> No; I just like looking stuff up. For specific drugs I'm not sure about,
> I check rxlist.com.
> > No; I just like looking stuff up. For specific drugs I'm not sure about,
> > I check rxlist.com.
>
> Well... I looked rxlist.com to check if it reported Aspirin as
> nephrotoxic and it doesn't! or I have not understood where to look exactly?
Well, Rxlist isn't the end-all and be-all; it's just one tool. Apsirin
(and all salicylates) are NSAIDs, and NSAIDs are nephrotoxic to some
degree or another. Here's the "Precautions" section from the Physician's
Desk Reference for aspirin:
"Precautions:
General: Renal Failure: Avoid aspirin in patients with severe renal
failure (glomerular filtration rate less than 10 mL/minute).
Hepatic Insufficiency: Avoid aspirin in patients with severe hepatic
insufficiency.
Sodium Restricted Diets: Patients with sodium-retaining states, such as
congestive heart failure or renal failure, should avoid
sodium-containing buffered aspirin preparations because of their high
sodium content.
Laboratory Tests: Aspirin has been associated with elevated hepatic
enzymes, blood urea nitrogen and serum creatinine, hyperkalemia,
proteinuria, and prolonged bleeding time."
See the last section, on laboratory tests? Proteinuria (and increased
proteinuria) is one of the biggest dangers with NSAID use in kidney
patients.
> >>> Clinoril
>
> Looking on the Internet I didn't find any statement of Clinoril being
> less nephrotoxic than the other NSAIDs, do you have a link?
I got the information from my internist and nephrologist, but here's
what the Physician's Desk Reference has to say on the subject:
"Renal Effects
As with other non-steroidal anti-inflammatory drugs, long-term
administration of sulindac to animals has resulted in renal papillary
necrosis and other abnormal renal pathology. In humans, there have been
reports of acute interstitial nephritis with hematuria, proteinuria, and
occasionally nephrotic syndrome.
A second form of renal toxicity has been seen in patients with prerenal
and renal conditions leading to a reduction in renal blood flow or blood
volume, where the renal prostaglandins have a supportive role in the
maintenance of renal perfusion. In these patients, administration of an
NSAID may cause a dose dependent reduction in prostaglandin formation
and may precipitate overt renal decompensation. CLINORIL may affect
renal function less than other NSAIDs in patients with chronic
glomerular renal disease (see CLINICAL PHARMACOLOGY ). Until these
observations are better understood and clarified, however, and because
renal adverse experiences have been reported with CLINORIL (see ADVERSE
REACTIONS ), caution should be exercised when administering the drug to
patients with conditions associated with increased risk of the effects
of non-steroidal anti-inflammatory drugs on renal function, such as
those with renal or hepatic dysfunction, diabetes mellitus, advanced
age, extracellular volume depletion from any cause, congestive heart
failure, septicemia, pyelonephritis, or concomitant use of any
nephrotoxic drug. Discontinuation of NSAID therapy is typically followed
by recovery to the pretreatment state."
http://www.drugs.com/pdr/clinoril_tablets.html
> FGCS:
> I read that the causes are not known.
Yes, I have idiopathic FSGS. It usually effects older Black men with
high blood pressure, but I am a young(ish) white chick with very low
blood pressure. Go figger! My biopsy was unusual; in addition to the
FSGS, I was also found to have very early diabetic nephropathy and maybe
Minimal Change Disease as well. I now have extensive scarring, too, from
a chronic kidney infection. I also pass a lot of stones. In other words,
I have really busy kidneys.
To my knowledge, such a statement
> means that there is a certain likelihood that it might be autoimmune
> (like in my case). I tell you this: I am currently trying LDN, low dose
> naltrexone, look it up on the internet. I don't think it's a scam
> because AFAIR I found lots of abstracts in Pubmed agreeing that it
> really works great for Multiple Sclerosis, and hence it might work for
> other autoimmune diseases as well. You might want to try it yourself.
I'm not sure how an opioid receptor antagonist would work for FSGS. I
can see how it might work for MS ... but I haven't read the studies yet,
just looked up what it is. Therapy with it would suck though - I take
narcotic analgesics!

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"Did Father shoot him? I will eat Grandfather for dinner."
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Robert CLS, MT(ASCP) - 18 May 2006 22:27 GMT
<Well, Rxlist isn't the end-all and be-all; it's just one tool. Apsirin
<(and all salicylates) are NSAIDs, and NSAIDs are nephrotoxic to some
<degree or another. Here's the "Precautions" section from the
Physician's
<Desk Reference for aspirin:
Chronic NSAID use is also associated with renal papillary necrosis.
http://www.emedicine.com/MED/topic2839.htm
REP - 18 May 2006 22:36 GMT
> <Well, Rxlist isn't the end-all and be-all; it's just one tool. Apsirin
>
[quoted text clipped - 4 lines]
>
> Chronic NSAID use is also associated with renal papillary necrosis.
Yes, but the OP has IgA Nephropathy - proteinuria is more of a concern.
I believe renal papillary necrosis is discusses in the section about
Clinoril.

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"Did Father shoot him? I will eat Grandfather for dinner."
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Spike - 19 May 2006 12:36 GMT
> I'm not sure how an opioid receptor antagonist would work for FSGS.
I don't think the effect against MS is due to the opioid receptor
antagonism, there must be some other effect of Naltrexone responsible
for the autoimmune fixing. Doses for LDN are 11-16 times less than those
of normal naltrexone, a dose at which the opioid receptor agonism would
not be significant. Also as you have probably read, more than 4.5 mg of
Naltrexone does not work for MS anymore, it's difficult to explain that
with opioid receptor antagonism.
> I
> can see how it might work for MS ... but I haven't read the studies yet,
> just looked up what it is. Therapy with it would suck though - I take
> narcotic analgesics!
Probably at the dose of LDN, the antinarcotic effect is close to zero...
Yesterday I found another interesting thing. Instead of Clinoril, one
might think about taking acetaminophen together with Erdosteine and/or
Propylthiouracil.
Look at these studies:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16532256&query_hl=7&itool=pubmed_docsum
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16354242&query_hl=7&itool=pubmed_docsum
REP - 19 May 2006 21:21 GMT
> Yesterday I found another interesting thing. Instead of Clinoril, one
> might think about taking acetaminophen together with Erdosteine and/or
[quoted text clipped - 6 lines]
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abst
> ract&list_uids=16354242&query_hl=7&itool=pubmed_docsum
The reason for taking Clinoril at all would be for its ati-inflammatory
properties. For some injuries/conditions, treatment with acetominophen
simply isn't "good enough" - bursitis, for one example, really needs an
anti-inflammatory. Sometimes, localized conditions may respond to
cortisone injections, which are less risky than oral steroids, but they
aren't always appropriate, and an oral steroid may be inappropriate for
whatever reason.
That said, Erdosteine sounds very interesting - I'll ask my doctor when
I see him in about half an hour!

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"Did Father shoot him? I will eat Grandfather for dinner."
- Helen Keller, on learning of the death of her grandfather