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Annals of Clinical and Experimental Hypertension

Approach of Hypertension in Autosomal Dominant Polycystic Kidney Disease

Editorial | Open Access | Volume 1 | Issue 1

  • 1. Department of Medicine A (M8), Charles Nicolle Hospital, North Africa
  • 2. Laboratory of Kidney Pathology (LR00SP01) Charles Nicolle Hospital, North Africa
  • 3. Faculty of Medicine, University of Tunis El Manar, North Africa
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Corresponding Authors
Imed Helal, Department of Medicine A (M8), Charles Nicolle Hospital. Bd 9 avril, BS 1006, Tunis-Tunisia, Tel: 00216-97-270-570; Fax: 00216-71-560-280;
Citation

Cite this article: Helal I, Gorsane I, Harzallah A, Zaziri F, Elgaied H, et al. (2013) Approach of Hypertension in Autosomal Dominant Polycystic Kidney Disease. Ann Clin Exp Hypertension 1(1): 1002.

EDITORIAL

In this Inaugural Issue of Annals of Clinical and Experimental Hypertension, we are interested by hypertension in autosomal dominant polycystic kidney disease (ADPKD). ADPKD is the most common, life threatening single-gene disease. It affects over 12.5 million worldwide [1] and responsible of 5 – 10% of end-stage renal disease (ESRD) [2]. Hypertension is a common and serious complication of ADPKD, often occurring early in the disease before appearance of renal dysfunction [3]. Early and effective treatment of hypertension is very important to decrease the morbidity and mortality of ADPKD patients. Patients with ADPKD have an increased incidence of hypertension, left ventricular hypertrophy (LVH) and cardiovascular abnormalities [4]. The reported relative mortality rate in patients with ADPKD ranges between 1.6-fold [95% confidence interval (CI) 1.3-2.0] and 3.2-fold higher [95% CI 2-4.8] in comparison to the general population [5]. Hypertension occurs in approximately 60% of the patients with ADPKD before any decline of renal function [3]. Hypertension is circumstance of diagnosis of ADPKD in 30%. Therefore, discover of hypertension in a young patient warrant lumbair examination and renal ultrasonography screening. Hypertension is associated with a faster progression to ESRD [6]. It has been demonstrated that better hypertension control leads to improvement in ADPKD outcomes [6]. However, cardiovascular disease still remains the main cause of death in ADPKD [7]. Also it has been demonstrated a significant decrease of kidney disease progression in ADPKD patients associated with attainment of better hypertension control and increased use of angiotensin converting enzyme inhibitors (ACEIs) [8]. Current published data confirm that patients with ADPKD in the United Sates [9], Denmark [10] and Great Britain [11] are having a better prognosis. There has been an earlier diagnosis, better control of blood pressure, more use of renin-angiotensin-aldosterone system (RAAS) inhibitors, better preservation of renal function, later onset of ESRD, and better survival. The improved survival no doubt involves factors in addition to the better control of blood pressure and preservation of renal function, and this issue therefore needs further study [9-11]. The pathogenesis of hypertension in ADPKD is complex and dependent on many factors that influence each other. Cyst growth, renal handling of sodium, activation of the RAAS, volume expansion, an elevated plasma volume, and increased plasma atrial natriuretic peptide and plasma endothelin levels have all been found to be associated with hypertension in ADPKD. Activation of the RAAS seems to have a major role in the pathogenesis of hypertension in ADPKD patients. Plasma renin activity and plasma aldosterone concentration are increased more in supine and upright positions in patients with ADPKD compared with patients with essential hypertension matched for age, sex, kidney function, sodium intake, and degree of hypertension [12]. All components of the RAAS system have been identified in kidneys from patients with ADPKD [13]. The question of whether treatment with either ACEIs and/or angiotensin receptor blockers (ARBs) is more effective on kidney disease progression in ADPKD will be answered by the HALT study [14].This study is a prospective clinical interventional study for adult ADPKD patients. This study will test whether intensive blockade of the RAAS with combination of ACEI and ARB therapy will slow renal progression in ADPKD patients, compared with ACEI monotherapy alone. In addition, the study will test whether rigorous versus moderate hypertension control will be more effective in slowing kidney progression in this population. In conclusion, Hypertension occurs early in ADPKD patients and before impairment of renal function. Hypertension is associated with a faster progression to ESRD and represents the most important potentially treatable factor in ADPKD. Hypertension plays also an important role in cardiovascular disease, which is the most frequent cause of death in ADPKD patients. Experimental and clinical data show that the RAAS is an important factor in the development of hypertension in ADPKD. Early and effective treatment of hypertension is very important to decrease the morbidity and mortality of ADPKD patients. Prospective randomized studies are needed to determine the most appropriate agents for the treatment of hypertension in these patients.

REFERENCES

1. Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet. 2007; 369: 1287-1301. 

2. U.S. Renal Data System: USRDS 2013 Annual Data Report, 2013.

3. Ecder T, Schrier RW. Hypertension in autosomal-dominant polycystic kidney disease: early occurrence and unique aspects. J Am Soc Nephrol. 2001; 12: 194-200.

4. Helal I, Reed B, Mettler P, Mc Fann K, Tkachenko O, Yan XD, et al. Prevalence of cardiovascular events in patients with autosomal dominant polycystic kidney disease. Am J Nephrol. 2012; 36: 362-370.

5. Florijin KW, Noteboom WM, Van Saase JL, Chang PC, Breuning MH, Vandenbroucke JP. A century of mortality in five large families with polycystic kidney disease. Am J Kidney Dis. 1995; 25: 370-374.

6. Ecder T, Edelstein CL, Fick-Brosnahan GM, Johnson AM, Duley IT, Gabow PA, et al. Progress in blood pressure control in autosomal dominant polycystic kidney disease. Am J Kidney Dis. 2000; 36: 266- 271.

7. Fick GM, Johnson AM, Hammond WS, Gabow PA. Causes of death in autosomal dominant polycystic kidney disease. J Am Soc Nephrol. 1995; 5: 2048-2056.

8. Schrier RW, McFann KK, Johnson AM. Epidemiological study of kidney survival in autosomal dominant polycystic kidney disease. Kidney Int. 2003; 63: 678-685.

9. Helal I, McFann K, Reed B, Yan XD, Schrier RW. Changing referral characteristics of patients with autosomal dominant polycystic kidney disease. Am J Med. 2013; 126: 832.e7-832.e11.

10.Orskov B, Rømming Sørensen V, Feldt-Rasmussen B, Strandgaard S. Improved prognosis in patients with autosomal dominant polycystic kidney disease in Denmark. Clin J Am Soc Nephrol. 2010; 5: 2034- 2039.

11.Patch C, Charlton J, Roderick PJ, Gulliford MC. Use of antihypertensive medications and mortality of patients with autosomal dominant polycystic kidney disease: A population-based study. Am J Kidney Dis. 2001; 57: 856-862.

12.Chapman AB, Johnson A, Gabow PA, Schrier RW. The reninangiotensin-aldosterone system and autosomal dominant polycystic kidney disease. N Engl J Med. 1990; 323: 091-1096.

13.Loghman-Adham M, Soto CE, Inagami T, Cassis L. The intrarenal reninangiotensin-system in autosomal dominant polycystic kidney disease. Am J Physiol Renal Physiol. 2004; 287: F775-788.

14.Chapman AB, Torres VE, Perrone RD, Steinman TI, Bae KT, Miller JP, et al. The HALT polycystic kidney disease trials: Design and implementation. Clin J Am Soc Nephrol. 2010; 5: 102-109.

Cite this article: Helal I, Gorsane I, Harzallah A, Zaziri F, Elgaied H, et al. (2013) Approach of Hypertension in Autosomal Dominant Polycystic Kidney Disease. Ann Clin Exp Hypertension 1(1): 1002.

Received : 30 Nov 2013
Accepted : 30 Nov 2013
Published : 02 Dec 2013
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