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Sir,

ACE inhibitors and angiotensin II receptor antagonists are cornerstones in the treatment of patients with renal disease and vascular disease. We agree that close monitoring of renal function is mandatory after the initiation of ACE inhibitors or angiotensin II receptor antagonists in patients with signs of vascular disease, and high grade renal artery stenosis should be ruled out where serum creatinine increases 30% after such therapy. We also agree that renal Doppler is the screening method of choice in such a work-up. However, patients with ACE inhibitor-induced acute renal failure are prevalent in hospitals, probably <20% of these patients have previously undiscovered renal artery stenoses, or non-significant stenoses rendered temporarily significant by concomitant dehydration [1]. Nevertheless, active thromboembolic disease is seldomly recognized in these patients. Our patient had persistent hypertension and experienced increasing diuresis up to day 11 when the second anuric episode and pulmonary congestion suddenly occurred, indicating a very active stimulus of the renin angiotensin system, and arguing against an ongoing thrombotic process from the time of hospital admission. It is well known that angiotensin II has prothrombotic effects, and that treatment with an ACE inhibitor may reduce thrombosis in rats [2] and PAI-1 in humans [3]. The literature is very inconclusive regarding the effects of ACE inhibitors on plasma fibrinolytic balance, and studies indicate different antithrombotic effects of ACE inhibitors and angiotensin II receptor antagonists [4]. In our case report we are very well aware that the coexistence of acute thromboembolic disease and a speculative surge of angiotensin II after withdrawal of an ACE inhibitor is highly speculative and may be coincidental. On the other hand, we do not believe that thrombosis evolves ‘on its own’, and after withdrawal of an ACE inhibitor, an exaggerated effect of angiotensin II as a facilitating mechanism for progressive thrombosis in selected cases with a stimulated renin angiotensin system is an interesting hypothesis. The presentation of such a hypothesis was the intent of our report. Recently, we also had a patient with high plasma renin levels, occluded renal artery and coexisting pulmonary embolus (personal observation). Such a potential interaction between the renin angiotensin system and prothrombotic mechanisms adds to the importance of a tight follow-up of risk patients, and anticoagulation should be considered part of the armamentarium in high risk patients with a stimulated renin angiotensin system.

Conflict of interest statement. None declared.

Einar Svarstad and Bjarne M. Iversen

Renal Unit Haukeland University Hospital Bergen Norway Email: einar.svarstad{at}med.uib.no

References

  1. Wynckel A, Ebikili B, Melin JP, Randoux C, Lavaud S, Chanard J. Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors. Am J Hypertens 1999; 12: 1049[CrossRef][ISI][Medline]
  2. Chabielska E, Pawlak R, Golatowski J, Buczko W. The antithrombotic effect of captopril and losartan on experimental arterial thrombosis in rats. J Physiol Pharmacol 1998; 49: 251–260[ISI][Medline]
  3. Vaughan DE, Rouleau JL, Ridker PM, Arnold JM, Menapace FJ, Pfeffer MA. Effects of ramipril on plasma fibrinolytic balance in patients with acute anterior myocardial infarction. Heart Study Investigators. Circulation 1997; 96: 442–447[Abstract/Free Full Text]
  4. Brown NJ, Vaughan DE. Prothrombotic effects of angiotensin. Adv Intern Med 2000; 45: 419–429[Medline]




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