Clinical Case 62: Answers and Summary

A 56 YEAR OLD FEMALE PRESENTS WITH NEPHROTIC SYNDROME AND RENAL VEIN THROMBOSIS. BIOPSY CONFIRMS MEMBRANOUS GN. HOW LONG WOULD YOU CONTINUE ANTI-COAGULATION?

6 months minimum    25%

Lifelong   13%

Till the albumin>2g/dl     21%

Till the remission of syndrome   35%

Not sure    3%

There is very low–quality evidence to suggest the use of 

prophylactic anticoagulation with warfarin in patients with 

idiopathic membranous GN and severe nephrotic syndrome. KDIGO recent glomerular disease recommendations suggests that it might be considered when the serum albumin concentration is <2.0–2.5 g/dl  with one or more of the following: proteinuria over 10g/day; BMI  over 35; prior history of thromboembolism; family history of thromboembolism with documented genetic predisposition; NYHA class III or IV congestive heart failure; recent abdominal or orthopedic surgery; prolonged immobilization.  Per recent KDIGO guidelines, the duration of prophylactic anti-coagulation needed for optimal benefit compared to risk is not known, but it seems reasonable to continue therapy for as long as the patient remains nephrotic with a serum albumin <3.0 g/dl.   Per glomerular disease experts " The treatment of overt thrombotic or embolic events in patients with nephrotic syndrome is relatively straightforward. Anticoagulation with sequential high or low molecular weight heparin and oral warfarin is the recommended. The duration of treatment needed to prevent recurrent events is unknown but is probably equal to the duration of the nephrotic state per se. "  Another article suggests that warfarin therapy is given for a minimum of 6 to 12 months. However, most experts feel that warfarin should be continued for as long as the patient remains nephrotic. So the best answer would be till the remission of the syndrome and following that perhaps 6 months minimum. The remission might be quicker than 6 months in some cases. 

Want to be an attending physician on the ward - or not??

Can Nephrologists be medicine attendings or co-attendings on ward months for residents?

One of the reasons that residents don't get a good flavor of nephrology is because nephrologists have started to back off on serving as medicine attendings at many places and are only focused on subspecialty care consultation services.  Although, studies have shown that replacement of specialists with general-hospitalists in the last 15 years on the wards has had a positive impact on trainees medical education. A recent editorial by Wachter and Verghese in JAMA suggests that specialty attendings might not be ideal in the current health care settings to serve as medicine ward attendings. But they do emphasize that their presence is important. Hence, their exposure to residents can be via conferences or even " short bursts of co-attending."

What does co- attending mean? Do you manage the patient together? What is the second attending's role? Certain academic centers to have two attendings that round with the teams. Perhaps that might work. This might be one of the reasons why many residents don't get exposed to nephrology related education or other specialty related education. A ward "work" attending along with a subspecialty " teaching attending" might be another approach that might work as well.

I wonder how many practicing academic nephrologist do inpatient medicine ward months in 2012?
Would love to hear from many that do and what their experience is compared to 1980s or 1990s?

Check out the full viewpoint in JAMA Sept 2012 issue. 
Check out the podcast that goes along with this topic as well on the main JAMA website

CJASN eJC: September discussion

CJASN's eJC is discussing an important topic regarding nephrology fellows. Please go comment and share your thoughts on the recent article on career choice and satisfaction of nephrology fellows in the Sept issue of CJASN. Use your ASN log in and password to get to the discussion board.

http://ejc.cjasn.org/phpBB3/

eAJKD updates: Medicine 2.0 coverage

Joel Topf, MD from eAJKD advisory board member's team has been live blogging and tweeting from the recent Medicine 2.0 conference in Boston.  Topics have been variable from interactive tools to patient outcomes data using web 2.0 applications.

Check out the live blogging posts on eAJKD.
http://ajkdblog.org/tag/medicine2conference/

In the News: The POWER of HERCULES

Renal artery stenosis has taken a story of the classic pendulum swinging.  Studies that were observational in the 1990s suggested benefit in stenting and angioplasty as a treatment of modality. Recent trials such as STAR and ASTRAL ( largest to date) have shown no significant benefit in interventional interventions for atherosclerotic renal artery stenosis(ARAS).

While CORAL is still underway, here comes HERCULES.  This is a large prospective multi-center single arm study of patients with significant RAS and uncontrolled HTN. This is in contrast to prior trails that had less sicker patients. Most were at least on 2 agents and 75% on ACEI or ARBS. The procedure related complications were only 1.5% compared to prior studies suggesting as high as 17%.  The results suggested drop in SBP significantly at 9 months, low in stent restenosis rate and complication rates.

While this is a positive study in terms of intervention- the fact that it is a single arm trial, makes it a major limitation.  HERCULES has limitations too. CORAL is still awaited.

Regardless- check out the full trial at Catheterization and cardiovascular interventions. 

Nephrotic Syndrome: Pathophysiology update

Why does edema happen in nephrotic syndrome?

There has been talk about this topic for decades. There is the underfill and the overfill concepts and both have had their share of evidence for and against it. A recent article in Kidney International describes the journey through the different players in the formation of edema in nephrotic syndrome.

Take home points that the article suggests after review of the basic science and clinical literature.

1. Hypoalbuminemia is not a cause of edema formation in nephrotic syndrome
2. Vascular permeability abnormalities are also less likely the major players
3. Proteinuria leads to increased activation of ENAC channels and leading to Na retention- this might be the major cause of edema. This might be the most active component regardless of the intravascular volume status of the patient.
4. Excess serum ADH levels might also help in water retention.
5. RAS system does not appear to be the primary mechanism of renal Na retention.

This leads us to believe that perhaps a combination of loop diuretic + K sparing diuretics might be a good combination to use in the treatment of the edema( although data is sparse)

Some interesting points from the article regarding edema physiology

1. Extracellular fluid volume expansion excess expands both the intravascular and interstitial space in chronic renal failure compared to nephrotic syndrome- where its largely confined to the interstitial space due to protective effects of interstitial protein washdown and washout.
2. Minimal Change disease or severe hypoalbuminemia might have true decrease in intravascular volume compared to other nephrotic syndromes that are more in the range of normal to expanded blood volume.

In the News: Kidney Transplant Chain- 1 year follow up

A recent publication in AJT describes the largest kidney transplant chain experience. They report the largest series of chain transplantation that were done at 57 centers in USA by pooling incompatible donor/recipient pairs.  Every recipient whose intended donor donated were transplanted. 46% percent included minorities who have hard time getting donors. One year follow up is excellent with mean crt of 1.3mg/dl. This is a remarkable success and a step forward in the field of transplantation.