No Effect of Angiotensin-Converting Enzyme Gene Polymorphism on Disease Progression and Left Ventricular Hypertrophy in Autosomal Dominant Polycystic Kidney Disease

2003 ◽  
Vol 23 (6) ◽  
pp. 466-470 ◽  
Author(s):  
Tevfik Ecder ◽  
Kimberly K. McFann ◽  
Mary V. Raynolds ◽  
Robert W. Schrier
Keyword(s):  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Autosomal Dominant ◽  
Left Ventricular ◽  
Angiotensin Converting Enzyme Gene ◽  
Converting Enzyme ◽  
Polycystic Kidney ◽  
Enzyme Gene ◽  
Autosomal Dominant Polycystic Kidney

scholarly journals Left ventricular hypertrophy in a contemporary cohort of autosomal dominant polycystic kidney disease patients

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Huanwen Chen ◽  
Terry Watnick ◽  
Susie N. Hong ◽  
Barry Daly ◽  
Yongfang Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Linear Regression ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Autosomal Dominant ◽  
Left Ventricular ◽  
Polycystic Kidney ◽  
Lv Mass ◽  
Autosomal Dominant Polycystic Kidney

Abstract Background Patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) often develop hypertension in childhood or early adulthood. Although this could result in left ventricular hypertrophy (LVH), a major risk factor for cardiovascular morbidity and mortality, prior studies of LVH in ADPKD have yielded conflicting results. We estimated the prevalence of LVH using consensus echocardiography criteria and examined the independent association of ADPKD severity with LV mass in a contemporary cohort of ADPKD patients. Methods Adults with ADPKD and eGFR> 15 ml/min/1.73m2 were enrolled in a single-center study. Left Ventricular Mass (LVM) was quantified using 2D echocardiography, and LVH was defined using gender-specific cut-points of LVM and LVM indexed to body surface area (LVMI) from consensus guidelines. Total Kidney Volume (TKV) was quantified using Magnetic Resonance Imaging, and GFR was estimated from serum creatinine using the CKD-Epi equation. Multiple linear regression was used to estimate the association of TKV and eGFR with LVM and LVMI, adjusting for potential confounders. Results Among 126 participants (78% with hypertension), median age was 46 years, median eGFR 63 ml/min/1.73 m2, and median [IQR] systolic blood pressure was 125 [116–133] mmHg. Prevalence of LVH was 21.4% as defined by LVMI and was not significantly different (p = 0.8) between those with and without HTN, and was similar (21.4%) after excluding those (N = 21) with known cardiac disease. Greater TKV and lower eGFR were directly correlated with greater LVMI (p = .016 and p < .001, respectively). In multiple linear regression models accounting for potential confounders including blood pressure, greater TKV was positively associated with LVM ($$ \hat{\beta} $$ β ̂ =0.19, p = 0.04). Conclusions In a contemporary cohort of ADPKD patients with well-controlled blood pressure, the prevalence of LVH is high, and ADPKD severity as reflected by TKV is independently associated with greater LV mass. These results may suggest a relationship between ADPKD pathophysiology and increased LV mass.

scholarly journals Left ventricular hypertrophy in autosomal dominant polycystic kidney disease.

1997 ◽  
Vol 8 (8) ◽  
pp. 1292-1297
Author(s):  
A B Chapman ◽  
A M Johnson ◽  
S Rainguet ◽  
K Hossack ◽  
P Gabow ◽  
...  
Keyword(s):  
Risk Factors ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Autosomal Dominant ◽  
Left Ventricular ◽  
Polycystic Kidney ◽  
Control Subjects ◽  
Healthy Control ◽  
Autosomal Dominant Polycystic Kidney

Cardiovascular complications are the most common cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). To understand this relationship, known cardiovascular risk factors were examined in ADPKD. Left ventricular hypertrophy (LVH) is a known, important risk factor for premature cardiovascular death in patients with essential hypertension. Hypertension is known to occur frequently and early in ADPKD patients. The frequency of LVH in ADPKD patients and its relation with hypertension and other risk factors, however, is not known. In this study, echocardiographic tests were performed in 116 consecutive adult ADPKD patients and 77 healthy control subjects. There was a significantly higher frequency of LVH in ADPKD men (46 versus 20%, P < 0.05) and women (37 versus 12%, P < 0.005) compared with control subjects. LVH in ADPKD patients was associated with higher systolic and diastolic arterial BP. There also was an association between LVH, diminished renal function, and increased renal volume. When comparing ADPKD patients with and without LVH, the former were older, weighed more, had a higher prevalence of hypertension, and had a lower hematocrit value and more renal impairment. LVH was also present in 23% of normotensive ADPKD patients and 16% of healthy control subjects (P = NS), but did not correlate with BP. The role of BP as a contributing factor to LVH in ADPKD patients may be due in part to earlier onset and inadequate treatment.

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