The role of medullary ischemia in acute renal failure

S. N. Heyman*, S. Fuchs, M. Brezis

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review


The introduction of new techniques for the determination of renal parenchymal oxygenation and intrarenal microcirculation has elucidated some important aspects in the pathophysiology of acute renal failure (ARF). Data accumulated over the last decade with these techniques, together with improved morphologic evaluation of the kidney, indicate that medullary damage may play a pivotal role in various forms of acute and chronic renal hypoxic and toxic insults. The outer medulla functions normally under hypoxic conditions, as a result of limited regional oxygen supply and high oxygen consumption for urinary concentration. Outer medullary oxygenation is critically balanced by mechanisms designed to adjust oxygen demand and supply, and their insufficiency may lead to ARF with hypoxic medullary damage. In this article, we outline our current concept of the physiologic control of medullary oxygenation and review the clinical conditions that predispose to hypoxic medullary damage, including rhabdomyolysis, hypercalcemia, or the exposure to endotoxin, nonsteroidal anti-inflammatory drugs, radiologic contrast agents, cyclosporine, FK506, and amphothericin. We shall indicate a possible role for medullary oxygen insufficiency in clinical conditions known to predispose to ARF, such as preexisting renal disease, diabetes mellitus, hypertension, atherosclerosis, effective volume depletion, urinary obstruction, or aging, and suggest potential strategies to preserve medullary oxygenation and integrity.

Original languageEnglish
Pages (from-to)597-607
Number of pages11
JournalNew Horizons: Science and Practice of Acute Medicine
Issue number4
StatePublished - 1995
Externally publishedYes


  • adenosine
  • endothelin
  • furosemide
  • laser-Doppler
  • medullary thick ascending limb
  • microcirculation
  • nitric oxide
  • oxygen microelectrode
  • prostaglandins
  • tubuloglomerular feedback


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