TY - JOUR
T1 - Clinical effects of calcium channel blockers and renin-angiotensin- aldosterone system inhibitors on changes in the estimated glomerular filtration rate in patients with polycystic kidney disease
AU - Mitobe, Michihiro
AU - Yoshida, Takumi
AU - Sugiura, Hidekazu
AU - Shiohira, Shunji
AU - Shimada, Katsunori
AU - Nitta, Kosaku
AU - Tsuchiya, Ken
N1 - Funding Information:
This work was supported by a grant from the Japan Research Promotion Society for Cardiovascular Diseases. We especially wish to thank Ai Munekawa, Mayuko Tsuboi and Atsuko Teraoka for their assistance.
PY - 2010/12
Y1 - 2010/12
N2 - Background: In the tubular cells of patients with polycystic kidney disease (PKD), a reduced intracellular Ca2+ level accelerates cell proliferation, resulting in cyst formation. Thus, whether calcium channel blockers (CCB) are useful for the treatment of hypertension in patients with PKD is questionable. Methods: Thirty-two outpatients with autosomal dominant PKD (ADPKD) were treated at Tokyo Women's Medical University between 2003 and 2008; these patients were studied retrospectively. Periods during which the antihypertensive drug prescriptions for CCB and/or renin-angiotensin-aldosterone system inhibitors (RAAS-I; including angiotensin converting enzyme inhibitor and angiotensin II receptor blocker) had not been changed for at least 1 year and during which time a diuretic agent had not been prescribed were selected from among the clinical histories of the 32 outpatients. Consequently, 31 periods of 31 patients were analyzed, and mean treatment duration was 2.4 years in this study. The estimated glomerular filtration rate (eGFR) was used to evaluate renal function. To evaluate the influence of CCB and RAAS-I with respect to the decrease of the eGFR, analysis of covariance (ANCOVA), including confounding factors [baseline eGFR, mean systolic blood pressure (SBP), mean diastolic blood pressure (DBP)], was used. Only CCB significantly contributed to a reduction in δeGFR in both a univariable ANCOVA and a multivariable ANCOVA. None of the confounding factors, RAAS-I, the baseline eGFR, or blood pressure, contributed to reductions in δeGFR. Conclusion: These results suggest that from a renoprotective perspective, CCB should possibly be avoided in patients with PKD unless treatment for resistant hypertension is necessary.
AB - Background: In the tubular cells of patients with polycystic kidney disease (PKD), a reduced intracellular Ca2+ level accelerates cell proliferation, resulting in cyst formation. Thus, whether calcium channel blockers (CCB) are useful for the treatment of hypertension in patients with PKD is questionable. Methods: Thirty-two outpatients with autosomal dominant PKD (ADPKD) were treated at Tokyo Women's Medical University between 2003 and 2008; these patients were studied retrospectively. Periods during which the antihypertensive drug prescriptions for CCB and/or renin-angiotensin-aldosterone system inhibitors (RAAS-I; including angiotensin converting enzyme inhibitor and angiotensin II receptor blocker) had not been changed for at least 1 year and during which time a diuretic agent had not been prescribed were selected from among the clinical histories of the 32 outpatients. Consequently, 31 periods of 31 patients were analyzed, and mean treatment duration was 2.4 years in this study. The estimated glomerular filtration rate (eGFR) was used to evaluate renal function. To evaluate the influence of CCB and RAAS-I with respect to the decrease of the eGFR, analysis of covariance (ANCOVA), including confounding factors [baseline eGFR, mean systolic blood pressure (SBP), mean diastolic blood pressure (DBP)], was used. Only CCB significantly contributed to a reduction in δeGFR in both a univariable ANCOVA and a multivariable ANCOVA. None of the confounding factors, RAAS-I, the baseline eGFR, or blood pressure, contributed to reductions in δeGFR. Conclusion: These results suggest that from a renoprotective perspective, CCB should possibly be avoided in patients with PKD unless treatment for resistant hypertension is necessary.
KW - Calcium channel blocker
KW - Hypertension
KW - Polycystic kidney disease
KW - Renin-angiotensin-aldosterone system inhibitor
KW - eGFR
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U2 - 10.1007/s10157-010-0329-5
DO - 10.1007/s10157-010-0329-5
M3 - Article
C2 - 20700620
AN - SCOPUS:78650953274
SN - 1342-1751
VL - 14
SP - 573
EP - 577
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
IS - 6
ER -