Talk:Hemolytic–uremic syndrome

Factor H
- even in atypical HUS (which is often familial), factor H is to blame for platelet deposition. JFW | T@lk  12:43, 26 May 2008 (UTC)

Prognosis
"About 9% may develop end stage renal disease. About one-third of persons with hemolytic-uremic syndrome have abnormal kidney function many years later, and a few require long-term dialysis." This seems inconsistent - is it saying "About one third of those diagnosed with hemolytic-uremic syndrome end up with some degree of Chronic Kidney Disease. Ultimately, 9% progress to stage 5 CKD with only a few progressing to stage 5 CKD proximate to the diagnosis."? BillpSea (talk • contribs) 03:21, 25 June 2008 (UTC)BillpSea (talk) 03:27, 25 June 2008 (UTC)

ADAM-TS13 involvement
It's mentioned in the pathophysiology part that STEC-HUS leads to a deficiency in ADAM-TS13 activity. There is no specific source for this. A couple lines further down, there's a linked source, with specifically states the contrary "In general, there is no evidence of ADAMTS13 deficiency among patients with shiga toxin-associated HUS". The source actually states that cleavage of ul-VWF multimers is increased "Large VWF multimers are decreased in patients with HUS, aortic stenosis or pulmonary arterial hypertension [2, 94, 95]. In these conditions, ADAMTS13 levels are normal or only mildly decreased. It is believed that large multimers are decreased because high levels of shear stress in these disorders enhance proteolysis of VWF by ADAMTS13. Consequently, the proteolytic fragments are increased.". Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3720712/ Pathophysiology of thrombotic thrombocytopenic purpura - this is reference [27].

I suggest that the statement concerning decreased ADAMTS13 activity in STEC-HUS should be removed, it's actually opposed by the primary data and is a pathognomic part of TTP and actually one of the primary lab-values that help discern TTP from (a)HUS

Here's the passage I would suggest should be removed:

"Additionally, the binding action of Shiga-toxin inactivates a metalloproteinase called ADAMTS13, the deficiency of which causes the closely related TTP. Once ADAMTS13 is disabled, multimers of von Willebrand Factor (vWF) form and initiate platelet activation, causing microthrombus formation. The activation of platelets resulting from inhibition of ADAMTS13 is due to the hyperactivity of large multimers of uncleaved vWF."

Treatment
I have some questions about the treatment section(s):

1. Why does the article have two? 2. Should we combine them? 3. Do we need the second? 4. Is the second one valid or useful? 5. Is there a better header for it than 'Treatment?'

The DarkArcher was here (talk) 21:27, 29 June 2008 (UTC)


 * As a first move, I've merged them into the same section. Beyond that, I'm not sure what all the correct answers are.  WhatamIdoing (talk) 16:39, 30 June 2008 (UTC)

- http://www.medicalnewstoday.com/articles/137365.php

Some info on some new clinical trial's on aHUS. My Englisch and Medical Background are not good enough to incorparate it in the article. I hoop someone will pick this up. —Preceding unsigned comment added by 81.207.2.46 (talk) 21:40, 12 February 2009 (UTC)

HUS
I had this when I was 13 months old. Had this dude: http://news.bbc.co.uk/1/hi/health/7542404.stm in charge of my case. What a hero. —Preceding unsigned comment added by 78.86.96.224 (talk) 21:07, 5 August 2008 (UTC)

What are the symptoms?
There should be a separate causes and symptoms section. I went to find the symptoms and can only find the causes listed under the symptoms.97.75.133.131 (talk) 04:37, 5 January 2012 (UTC)

pathogenesis
Info on pathogenesis would be much appreciated!--Xris0 (talk) 20:56, 31 January 2012 (UTC)
 * It's good that you're trying to improve the article, but have you got a reference for what you're writing? There are some sources that may be helpful in the reference list, otherwise Pubmed would be a good place to try. Watermelon mang (talk) 21:37, 31 January 2012 (UTC)

Lancet seminar
10.1016/S0140-6736(17)30062-4 JFW &#124; T@lk  16:42, 14 August 2017 (UTC)

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Pathophysiology
10.1111/jth.13956 JFW &#124; T@lk  13:00, 11 April 2018 (UTC)

Problems with discussion of aHUS
Much of the aHUS content should be removed since it's already covered on the aHUS article and it's potentially misleading here. The article seems to conflate the two in places, and in terms of content, it seems very imbalanced toward genetic pathologies, considering their extreme rarity relative to infectious HUS. My recent edit fixed a paragraph that discussed aHUS prognostic statistical figures in the middle of a paragraph about both infectious HUS prognosis and (I think) HUS prognosis overall, and it wasn't written in a way as to draw attention to a comparison or contrast between them. The whole article is like that, to a lesser extent. So, anyone reading this article is prone to conflating aHUS with infectious HUS with HUS overall.

Infection-induced HUS is many, many orders of magnitude more common than aHUS, so aHUS shouldn't be receiving more air time on this article than infectious HUS. It already has its own article, while infectious HUS does not. It seems like some editors are thinking this article is about the group of disorders called HUS, while other editors are thinking this article is about the infectious disorder called HUS that is by far the most common and well-known disorder with that name. Well, an article for infection-induced HUS could be created. But until then, I think this article should 1) discuss HUS as a whole, 2) list the many causes of HUS, and 3) discuss infectious HUS. Specific discussion about non-infectious disorders called HUS should be reserved for the aHUS article. To avoid confusion, the term "infectious HUS" can be used in the headings of sections that specifically describe infectious HUS. This article should of course include a link to the aHUS article, plus some brief discussion.

If instead it is considered imperative to refer to HUS as a group of disorders connected only by common clinical symptoms with common lower-order mechanisms, then the article is still very inadequate, because there are many distinct HUS etiologies. It's not just infectious HUS and genetic HUS (this article describes atypical HUS as "largely" genetic in origin, whatever that means). Here is a list from a comprehensive article, which this Wiki article cites:
 * HUS infection-induced (Shiga and strep)
 * HUS induced by disorders of complement regulation (genetic and acquired)
 * ADAMTS13 deficiency (genetic and acquired)
 * Defective cobalamin metabolism
 * HIV infection
 * Malignancy
 * Cancer chemotherapy or ionizing radiation
 * Calcineurin inhibitors and transplantation
 * Pregnancy, HELLP syndrome, contraceptive pill
 * Systemic lupus erythematosus, anti-phospholipid antibody syndrome
 * Glomerulopathy
 * Drug induced

So I would propose that a section be added near the top that briefly lists all the rarer etiologies (or just the well-established ones), along with inline links to any corresponding articles (currently existing or otherwise). Genetic HUS isn't especially more notable than any of the other above mentioned etiologies, so if genetic causes are to be mentioned then so should the others. Then, the rest of the article can get on with describing the subject of the article as a single thing — either infectious HUS or HUS considered as a whole, where appropriate.

Specific details (especially statistical figures) that concern atypical HUS in particular should not be added unless they're really important or offer some kind of affordance to open the aHUS article. Each section could have like, one sentence max about atypical HUS, with a link to direct the user to the atypical HUS article. I think in this case it's perfectly reasonable to have multiple inline links to the aHUS article, because not everyone is going to read the whole article from top to bottom. Some readers may just skip to the prognosis section. Aminomancer (talk) 13:47, 16 May 2022 (UTC)