Thursday, January 28, 2016

Perspective: How an Ultrasound machine has changed my practice?


My new instrument in the last 2 years has been the ultrasound probe.  It adds tremendous value to my physical exam. Residents in our program have traditionally been learning ultrasound skills as part of examining the patient: especially in the ICU.  Lungs look wet, kidneys look ok, bladder is full and IVC is plump.. We have now gotten information that can really make the care of the patient really swift. Official ultrasounds are still obtained but a quick and important organ examination can save lives and critical time..



Besides, I now feel that as nephrologists, this might be an important skill that we need to develop and gain acceptance too.  A patient calls and says he cannot urinate and he is having pain and he has known CKD. You see him but you are concerned about potential distal obstruction:- A quick bladder sonogram in the office can reveal the obstruction or distended bladder with urine and rather than an ER visit, you can promptly send this patient to the Urologist for foley insertion and home.

A dialysis patient tends not usually gain weight ( maybe 1kg between treatments) , comes in slightly short of breath. A lung ultrasound done by you reveal kerley B lines and in multiple views suggesting fluid overload.  This allows you to take off 2kg today and patient feels better.  Alternatively, you would have done that anyway but also perhaps exposed the patient to an X-ray that might have not been necessary. 

My practice has changed with this revelation. Training our faculty and fellows in this important skill- sonogram of the bladder and kidney and lung US and IVC for volume status is important. In the era of declining interest in nephrology, perhaps this skill might shed some excitement in the field of nephrology.   Lung US compares favorably to CT scan for detection for pulmonary edema and might be better than CXR.

The Emory course on sonogram might be the excellent course. What I envision is more of a short burst of courses that can really help us use this in clinical practice like we use our stethoscope, and not focus on using it for billing/coding etc. purposes.  Let’s save lives by making a difference in our patients in a fast paced manner , avoid ER visits and giving them a more comprehensive care in the Nephrology clinic.

Here are some interesting references !


Tuesday, January 26, 2016

Kidney Education Website in over 20 languages for patients around the world

The Kidney Education Foundation is an organization founded by Dr Sanjay Pandya from India. The website is currently engaged in spreading the information by preparing books and websites for the prevention of kidney diseases in different languages. Check out the website in various languages.

These educational websites are created to explain the goal of the kidney and what kidney disease is in very simple terms for the patients.  It is completely free. It is ISN endorsed!

http://www.kidneyeducation.com/

Sunday, January 24, 2016

Consult Rounds: High renal arterial resistive index

The renal arterial resistive index (RI) is a sonographic index to assess for renal arterial disease.
RI = (peak systolic velocity - end diastolic velocity ) / peak systolic velocity
  • The normal value is ≈ 0.60
  • With 0.8-0.9 being elevated
  • The RI measures the resistance of renal arterial flow to the kidney. In cases that cause elevated RI levels, there is reduced flow through the renal artery during diastole and sometimes even reversal of flow during diastole. 
We classically see this in the transplant kidney when there is concern for rejection

What is the differential diagnosis of this finding in a native kidney?
ATN
Obstruction
Renal artery stenosis
Renal vein thrombosis
Pyelonephritis
Severe hypotension

Tuesday, January 12, 2016

In the NEWS: Cardiotrophin like cytokine factor-1 and the podocyte?

What is CLCF1 and how does it matter to the podocyte?

CLCF-1( Cardiotrophin like cytokine factor-1) is  a  member of the interleukin 6 (IL-6) family of cytokines, is also known as novel neurotrophin 1 and B cell–stimulating factor-3.
CLCF1 is believed to be secreted and present in circulation as a heterodimeric composite cytokine with either of 2 proteins, namely cytokine receptor-like factor  (CRLF1) or soluble ciliary neurotrophic factor receptor alpha (sCNTFRa).
The role of CLCF1 in the regulation of podocyte structure and function is not known. Studies have shown it’s interaction though with the activation of  the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway.
The investigators in a recent study published detected CLCF1 in the plasma from patients with recurrent FSGS.  They studied the effect of CLCF1 on isolated rat glomeruli using an in vitro assay of albumin permeability (Palb).  The CLCF-1 did cause maximal increase in Palb. It was similar to an effect of having a FSGS serum.  If they blocked the CLCF-1, the increase in Palb was attenuated.  The available JAK2 inhibitor blocked the effect of CLCF-1 or FSGS serum on Palb.  STAT3 inhibitors also blocked this effect.  

What do these findings mean?

1.      Could this be the permeability factor that we are searching for fSGS?
2.      More needs to be understood regarding this factor before making any strong conclusions
3.      Interestingly, could STAT3 or JAK2 inhibitors could be potentially used to treat FSGS?



Wednesday, December 16, 2015

AVG thrombosis-- can any drug prevent it?


AVG can clot and certain patients, they clot frequently.  What is the data on pharmacological interventions to improve AVG outcomes in terms of preventing further clots?


A recent article in CJASN discusses this nicely via a case of a patient who has numerous AVG and most clot within weeks  of creation. The authors discuss patho-physiology of thrombosis of AVG but then discuss the potential pharmacological options.  I encourage all to look at Table 1 as it summarizes the randomized controlled trials on major agents that we consider are useful in preventing clots.

Apparently, warfarin, ASA + clopidogrel showed no difference and were more harmful in causing bleeding. 

Lowering homocysteine levels by folic acid didn’t do much either. Only trials that showed benefit were the ones that used Fish oil.  One is a small single center trial that showed decrease in thrombosis and other was a multicenter trial that showed that fish oil (four 1-g capsules/day) halved the frequency of the AVG thrombosis and angioplasty.

Worth a read for all nephrologists!

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