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Here's the latest review of Acute Renal Failure:

Acute renal failure: definitions, diagnosis, pathogenesis, and therapy
Robert W. Schrier, Wei Wang, Brian Poole and Amit Mitra
J. Clin. Invest. 114:5-14 (2004). doi:10.1172/JCI200422353.
http://www.jci.org/cgi/content/full/114/1/5

Anyone interested in extracting the good info from this review ? -- PFHLai 19:26, 2004 Jul 2 (UTC)

Hey, you noticed it as well! The historical stuff is very nice. The material about pathogenesis still needs to be worked into this article. JFW | T@lk 21:47, 27 July 2005 (UTC)[reply]

Lancet

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When I get the time, I will cite more from the Lancet review. It doesn't really matter if it's free or not - it is the best review I've read on ARF for years. JFW | T@lk 06:47, 28 July 2005 (UTC)[reply]

Contrary to your claim, it does matter. The article I found had exactly the same information.
Since Wikipedia is a free-for-all in terms of who can edit it-- I think references that are available to the general public are a huge bonus, as checking a fact is just a click or two. Also, citing open journals is a small way to encourage more journals to open up. Biomed central has gone open. The CMAJ (which is #5, after JAMA, N Engl J Med, Lancet & BMJ) is totally open-- no registration & no sign-in. BMJ was open... but decided to close-up again.
I don't think one should compromise quality for politics; so, by all means use the Lancet article. That said, I think you should keep an eye open for free... information wants to be free.
Have you taken a look at emedicine? eMedicine - Renal Failure, Acute : Article by Richard Sinert, DO (from Jan) eMedicine - Acute Renal Failure : Article by Mahendra Agraharkar MD (from April) eMedicine is free, peer-review and, I think you'll agree, fairly good. Also, the format of all the emedicine articles is pretty much standard, which makes 'em easy to read if you've seen a few of 'em. Nephron

Nephron, you are free to include whatever you like. When I work on clinical articles I usually go by one good systematic review. Whether that is free-access or not is immaterial. If you want to ditch the Lameire review in favour of a free resource I will not stop you. The Schrier review is free, and covers pretty much everything as well. JFW | T@lk 18:57, 28 July 2005 (UTC)[reply]

Edits

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I've made some minor changes, about renal biopsy-which is often performed for ARF in renal units (rather than on ITU) I've added acute GN to the intra-renal causes, and removed hyperparathyroidism for a cause of ARF (which is preposterously obscure),I've also removed the partial list of specific blood tests, which vary from place to place and are irrelevant in terms of the content of the article.Felix-felix 17:39, 15 January 2006 (UTC)[reply]

Some blood tests should be mentioned. JFW | T@lk 13:25, 16 January 2006 (UTC)[reply]

Merging Renal shutdown

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I think the two ought to be merged. Renal shutdown is used in the medical literature.[1][2][3] As far as I know it is the same thing as acute renal failure, (see [4]) which is used much more frequently. Ergo Merge Renal shutdown into Acute renal failure. Nephron  T|C 02:12, 12 June 2006 (UTC)[reply]

pre-renal, renal, post-renal -- ARF & CRF

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I think the pre-renal, renal, post-renal subdivision is not that useful in CRF. Also, a discussion of how to diagnose/categorize CRF is not relevant to the article. Nephron  T|C 15:57, 16 September 2007 (UTC)[reply]

RRT in ARF

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http://jama.ama-assn.org/cgi/content/abstract/299/7/793

The conclusions from this review are basically that filtration and dialysis are equally effective as long as CVVHF is provided at reasonable rates. But trial data is not great. JFW | T@lk 16:10, 24 February 2008 (UTC)[reply]

Acute Kidney Disease

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I would be in favor of rewriting using the term Acute Kidney Disease. The severity of the disease depends on GFR, etc. only Acute Kidney Disease Stage 5 is Acute Renal Failure. If someone presents (poisoning) with a GFR of 40 they would have Acute Kidney Disease Stage 3. Acute Renal failure is sometimes used in that situation but it is not entirely accurate. BillpSea (talk) 05:03, 18 March 2008 (UTC)[reply]

Do you have a source for this classification? If anything is hard, it is measuring the GFR in someone with sudden fluid shifts and oliguria/anuria. The RIFLE criteria seem to have a much wider support base. JFW | T@lk 12:49, 24 March 2008 (UTC)[reply]

What and how to RRT

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A systematic review on RRT modalities: http://jama.ama-assn.org/cgi/content/abstract/299/7/793?etoc

It turns out the evidence is limited. JFW | T@lk 12:49, 24 March 2008 (UTC)[reply]

In AKI in acutely ill patients, intensive RRT doesn't make much difference compared to less-intensive RRT. doi:10.1056/NEJMoa0802639 JFW | T@lk 05:39, 25 May 2008 (UTC)[reply]

ARF and hypouricemia

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Would someone with ready access to the literature please write an explanation of the "association" between ARF and hypouricemia? Eg PMID 15150354 reports patients in exercise-induced ARF had nearly normal levels of serum uric acid; in recovery, the levels were extremely low. --Una Smith (talk) 05:28, 25 December 2008 (UTC)[reply]

ARF pathogenesis

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May I know why were my flow charts on the pathogenesis of acute renal failure deleted? Please provide solid arguements since I failed to see any strong explanation on the topic. The current explanation on its pathogenesis is very poorly written and it doesn't include the role of inappropriate tubular adhesion and exfoliation in the development of ARF. You can't possibly explain how renal calculi may cause ARF without the tubular part. —Preceding unsigned comment added by Broississy (talk • contribs) 23:48, 29 May 2009 (UTC)[reply]

Contradiction

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Guys, this doesn't make any sense: "..reduction of angiotensin II leads to vasodialation which in turn reduces GFR." "..reduction in prostaglandin leads to vasoconstriction thus reducing GFR."

Both vasodilation and vasoconstriction cause reduced GFR? Needs clarification! —Preceding unsigned comment added by 90.233.192.82 (talk) 17:08, 15 October 2009 (UTC)[reply]

Staging criteria

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The RIFLE criteria also included change in GFR (however measured) and not merely the surrogate of change in creatinine. Should not this be included (along with the correction to the maths of the original paper)? Kiwiski (talk) 06:57, 27 December 2009 (UTC)[reply]

Signs and symptoms

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I struggled to find a source for acute uraemia. I simply used the CKD chapter in Harrison's. JFW | T@lk 17:04, 17 April 2011 (UTC)[reply]

Causes

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"These causes [sic] the inadequate cardiac output and hypovolemia or vascular diseases causing reduced [suggest 'reducing'] perfusion of both kidneys."

Renal disease causes reduced cardiac output? Am not doctor or physiologist, so am not confident in tweaking this. — Preceding unsigned comment added by 194.176.105.150 (talk) 20:45, 15 January 2013 (UTC)[reply]

New (Post-2011) Research on Other Markers?

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Does anyone know if any of the potential markers listed (NGAL, KIM-1, IL-18, cystatin C, others?) has been verified - either positively or negatively? I probably added too many "time templates" as the citation needed tag was in 2011, which might make it a dated statement that's true nonetheless.. Or it might have been found to be definitely false by someone in the meantime. I don't know and don't care to go tromping through PubMed just now..) Jimw338 (talk) 08:38, 18 April 2013 (UTC)[reply]

2012 KDIGO recommendations

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doi:10.1038/kisup.2012.1 JFW | T@lk 10:48, 11 February 2014 (UTC)[reply]

FENA clarifications

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Hi all, I was comparing the FENa in the chart on this page ("classic laboratory findings in AKI" section) to the FENa (fractional sodium excretion) page and the numbers do not add up. There are also no references to the table. Any ideas? Elliotelliotf (talk) 21:29, 21 May 2014 (UTC)[reply]

Prevention in cardiac surgery

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doi:10.1186/s13054-014-0517-x bicarbonate solution doesn't work. Crit Care 2014, something to mention in the "prevention" section together with the various efforts to reduce contrast nephropathy. JFW | T@lk 14:00, 17 September 2014 (UTC)[reply]

Long-term impact on other organs

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AKI and temporary RRT can impact remote organ function doi:10.1186/s13054-015-1149-5 JFW | T@lk 12:46, 4 January 2016 (UTC)[reply]

AKI 2016

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Intensive care perspective: doi:10.1186/s13054-016-1478-z JFW | T@lk 09:12, 7 October 2016 (UTC)[reply]

Prevention and early detection

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doi:10.1016/S0140-6736(17)31329-6 (doi not yet registered). JFW | T@lk 08:23, 28 May 2017 (UTC)[reply]

ICM

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Entire issue about AKI: https://link.springer.com/journal/134/43/6 JFW | T@lk 18:48, 14 June 2017 (UTC)[reply]

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Postoperative AKI

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QJM doi:10.1093/qjmed/hcw175 JFW | T@lk 17:15, 5 December 2017 (UTC)[reply]

Pediatrics

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It may interesting to include some pediatric specific material on AKI. For example, in the post-renal section, bladder outlet obstruction is a very common cause of neonatal AKI. Also missing in the renal replacement therapy, is the fact that some pediatric centers use peritoneal dialysis as a form of renal replacement therapy, particularly in the post-operative cardiac patient population. Hwoollen16 (talk) 16:41, 15 September 2018 (UTC)[reply]

clinical features & presentation

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how long it takes before the patient went into coma or become disoriented ? how long a comatose patient with ARF has before he dies if he does not get dialysis (assume the injury is permanent). you said patient can have normal blood pressure and at other possibility he may be thirsty, does these two conditions possible to come together (if he is thirsty won't he have hypotension?). — Preceding unsigned comment added by Yasir muhammed ali (talk • contribs) 07:58, 12 January 2019 (UTC)[reply]

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