NephMADNESS 2014

March Madness and Nephrology
Fun and learning mixed together.

This time: More new brackets, world experts contributing and a fancy website and tool to allow you to submit your brackets. In addition, there are prizes to be won as well

To submit your picks in NephMadness 2014 go to the NephMadness site. After you submit your picks you will need to register with your full name, username, email and passsword.  Deadline for completing your bracket is Wednesday March 26th at Noon EST. After that you will not be able to submit a bracket.

Detailed scouting reports on all 64 nephrology concepts can be found on the eAJKD website. eAJKD is also where the winners and losers will be announced and news about the contest will be posted.

Most of the content and resources for NephMadness are also available at NephMadness.com.

Interact with NephMadness content by following eAJKD on twitter or by following the#NephMadness hashtag.

TOPIC DISCUSSION: ANCA negative pauci immune vasculitis- what is it?

Approximately 10% of systemic vasculitis patients test negative for ANCA( PR3 or MPO). This group has been studied only infrequently.  It appears that evidence suggests that ANCA negative disease is more renal limited and more severe to the kidney. Some data suggesting that anti endothelial antibodies might be associated with ANCA negative vasculitis.

 Hedger et al. investigated over 30 patients with ANCA-negative rapidly progressive glomerulonepritis and found that they had fewer respiratory findings compared to ANCA positive patients. Eisenberger et al. have identified 20 cases with ANCA negative vasculitis. The renal histology revealed a high percentage of active glomerular lesions (50%), mainly cellular crescents, whereas only 28% of them had glomerular necrosis. Chronic tissue damage with glomerulosclerosis (21%) and diffuse interstitial fibrosis (40%) were already present at diagnosis, more prominent than in historical ANCA positive patients.  Age over 65 was found to be predictor of mortality in this study.

In another study, they found that the level of urinary protein and the prevalence of nephrotic syndrome were significantly higher in ANCA-negative patients than that in ANCA-positive patients. The renal pathology was more severe in ANCA negative groups and the renal survival was poorer as per prior studies.  Treatment has been focused on using combo therapy of either cytoxan+steroids or MMF+steroids.

Nephrology: Salary and compensation

Salary and compensation myths in Nephrology

There is a misconception that salaries of nephrologists are low.  One needs to look at actual data before making such conclusions.  Salaries of physicians in general are being disturbed by variety of factors that are currently not under our control.  Besides that, here is some data from peer reviewed publications talking about different compensations and comparative earnings.  This first publication by Leigh JP et al looked at life time earnings of medical specialties.

This figure suggests that life time earnings of a nephrologists are not that bad. We are right in the middle and actually close to dermatologists and allergists. For a limited procedural field, we are actually not doing that bad.  

This figure from an  article that had looked at work hours spent less or more than family practice as bench mark and we do spend more time ( hours) but so does some of the other specialties.  But overall, we are not that far off from the center.  So far, to me – nephrology is not looking that bad based on this data( which compiles not just academic but private practices as well). One has to keep in mind that the private practice nephrologists can earn substantially more than academic counterparts. Some of my fellows over the last few years have gone into practice in private settings all around the country and are very satisfied with their compensation. 

A different  study compared mean hourly wages of nephrologists to other fields and general surgery was the bench mark.  Also the table below shows the mean number of hours.

We are right up there after GI and Cards in medical subspecialties. 

I think the three tables from articles in the fairly recent era suggest that myths of poor compensation is exactly what it is- a myth.  

Nephmadness 2014:

March madness fever has begun. This month is National Kidney month. In spirit of nephrology education and kidney centric month, eAJKD and nephrology blogsphere presents Nephmadness 2014 to all of you.
This year, its more sophisticated with newer brackets, more interactive online platform and moderators that are experts in the field.

Check out the official website of Nephmadness at www.nephmadness.com
Select your brackets starting this sunday March 16th 11:00AM onwards.
eAJKD will also host the discussions and bracket details on the blog site as well.

Let the educational game begin!!

Detective Nephron: Next venture

Take a look at the March 2014 ASN Kidney News for the next Detective Nephron venture as the detective tackles an AKI case.
http://onlinedigeditions.com/publication/?i=200100

Clinical case and answers 81

What leads to hyponatremia in adrenal crisis?

Pre renal state due to low cortisol	5 (26%)
CRH release leads to hyponatremia	2 (10%)
Cortisol normally suppresses ADH and in adrenal insuff, this doesn't happen	11 (57%)
The mechanism is not known	6 (31%)

The hypersecretion of ADH seen in low cortisol states may be due in part to the reductions in blood pressure and cardiac output. However, a more important mechanism may be that cortisol deficiency lead to increase CRH production leading to increase ADH state.  Cortisol feeds back negatively on CRH and ACTH, an inhibitory effect that is removed with adrenal insufficiency. In addition, cortisol appears to directly suppress ADH secretion. Thus, ADH levels increase when plasma cortisol levels are low.  Alternatively, the hypersecretion of ADH induced by aldosterone deficiency is caused by renal salt wasting with resultant volume depletion. Many studies support the concept that hyponatremia in patients with hypopituitarism is mainly caused by failing inhibition of ADH secretion because of hypocortisolism.

http://jasn.asnjournals.org/content/17/7/1820.long is an amazing reference from JASN that looks at water homeostasis in adrenal disorders. 

IN the NEWS: Is this the end of suPAR?

Clinical and experimental evidence suggests the pathogenic role of circulating permeability factors, including soluble urokinase plasminogen activating receptor (suPAR). Serum suPAR levels were found to be elevated in Caucasian adults with primary FSGS and in two cohorts of children with FSGS from Europe and the United States. 

          This new study in KI March 2014 issue from India looked at the role of suPAR in all children with nephrotic syndrome. Compared to controls, suPAR levels were highest in FSGS and then other nephrotic syndromes from MCD and other congenital diseases. Interestingly, the study failed to show that this circulating factor that was really hallmark of FSGS diagnosis was specific for FSGS. Rather, it might be a biomarker for nephrotic syndrome in general.  Interestingly, levels of suPAR significantly correlated inversely with eGFR and CRP.

          So what this study is telling us is that suPAR gets elevated with downtrending GFR- perhaps it’s just a renal clearance marker. In addition, suPAR has been found to be elevated in sepsis, malaria and chronic infections such as Hepatitis and HIV. So it’s unclear if suPAR really is a marker of podocyte injury but rather a marker of generalized inflammation. 

          So, suPAR doesn’t answer our question for FSGS permeability factor anymore.  This study really highlighted the non specificity of suPAR for FSGS and even perhaps podocyte injury.