GAPDH as housekeeping gene at renal level

Abstract

glomerular injury [5]. It could be supposed that tubu-lointerstitial inflammation yields cytokines, growth fac-tors, vasoactive molecules, and free oxygen radicals that contribute to the development of arteriolar and glomeru-lar lesions. Some authors go further and extend this hy-pothesis, assuming that subtle interstitial injury is not so much the manifestation of hypertensive kidney disease, but rather the underlying reason for hypertension [6]. Further studies are necessary to clarify this issue. LESZEK TYLICKI and BOLESLAW RUTKOWKI Gdá nsk, Poland REFERENCES 1. SANCHEZ-LOZADA LG, TAPIA E, JOHNSON RJ, et al: Glomerular hemo-dynamic changes associated with arteriolar lesions and tubulointer-stitial inflammation. Kidney Int 64(Suppl 86):S9–S14, 2003 2. TYLICKI L, RUTKOWSKI B, HORL WH: Multifactorial determination of hypertensive nephroangiosclerosis. Kidney Blood Press Res 25:241– 353, 2002 3. MAI M, GEIGER H, HILGERS KF, et al: Early interstitial changes in hypertension-induced renal injury. Hypertension 22:754–765, 1993 4. BAPAT S, POST JA, BRAAM B, et al: Visualizing tubular lipid peroxi-dation in intact renal tissue in hypertensive rats. J Am Soc Nephrol 12:2990–2996, 2002 5. TYLICKI L, MANITIUS J, LYSIAK-SZYDLOWSKA W, RUTKOWSKI B: Tubular injury: The first symptom of hypertensive kidney involvement? Med Sci Monit 9:CR135–CR41, 2003 6. JOHNSON RJ, HERRERA-ACOSTA J, SCHREINER G, RODRIGUEZ-ITURBE B: Subtle acquired renal injury as a mechanism of salt-sensitive hy-pertension. N Engl J Med 346:913–923, 2002 Reply from the Authors Our paper [1] focused primarily on the relationship of arteriolar disease and tubulointerstitial inflammation in renal progression. With renal mass reduction there is an increase in systemic blood pressure with glomerular hy-perfiltration, glomerular hypertension, and proteinuria. Tubulointerstitial inflammation results and appears to mediate afferent arteriolar disease, which further impairs autoregulation, resulting in further increases in glomeru-lar pressure and acceleration of glomerulosclerosis. Ar-teriolopathy in other conditions is also associated with glomerular hypertension, reduced plasma flow, ischemia, and fibrosis. Drs. Tylicki and Rukowski ask about the relationship of arteriolopathy and tubulointerstitial inflammation in essential hypertension. This is an area of special inter-est to us because we have proposed that these changes are responsible for the development of salt-sensitive hy-pertension [2, 3]. As we have proposed, renal injury is initiated by vasoconstriction and glomerular hyperten-sion induced by sympathetic nervous system overactivity, endothelial dysfunction, hyperuricemia, or activation of the renin-angiotensin system; this leads to tubulointersti-tial inflammation, intrarenal oxidant and angiotensin II generation, and afferent arteriolar disease [4]. The arte-riolopathy results in impaired autoregulation and