TY - JOUR
T1 - Determinants of progression in early autosomal dominant polycystic kidney disease
T2 - Is it blood pressure or renin-angiotensin-aldosterone-system blockade?
AU - HALT PKD Investigators
AU - Brosnahan, Godela M.
AU - Abebe, Kaleab Z.
AU - Moore, Charity G.
AU - Bae, Kyongtae T.
AU - Braun, William E.
AU - Chapman, Arlene B.
AU - Flessner, Michael F.
AU - Harris, Peter C.
AU - Hogan, Marie C.
AU - Perrone, Ronald D.
AU - Rahbari-Oskoui, Frederic F.
AU - Steinman, Theodore I.
AU - Torres, Vicente E.
N1 - Publisher Copyright:
© 2018 Bentham Science Publishers.
PY - 2018
Y1 - 2018
N2 - Background: The HALT PKD trial in early autosomal dominant polycystic kidney disease (ADPKD) showed that intensive control of systolic blood pressure to 95-110 mmHg was associated with a 14% slower rate of kidney volume growth compared to standard control. It is unclear whether this result was due to greater blockade of the renin-angiotensin-aldosterone system (RAAS) by allowing the use of higher drug doses in the low blood pressure arm, or due to the lower blood pressure per se. Methods: In this secondary analysis of HALT PKD Study A, we categorized participants into high and low dose groups based on the median daily equivalent dose of RAAS blocking drugs used after the initial dose titration period. Using linear mixed models, we compared the percent change in total kidney volume and the slope of estimated glomerular filtration rate (eGFR) between the 2 groups. We also assessed the effects of time-varying dose and time-varying blood pressure parameters on these outcomes. Results: Subjects in the high dose group (n=252) did not experience a slower increase in total kidney volume than those in the low-dose (n=225) group, after adjustment for age, sex, genotype, and BP arm. The chronic slope of eGFR decline was similar in the 2 groups. Higher time-varying systolic blood pressure was associated with a steeper decline in eGFR. Conclusion: ADPKD progression (as detected by eGFR decline and TKV increase) was ameliorated by intense blood pressure control as opposed to pharmacologic intensity of RAAS blockade.
AB - Background: The HALT PKD trial in early autosomal dominant polycystic kidney disease (ADPKD) showed that intensive control of systolic blood pressure to 95-110 mmHg was associated with a 14% slower rate of kidney volume growth compared to standard control. It is unclear whether this result was due to greater blockade of the renin-angiotensin-aldosterone system (RAAS) by allowing the use of higher drug doses in the low blood pressure arm, or due to the lower blood pressure per se. Methods: In this secondary analysis of HALT PKD Study A, we categorized participants into high and low dose groups based on the median daily equivalent dose of RAAS blocking drugs used after the initial dose titration period. Using linear mixed models, we compared the percent change in total kidney volume and the slope of estimated glomerular filtration rate (eGFR) between the 2 groups. We also assessed the effects of time-varying dose and time-varying blood pressure parameters on these outcomes. Results: Subjects in the high dose group (n=252) did not experience a slower increase in total kidney volume than those in the low-dose (n=225) group, after adjustment for age, sex, genotype, and BP arm. The chronic slope of eGFR decline was similar in the 2 groups. Higher time-varying systolic blood pressure was associated with a steeper decline in eGFR. Conclusion: ADPKD progression (as detected by eGFR decline and TKV increase) was ameliorated by intense blood pressure control as opposed to pharmacologic intensity of RAAS blockade.
KW - Angiotensin receptor blockers
KW - Angiotensin-converting enzyme inhibitors
KW - Autosomal dominant polycystic kidney disease
KW - Estimated glomerular filtration rate
KW - HALT PKD trials
KW - Total kidney volume
UR - http://www.scopus.com/inward/record.url?scp=85048985225&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85048985225&partnerID=8YFLogxK
U2 - 10.2174/1573402114666180322110209
DO - 10.2174/1573402114666180322110209
M3 - Article
C2 - 29564978
AN - SCOPUS:85048985225
SN - 1573-4021
VL - 14
SP - 39
EP - 47
JO - Current Hypertension Reviews
JF - Current Hypertension Reviews
IS - 1
ER -