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Published ahead of print on May 3, 2006
J Am Soc Nephrol 17: 1703-1709, 2006
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2005080872
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Hemodynamics and Vascular Regulation

Impact of Renin Angiotensin System Modulation on the Hyperfiltration State in Type 1 Diabetes

Etienne B. Sochett*, David Z.I. Cherney{dagger}, Jacqueline R. Curtis*, Maria G. Dekker*, James W. Scholey{dagger} and Judith A. Miller{dagger}

* Division of Endocrinology, Hospital for Sick Children; and {dagger} Division of Nephrology, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada

Address correspondence to: Dr. Judith A. Miller, Toronto General Hospital, 585 University Avenue, 8N-846, Toronto, Ontario, M5G 2N2, Canada. Phone: 416-340-4966; Fax: 416-340-4951; E-mail: judith.miller{at}utoronto.ca

Received for publication August 22, 2005. Accepted for publication March 23, 2006.

The initial stages of diabetic nephropathy are characterized by glomerular hyperfiltration and hypertension, processes that have been linked to initiation and progression of renal disease. Renin angiotensin system (RAS) blockade is commonly used to modify the hyperfiltration state and delay progression of renal disease. Despite this therapy, many patients progress to ESRD, suggesting heterogeneity in the response to RAS modulation. The role of the RAS in the hyperfiltration state in adolescents with uncomplicated type 1 diabetes was examined, segregated on the basis of the presence of hyperfiltration. Baseline renal hemodynamic function was characterized in 22 patients. Eleven patients exhibited glomerular hyperfiltration (GFR ≥ 135 ml/min), and in the remaining 11 patients, the GFR was <130 ml/min. Renal hemodynamic function was assessed in response to a graded angiotensin II (AngII) infusion during euglycemic conditions and again after 21 d of angiotensin-converting enzyme (ACE) inhibition with enalapril. AngII infusion under euglycemic conditions resulted in a significant decline in GFR and renal plasma flow in the hyperfiltration group but not in the normofiltration group. After ACE inhibition, GFR fell but did not normalize in the hyperfiltration group; the normofiltration group showed no change. These data show significant differences in renal hemodynamic function between hyperfiltering and normofiltering adolescents with type 1 diabetes at baseline, after AngII infusion and ACE inhibition. The response to ACE inhibition and AngII in hyperfiltering patients suggests that vasodilation may complement RAS activation in causing the hyperfiltration state. The interaction between glomerular vasoconstrictors and vasodilators requires examination in future studies.




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