Journal of Onconephrology

Announcing the first of it's kind
Journal of Onconephrology, the official journal of C-KIN
We are hoping this journal will become THE place for the articles related to cancer and the kidney be published,

First article from 1966 that inaugurated the ASN

The field of Nephrology is not that old. ASN is going to be celebrating the 50th year of creation of the American Society of Nephrology this Fall 2016. I wanted to share the first article ever published in 1966 introducing ASN to the world. It was recently linked in ASN Kidney News.  Worth a read.
Even back then in 1966, a plea was made for early referrals for CKD, and not wait too long...

Check it out here...

IN THE NEWS: Cardiac output out and renal congestion in? what is the real cause of renal failure in CHF?

A dynamic study published in JACC might throw a curve on our thinking on heart failure and renal dysfunction. Chronic CHF( not cardiogenic shock) related renal dysfunction has been attributed by many to hypoperfusion due to impairment of cardiac output. Hanberg et al disprove this concept via an elegantly done analysis of cardiac index and renal dysfunction a registry database of CHF patients. There was no relationship that was significantly noted with cardiac index and renal dysfunction.  In this study , the patients were hospitalized for CHF, cardiac index was NOT the primary driver of renal dysfunction.

What is the major player then in the negative renal function?

Systolic Blood pressure might being low
High abdominal pressures – abdominal compartment syndrome
Renal vein congestion
Neurohormonal activation

An editorial in the same issue proposes alternate mechanism? But yet again physiology has not helped us. What was taught in textbooks and prior reviews was intuitive and perhaps it’s not that simple.  Improving forward flow might not be as important as providing “decongestion” from a kidney’s perspective.

Worth a read for the cardio-renal folks out there

In the News: Will the smart phone change Nephrology Care?

While smartphone apps have flourished in the general world we live in, Nephrology hasn’t seen direct patient care related smartphone apps. There are some great educational apps and a list of them are provided in a prior post on AJKD Blog. A survey done that was mentioned in that post focused mainly on educations of nephrology related apps.
The most recent CJASN issue presents perhaps one of the first( there might be more but not published) nephrology app that can be used in clinical practice. While this is not a randomized control trial, nor there was sustained long term follow up of these patients, this is a good start for a proof of concept for perhaps work in this area. This smartphone app targeted four behavioral elements in patients with CKD stage 4 or 5, it targeted BP, medication management, symptom assessment, and tracking laboratory results. The mean reductions in home BP readings between baseline and exit were statistically significant  and  27% with normal clinic BP readings had newly identified masked hypertension. In addition, medication errors were also identified.  An accompanying editorial also sheds some interesting thoughts on this concept. The editorial rightly addresses the downloadability of such apps. 
How many of your CKD patients own a smart phone?
If they do, how many are “techy” enough to download the app?
Mass use of such apps might be tough given the socio-economic barriers some of our patients might face.  Regardless, we need such apps and available for free for patients. Perhaps, we can teach them to download them and use them effectively to prevent re-hospitalization, medication errors, and offer and provide better patient care. 

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 22^st century.
Let’s please stop this madness!!

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

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