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Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Trivandrum 695 011, India
To the Editor:
I read with interest the article by Marie- Laurie Cittanova et al. (1). They have studied prospectively, the possible preoperative risk factors for predicting postoperative renal dysfunction.
Multiple factors may influence a patient’s perioperative renal function (2). Hypovolemia, which can occur in the presence or absence of hypotension, causes redistribution of renal blood flow (RBF) from the outer cortex to the inner cortex and the medulla, which may affect renal functional reserve (3). Although the authors have studied ‘hypotension’ as one of the risk factors, ‘hypovolemia’ has not been addressed as a separate factor. Another important factor, which has not been addressed in this study, is exposure to salicylates and non-steroidal anti-inflammatory drugs (NSAIDs). These drugs are inhibitors of prostaglandin synthesis and are known to cause deterioration of RBF and glomerular filtration rate (GFR) in patients with decreased effective blood volume (4,5).
It is possible that the result of this study, i.e., the chronic inhibition of angiotensin converting enzyme (ACE) impairs postoperative renal function, could have been confounded by these variables if the patients on ACE inhibitors also had exposure to NSAIDs or suffered hypovolemia perioperatively.
References
Dept. D’Anesthesie-Reanimation, Groupe Hospitalier Pitie-Salpetriere, Paris, France
In Response:
Concerning hypovolemia, we agree that hypovolemia has not been addressed as a separate factor. However, we analyzed separately the need for intraoperative administration of catecholamines. Since the stepwise logistic regression included these two factors: hypotension and catecholamines, the occurrence of hypovolemia with none of these factors was very unlikely. Nevertheless, the main point to maintain the glomerular filtration rate is not the renal blood flow but, according to Starling equation, the net balance between the transcapillary hydraulic pressure gradient, the transcapillary colloid osmotic pressure gradient, and the hydraulic permeability of the filtration barrier (1). Consequently, hypovolemia has a deleterious on the glomerular filtration rate mainly because of the decrease in perfusion pressure, and not because of the decrease in renal blood flow (2).
On the other hand, one must admits that the diagnostic of intraoperative hypovolemia is difficult in clinical practice. The normal volemic status of a patient is difficult to define and impossible to evaluate. Instead of trying to determine subjectively whether the patients were or not hypovolemic, we included in the analysis objective parameters of hypovolemia: hypotension and the need for vasopressors.
A very few patients were receiving nonsteroidal antiinflammatory drug treatment, in the perioperative period. Many patients were receiving antiplatelet doses of aspirin, which are much smaller than the antiinflammatory class.
Thus, since all the confounding factors pointed out in your letter have been considered in our study, the conclusion concerning the deleterious effect of ACEIs on renal function in this period is maintained (3).
References
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