Lithium Induced Nephrogenic Diabetes Insipidus

[zedx]

So i've been looking at a couple books and can't seem to get any sort of consensus. For Lithium Induced Nephrogenic Diabetes Insipidus, is the current to give the patient a Thiazide Diuretic or Amiloride? I was under the impression that thiazides would decrease the secretion of lithium in the kidneys; but it seems like it is used according to certain sources (e.g. emedicine) but certain texts refer to the use of amiloride as a treatment (e.g. Lippencott's).

Anyone have an idea as to whether one is more "ideal" than the other?

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[___Doctor786___]

So i've been looking at a couple books and can't seem to get any sort of consensus. For Lithium Induced Nephrogenic Diabetes Insipidus, is the current to give the patient a Thiazide Diuretic or Amiloride? I was under the impression that thiazides would decrease the secretion of lithium in the kidneys; but it seems like it is used according to certain sources (e.g. emedicine) but certain texts refer to the use of amiloride as a treatment (e.g. Lippencott's).

Anyone have an idea as to whether one is more "ideal" than the other?

From what I understand, both Thiazides and Amiloride are used for Lithium Induced Diabetes Insipidus. Remember, Amiloride is a K+ sparing agent, so they are used along with other diuertics. So, in the case of Lithium induced diabetes inspidus, both could be used. I'm not which one is the "ideal" one. If I am wrong, someone please correct me.

 

[sanche60]

id guess thiazides.

 

[HIJay]

i have always read and been taught thiazides

 

[MikeyLu2010]

i always thought thiazides as well

 

[Substance]

http://ndt.oxfordjournals.org/cgi/reprint/21/4/869

From the looks of the abstract, nobody completely understands the renal physiology of lithium.

I will venture the following hypotheses of treatment of lithium toxicity:

1. Amiloride: according to that article, the amiloride sensitive Na+ channel in the distal tubule is also the entry-point for lithium. Thus, if you block this with amiloride, the lithium cannot enter the cell and bind to the V2 Aquaporin channel.

2. Thiazides: since the Amiloride sensitive Na+ channel is the entry point for lithium as well, and ASSUMING that the entry of these ions is COMPETITIVE, then perhaps using the thiazides increases distal delivery of sodium, which outcompetes the lithium for the transporter channel.

 

[drgreeneatutk]

When we covered this in pharm a few weeks ago our prof said that in general for nephrogenic DI, thiazides were #1. But when it is specifically Lithium induced, Amiloride was #1

 

[HIJay]

actually had a q on this on my step 1 today

they used thiazide as the example

 

[crys20]

actually had a nephrologist do a lecture on this this week - here's what he said.

Li gets into the distal tubular cell using the Na channel which is blocked by amiloride - thus, amiloride blocks its entry into the cell so it can't affect aquaporin mobilization. This will prevent the diabetes insipidus to some extent.

With Li induced nephrogenic DI or other causes of nephrogenic DI, using thiazides works by decreasing Na reabsorpton and thus increasing Na excretion and causing an ECF volume contraction - which will decrease the GFR allowing increased time for Na and H20 reabsoprtion which means less H20 and Na excretion.

I don't know which is 1st line or if you combine both in Li induced nephrogenic DI but just thought I would add those facts!

 

[agranulocytosis]

FYI, in Kaplan it states Li-induced NDI is managed with amiloride, with no other mention of thiazides.