRD heart has not been reported previously.
Treatment of anaemia and hyperparathyroidism cannot explain the regression of LVH in this patient. Normalizing haemoglobin with erythropoietin can reduce LVH and improve LV geometry, but this patient's haemoglobin levels were significantly lower after nephrectomy. The decrease in haemoglobin may have been due to surgical blood loss, or loss of pathological erythropoietin produced by the resected renal tumours. Normalization of serum calcium and PTH after parathyroidectomy can promote regression of LVH, but PTH levels did not change. The goal weight and the degree of extracellular volume expansion were not appreciably different before and after nephrectomy, and cannot explain the dramatic decrease in BP and LVH.
Regression of echocardiographic LVH has been described after therapy with ACE-Is and ARBs, independent of BP reduction [3,4]. The renin–angiotensin–aldosterone system (RAAS) has been implicated as an important factor in the pathogenesis of hypertension in ESRD. Bilateral nephrectomy, which removes the anatomic site of the RAAS, has been employed in the past as salvage therapy for refractory hypertension in ESRD [7], although nephrectomy became obsolete when pharmacologic blockade of the RAAS emerged as an alternative treatment. ACE-Is, ARBs, and aldosterone antagonists all block the RAAS, at different steps. The impact of aldosterone blockade on LVH is being actively researched [8], although most studies of spironolactone or eplerenone exclude the ESRD population.
Hypertension persisted in this patient despite a substantial dose of lisinopril. The failure of ACE inhibition could have been related to medication compliance issues, or could perhaps indicate a state in which a chronically activated RAAS was not amenable to ACE-Is at conventional doses. The contribution of the neoplasm to activation of the RAAS is unknown. Renin and aldosterone levels were not measured prior to nephrectomy. Renin, angiotensin and aldosterone may not be the only factors to play a role in the genesis of hypertension and LVH in ESRD. The presence of non-functioning ESRD kidneys has been shown to chronically increase sympathetic tone in renal transplant patients. Removal of native kidneys has been shown to decrease post-transplantation BP [9,10].
Regression of LV mass following nephrectomy was as rapid as it was dramatic, with a decrease of 54 g over only 4 months. LV mass index decreased by 32 g/m2. In the LIFE trial, LV mass reductions of 30 and 45 g were achieved over 12 and 48 months with losartan [11]. LV mass index was reduced by 16 and 24 g/m2 at 12 and 48 months, respectively. In the 4E-Left Ventricular Hypertrophy Study, LV mass reduction of 27 g was demonstrated at 9 months in patients taking both eplerenone and enalapril [8]. Surgical removal of the kidneys achieved more rapid and effective regression than pharmacologic blockade of the RAAS.
We report a case in which rapid and dramatic reduction in the LV mass, LV relative wall thickness and LV mass–volume ratio of a chronic dialysis patient was documented on cardiac MRI after bilateral nephrectomy. Although nephrectomy is no longer employed for the management of hypertension in ESRD and the anephric state is considered by many clinicians to be clinically disadvantageous, this patient has incurred a clinical benefit that may impact upon his cardiovascular longevity. We hypothesize that eradication of a chronically activated RAAS may explain both the improvement in BP control, and the rapid and dramatic improvement in myocardial geometry. Nephrectomy may merit renewed consideration as a means to control LVH in patients who cannot tolerate or will not take ACEs or ARBs, or for whom pharmacological inhibition of the RAAS is ineffective or contraindicated. Important information may be obtained by examination of the ESRD ventricle by MRI.
Conflict of interest statement. None declared.
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References |
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- Paoletti E, Specchia C, Di Maio et al. The worsening of left ventricular hypertrophy is the strongest predictor of sudden cardiac death in haemodialysis patients: a 10 year survey. Nephrol Dial Transplant 2004; 19: 1829–1834
[Abstract/Free Full Text] - Zoccali C, Benedetto FA, Mallamaci F et al. Left ventricular mass monitoring in the follow-up of dialysis patients: prognostic value of left ventricular hypertrophy progression. Kidney Int 2004; 65: 1492–1498[CrossRef][Medline]
- Kanno Y, Kaneko K, Kaneko M et al. Angiotensin receptor antagonist reduces left ventricular hypertrophy associated with diabetic nephropathy in dialysis patients. J Cardiovasc Pharmacol 2004; 43: 380–386[CrossRef][Web of Science][Medline]
- Suzuki H, Kanno Y, Kaneko M et al. Comparison of the effects of angiotensin receptor antagonist, angiotensin converting enzyme inhibitor, and their combination on regression of left ventricular hypertrophy of diabetes type 2 patients on recent onset hemodialysis therapy. Ther Apher Dial 2004; 8: 320–327[CrossRef][Web of Science][Medline]
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- Stewart GA, Foster J, Cowan M et al. Echocardiography overestimates left ventricular mass in hemodialysis patients relative to magnetic resonance imaging. Kidney Int 1999; 56: 2248–2253[CrossRef][Web of Science][Medline]
- Lee C, Neff MS, Slifkin RF, Leiter E. Bilateral nephrectomy for hypertension in patients with chronic renal failure on a dialysis program. J Urol 1978; 119: 20–22[Medline]
- Pitt B, Reichek N, Willenbrock R et al. Effects of eplerenone, enalapril, and eplerenone/enalapril in patients with essential hypertension and left ventricular hypertrophy: the 4E-left ventricular hypertrophy study. Circulation 2003; 108: 1831–1838
[Abstract/Free Full Text] - Hausberg M, Kosch M, Harmelink P et al. Sympathetic nerve activity in end-stage renal disease. Circulation 2002; 106: 1974–1979
[Abstract/Free Full Text] - Curtis JJ, Luke RG, Dustan HP et al. Remission of essential hypertension after renal transplantation. N Engl J Med 1983; 309: 1009–1015[Abstract]
- Devereaux RB, Dahlöf B, Gerdts E et al. Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the losartan intervention for endpoint reduction in hypertension (LIFE) trial. Circulation 2004; 110: 1456–1462
[Abstract/Free Full Text]
Accepted in revised form: 16.11.05
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