Department of Medicine

Faculty

Richard J Johnson, M.D.
Professor & Chief,
Division of Nephrology, Hypertension and Renal Transplant

Dr. Richard J Johnson is currently the J. Robert Cade Professor of Medicine and Chief of the Division of Nephrology, Hypertension, and Renal Transplantation at the University of Florida. Dr Johnson received his undergraduate degree in Anthropology in 1975 from the University of Wisconsin, and his M.D. degree in 1979 from the University of Minnesota in Minneapolis. He completed an internal medicine residency and nephrology and infectious diseases fellowships at the University of Washington Medical Center in Seattle. Dr. Johnson joined the faculty at the University of Washington in 1986, and in 2000 moved to Baylor College of Medicine in Houston, Texas where he was the Chief of Nephrology. In September 2003 he joined the faculty at the University of Florida to take on his current position. Dr. Johnson is nationally and internationally renowned for his work on mechanisms of renal injury and progression, including in glomerulonephritis, diabetes, and hypertension. Recent studies have focused on the pathogenesis of essential hypertension and the role of subtle renal injury. He has published over 300 articles, lectured in over 25 countries, and is currently coeditor with John Feehally of the very successful clinical textbook, Comprehensive Clinical Nephrology. He received the American Society of Nephrology Young Investigator Award in 1994, is a member of the American Society for Clinical Investigation, and will be giving the endowed “Brenner” lecture at the American Society of Nephrology meeting in San Diego in November, 2003.

Research Interest

Dr Johnson’s laboratory has focused on several areas of investigation. First, his group has examined mechanisms involved in renal progression, including the role of mesangial activation, tubulointerstitial disease, and involvement of the microvasculature. His most recent studies have focused on the loss of vascular endothelium due to an impairment in angiogenesis, and the use of angiogenic growth factors to accelerate recovery of renal damage in diseases such as hemolytic uremic syndrome and renal progression. A second major area of research has focused on the hypothesis that essential hypertension may be due to acquired renal injury that causes a defect in sodium handling, and he has explored these mechanisms in detail, linking renal microvascular disease and tubulointerstitial injury and T cell infiltration to the development of this important medical problem. A third area has been studies focusing on the role of uric acid in renal disease and hypertension, with studies involving both basic and clinical research to investigate the pathogenic mechanisms by which uric acid may have deleterious effects. Finally, he also has been involved in international research projects, particularly in Peru, where he has studied the etiology of kidney diseases, including those that develop at high altitude.Dr Johnson has trained many nephrology and postdoctoral fellows, with more than 25 of them currently in academic positions throughout the world. He is the Director of the Nephrology Research Training Program (NIH funded) and is well versed at mentoring fellows for a career in academic medicine.

Publications:

• Sanchez-Lozada LG, Tapia E, Nepomuceno T, Soto V, Avila-Casado C, Nakagawa T, Johnson RJ, Herrera-Acosta J, Franco M. Effects of acute and chronic L-arginine treatment in experimental hyperuricemia Am J Physiol 2007 Apr;292(4):F1238-44
• Heinig M, Johnson RJ. Medical Grand Rounds. Role of uric acid in hypertension, renal disease, and metabolic syndrome. Cleveland Clinic Journal of Medicine 2006 Dec;73(12):1059-64
• Cirillo P, Sato W, Reungjui S, Heinig M, Gersch M, Sautin Y, Nakagawa T, Johnson R.
  Uric Acid, the Metabolic Syndrome, and Renal Disease. Kidney Int (Supplement). 2006 Dec;17(12 Suppl 3):S165-8
• Schold J, Srinivas TR, Guerra G, Reed JV, Johnson RJ, Weiner ID, Oberbauer R, Harman JS, Hemming AW, Meier-Kriesche HU. A 'Weight-Listing' Paradox for Candidates of Renal Transplantation? Am J Transplant. 2007 Mar;7(3):550-9
• Germain AM, Romanik MC, Guerra I, Sandra S, Reyes MS, Johnson RJ, Price K, Karumanchi A, Valdes G. Endothelial dysfunction: a link among preeclampsia, recurrent pregnancy loss, and future cardiovascular events? Hypertension. 2007 Jan;49(1):90-5
• Suliman ME, Johnson RJ, Garcia-Lopez E, Qureshi AR, Molinai H, Carrero JJ, Heimburger O, Barany P, Axelsson J, Lindholm B, Stenvinkel P. J-Shaped mortality relationship for uric acid in chronic kidney disease. Am J Kid Dis. 2006 Nov;48(5):761-771
• Feig DI, Johnson RJ. The Role of Uric Acid in Pediatric Hypertension. J Ren Nutr. 2007 Jan;17(1):79-83
• Garcia GE, Truong LD, Li P, Zhang P, Johnson RJ, Wilson CB, Feng L. Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis. Am J Pathol. 2007 May;170(5):1485-96
• Abboud O, Barsoum R, Berthoux F, Field M, Johnson R, Lin S, Massari P. European Best Practice Practice Guidelines for Peritoneal Dialysis acknowledged by ISN. Nature Clinical Practice Nephrology 2007; 3:6-7.
• Adrogue HE, Borillo J, Torres L, Kale A, Zhou C, Feig D, Merszei J, Johnson RJ, Lou YH. Coincident activation of Th2 T cells with onset of the disease and differential expression of GRO-gamma in peripheral blood leukocytes in minimal change disease Am J Nephrol 2007;27(3):253-61
• Johnson RJ, Segal M, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, and Sanchez-Lozada LG. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86(4):899-906
• Sautin YY, Nakagawa T, Zharikov S, Johnson RJ. Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol. 2007 Aug;293(2):C584-96.
• Franco M, Martínez F, Quiroz Y, Galicia O, Bautista R, Johnson RJ, Rodríguez-Iturbe Renal angiotensin II concentration and interstitial infiltration of immune cells are correlated with blood pressure levels in salt-sensitive hypertension. Am J Physiol Integr Com Physiol 2007; 293:R251-6
• Rodriguez-Iturbe B, Romero F, Johnson RJ. Pathophysiological mechanisms of salt-dependent hypertension. Am J Kidney Dis. 2007 Oct;50(4):655-72.
• Reungjui S, Roncal CA, Mu W, Sriniva TR, Sirivongs D, Johnson RJ, Nakagawa T. Thiazide diuretics exacerbate fructose-induced metabolic syndrome. J Am Soc Nephrol. 2007 Oct;18(10):2724-31
• Tantravahi J, Srinivas TR, Johnson RJ. Hyperfiltration: A sign of poor things to come in individuals with metabolic syndrome. Nature Clinical Practice Nephrology 2007; 3:474-5
• Nakagawa T, Segal MS, Croker B, Johnson RJ. A breakthrough in diabetic nephropathy: the role of endothelial dysfunction. Nephrol Dial Transplant. 2007 Oct;22(10):2775-7
• Gersch MS, Mu W, Cirillo P, Reungjui S, Li Z, Roncal CA, Sautin YY, Johnson RJ, Nakagawa T. Fructose, but not dextrose, accelerates the progression of chronic kidney disease. Am J Physiol Renal Physiol. 2007 Oct;293(4):F1256-61
• Reungjui S, Hu H, Mu W, Roncal CA, Croker BP, Patel JM, Srinivas TR, Byer K, Simoni J, Wesson D, Sitprija V, Johnson RJ. Thiazide-induced subtle renal injury not observed in states of equivalent hypokalemia Kidney Int 2007 Dec;72(12):1483-92
• Roncal C, Mu W, Reungjui S, Kim KM, Henderson GN, Ouyang X, Nakagawa T, Johnson RJ. Lead, at low levels, accelerates arteriolopathy and tubulointerstitial injury in chronic kidney disease. Am J Physiol Renal Physiol. 2007 Oct;293(4):F1391-6