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Clinical Nephrology |
,a
* Department of Nephrology and Hypertension, Cleveland Clinic Foundation, Cleveland, Ohio; Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin; Department of Medicine, University of Grenoble, Grenoble, France; Department of Medicine, Hospital la Paz, Madrid, Spain; || Department of Internal Medicine, University of Genova, Genova, Italy; ¶ Department of Internal Medicine, Washington Hospital Center, Washington, DC; # Hospital Clinicoy Provincial, Barcelona, Spain; ** Department of Medicine, University of Melbourne, Fitzroy, Victoria, Australia; Department of Medicine, University of Iowa, Iowa City, Iowa; Department of Medicine, University of Campinas, Campinas, Brazil; Department of Medicine, Hospital Bolognini, Seriate, Italy; |||| Department of Medicine, Washington Hospital Center, Washington, DC; ¶¶ Department of Medicine, Louisiana State University Medical Center, New Orleans, Louisiana; ## Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany; *** Department of Internal Medicine, Rudolphstiftung Hospital, Vienna, Austria; Department of Internal Medicine, Brookdale Hospital Medical Center, Brooklyn, New York; Department of Diabetes, North Middlesex Hospital, London, United Kingdom; and Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois
Address correspondence to: Dr. Marc A. Pohl, Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk A51, Cleveland, OH 44195. Phone: 216-444-6776; Fax: 216-444-9378; E-mail: pohlm{at}ccf.org
Received for publication November 8, 2004. Accepted for publication July 9, 2005.
Elevated arterial pressure is a major risk factor for progression to ESRD in diabetic nephropathy. However, the component of arterial pressure and level of BP control for optimal renal outcomes are disputed. Data from 1590 hypertensive patients with type 2 diabetes in the Irbesartan Diabetic Nephropathy Trial (IDNT), a randomized, double-blind, placebo-controlled trial performed in 209 clinics worldwide, were examined, and the effects of baseline and mean follow-up systolic BP (SBP) and diastolic BP and the interaction of assigned study medications (irbesartan, amlodipine, and placebo) on progressive renal failure and all-cause mortality were assessed. Other antihypertensive agents were added to achieve predetermined BP goals. Entry criteria included elevated baseline serum creatinine concentration up to 266 µmol/L (3.0 mg/dl) and urine protein excretion >900 mg/d. Baseline BP averaged 159/87 ± 20/11 mmHg. Median patient follow-up was 2.6 yr. Follow-up achieved SBP most strongly predicted renal outcomes. SBP >149 mmHg was associated with a 2.2-fold increase in the risk for doubling serum creatinine or ESRD compared with SBP <134 mmHg. Progressive lowering of SBP to 120 mmHg was associated with improved renal and patient survival, an effect independent of baseline renal function. Below this threshold, all-cause mortality increased. An additional renoprotective effect of irbesartan, independent of achieved SBP, was observed down to 120 mmHg. There was no correlation between diastolic BP and renal outcomes. We recommend a SBP target between 120 and 130 mmHg, in conjunction with blockade of the renin-angiotensin system, in patients with type 2 diabetic nephropathy.
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