Differences in Cardiac Structure Assessed by Echocardiography Between Renal Transplant Recipients and Chronic Kidney Disease Patients

BackgroundCardiovascular disease (CVD) is the leading cause of death in predialysis chronic kidney disease (CKD) and dialysis patients as well as in renal transplant recipients (RTRs). Left ventricular hypertrophy (LVH) starts early during the course of CKD and is a strong predictor of CVD in this population. Regression of LVH after a successful renal transplantation remains a debatable issue among investigators, whereas there is little data comparing echocardiographic measurements between patients with predialysis CKD and RTRs.AimThe aim of this study was to compare echocardiographic measurements of LV structure and function between predialysis CKD patients and RTRs of similar renal function level.Patients and MethodsWe conducted a case control study with individual (1:2) matching from the Renal Transplant and the predialysis CKD Outpatient Clinic. For each of the 36 RTRs, two matched for gender, age and estimated glomerular filtration rate (eGFR) predialysis CKD outpatients (72 patients) were included. All patients underwent transthoracic echocardiography and LV mass, LV mass index [LVM and LVMI = LVM/BSA g/m²] and indices of systolic function were measured. In a subgroup of 12 RTRs we retrospectively assessed and compared the LVMI measurements at three different time points, during predialysis, dialysis and post transplant period.ResultsThe prevalence of LVH was 33% in RTRs and 52% in CKD patients (ns). RTRs had significantly lower LVM and LVMI levels compared with predialysis CKD patients (P = .006 and P = .008) while the other echocardiographic indices did not differ. In the subgroup of 12 RTRs, post-transplant LVMI levels (105 ± 25 g/m²) were significantly lower in comparison with predialysis (147 ± 57 g/m²) and dialysis LVMI levels (169 ± 72 g/m²) (P = .01, P = .01, respectively).ConclusionRTRs had significantly lower LVMI compared with predialysis CKD patients of similar age, renal function, hemoglobin and blood pressure level.     

Plasma adiponectin concentration and left ventricular hypertrophy in kidney transplant patients

Adamczak M, B?ach A, Kolonko A, Szotowska M, Chudek J, Franek E, Wi?cek A. Plasma adiponectin concentration and left ventricular hypertrophy in kidney transplant patients.
Clin Transplant 2011: 25: 561–568. © 2010 John Wiley & Sons A/S. Abstract: Background: Low plasma adiponectin concentration is associated with more frequent occurrence of left ventricular hypertrophy (LVH) and more exaggerated intima‐media thickness of common carotid artery (IMT). IMT is an early surrogate marker of atherosclerosis. This study aimed to assess the relationship between plasma adiponectin concentration and left ventricular mass index (LVMI) and IMT in kidney transplant patients (KTP). Methods: In 88 adult KTP, plasma adiponectin concentration, LVMI, and IMT were estimated. LVH was defined as LVMI >110 or >125 g/m² for females and males, respectively. Data presented are means and 95% CI. Results: Plasma adiponectin concentration was similar in KTP with (n = 42) or without LVH (n = 46) (13.5 [11.4–15.6] vs. 13.1 [11.6–14.6] μg/mL, respectively), as well as in KTP subgroups divided according to the IMT value tertiles (p = 0.42) (11.7 [10.0–13.3], 14.2 [11.7–16.6], and 14.0 [11.7–16.4] μg/mL in the lowest, middle, and highest tertiles, respectively). Plasma glucose concentrations were similar in KTPs with LVH or without LVH. No significant correlation was found between plasma adiponectin concentration and both LVMI (R = ?0.02; p = 0.87) and IMT (R = 0.09; p = 0.38), respectively. Conclusion: Results of this cross‐sectional study do not confirm the roles of low adiponectin and high glucose in the pathogenesis of LVH and atherosclerosis in KTP.     

Influence of cyclosporine and tacrolimus on serum uric acid levels in stable kidney transplant recipients

Although hyperuricemia is a well-known adverse effect of cyclosporine (CsA) treatment, there are contradictory data regarding the effect of tacrolimus on uric acid levels. The aim of this study was to examine the influences of CsA and tacrolimus-based treatment regimens on serum uric acid levels in 155 renal transplant recipients with normal allograft function who underwent renal transplantation between 1999 and 2002. Serum uric acid levels were recorded at 1, 6, 12, 18, and 24 months follow-up. The patients were treated with CsA-based (n = 73), tacrolimus-based (n = 47), or conversion from CsA-based to tacrolimus-based (n = 35) immunosuppressive regimens. Serum uric acid levels for patients in the CsA and tacrolimus groups were 6.3 +/- 1.6 versus 7.9 +/- 1.9 mg/dL and 6.5 +/- 1.8 versus 8.0 +/- 1.8 mg/dL at the study outset and 24 months, respectively. Both of the treatment regimens showed progressively increasing serum uric acid levels (P < .001). Serum uric acid levels of patients with treatment conversion from CsA to tacrolimus were 8.6 +/- 2.8 mg/dL before conversion and 8.1 +/- 1.9 mg/dL after conversion. There was no alteration in serum uric acid levels after the change of treatment (P > .05). These findings indicate that, compared with CsA, tacrolimus offers no advantage for serum uric acid levels in renal transplant recipients.     

Time-dependent changes in cardiac growth after kidney transplantation: the impact of pre-dialysis ventricular mass.

BACKGROUND: Left ventricular hypertrophy (LVH) is common in chronic kidney disease (CKD), including kidney transplant recipients. However, time-related left ventricular mass changes (DeltaLVM) from pre-dialysis stage to beyond the first post-transplant year have not been clearly identified. METHODS: We studied a cohort of 60 stages 4-5 CKD patients without overt cardiac disease, who underwent three echocardiograms during follow-up: at pre-dialysis stage, on dialysis and after kidney transplantation (KT). Multiple linear regression was used to model DeltaLVM from baseline study. Cox proportional analysis was used to determine risk factors associated with either de novo LVH or>20% DeltaLVMI over time. RESULTS: Patients with baseline LVH (n=37; 61%) had a higher body mass index (BMI) than those without LVH (n=23; 39%) (P=0.013). BMI, haemoglobin levels (P=0.047) and non-use of angiotensin-converting enzyme inhibitors (ACEI) (P=0.057) were associated with baseline left ventricular mass index (LVMI). Twelve out of 23 patients (52%) with normal LVM at baseline, developed either de novo LVH or>20% DeltaLVMI at follow-up. On the other hand, 29 (78%) of those with initial LVH maintained this abnormality, and 8 (22%) normalized LVM post-transplantation. Factors associated with DeltaLVMI were age (P=0.01), pre-dialysis LVMI (P<0.0001), serum creatinine (P=0.012) and the use of ACEI post-transplantation (P=0.009). In Cox analysis, pre-dialysis LVMI was associated with de novo LVH or>20% DeltaLVMI over time (hazard ratio 1.009; 95% confidence interval 1.004 to 1.015; P=0.001). CONCLUSIONS: Successful KT may not completely normalize LVM post-transplantation. Pre-dialysis LVMI, traditional risk factors and no use of ACEI may perpetuate cardiac growth following KT.     

Vitamin D receptor (VDR) gene polymorphism is associated with left ventricular (LV) mass and predicts left ventricular hypertrophy (LVH) progression in end‐stage renal disease (ESRD) patients

Left ventricular hypertrophy (LVH) is a strong cardiovascular risk marker in end‐stage renal disease (ESRD) patients. Vitamin D deficiency and/or disturbed vitamin D signaling has been implicated in LVH in experimental models. Because the BsmI vitamin D receptor VDR gene polymorphism may alter VDR function, we performed a cross‐sectional and longitudinal study in a cohort of 182 dialysis patients to investigate (1) the relationship between BsmI VDR gene polymorphism and left ventricular mass index (LVMI) measured by echocardiography and (2) the predictive power of this polymorphism for progression in LVH over a 18 ± 2 months of follow‐up. As a reference group, we used 175 healthy subjects matched to the study population as for age and sex. The distribution of BsmI genotypes did not significantly deviate from Hardy‐Weinberg equilibrium either in patients or in the control group of healthy subjects. The frequency of the B allele of BsmI polymorphism (40.4%) in dialysis patients was similar to that of healthy control subjects (38.6%), and the number of B alleles was directly related to LVMI (r = 0.20, P = .007). This relationship remained robust (β = 0.19, P = .006) in multivariate analysis adjusting for traditional and nontraditional risk factors and antihypertensive and calcitriol treatment. In the longitudinal study, LVMI rose from 60.1 ± 17.9 to 64.2 ± 19.3 g/m^2.7 (P < .001), and again, the number of B alleles was associated with LVMI changes both in crude and in fully adjusted analyses. These cross‐sectional and longitudinal observations coherently support the hypothesis that altered vitamin D signaling is implicated in LVH in ESRD patients. © 2010 American Society for Bone and Mineral Research     

Prevalence and Risk Factors of Myocardial Remodeling in Hemodialysis Patients

Background. Left ventricular hypertrophy (LVH) is an independent risk factor for morbidity/mortality in patients with end stage renal disease (ESRD). Our study aimed to identify prevalence as well as independent risk factors that contribute to the development of LV geometric remodeling in our HD patients. Methods. The left ventricles of 116 HD patients were classified echocardiographically into four different geometric patterns on the basis of LV mass and relative wall thickness. Furthermore, we measured inferior vena cava (IVC) diameter and its collapsibility index (CI) by echocardiography. Finally, we modeled a stepwise multiple regression analysis to determine the predictors of LV geometry.?Results. Our study provides evidence that HD patients had a prevalence of abnormal LV geometry in 92% and LVH in 81%. We found all four geometric models of LV. Most dominant were eccentric LVH. Concentric LVH was observed in 37, normal geometry (NG) in 9, and concentric remodeling (CR) in 13 of HD patients. Mean arterial blood pressure was significantly higher in the cLVH group (95 ± 10 mmHg) than in the NG and CR groups (81.6 ± 12.3 and 80 ± 11.8, respectively, p < 0.001). The cLVH and eCLVH groups had significantly lower mean hemoglobin (10.3 ± 1.4g/dL and 10.6 ± 1g/dL, respectively) compared with the NG group (11.9 ± 1.4g/dL), p < 0.001. Furthermore, interdialytic weight gain (kg) was significantly higher in eCLVH group (3.13 ± 0.8) than in NG group (2.3 ± 1.1), p < 0.001. Mean IVC index of the eLVH group (10.83 ± 2.07 mm/m²) was significantly higher than corresponding indexes of NG (10.83 ± 2.07 mm/m²), CR (8.31 ± 1.32 mm/m²) and cLVH (8.12 ± 2.06 mm/m²) groups (p < 0.001 for each comparisons). Conclusion. Mean arterial pressure, hemoglobin, IVC index, and interdialytic weight gain were found to be independent predictors of LV geometry (R² = 0.147; p < 0.001) in HD patients.     

Increased serum renalase in hemodialysis patients: is it related to left ventricular hypertrophy?

Introduction: Left ventricular hypertrophy (LVH) is one of the most common cardiac abnormalities in patients with end stage renal disease (ESRD). Hypertension, diabetes, increased body mass index, gender, age, anemia, and hyperparathyroidism have been described as risk factors for LVH in patients on dialysis. However, there may be other risk factors which have not been described yet. Recent studies show that renalase is associated with cardiovascular events. The aim of this study was to reveal the relation between renalase, LVH in patients under hemodialysis (HD) treatment.

Methods: The study included 50?HD patients and 35 healthy controls. Serum renalase levels and left ventricle mass index (LVMI) were measured in all participants and the relation between these variables was examined.

Findings: LVMI was positively correlated with dialysis vintage and C-reactive protein (CRP) (r?=?0.387, p?=?0.005 and r?=?0.597, p?r?=??0.324, p?=?0.022 and r?=??0.499, p?r?=?0.263, p?=?0.065). Serum renalase levels were significantly higher in HD patients (212?±?127?ng/mL) compared to controls (116?±?67?ng/mL) (p?r?=?0.677, p?r?=?0.625, p?Discussion: In our study, LVMI was correlated with dialysis vintage, residual diuresis, CRP, and hemoglobin. LVMI tends to correlate with renalase and this correlation may be significant in studies with more patient numbers. The main parameters affecting renalase levels are dialysis vintage and serum creatinine.     

The Prevalence of Hypertension, Valve Calcification and Left Ventricular Hypertrophy and Geometry in Peritoneal Dialysis Patients

Background/Aims: Cardiac valve calcification (CVC) and left ventricular (LV) abnormalities are common indicators of a poor prognosis in dialysis patients. We determined the prevalence of hypertension, CVC, LV hypertrophy (LVH) and LV geometry in peritoneal dialysis (PD) patients. Methods: Eighty-seven patients (50 female; mean age 42 ± 13 years; mean dialysis duration 46 ± 24 months) on strict salt and volume restriction, none of whom were receiving antihypertensives, were included in the study. Blood pressure (BP), biochemical parameters, CVC, LVH and LV geometry were determined. Results: Most patients were normotensive. CVC of the mitral and aortic valves and of both valves were noted in 22, 23 and 15% of patients, respectively. Patients with CVC had significantly higher diastolic BP (p = 0.023), cardiothoracic index (CTI; p = 0.037) and LV mass index (LVMI; p = 0.002). LVH, noted overall in 44% of cases, was present in 62 and 36% of the patients with and without CVC, respectively (p = 0.028). Of the whole group, only 50.6% had normal LV geometry. LVH was associated with lower serum albumin (p = 0.002), higher CTI (p = 0.027) and more frequent CVC (p = 0.028). LVMI was greater in patients with CVC (p = 0.002). Conclusion: Strict salt restriction and the achievement of ideal dry weight result in normotension in PD patients. CVC is associated with LVH, both of which are lower in normotensive patients.     

An Association Between Inflammatory State and Left Ventricular Hypertrophy in Hemodialysis Patients

This study was performed to investigate the potential relationship between left ventricular hypertrophy (LVH) and proinflammatory cytokines in hemodialysis (HD) patients and the effect of HD on cytokine production. Serum interleukin 1 beta (IL-1 β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) measurements and echocardiographic studies were performed in 35 stable HD patients. A variety of probable risk factors for LVH including age, HD duration, blood pressure (BP), body mass index, lipid profile, hemoglobin, albumin, parathormone and homocysteine levels were also investigated. Additionally, the effect of HD procedure on cytokine levels was evaluated. Predialysis serum levels of IL-1β, IL-6, TNF-α, and homocysteine in HD patients were compared with 12 healthy subjects. Left ventricular hypertrophy was demonstrated in 20 (57%) of HD patients by echocardiography. Left ventricular mass index (LVMI) was correlated positively with systolic BP (r = 0.556, p = 0.001), diastolic BP (r = 0.474, p = 0.004), and serum levels of TNF-α (r = 0.446, p = 0.009).Multiple regression analysis showed that systolic BP and TNF-α levels were significant independent predictors of LVH. No relationship was observed between LVH and other parameters. The mean predialysis serum level of IL-6 was significantly higher in HD patients compared to healthy controls (15.7 ± 8.7 vs. 7.3 ± 0.7 pg/mL, p = 0.001). Predialysis serum levels of TNF-α in HD patients were higher when compared to healthy subjects, but the difference was not statistically significant (8.3 ± 3 vs. 7 ± 1.45 pg/mL, respectively, p > 0.05). However, serum levels of IL-6 and TNF-α significantly elevated after HD, when compared to predialysis levels (from 15.7 ± 8.7 to 17.8 ± 9.5 pg/mL, p = 0.001 and from 8.3 ± 3.0 to 9.9 ± 3.5 pg/mL p = 0.004, respectively). As a conclusion, in addition to BP, proinflammatory cytokines, TNF-α in particular, seem to be associated with LVH in ESRD patients.     

A J‐Shaped Association Between Serum Uric Acid Level and Allograft Outcomes After Living Donor Kidney Transplantation

Hyperuricemia following kidney transplantation (KT) may contribute to a decline in allograft renal function, but be affected by KT‐related confounding factors. Some studies have even suggested that a reduction in serum uric acid (UA) is associated with poor patient outcomes. Thus, we retrospectively analyzed the impact of serum UA on allograft outcomes in 281 KT recipients. KT recipients were divided into five groups according to serum UA level (mg/dL): Group I (n = 46), ≤ 5; Group II (n = 62), >5 and ≤6; Group III (n = 70), >6 and ≤7; Group IV (n = 53), >7 and ≤8; Group V (n = 50), >8. Regression analysis showed that serum UA level was significantly associated with future allograft function. In a Kaplan–Meier analysis, the dialysis‐free survival of Group II recipients was better than that of the other groups (Group I, 140 ± 5 months; Group II, 208 ± 7 months; Group III, 148 ± 4 months; Group IV, 185 ± 12 months; Group V, 164 ± 11 months; P = 0.0164). In Cox proportional hazard models adjusting for estimated glomerular filtration rate, the relative risk of allograft loss still tended to be elevated in Group I (HR=3.417, 95% CI 1.138–10.258) and Group V (HR=2.793, 95% CI 1.108–7.041), using Group II as the reference. Our results suggest that there is a J‐shaped association between serum UA levels and allograft outcomes in living donor KT recipients.     

Is uric acid a predictive factor for graft dysfunction in renal transplant recipients?

Hyperuricemia is a common complication in renal transplant recipients, and uric acid (UA) may play a role in renal dysfunction. The aim of this study was to evaluate the effects of UA on chronic allograft nephropathy (CAN) in renal transplant recipients. The 133 study subjects included 34 women and 99 men of overall mean age of 34.7 +/- 9.9 years. They underwent renal transplantation between 1998 and 2000. Serum UA levels were measured in the first month after transplantation and then at yearly intervals throughout a 3-year follow-up. In the first month after transplantation, 55.3% of recipients had hyperuricemia (UA >7 mg/dL in men; UA >6 mg/dL in women), but, 3 years after transplantation, 84.6% of the subjects had that disorder (P<.001). CAN was diagnosed in 31.5% of the patients at a mean onset of 31.8 +/- 14.3 months after transplantation. Fifty-two percent of these individuals experienced graft failure within 43.3 +/- 20.8 months after transplantation. UA levels were recorded before the development of CAN. There was no association between UA levels and CAN according to a Cox regression analysis (P>.05; relative risk, 1.082; 95% confidence interval [CI] 0.9-1.3). We concluded that the prevalence of hyperuricemia was higher among recipients than in healthy individuals, but that the UA level did not affect the development of CAN during first 3 years after transplantation.     

Effects of erythropoietin on left ventricular hypertrophy in adults with severe chronic renal failure and hemoglobin <10 g/dL

BACKGROUND: Left ventricular hypertrophy (LVH) frequently complicates chronic renal insufficiency. Anemia is also common in these patients and may contribute to LVH. METHODS: We conducted an open-label interventional trial to evaluate the effect of recombinant erythropoietin (rhEPO) on left ventricular mass index (LVMI) in anemic patients with renal insufficiency. Adults with creatinine clearance 10 to 30 mL/min (nondiabetics) or 20 to 40 mL/min (diabetics) were recruited, and rhEPO was given to those with anemia (hemoglobin level <10 g/dL). Baseline and 6-month LVMI and LVH (LVMI >130 g/m(2) in men and >100 g/m(2) in women), hemoglobin levels, creatinine clearance, blood pressure, medications, and medical history were obtained. Forty anemic and 61 nonanemic control subjects were enrolled. RESULTS: Overall, the prevalence of LVH was 68.3% (95% CI 58.3-77.2), and entry hemoglobin level was the only significant predictor of baseline LVH (adjusted OR 0.69 per g/dL increase in hemoglobin, 95% CI 0.50-0.94). After 6 months, LVMI decreased in anemic patients receiving rhEPO (142 +/- 56 vs. 157 +/- 56 g/m(2)) (P= 0.007), with an increase in hemoglobin (11.3 +/- 1.9 vs. 9.1 +/- 0.7 g/dL) (P= 0.001). There were no changes in LVMI or hemoglobin level among controls. After adjusting for confounders and change in hemoglobin, receipt of rhEPO was associated with a significant reduction in LVMI (P= 0.01). CONCLUSION: Treatment with rhEPO was not independently associated with significant changes in blood pressure or renal function. LVH is a common finding in chronic renal insufficiency and is associated with lower hemoglobin levels. Treatment with rhEPO may decrease LVH in patients with severe renal insufficiency and anemia.     

Hypoalbuminemia as a risk factor for progressive left-ventricular hypertrophy in hemodialysis patients

BACKGROUND: This study was performed to evaluate the changes in left-ventricular (LV) mass in the patients starting maintenance hemodialysis and the risk factors for the progression of LVH. METHODS: From June 1994 to February 1997, baseline echocardiography was obtained within six months after the initiation of hemodialysis in 111 patients with end-stage renal disease. Of the patients who had LVH on baseline echocardiography, 32 patients underwent follow-up echocardiography after 15 months (range: 9-24 months). LVH was defined as a left-ventricular mass index (LVMI) greater than 131 g/m(2) in males and 100 g/m(2) in females. Progressive LVH was defined as a follow-up LVMI greater than 105% of the baseline value. Hemoglobin, blood urea nitrogen, creatinine, cholesterol, albumin, prealbumin, parathyroid hormone, Kt/V, nPCR, fibrinogen, homocysteine and ACE gene polymorphism were also measured. RESULTS: LVH was detected in 91 of 111 (82%) ESRD patients starting maintenance hemodialysis. Of the 32 patients in whom follow-up echocardiography was performed, progressive LVH occurred in 19 patients (M:F = 12:7). Progressive LVH was associated with lower diastolic blood pressure (81 +/- 11 vs. 90 +/- 12 mm Hg, p = 0.036) and lower serum albumin (3.5 +/- 0.4 vs. 3.9 +/- 0.4 g/dl, p = 0. 009). Serum albumin was negatively (r = -0.420, p = 0.017) correlated to Delta LVMI (follow-up LVMI minus baseline LVMI). Hypoalbuminemia was an independent risk factor for progressive LVH in multiple logistic regression analysis (R.R. = 1.29, p = 0.046). The association of progressive LVH with age, gender, diabetes mellitus, smoking history or other laboratory parameters was not significant. CONCLUSION: LVH was highly prevalent in the patients starting maintenance hemodialysis for ESRD. In the follow-up echocardiography, LVH progressed in a substantial portion of the patients, and hypoalbuminemia was a risk factor for progressive LVH.     

Inverse association of serum long-acting natriuretic peptide and bone mineral density in renal transplant recipients

Hsu B‐G, Ho G‐J, Lee C‐J, Yang Y‐C, Chen Y‐C, Shih M‐H, Lee M‐C. Inverse association of serum long‐acting natriuretic peptide and bone mineral density in renal transplant recipients.
Clin Transplant 2011 DOI: 10.1111/j.1399‐0012.2011.01575.x.
© 2011 John Wiley & Sons A/S. Abstract: Objective: Our aim was to evaluate the relationship between bone mineral density (BMD) and fasting serum long‐acting natriuretic peptide (LANP) concentration in renal transplant recipients. Patients and methods: Fasting blood samples were obtained from 65 renal transplant recipients. BMD was measured using dual energy X‐ray absorptiometry in lumbar vertebrae (L2–L4). Serum LANP levels were measured using a commercial enzyme immunoassay kit. Results: Six patients (9.2%) had osteoporosis and 28 patients (43.1%) had osteopenia in renal transplant recipients. Increased serum LANP (p < 0.001) was significantly correlated with low lumbar T‐score cut‐off points between groups (normal, osteopenia, and osteoporosis) in renal transplant recipients. Female patients had lower lumbar BMD than male renal transplant recipients (p = 0.027). Univariate linear regression analysis indicated that lumbar BMD were positively correlated with height (p = 0.038), body weight (p = 0.003), and body mass index (BMI; p = 0.019), whereas negatively correlated with LANP (p = 0.004) among the renal transplant recipients. Multivariate forward stepwise linear regression analysis of the significant variables revealed that body weight (R² change = 0.132; p = 0.006) and LANP (R² change = 0.093; p = 0.008) were the independent predictors of lumbar BMD values in the renal transplant recipients. Conclusion: Serum LANP concentration correlates negatively with lumbar BMD values in renal transplant recipients.     

Influence of chronic renal insufficiency on left ventricular diastolic function in hypertensives without left ventricular hypertrophy

BACKGROUND: Patients with chronic renal insufficiency (CRI) have a much greater cardiovascular risk than the general population. Moreover, hypertension is common in these patients, as is left ventricular hypertrophy (LVH) and diastolic dysfunction, which contribute to a worse prognosis. While these findings are well established for end-stage renal disease, fewer data are available in mild to moderate CRI. Furthermore, little is known about diastolic function in CRI patients without LVH. METHODS: We performed a cross-sectional study to evaluate LV structure and function in hypertensives with CRI, compared with hypertensives with normal renal function (EH), by means of mitral inflow and tissue Doppler echocardiography. Patients with LVH were excluded from both groups. RESULTS: CRI patients had higher left ventricular end-diastolic diameter, end-systolic diameter (p<0.0001 and p=0.0001, respectively) and left ventricular mass index (LVMI) (p<0.0001) than EH patients. The CRI group also showed greater alterations of the diastolic function indexes than hypertensives: lower E-wave peak velocity (p=0.02), E-wave peak velocity to A-wave peak velocity ratio (p=0.03) and early diastolic myocardial velocity (p=0.04), higher A-wave peak velocity (p=0.07), E-deceleration time (p=0.02) and isovolumic relaxation time (p=0.0001). Multiple regression analysis demonstrated that renal function was a predictor of LVMI and diastolic function independently of age, sex, pulse pressure, body mass index and duration of hypertension. CONCLUSIONS: Our data showed a greater alteration of diastolic function in the CRI group, in part independent of LVMI. In CRI, factors other than LVMI and blood pressure seem to play an important role in causing early diastolic dysfunction.     

Cardiac impact of the arteriovenous fistula after kidney transplantation: a case‐controlled,match‐paired study

In kidney transplant (KT) recipients, cardiac impact of the persistence of an asymptomatic arteriovenous fistula (AVF) for hemodialysis has not been fully elucidated. Seventy‐six patients (mean age: 49 years) without history of diabetes or cardiovascular disease underwent an echocardiography. Thirty‐eight had a functioning AVF and were match‐paired for age, gender and KT duration. Left ventricular mass index (LVMI) was significantly higher in patients with functioning AVF: 135.1 ± 30.3 vs. 112.4 ± 28 g/m² (P = 0.001). Exposure to AVF increased the risk of developing high LVH fourfold. Search for a dose‐effect of AVF flow revealed a trend towards increasing LVMI with higher flow: 142.6 ± 30 vs. 126.9 ± 23.9 g/m² (P = 0.084) (median flow of the population as cut‐off). Other significant changes were observed in left ventricular dimensions: greater end diastole‐ and systole diameters, both larger left and right atria, and left atrium diameter. Our study suggests that, in stable asymptomatic KT patients, functioning AVF has significant impact on cardiac mass, cardiac index and left ventricular dimensions. The effects on morbidity and mortality were to be investigated.     

Regression of left ventricular hypertrophy by lisinopril after renal transplantation: role of ACE gene polymorphism

BACKGROUND: Cardiac complications are the main cause of death in renal transplantation (RT), and left ventricular hypertrophy (LVH) may play an important role in these patients. The unfavorable genotype of the angiotensin-converting enzyme (ACE) gene has been associated with cardiovascular disease, including LVH. ACE inhibitors (ACEIs) reduce LVH, but little is known about the effects of ACEIs on LVH in RT patients with different insertion/deletion (I/D) genotypes of the ACE gene. METHODS: We prospectively studied 57 stable nondiabetic RT patients with hypertension and echocardiographic LVH as well as a functional graft for 69.5 +/- 5.6 months. Patients randomly received either lisinopril 10 mg/day (group A, N = 29; 5 were excluded due to reversible acute renal failure) or placebo (group B, N = 28) for 12 months. Echocardiography (M-mode, 2-B, and color flow Doppler) was performed at baseline and 6 and 12 months later by the same examiner without previous knowledge of the genetic typing. The ACE genotype (I or D alleles) was ascertained by polymerase chain reaction (PCR; group A, DD = 10 and ID/II = 14; group B, DD = 15 and ID/II = 13). RESULTS: All patients maintained a good renal function (serum creatinine <2.5 mg/dL) during the follow-up and both groups received a similar proportion of antihypertensive drugs (beta-blockers 83 vs. 79%; Ca antagonists 66 vs. 68%; alpha1-adrenoreceptor antagonists 50 vs. 67%) during the study. As expected, mean arterial blood pressure and hemoglobin levels showed a higher percentage reduction in group A versus group B (-4 +/- 2.8 vs. 2.1 +/- 2.6%, P = 0.07, and -11.5 +/- 1.5 vs. -0.5 +/- 2.3%, P < 0.01, respectively). Group A patients showed a significantly higher decrement in LV mass index (LVMI) than group B at the end of follow-up, after adjusting for age, baseline LVMI, time after grafting and changes in systolic blood pressure, renal function, and hemoglobin levels (group A, -9.5 +/- 3.5% vs. group B, 3 +/- 3.2%, P < 0.05). As a result, 46% of group A and only 7% of group B patients showed a reduction of LVMI >/=15% (P < 0.01). The beneficial effect of lisinopril on LVMI reduction was more evident in DD patients (placebo DD, 8.4 +/- 4.1% vs. lisinopril DD, -7.2 +/- 5.3, P < 0.05), and a trend was observed in patients with other genotypes (placebo ID/II, 2.8 +/- 5.4% vs. lisinopril ID/II, -11.4 +/- 5%, P = 0.33). CONCLUSIONS: Lisinopril decreases LVM in renal transplant patients with hypertension and LVH, and the ACE gene polymorphism may predict the beneficial effect of this therapy. This finding may be important in targeting prophylactic interventions in this population.     

Diagnostic potential of circulating natriuretic peptides in chronic kidney disease.

BACKGROUND: Measurement of natriuretic peptides, particularly brain natriuretic peptide (BNP) is an established method for the diagnosis of cardiovascular disorders, chiefly left ventricular (LV) dysfunction. The influence of renal function on the diagnostic utility of natriuretic peptides is unclear. METHODS: We performed a cross-sectional study of 296 patients with renal disease but no history of cardiac disease using echocardiography to assess LV mass and function. Circulating levels of atrial natriuretic peptide (ANP) and BNP were also measured. RESULTS: The incidence of LV hypertrophy increased with progressive renal dysfunction; from 39% in patients with near-normal renal function, to 80% in renal transplant patients. There was a negative correlation between both ANP and BNP, and glomerular filtration rate (GFR) (ANP: r = -0.28, P<0.001; BNP: r = -0.40, P<0.001). Serum ANP and BNP had sensitivity and specificity for LV hypertrophy of 39.9%, 87.4% (ANP) and 61.4%, 67.6% (BNP) respectively. Sensitivity and specificity for LV dysfunction was 77.2%, 32.4% (ANP) and 71.8%, 40.0% (BNP). Significant confounders in determining serum ANP were haemoglobin, beta blockade and albumin, while serum BNP levels were significantly confounded by GFR, albumin, haemoglobin, beta blockade and age. CONCLUSIONS: Across a spectrum of renal dysfunction, GFR is a more important determinant of serum BNP than ventricular function, and several factors are predictors of natriuretic peptide levels. In chronic kidney disease, the use of natriuretic peptides to diagnose LV hypertrophy must be interpreted in light of these other factors. The use of these peptides in renal dysfunction to diagnose LV dysfunction may be of limited value.     

Regression of Left Ventricular Hypertrophy After Arteriovenous Fistula Closure in Renal Transplant Recipients: A Long-Term Follow-Up

The long-term effects of hemodialysis arteriovenous fistula (AVF) closure on left ventricular (LV) morphology are unknown. Using echocardiography, we prospectively studied 17 kidney transplant recipients before, 1, and, 21 months after AVF closure (mean fistula flow 1371 +/- 727 mL/min). Eight kidney transplant recipients with a patent AVF, matched for age, time after AVF creation, and time after transplantation, served as controls. LV mass index (LVMI) decreased from 139 +/- 44 g/m2 before AVF closure to 127 +/- 45 g/m2 and 117 +/- 40 g/m2 at 1 and 21 months post-closure, respectively (p < 0.001), but remained unchanged in controls. LV hypertrophy prevalence (LVMI > 125 g/m2) decreased from 65% before, to 41% early, and 18%, late, after surgery (p = 0.008), mostly from a decrease in LV end-diastolic diameter. Consequently, the prevalence of LV concentric remodeling (relative wall thickness > 0.45 without hypertrophy) increased from 12% before, to 35% early, and 65% late, after surgery (p = 0.003). Diastolic arterial blood pressure increased from 78 +/- 15 mmHg before, to 85 +/- 13 mmHg early, and 85 +/- 10 mmHg late, after surgery (p < 0.015). In conclusion, closure of large and/or symptomatic AVF induces long-term regression of LV hypertrophy. However, residual concentric remodeling geometry as well as diastolic blood pressure increase may blunt the expected beneficial cardiac effects of the procedure.     

Association of Serum Uric Acid With Graft Survival After Kidney Transplantation: A Time‐Varying Analysis

The association of serum uric acid (UA) with kidney transplant outcomes is uncertain. We examined the predictive value of UA during the first year posttransplant as a time‐varying factor for graft survival after adjustment for time‐dependent and independent confounding factors. Four hundred and eighty‐eight renal allograft recipients transplanted from January 2004 to June 2006 and followed for 41.1 ± 17.7 months were included. Data on UA, estimated glomerular filtration rate (eGFR), tacrolimus level, mycophenolate mofetil (MMF) and prednisone doses, use of allopurinol, angiotensin‐converting enzyme‐inhibitor/angiotensin‐receptor‐blocker (ACEi/ARB) and diuretics at 1, 3, 6, 9 and 12 months were collected. Primary endpoint of the study was graft loss, defined as graft failure and death. Cox proportional hazard models and generalized estimating equations were used for analysis. UA level was associated with eGFR, gender, retransplantation, decease‐donor organ, delayed graft function, diuretics, ACEi/ARB and MMF dose. After adjustment for these confounders, UA was independently associated with increased risk of graft loss (HR: 1.15, p = 0.003; 95% CI: 1.05–1.27). Interestingly, UA interacted with eGFR (HR: 0.996, p < 0.05; 95% CI: 0.993–0.999 for interaction term). Here, we report a significant association between serum UA during first year posttransplant and graft loss, after adjustment for corresponding values of time‐varying variables including eGFR, immunosuppressive drug regimen and other confounding factors. Its negative impact seems to be worse with lower eGFR.