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New guidelines for drive-by renal arteriography may lead to an unjustifiable increase in percutaneous intervention
  1. James W Dear1,
  2. Paul L Padfield2,
  3. David J Webb1
  1. 1
    Clinical Pharmacology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, UK
  2. 2
    Metabolic Unit, Western General Hospital, Edinburgh, UK
  1. Professor D J Webb, Clinical Pharmacology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Room E3.22, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; d.j.webb{at}ed.ac.uk

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Narrowing of the lumen of the renal artery is termed renal artery stenosis (RAS) and can be a cause of hypertension and chronic kidney disease (CKD).1 When hypertension is caused by RAS the term renovascular hypertension is used, but the only way to be certain of the diagnosis is to demonstrate that relief of the renal artery narrowing results in a return to a normal blood pressure. This is because essential hypertension is considerably more common than, and a risk factor for, RAS so the coexistence of RAS and hypertension in a patient does not infer causality. In addition, even where clinically significant RAS is the initial cause of hypertension, reversal of the stenosis may not result in a normal blood pressure or renal function if longstanding hypertension has produced irreversible contralateral renal injury.2

RAS is most commonly due to atherosclerotic renal artery stenosis (ARAS) and has been reported to be present in around 30% of patients having routine coronary angiography and up to 50% of patients undergoing peripheral angiography.2 The presence and anatomical location of RAS can be confirmed by non-invasive imaging with duplex ultrasound, …

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