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I recently was reading notes on the website of the American Society of Nephrology and came across an unfamiliar statement. These notes reference Theodore I. Steinman for the ASN Board Review, so this not information from an unreliable source. These conference cast notes on Polycystic Kidney Disease dated August 1, 2016, on page 15, under Management Issues, state “Avoid drugs that stimulate release of Vasopressin or potentiate its action –SSRI –TCA”. I have tried without success to find information in this regard. I would like to find literature specifically addressing the use of specific antidepressants in PKD patients. Any information you may be able to provide in this regard would be greatly appreciated.
http://conference-cast.com/asn/media/ASN16BRCU_24/BRCU16-26-30/BRCU16-28/BRCU16-28.pdf
http://conference-cast.com/asn/media/ASN16BRCU_24/BRCU16-26-30/BRCU16-28/BRCU16-28.pdf
Accepted Answer
The role of SSRI –TCA on vasopressin release is circumstantial based on a few case reports and observational studies documenting an association of occurrence of hyponatremia in some (esp. elderly) but not all patients on these medications. However, the occurrence of hyponatremia in this setting is complex and primarily affects elderly females who may have other risk factors (e.g. thiazide, anti-epileptics, disease states associated with low effective circulation). Moreover, the prevalence of as high as 9% of the study subjects is likely an over-estimate when compared to that in the general population. Nonetheless, SSRI may be associated with higher risk of hyponatremia than TCA.
If we extrapolate to say that SSRI-TCA is detrimental in patients with ADPKD we will be in even more uncertain ground. So I would regard Dr. Steinman’s statement as a soft recommendation.
Personally, I do not restrict the use of antidepressant in ADPKD patients but make sure that it is clinically indicated – TCA may be preferred in this case. I would monitor serum sodium in the treated patients given our practice of recommending high water intake in the PKD patients.
If we extrapolate to say that SSRI-TCA is detrimental in patients with ADPKD we will be in even more uncertain ground. So I would regard Dr. Steinman’s statement as a soft recommendation.
Personally, I do not restrict the use of antidepressant in ADPKD patients but make sure that it is clinically indicated – TCA may be preferred in this case. I would monitor serum sodium in the treated patients given our practice of recommending high water intake in the PKD patients.
Hello,
That is a very interesting question and one which is referencing the role of ADH in the pathogenesis of renal cysts. Unfortunately, I am not a psychiatrist and am not familiar with the pharmacology of all anti-depressants to sufficiently answer the question. But I will look in to it.
Dr. Jordan Weinstein
That is a very interesting question and one which is referencing the role of ADH in the pathogenesis of renal cysts. Unfortunately, I am not a psychiatrist and am not familiar with the pharmacology of all anti-depressants to sufficiently answer the question. But I will look in to it.
Dr. Jordan Weinstein
Thank you for any assistance you may be able to provide. Unfortunately, not even all nephrologists are experts in PKD. There can be a tendency to treat PKD patients the same as any patient with chronic kidney disease. Certainly there are recommendations that are universal for all kidney patients, but there are unique components to PKD.
You are correct.
In the US, interest and expertise in ADPKD will increase once Tolvaptan is approved for use. In Canada (where I practice and where Tolvaptan is approved for use) nephrologists have become very interested in this disorder now that we have a viable treatment for it..
Dr. Jordan Weinstein
In the US, interest and expertise in ADPKD will increase once Tolvaptan is approved for use. In Canada (where I practice and where Tolvaptan is approved for use) nephrologists have become very interested in this disorder now that we have a viable treatment for it..
Dr. Jordan Weinstein
My own feeling on this is that the increase in ADH levels associated with certain drugs would become less relevant in the context of tolvaptan therapy which blocks the horomone's actions. Furthermroe, ADPKD is not caused by increased ADH levels, even if blocking it is helpful in delaying progression. Therefore, in the absence of tolvaptan while there might be some elevation in ADH-mediated progression of ADPKD, I am not convinced that the impact would be large. But as you point out, there is a paucity of data on this subject.
I will also forward your question to Dr. York Pei, another expert (like Dr. Torres) on ADPKD.
Dr. Jordan Weinstein
I will also forward your question to Dr. York Pei, another expert (like Dr. Torres) on ADPKD.
Dr. Jordan Weinstein
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