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Progression of Chronic Kidney Disease: The Role of Blood Pressure Control, Proteinuria, and Angiotensin-Converting Enzyme Inhibition: A Patient-Level Meta-Analysis

Tazeen H. Jafar, MD, MPH; Paul C. Stark, ScD; Christopher H. Schmid, PhD; Marcia Landa, MA; Giuseppe Maschio, MD; Paul E. de Jong, MD, PhD; Dick de Zeeuw, MD, PhD; Shahnaz Shahinfar, MD; Robert Toto, MD; Andrew S. Levey, MD, AIPRD Study Group*
[+] Article and Author Information

From Tufts–New England Medical Center, Boston, Massachusetts; The Aga Khan University, Karachi, Pakistan; Ospedale Civile Maggiore, Verona, Italy; University of Groningen, Groningen, the Netherlands; Merck Research Laboratories, West Point, Pennsylvania; and University of Texas at Southwestern Medical Center, Dallas, Texas.


Grant Support: By grant RO1 DK53869A from the U.S. National Institute of Diabetes and Digestive and Kidney Diseases (Dr. Levey); grant RO1 HS 10064 from the Agency for Healthcare Research and Quality (Dr. Schmid); a grant from Dialysis Clinic, Inc., Paul Teschan Research Fund 1097-5 (Dr. Jafar); New England Medical Center St. Elizabeth's Hospital Clinical Research Fellowship, Boston, Massachusetts (Dr. Jafar); and an unrestricted grant from Merck Research Laboratories, West Point, Pennsylvania (Dr. Levey).

Potential Financial Conflicts of Interest:Employment: S. Shahinfar (Merck & Co.); Stock ownership or options (other than mutual funds): S. Shahinfar (Merck & Co.); Consultancies: R.D. Toto (Merck & Co.); Honoraria: R.D. Toto (Merck & Co.); Grants received: R.D. Toto (Merck & Co.), A.S. Levey (Merck & Co.).

Requests for Single Reprints: Andrew S. Levey, MD, Division of Nephrology, Tufts–New England Medical Center, 750 Washington Street, Box 391, Boston, MA 02111.

Current Author Addresses: Dr. Jafar: Department of Medicine, The Aga Khan University, Stadium Road, PO Box 3500, Karachi, Pakistan.

Drs. Stark and Schmid: Division of Clinical Care Research, Biostatistics Research Center, Tufts–New England Medical Center, Box 63, 750 Washington Street, Boston, MA 02111.

Dr. Landa: Division of Clinical Care Research, Tufts–New England Medical Center, 35 Kneeland Street #827, Boston, MA 02111.

Dr. Maschio: Division Nefrologia, Ospedale Civile Maggiore, 37126 Verona, Italy.

Drs. Jong and de Zeeuw: University of Groningen, Oostersingel 59, 9713 EZ Groningen, the Netherlands.

Dr. Shahinfar: Merck Research Labs, 10 Sentry Parkway, Walton and Stenton Avenue, BL-1, Blue Bell, PA 19422.

Dr. Toto: Patient-Oriented Research in Nephrology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8856.

Dr. Levey: Division of Nephrology, Tufts–New England Medical Center, 750 Washington Street, Box 391, Boston, MA 02111.

Author Contributions: Conception and design: C.H. Schmid, A.S. Levey.

Analysis and interpretation of the data: T.H. Jafar, P.C. Stark, C.H. Schmid, A.S. Levey.

Drafting of the article: T.H. Jafar, P.C. Stark, C.H. Schmid, G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto, A.S. Levey.

Critical revision of the article for important intellectual content: T.H. Jafar, P.C. Stark, C.H. Schmid, G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto, A.S. Levey.

Final approval of the article: P.C. Stark, C.H. Schmid, G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto, A.S. Levey.

Provision of the study materials or patients: G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto.

Statistical expertise: P.C. Stark, C.H. Schmid, A.S. Levey.

Obtaining of funding: T.H. Jafar, C.H. Schmid, A.S. Levey.

Administrative, technical, or logistic support: P.C. Stark, C.H. Schmid, A.S. Levey.

Collection and assembly of the data: T.H. Jafar, P.C. Stark, C.H. Schmid, M. Landa, G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto.


Ann Intern Med. 2003;139(4):244-252. doi:10.7326/0003-4819-139-4-200308190-00006
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Our results show independent, strong, graded relationships between higher levels of current systolic blood pressure and urine protein excretion and the risk for kidney disease progression during antihypertensive therapy with or without ACE inhibitors in patients with nondiabetic kidney disease. After adjustment for systolic blood pressure, diastolic pressure was not a risk factor. The lowest risk for kidney disease progression seemed to be at levels of current systolic blood pressure of 110 to 129 mm Hg and urine protein excretion less than 2.0 g/d. However, the relationship of the level of current systolic blood pressure with the risk for kidney disease progression varied with the level of current urine protein excretion. At levels of current urine protein excretion greater than 1.0 g/d, the risk for kidney disease progression increased steeply at current systolic blood pressures greater than 120 to 130 mm Hg; however, at levels of current urine protein excretion less than 1.0 g/d, there was little relationship between risk for kidney disease progression and current systolic blood pressure from 110 to 159 mm Hg. At both levels of current urine protein excretion, a current systolic blood pressure less than 110 mm Hg was associated with a higher risk for kidney disease progression. The findings were similar in patients receiving antihypertensive regimens with or without ACE inhibitors.

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Figure.
Relative risk for kidney disease progression based on current level of systolic blood pressure and current urine protein excretion.

The relative risk for patients with a current urine protein excretion of 1.0 g/d or greater represents 9336 patients (223 events), and the relative risk for patients with a current urine protein excretion less than 1.0 g/d represents 13 274 visits (88 events). The reference group for each is defined at a systolic blood pressure of 110 to 119 mm Hg. Confidence intervals are truncated, as shown. Results are from a single multivariable model including two levels for urine protein excretion, six levels for systolic blood pressure, and the interaction of current systolic blood pressure and current urine protein excretion. Covariates include assignment to angiotensin-converting enzyme inhibitor versus control group, sex, age, baseline systolic blood pressure, baseline diastolic blood pressure, baseline urine protein excretion, baseline serum creatinine concentration (<2.0 or ≥ 2.0 mg/dL [<177 or ≥ 177 µmol/L]), interaction of baseline serum creatinine and baseline urine protein excretion, interaction of baseline serum creatinine and current urine protein excretion, and study terms.

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Summary for Patients

Blood Pressure and Urine Protein Levels with the Least Risk for Worsening Kidney Disease

The summary below is from the full report titled “Progression of Chronic Kidney Disease: The Role of Blood Pressure Control, Proteinuria, and Angiotensin-Converting Enzyme Inhibition. A Patient-Level Meta-Analysis.” It is in the 19 August 2003 issue of Annals of Internal Medicine (volume 139, pages 244-252). The authors are T.H. Jafar, P.C. Stark, C.H. Schmid, M. Landa, G. Maschio, P.E. de Jong, D. de Zeeuw, S. Shahinfar, R. Toto, and A.S. Levey, for the AIPRD Study Group.

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