Wednesday, April 13, 2016

Perspective: Broken Medicine


Here is a question for you:




















A 55 y old male with HTN is here for follow up.  He has no other medical problems.  Medications include losartan, metoprolol, amlodipine, and HCTZ.  Blood pressure is 160/100 mm HG.  What is the next best step for his blood pressure control?

A.      Dietary history
B.      Check Renin/Aldosterone levels
C.      Check secondary workup
D.      Make sure the patient is taking all medications properly
E.       Obtain a 24 hour ABPM
Any of the above or all of the above would be good choices and one can start with either one. Here are the real world choices…
A.      Obtain Renal consult
B.      Obtain Endocrine consult
C.      Obtain Cardiology consult

Here is where the fragmentation begins. Why does this happen?
Here are the top reasons in my opinion
Not enough time to think
Inertia to think
Patient satisfaction( I want a HTN specialist)
Training not adequate
Trainers were not master clinicians and hence they believed in panconsultemia as well

Once consults are obtained: - more confusion as cardiology and nephrology don’t agree on drug choices. Endocrine wants more tests. Now more accidental findings…. And it continues. 

Welcome to medicine in 22st century.
Let’s please stop this madness!!

Tuesday, April 12, 2016

Topic Discussion: Anticoagulation related nephropathy(ARN)


Anticoagulation-related nephropathy (ARN) is a significant but under-diagnosed complication of anticoagulation  We have heard of cases of warfarin nephropathy but why can't this happen with any anti coagulation.  A recent review illustrates the data for us.  Check out this review here.  ARN is currently defined as acute kidney injury (AKI) without obvious etiology in the setting of an International Normalized Ratio (INR) of > 3.0. Prior investigations into ARN have almost universally focused on anticoagulation with warfarin; however, recent case reports and animal studies

suggest that it can also occur in patients taking novel oral anticoagulants. 
It is important to consider this entity in our differential. Biopsy is not always possible as most of the cases present with high INR levels and risk of bleeding could be high. But in certain cases, perhaps possible too make a more distinct diagnosis.  The authors make some interesting and important recommendations for patients at risk for ARN

1. INR and renal function to be monitored every 3-4 weeks in first 3 months of starting anticoagulation as most of the ARN happens in 6-8 weeks following therapy.
2. Rapid increases in INR can cause AKI
3. Patients with moderate to severe CKD should have their renal function checked even more frequently.
4. If INR is supratheurapeutic, renal function should be checked more closely
5. Workup should include Urinalysis, urine electrolytes, renal sonogram and if negative and only finding is hematuria- ARN should be in the differential diagnosis. 
6. The data on the newer direct oral AC is minimal in CKD patients.  Renal function should be monitored in those patients closely as well as dosing might depend on crcl as well for those agents.

While the data is mostly in warfarin, the newer agents and the kidney might be at risk. Thus far only 1 case report as I linked earlier is noted with dabigatran but was also clouded with hx of IgA nephropathy and warfarin use.  Some of the complications of dabigatran related bleeding are due to the AKI or low clearance. Which came first? 

Regardless, AKI can be seen with glomerular bleeding and I have noted crt rising with INR rising and considered it in many cases.  Let's see if the newer oral ACs have this complication.  Uptodate even has a section on this now listed under ARN. 
My prior post on WRN in 2011 when it was first described.
Check out this other review as well
http://www.krcp-ksn.com/article/S2211-9132(14)00131-4/abstract

Tuesday, March 22, 2016

A novel look at hyponatremia in the alcoholics

Tavare and Murray in a recent NEJM image had an interesting case of hyponatremia correction. The case highlights development of central pontine myelinolysis(CPM) despite slow correction of hyponatremia.  CPM is known to occur in alcoholism, liver disease and malnourishment in the absence of hyponatremia, hypokalemia or hypophosphatemia. 

We wanted to suggest an algorithm that can be used in settings where alcoholics present with moderate to severe hyponatremia with similar symptoms as presented in this case and are at risk of CPM.  The figure below is a novel algorithm that uses brain imaging to help us guide the therapy for moderate to severe hyponatremia in alcoholics.  



If the patient is symptomatic with seizures, the correction of hyponatremia should be promptly started.  If the patient is asymptomatic  or with milder symptoms and is encephalopathic ( with several  confounding  etiologies : hyponatremia, alcoholism, liver disease), a MRI of the brain should be performed. If the MRI confirms cerebral edema, hyponatremia should be treated with the usual slow rate of correction of 6-9mmol/L per 24 hours.  If the MRI confirms CPM, the correction of hyponatremia should be put on hold.  

We hypothesize that often the hyponatremia  in alcoholics is  chronic  and correction, regardless of the rate, might cause harm in these patients.

We welcome comments from experts on this concept. 

Kenar D. Jhaveri, MD
Rimda Wanchoo, MD
Alessandro Bellucci, MD


Friday, March 11, 2016

Nephrologists as Super Heroes


When somebody asks me what nephrologists are, I usually respond with ‘superheroes.’ Sure, my perspective may be a bit skewed since I write for a comic series, and yes, superheroes may not be the first thing that pops into one’s mind when discussing the kidney. But in clinical practice, nephrology is a multidisciplinary field within medicine that requires deep knowledge of numerous organ systems. Acid-base disorders, dialysis, oncology, rheumatologic diseases, and transplantation are just some of the subjects in which a budding nephrologist gains expertise. Combine this prowess with the everyday challenges of providing primary care to chronic kidney disease patients, one can’t help but think of nephrologists as ‘superheroes’ in medicine.

When intensivists are struggling with an ABG, who do they call? The nephrologist. When cardiologists are struggling with hypertension and volume management, who do they call? The nephrologist. When endocrinologists are baffled by unexplained hypercalcemia, who do they call? You get the picture. Superheroes are wanted---and needed---in order to save the day.
You would think that young residents would be clamoring to don their capes and join the field of nephrology. But on the contrary, interest in nephrology has steadily been declining in recent years. According to Dr. Warren Kupin of U-Miami, the field of nephrology is suffering from an ‘acute fellowship insufficiency’, with fewer than 50% of programs filling their open fellowship positions, and some large academic programs going without even a single fellow. This lack of interest can be attributed to perceptions that this field is too complex, or perhaps to a lack of exposure to nephrology in residency. We may see ourselves as superheroes, but in actuality we are perceived more as “mutants” by the rest of the medical profession.

The mutants of X-Men are a group of individuals that were born with superhuman powers, but needed guidance, direction and purpose in order to flourish. They were constantly being targeted for their distinct abilities and talents that no humans could ever dream of possessing. The X-Men frequently had to fight for their mere survival. While on the pathway to annihilation, a bright light shined over these mutants. A gentleman by the name of Professor X would fill the void and provide mentorship to these troubled youth. He was a scholar and a role model for his students. It was through him alone that the X-Men were able to hone their powers for the good of mankind and recruit other mutants to Xavier’s Academy for Gifted Youngsters. Had it not been for the mentorship of Professor X, the mutants would have surely fallen into extinction.
Simply stated, we need more Professor Xs in nephrology. There needs to be a drive from within the field itself to demonstrate the attractiveness of our specialty. A systematic approach towards creating interest in our field must be undertaken to draw in the next generation of renal specialists. One way to make nephrology appealing to medical students and residents is through effective mentorship and education from the people within.
            When I was in medical school, I was assigned to a nephrologist as my attending physician for much of my internal medicine rotation. This was my first real exposure to what I would come to find as my life’s calling. I was intrigued by the complexities of renal physiology and its application in practice. I was excited by the life saving procedures of catheter placement and emergent hemodialysis in the emergency room and ICU. I was challenged by the detective work involved with diagnosing glomerular diseases. Now, in fellowship, my passion for the field has been furthered by being a part of the kidney transplant team.
            It is time we all do our part and take on the tradition of actively engaging and mentoring young physicians in the field of nephrology. Medical students and residents should be encouraged to rotate through nephrology electives with inspiring clinicians and passionate educators. By motivating a new trainee to consider a career in nephrology, you become more than a role model- you become a superhero. In the words of Professor X, “when you can access all that, you’ll possess a power no one can match. Not even me.”

Post by Dr. Khurram Mehtabdin, NSMC intern, who is a graduate of Syracuse University and TouroCOM NY. He completed his residency in internal medicine at Flushing Hospital Medical Center and is in his nephrology fellowship at the Northwell Health and Hofstra Northwell School of Medicine. Khurram is the co-creator of the comic book series Zindan, available at TheLastAnsaars.com





Nephmadness 2016 Begins today

As each of you might be aware, NephMadness (now in its 4th year) is a way to promote our field to residents and medical students while each of us learn at the same time. NephMadness celebrates all things nephrology during the entire month of March (National Kidney Month). NephMadness (brought to you by the AJKD blog, the official blog of the American Journal of Kidney Diseases) is an online game that invites everyone to predict the "winners" of competing medical concepts.
Like in March Madness, where fans try to pick the winner of the NCAA Basketball Tournament, NephMadness provides brackets for participants to fill out online (click here for the submission site) and then compete with a worldwide community of peers. Winners of each “game” are determined by a majority vote of nephrologists we call the “blue ribbon panel”


  • Dan Weiner
  • Scott Gilbert
  • Nancy Adams
  • Jeffrey Berns
  • David S. Goldfarb
  • Melanie Hoenig
  • Roger Rodby
The medical concepts—or "teams"—are divided into eight regions highlighting different aspects of nephrology. They are:
  1. Hypertension Region: Raymond Townsend
  2. International Nephrology Region: Professor Vivekanand Jha
  3. Missteps in Nephrology Region: Mark Rosenberg, MD
  4. Transplant Nephrology Science Region: Milagros (Millie) Samaniego, MD
  5. Recreational Drugs and the Kidney Region: Mark A. Perazella, MD, FACP
  6. Pediatric Nephrology Region: John D. Mahan, MD
  7. Statistics in Nephrology Region: Perry Wilson, MD MSCE
Detailed scouting reports with background information is all provided at the blog. How do you pick the winner of each match. Simple, just select the medical concept that in his/her best medical judgment holds the most significant and promising benefit for the future of nephrology, weighting evidence-based medicine over eminence-based medicine.
NephMadness begins March 10th (World Kidney Day) and entries are collected until March 23rd when the game begins at roughly the same pace as the real NCAA tournament.
Winners of the concept matchups will be determined by a blue-ribbon panel of nephrologists and physicians. Those who guess the most correct matchups correctly will have a chance to win AJKD/NephMadness swag, textbooks, and fame!
Go to www.ajkdblog.org to review the scouting reports for each concept or go to the bracket submission site to place your votes.

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Sunday, February 21, 2016

Monoclonal Gammopathy and end organ damage ( Skin, Nerves, Cornea and more):- it’s not just the kidney.



While MGUS and Kidney disease is now a finding well described in the literature, why not other organs?

It is quite possible that there is end organ damage to other organs from these small set of B cell or plasma cell clones if there is kidney damage.
A recent review in the corneal world found a case series of what we could call MIDD in the cornea. Seven patients were identified with corneal immunoglobulin deposition. The structures they found are similar to crystalline structures. Some of them looked like immunotactoid, some fibrillary and some amyloid. All patients had evidence of paraproteinemia in a setting of monoclonal gammopathy of undetermined significance, smoldering plasma cell myeloma, or Waldenström macroglobulinemia. Authors suggest treating underlying MGUS or paraprotein disease. Few patients, this was the first systemic presentation of the disease.  What a great observation!!  If it can effect small renal vessels, why not the eye!

What other organs?

Skin: The association between Necrobiotic xanthogranuloma(NXG) and paraproteinemia is well documented in 2009. 11-48% had paraprotein disease as myeloma. The most common is IgG kappa more than lambda. However, the skin lesions in NXG could represent reactive inflammation and are not associated with the presence of monoclonal plasma cells or multiple myeloma.


Powell et al also described initially eight patients with pyoderma gangrenosum and monoclonal gammopathy showed that all patients except one had an IgA paraproteinemia. Seven patients have had a benign course and multiple myeloma has developed in one. In seven patients, the onset of thepyoderma gangrenosum preceded the detection of the monoclonal gammopathy. Since then, more cases have been associated with MGUS.

Syndromes:
Besides POEMS syndrome, which has been well described in the literature, others are :

TEMPI syndrome, a syndrome that was mentioned in NEJM that had a constellation of findings: Telangiectasias,elevated erythropoietin level and erythrocytosis, monoclonal gammopathy(IgG kappa), perinephric fluid collections and intrapulmonary shunting.  Since it’s initially discovery, chemotherapy and HSCT have been used for treatment of this entity.

Schnitzler's syndrome, initially described in 1974 is an uncommon condition defined by chronic urticaria and monoclonal IgM gammopathy. A study done in 2002 found 56 cases of Schnitzler's syndrome reported to date. The absence of lymphoproliferative disease in this condition is typical, but nine patients have progressed to develop lymphoplasmacytic neoplasias, particularly waldenstrom's macroglobulinemia.

So, besides MGRS, MGUS might have other distant organ effects from small noxious B cell clones. Perhaps, this needs to be defined more and treated more like MGRS.  It might be interesting to see the cases of ITG and fibrillary GN – if they have corneal findings and other end organ damages that we might be missing given these novel associations. We might be looking at a more systemic disease. 


We might be entering a new era in the paraprotein world.

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