Biventricular diastolic dysfunction in patients with autosomal-dominant polycystic kidney disease

Oflaz, Hüseyin; Alışır, Sabahat; Büyükaydın, Banu; Kocaman, Orhan; Turgut, Faruk; Namli, Sule; Pamukçu, Burak; Öncül, Aytaç; Ecder, Tevfik

doi:10.1111/j.1523-1755.2005.00682.x

Cited by 51 publications

(35 citation statements)

References 39 publications

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“…[2] Increased left ventricular mass indexes, biventricular diastolic dysfunction, ED, increased carotid intima-media thickness, and exaggerated blood pressure response during exercise have been reported even in young normotensive patients with ADPKD with well-preserved renal function. [4,[14][15][16][17][18][19][20][21] Ambulatory blood pressure and non-dipping pattern have been shown to be more closely associated with target organ damage and a worsened cardiovascular outcome than clinic blood pressure in patients with essential hypertension. [22] Li Kam Wa et al [8] have reported that hypertensive patients with ADPKD have significantly less nocturnal fall in blood pressure compared to patients with essential hypertension.…”

Section: Discussionmentioning

confidence: 99%

Ambulatory Blood Pressure and Endothelial Dysfunction in Patients with Autosomal Dominant Polycystic Kidney Disease

et al. 2007

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Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Endothelial dysfunction (ED), which is an early manifestation of vascular injury, has been shown in patients with ADPKD. However, the association between ambulatory blood pressure and ED has not been investigated in these patients. Forty-one patients with ADPKD having well-preserved renal function were included in the study. Ambulatory blood pressure monitoring was performed in all patients. Patients were divided into dipper and non-dipper groups. Endothelial function of the brachial artery was evaluated by using high-resolution vascular ultrasound. Endothelial-dependent dilatation was expressed as the percentage change in the brachial artery diameter from baseline to reactive hyperemia. The mean 24-hour systolic blood pressure was similar in both groups (125.5 ± 10.7 mmHg in dippers and 121.2 ± 14.3 in non-dippers, p > 0.05). There was also no significant difference between the mean 24-hour diastolic blood pressures in both groups (82.3 ± 9.6 mmHg in dippers and 77.1 ± 8.6 mmHg in non-dippers, p > 0.05). The nocturnal fall rate in systolic blood pressure was 11.1 ± 1.2% in dippers and 0.98 ± 0.9% in non-dippers (p = 0.001). The nocturnal fall rate in diastolic blood pressure was 14.0 ± 0.9% in dippers and 3.8 ± 0.8% in non-dippers (p = 0.001). Endothelial-dependent dilatation was significantly higher in dippers compared to non-dippers (6.22 ± 4.14% versus 3.57 ± 2.52%, p = 0.025). Non-dipper patients with ADPKD show significant ED, which has an important impact on cardiovascular morbidity and mortality.

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Section: Discussionmentioning

confidence: 99%

Ambulatory Blood Pressure and Endothelial Dysfunction in Patients with Autosomal Dominant Polycystic Kidney Disease

et al. 2007

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“…Hypertension in ADPKD is characterized by relative activation of the reninangiotensin-aldosterone system (RAAS) (20 -22), the sympathetic nervous system (23), endothelin (24), and vasopressin (25,26). Abnormalities in endothelial function, left and right ventricular function, and kidney blood flow are present before loss of kidney function and the development of hypertension, and renal excretion of sodium is reduced early in ADPKD (27)(28)(29)(30)(31)(32)(33)(34)(35). These observations suggest that defects as a result of mutations in the polycystins may result in a vascular phenotype that is specific to ADPKD.…”

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Autosomal Dominant Polycystic Kidney Disease

Chapman

2007

Journal of the American Society of Nephrology

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Diagnosis and treatment of autosomal dominant polycystic kidney disease (ADPKD) is rapidly changing. Cellular pathways that involve the polycystins are being mapped and involve the primary cilium, intracellular calcium and cAMP regulation, and the mammalian target of rapamycin (mTOR) pathway. With the use of new imaging approaches, earlier diagnosis of hepatic cystic disease is possible, and measurement of kidney and cystic growth as well as kidney blood flow is possible over relatively short periods. PKD gene type, gender, proteinuria, and the presence of hypertension relate to the rate of kidney growth in ADPKD. On the basis of risk factors for progression to ESRD and the pathogenic roles that intracellular cAMP and mTOR play in cystogenesis, novel therapies are now being tested, including maximal inhibition of the renin-angiotensin system, inhibition of renal intracellular cAMP using vasopressin V2 receptor antagonists, and somatostatin analogues, as well as inhibitors of mTOR. This review addresses the current understanding of the pathogenesis and the natural history of ADPKD; accuracy and reliability of diagnostic approaches in utero, childhood, and adulthood; the value of reliable magnetic resonance imaging to measure disease progression early in the course of ADPKD; and novel therapeutic approaches that are being evaluated in ADPKD.

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“…The RAS activation plays an important role in atherosclerosis, LVH heart failure, and end stage renal failure. 14,16 Hereditary factors and myocardial collagen matrix failure as well as RAS activation are the factors blamed for LVH etiology in normotensive polycystic kidney patients. 14,17 In the study by Valero et al 14 the contribution of ambulatory BP change to LVH in normotensive polycystic kidney patients was evaluated.…”

Section: Discussionmentioning

confidence: 99%

“…14,15 In a study, compared to control group, 23% higher LVH was identified in normotensive polycystic kidney patients. 16 One of the mechanisms highlighted that ischemia occurs as a result of cyst pressure to nearby tissues because of expansion. The RAS activation starts at early stages of the disease before hypertension and renal damage are seen.…”

Section: Discussionmentioning

confidence: 99%

A comparison of the effects of ramipril and losartan on blood pressure control and left ventricle hypertrophy in patients with autosomal dominant polycystic kidney disease

et al. 2010

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Background: Hypertension is frequently seen in autosomal dominant polycystic kidney disease (ADPKD), and it has a negative effect on renal progression. Hypertension and left ventricle hypertrophy (LVH) are related in terms of pathogenesis and their effects on renal progression. In this study, we aimed to compare the effects of losartan and ramipril on blood pressure (BP) control, LVH, and renal progression in patients with hypertensive ADPKD. Methods: Thirty-two ADPKD patients with ages ranging between 18 and 70 years who were stage 1-2 hypertensive were included in this study. Routine biochemical tests and echocardiography were obtained at first examination of the patients. Following these, the patients were randomized. One group was given losartan and the other ramipril. They were followed up for 1 year, and their echocardiographies and routine biochemical tests were repeated at the end of the year. Results: BP values decreased in both the groups at the end of the first year (p < 0.001). There was a statistically significant difference in LVH in both the groups at the end of the first year than at the beginning (losartan, p = 0.007; ramipril, p < 0.001). Conclusions: In this study, effective BP control was obtained with losartan and ramipril and LVH was found to be regressed significantly in the hypertensive patients with ADPKD. These two groups of antihypertensive drugs may also have beneficial effects on the retardation of renal progression and in reducing cardiovascular mortality in hypertensive patients with ADPKD.

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Biventricular diastolic dysfunction in patients with autosomal-dominant polycystic kidney disease

Abstract: Both hypertensive and normotensive patients with ADPKD show significant biventricular diastolic dysfunction, suggesting cardiac involvement very early in the course of ADPKD.

Cited by 51 publications

References 39 publications

Ambulatory Blood Pressure and Endothelial Dysfunction in Patients with Autosomal Dominant Polycystic Kidney Disease

Ambulatory Blood Pressure and Endothelial Dysfunction in Patients with Autosomal Dominant Polycystic Kidney Disease

Autosomal Dominant Polycystic Kidney Disease

A comparison of the effects of ramipril and losartan on blood pressure control and left ventricle hypertrophy in patients with autosomal dominant polycystic kidney disease

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