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Biomedical Sciences

Quillen College of Medicine

Dr. Aaron Polichnowski
Polichnowski pic

Dr. Aaron Polichnowski

Assistant Professor Department of Biomedical Sciences

Curriculum Vitae

Contact Information:

Aaron Polichnowski, Ph.D.
Assistant Professor
Department of Biomedical Sciences
Carl A. Jones Hall (VA Bldg 1 & 119)
Office: VA Bldg. 1, Room 132
Lab: VA Bldg. 119, Rooms 320 & 322
James H. Quillen College of Medicine
East Tennessee State University
PO Box 70577
Johnson City, TN 37614
Phone: 423-439-5625
Fax: 423-439-8044


Education and Professional Background:

1999 -  B.S., Exercise Science, East Tennessee State University
2001 -  M.S., Exercise Physiology, University of Wisconsin Milwaukee
2009 -  Ph.D., Physiology, Medical College of Wisconsin
2011 -  Postdoctoral Fellowship, Nephrology, Loyola University Chicago

Research/Teaching Interests:

  1. Acute kidney injury and chronic kidney disease.
  2. Reduced nitric oxide availability and susceptibility to hypertensive kidney disease.
  3. Regulation of renal blood flow.

Current Research Support:

Veterans Administration, Career Development Award 2
IK2 BX001285 (Polichnowski) 4/1/2011 9/30/2016
Title: Nitric Oxide Deficiency in Hypertensive Nephropathies
This project examines the blood pressure dependent and independent mechanisms by which reduced nitric oxide availability increases the susceptibility to renal injury.

Recent Publications:

  1. Picken MM, Long J, Williamson GA, Polichnowski AJ. Progression of Chronic Kidney Disease Following Acute Kidney Injury: Role of Self-perpetuating vs. Hemodynamic-induced Fibrosis. Hypertension 68(4):921-928, 2016.

  2. Polichnowski AJ, Licea-Vargas H, Picken MM, Long J, Bisla R, Williamson GA, Bidani AK, Griffin KA. Glomerulosclerosis in the diet-induced obesity model correlates with sensitivity to nitric oxide inhibition but not glomerular hyperfiltration or hypertrophy. Am J Physiol Renal Physiol. 309(9):F791-799, 2015.

  3. Griffin KA, Pothugunta K, Polichnowski AJ, Bidani AK. The role of systemic blood pressure in the progression of chronic kidney disease. Current Cardiovascular Risk Reports. May; 9(5), 2015.

  4. Polichnowski AJ, Griffin KA, Picken MM, Licea-Vargas H, Long J, Williamson GA, Bidani AK. Hemodynamic basis for the limited renal injury in rats with angiotensin II-induced hypertension. Am J Physiol Renal Physiol. 308(3):F252-260, 2015.

  5. Griffin KA, Polichnowski A, Litbarg N, Picken M, Venkatachalam MA, Bidani AK. The critical BP threshold dependence of hypertensive injury and repair in a malignant nephrosclerosis model. Hypertension 64(4):801-807, 2014.

  6. Polichnowski AJ, Lan R, Geng H, Griffin KA, Venkatachalam MA, Bidani AK. Severe renal mass reduction impairs recovery and promotes fibrosis after AKI. J of Am Soc Nephrol. 25(7):1496-1507, 2014.

  7. Polichnowski AJ, Griffin KA, Long J, Williamson GW, Bidani AK. Blood pressure renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats. Am J Physiol Renal Physiol. 305(7): 1074-1084, 2013.

  8. Bidani AK, Polichnowski AJ, Loutzenhiser R, Griffin KA. Renal microvascular dysfunction, hypertension and CKD progression. Curr Opin Nephrol Hypertens 22(1):1-9, 2013.

  9. Lan R, Geng H, Polichnowski AJ, Singha PK, Saikumar P, McEwen DG, Griffin KA, Koesters R, Weinberg JM, Bidani AK, Kriz W, Venkatachalam MA. PTEN loss defines a TGF induced tubule phenotype of failed differentiation and JNK signaling during renal fibrosis.
    Am J Physiol Renal Physiol 302(9): 1210-1223, 2012.

  10. Griffin K, Polichnowski A, Licea-Vargas H, Picken M, Long J, Williamson G, Bidani A. Large BP-dependent and independent differences in susceptibility to nephropathy after nitric oxide inhibition in Sprague-Dawley rats from two major suppliers. Am J Physiol Renal Physiol 302(1): 173-182, 2012.

PubMed publications

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