Sunday, February 2, 2020

Gender equality for invited speakers in Nephrology, comparing to other fields in medicine.

How does Nephrology do compared to other fields in Medicine in terms of female representation at academic conferences?

Here is a breakdown from articles all published in the last 2 years in medicine/surgery

In general medicine vs surgery,  in one study 181 conferences with 701 individual meetings were analyzed, including 100 medical and 81 surgical specialty conferences. The proportion of women ranged from 0% to 82.6% of all speakers. The mean (SD) proportion of female conference speakers for all meetings analyzed significantly increased from 24.6% (14.6%) for 40 meetings in 2007 to 34.1% (15.1%) for 181 meetings in 2017 (P < .001). The mean proportion of female speakers at medical specialty conferences was 9.8% higher (SE, 1.9%; P < .001) than the mean proportion of female speakers at surgical specialty conferences for all years analyzed. 

In dermatology, women spoke less than men at their main conferences. 
In Anesthesiology, when studied in Canada, the representation of women speakers at the their annual meeting was similar to the representation of women in the anesthesiology workforce in Canada over the study period. Gender representation varied widely by subspecialty symposia, subject area, and women were absent from nearly half of all symposia at the annual meetings.
In General Surgery, women remain in the minority of panelists and moderators at their main meetings, and approximately 1 in 5 panels are composed entirely of men. 
In Neurology, at Stroke conferences, women are less likely to be invited speakers.

In colo-rectal conferences, program representation of women was similar to meeting demographics, although with low numbers in some topics. An imbalance in the formality of speaker introductions between genders was observed. This introduction concern was also raised recently at ASCO(Oncology meetings)

Interestingly, at the Critical care conferences, Over the 7 years, Society of Critical Care Medicine had the highest representation of female (27% overall) and nursing/allied health professional (16-25%) speakers; notably, male physicians substantially outnumbered female physicians in all years (62-70% vs 10-19%, respectively)

In our analysis recently published in CJASN time series analyses showed that the proportion of women moderators increased significantly by 3.5% per year (p=0.009, CI 1.2% - 5.9 %), and women speakers increased by 2.3% per year (p=0.001, CI 1.3% - 3.3%). This is impressive and kudos to nephrology leadership and association. Comparing to other specialities outside of internal medicine and within internal medicine( nephrology clearly is leading the way in terms of gender equality in invited speakers are conferences). 


Tuesday, January 28, 2020

Concept map: Copeptin in Natremias



The above figure summarizes the best data on use of serum copeptin level for diagnosis of diabetes inspidus and primary polydipsia. Copeptin derives from the precursor protein of AVP and has been correlated well with AVP production

What about in cases of increased ADH- such as SIADH? Data on that is poor and only one large study of >200+ patients showed that in hypovolemic hyponatremia ( appropriate ADH), the copeptin levels were >84pmol/L ( spec 90%, sens 23%) and SIADH fell in the 10-30pmol/L categories( not helping much) and hypervolemic and diuretic induced fell in 30-65pmol/L category. Use of this test is currently not recommended in diagnosis of increased AVP production disorders. 

Finally in patients with nephrogenic syndrome of inappropriate anti diuresis, copeptin levels were are low or suppressed. 

This article is an excellent summary of the use of copeptin in Na related disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850413/ 


Monday, January 20, 2020

Topic Discussion: Hypertension and TMA- chicken or the egg?

A recent discussion on twitter and ASN Communities has sparked this age old battle if HTN related TMA exists? Some believe that TMA is the initial insult and that leads to endothelial damage and HTN is a symptom and not the disease. Some believe that HTN is the start - leading to sheer stress and endothelial damage and in severe cases-- TMA

Check out the amazing twitter discussion by TMA experts on this topic.
What i found was this amazing image
Image
As one can see in this image- with some data existing on this - that malignant HTN can lead to endothelial dysfunction and some complement activation but not as severe as aHUS.

So if HTN does cause TMA, how does one distinguish that from a complement mediated TMA or aHUS? What if we are missing a mutation or an antibody that we haven't discovered.

1) Kidney biopsy cannot distinguish HTN induced TMA from complement mediated TMA 2) C3 being low is more valuable for an over active complement cascade compared to C5b-9 as even HTN can cause that to be elevated
3)) Doing a fundus exam can help significantly- there is no value in genetic testing in grade 3/4 retinopathy and especially with DBP>130mm Hg 4) No value in genetic testing in those that have a good response to bp control and eventually stabilized kidney function.
5) Ongoing TMA despite bp control and recovering of renal function- likely is then not HTN mediated and additional complement testing should be done.

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