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Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia.

S E Thomas, S Anderson, K L Gordon, T T Oyama, S J Shankland and R J Johnson
JASN February 1998, 9 (2) 231-242;
S E Thomas
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S Anderson
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K L Gordon
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T T Oyama
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S J Shankland
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R J Johnson
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Abstract

Aging is associated with a progressive decline in renal function and the development of glomerulosclerosis and interstitial fibrosis. Although many studies have addressed the cellular mechanisms of age-related glomerulosclerosis, less is known about the tubulointerstitial fibrosis. In this study, aging (24 mo) rats develop tubulointerstitial fibrosis characterized by tubular injury and focal tubular cell proliferation, myofibroblast activation, macrophage infiltration with increased immunostaining for the adhesive proteins osteopontin and intercellular adhesion molecule-1, and collagen IV deposition. Aging rats demonstrated immunostaining for endothelial nitric oxide synthase (eNOSIII) in renal tubular epithelial cells and infiltrating mononuclear cells in areas of tubulointerstitial injury, with a relative loss of staining of the peritubular capillaries compared with young rats. The aging rats also displayed focal loss of peritubular capillaries (as noted by focally decreased RECA-1 and OX-2 staining) in areas of tubulointerstitial injury. The areas of fibrosis and hypocellularity were associated with increased apoptosis of tubular and interstitial cells compared with young (3 mo) rats (25.4 +/- 5.3 versus 3.5 +/- 2.5 TUNEL-positive cells/0.25 mm2 in old versus young rats, P = 0.0001). It is concluded that tubulointerstitial fibrosis in aging is an active process associated with interstitial inflammation and fibroblast activation. The progressive loss of cells in areas of fibrosis may be due to accelerated apoptosis. Furthermore, the tubulointerstitial injury may be the consequence of ischemia secondary to peritubular capillary injury and altered eNOS expression.

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Journal of the American Society of Nephrology
Vol. 9, Issue 2
1 Feb 1998
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Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia.
S E Thomas, S Anderson, K L Gordon, T T Oyama, S J Shankland, R J Johnson
JASN Feb 1998, 9 (2) 231-242;

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Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia.
S E Thomas, S Anderson, K L Gordon, T T Oyama, S J Shankland, R J Johnson
JASN Feb 1998, 9 (2) 231-242;
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Cited By...

  • Mechanisms of Tubulointerstitial Fibrosis
  • Mobilized Human Hematopoietic Stem/Progenitor Cells Promote Kidney Repair After Ischemia/Reperfusion Injury
  • Zag Expression during Aging Suppresses Proliferation after Kidney Injury
  • Thrombospondin 2 Functions as an Endogenous Regulator of Angiogenesis and Inflammation in Experimental Glomerulonephritis in Mice
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  • Delayed Chemokine Receptor 1 Blockade Prolongs Survival in Collagen 4A3-Deficient Mice with Alport Disease
  • Hypoperfusion of Peritubular Capillaries Induces Chronic Hypoxia before Progression of Tubulointerstitial Injury in a Progressive Model of Rat Glomerulonephritis
  • Glomerulosclerosis and Tubulointerstitial Fibrosis are Attenuated with 17{beta}-Estradiol in the Aging Dahl Salt Sensitive Rat
  • Angiotensin II and Oxidative Stress in Dahl Salt-Sensitive Rat With Heart Failure
  • Peritubular Capillary Regression during the Progression of Experimental Obstructive Nephropathy
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  • Impaired Angiogenesis in the Remnant Kidney Model: I. Potential Role of Vascular Endothelial Growth Factor and Thrombospondin-1
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  • Peritubular Capillary Injury during the Progression of Experimental Glomerulonephritis in Rats
  • Renal Injury and Salt-Sensitive Hypertension After Exposure to Catecholamines
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