Tubulointerstitial disease: Role of ischemia and microvascular disease

Takahiko Nakagawa, Duk Hee Kang, Ryuji Ohashi, Shin Ichi Suga, Jaime Herrera-Acosta, Bernardo Rodriguez-Iturbe, Richard J. Johnson

Research output: Contribution to journalReview articlepeer-review

74 Scopus citations


Purpose of review: Tubulointerstitial injury is characteristic of aging-associated renal injury and progressive renal disease. Salt-sensitive hypertension is also associated with tubulointerstitial inflammation, especially when accompanied by microvascular disease. Here we summarize recent studies on the pathogenesis and consequences of tuburointerstitial disease, emphasizing the role of ischemia and the microvasculature. Recent findings Tuburointerstitial injury occurs via several mechanisms of which one of the most important is chronic ischemia. Recent studies suggest that chronic vasoconstriction may contribute to the renal injury associated with angiotensin II, catecholamines, nitric oxide inhibition, hypokaremia, hyperuricemia, and cyclosporine nephropathy. Salt-sensitivity may result as a consequence of the tubulointerstitial inflammatory response to these conditions, and this appears to be perpetuated by the development of preglomerular vascular disease. With progression of tuburointerstitial disease there is also a loss of peritubular capillaries, and stimulating microvascular growth with angiogenic factors can stabilize renal function in these models. Summary: Ischemia secondary to vasoconstriction or to structural changes of the renal vasculature may have important consequences both in terms of mediating salt-sensitive hypertension and renal progression. Angiogenic factors may have potential benefit in preventing or treating these conditions.

Original languageEnglish
Pages (from-to)233-241
Number of pages9
JournalCurrent Opinion in Nephrology and Hypertension
Issue number3
StatePublished - May 2003


  • Angiogenesis
  • Inflammation
  • Salt-sensitive


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