Virtual Grand Rounds in Nephrology- E nephrology

As we are seeing, there is a blossoming of E -Nephrology tools and one such is the Pediatric Nephrology website and what they refer to as Grand Rounds. It is a fascinating feature of their blog and we have been pasting links of their ongoing grand rounds that helps not only the pediatric but adult nephrology field as well.  Take a look a fascinating article on this very concept.

http://www.springerlink.com/content/h523q12p6t1r8265/

ASN's review on the ESRD bundling

The ASN has created a special website and a pdf summary of the ESRD bundling and will continue to review the 900+ article.

http://asn-online.org/policy_and_public_affairs/esrd-bundling.aspx

Please have a look at the website. The summary is helpful.

TOPIC DISCUSSION: EFFECT OF PROTEINURIA on combination treatment

The role of combination blockade has been now come to question at least in the non nephrotic proteinuria world.
But there were some simple questions we wanted answered?
When you have someone on ACEI, and you add an ARB, what additional reduction in proteinuria do you get?
--> It actually is around 25% more reduction or 0.5g/dl additional reduction in proteinuria. This was extensively studied in one paper listed below. In another study, it was around 39% compared to ACEI monotherapy.
What about the effect on GFR?
--->Usually the fall is 4 ml/min
What about the effect on SBP and DBP?
--->Usually fall of 5mm/hg in both with the addition.

http://www.ncbi.nlm.nih.gov/pubmed/17367311
http://www.ncbi.nlm.nih.gov/pubmed/16797382
http://www.ncbi.nlm.nih.gov/pubmed/18468748

Poem from Pediatric Nephrologist

Check this out on CKD

https://www.pediatric-nephrology.com/daily-updates/2010/07/30/252-ckdpoem1.html

TOPIC DISCUSSION: ACE induce angioedema replaced by an ARB

Th e questions stems from the fact that many of us struggle to use or refrain from using an ARB in patients who have ACE induced allergic reaction specifically angioedema. Here is the data with references --

1) http://www.ncbi.nlm.nih.gov/pubmed/15111379 - Arch Intern Med. 2004 Apr 26;164(8):910-3. "Only a small percentage of patients with ACE inhibitor-related angioedema continue with this symptom when switched to an ARB."

2) http://www.ncbi.nlm.nih.gov/pubmed/17225721 - Ann Allergy Asthma Immunol. 2007 Jan;98(1):57-63. " The mean time to onset of angioedema after initiation of therapy in 51 patients was 1.8 years. Also, none of the 6 patients, whose angioedema was attributed to an ACE-I who then received an ARB, developed recurrent angioedema in more than 8.1 patient-years of follow-up. "

3) http://www.ncbi.nlm.nih.gov/pubmed/19055203 - Ann Allergy Asthma Immunol. 2008 Nov;101(5):495-9. This is the meatanalysis I was referring to - " Any article that described a cohort of patients who had angioedema after taking an ACE-I, were subsequently exposed to an ARB, and were followed for a least 1 month were included. The risk of angioedema was 9.4% (95% confidence interval, 1.6%-17%) for possible cases and 3.5% (95% confidence interval, 0.0%-9.2%) for confirmed cases. CONCLUSIONS: Limited evidence suggests that for patients who develop angioedema when taking an ACE-I, the risk of development of any subsequent angioedema when taking an ARB is between 2% and 17%; for confirmed angioedema, the risk is 0% to 9.2%. This information will aid clinicians in counseling patients regarding therapy options after development of angioedema due to ACE-Is."

Please feel free to share or comment if you have some other ideas or data to share.

Thanks,

Arun Chawla, MD

Nephsap review: Chronic Kidney Disease : CKD patients are more likely to have proximal coronary lesions???

Did you know that patients with CKD are more likely to have proximal coronary lesions on coronary angiography? This is well summarized in Charytan,et al study in KI 2008. This is in comparison to distal lesions
the pathogenic mechanism behind it might the time that is not enough to form collaterals, uremic mileau, and perhaps other unknown reasons.

Interesting

http://www.ncbi.nlm.nih.gov/pubmed/18818684

Nephsap review: Chronic Kidney Disease: Troponin T vs I in CKD

On review of Nephsap 2009 CKD, here is an interesting topic of discussion that came up after a question we reviewed.
Hayeshi, et al studied the utility of using cardiac troponin t as a tool for predicting asymptomatic coronary artery stenosis in CKD patients on renal replacement therapy. The primary finding was that cardiac troponin t was a more potent independent predictor of asymptomatic multivessel coronary artery disease in late stage CKD patients. This raises an important point and makes us wonder will we be using troponin t as a screening tool for asymptomatic coronary artery disase in the future? Further studies are needed to help us with this.
First we need to understand the different troponins in the picture.

Troponin is a component of thin filaments and is the protein to which calcium binds to accomplish this regulation. Troponin has three subunits, TnC, TnI, and TnT. 

• Troponin C binds to calcium ions to produce a conformational change in TnI
• Troponin T binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex
• Troponin I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place.

Some centers use Tropnin I and some T, both are very sensitive and specific for cardiac events.

The question is which one is better in CKD patients.

Another study by Fehr et al in Clinical Nephrology showed that for diagnosis of ACS in HD patients, a combination of cTnT and cTnI may be used, since the former has higher sensitivity and the latter higher specificity. A higher threshold value for cTnT in HD patients could further increase its diagnostic accuracy.

Interesting the differences in the studies, one with CKD and other with ESRD.

http://www.ncbi.nlm.nih.gov/pubmed/18403432

http://www.ncbi.nlm.nih.gov/pubmed/12572929