Thursday, January 18, 2018

Register for Nephrology Business Leadership University (NBLU)


Nephrology Fellows - Nephrology Business Leadership University (NBLU) is in its 3rd year. This is a must for graduating fellows.

Read this review from Mona Shaban and Natasha Dave from RFN from last years.

NBLU is a unique week long program that brings together a diverse faculty of practicing Nephrologists, hospital and dialysis provider executives, and other healthcare professionals who will share their insights on leadership, the business of nephrology, and the evolving healthcare landscape. 

Most sessions are held in a workshop format and are highly interactive and individualized.

Fellows attending a NBLU rotation can expect to leave with:

  1. Ability to evaluate potential employers for the ultimate fit 
  2. Enhanced leadership and business understanding to bring to potential employers 
  3. An understanding of the ever-changing payment / reimbursement landscape 
  4. The know-how to embark as a solo practitioner or as a high impact member of a group practice  
  5. Confidence approaching the interview process 
  6. Knowing you have the tools to start your career in the right direction 
Topics Covered:

  • Billing and Coding Workshop
  • CV and Interview Workshop
  • ACOs, ESCOs Basics
  • How to find the right job
  • Growth Strategies for your practice
  • Marketing 101
  • Practice Management
  • How to Review Employment Contracts 
  • Financial Planning
  • POC Ultrasound
  • Much Much More....... 
When: August 6th to August 10, 2018
Where: Plano, Texas.

Since we would like to keep the sessions very interactive space is limited.
Registration is free and can be done on the website NBLuniv.com

Travel support, hotel accommodations, and most meals are provided to all fellows that are attending. There should be little to no out of pocket expenses to the fellow or their training program.

Program Organizers -
University of California San Diego Division of Nephrology and Hypertension
Dallas Renal Group
US Renal Care

View the testimonial videos from prior years 

The NBLU team looks forward to seeing you in August!

Cindy Miracle

Friday, January 12, 2018

Azathioprine Toxicity

Azathioprine is one of the oldest immunosuppressant medications, which has been used in the field of solid organ transplantation over the past 5 decades. It is metabolized into its inactive forms by the enzyme thiopurine methyltransferease (TPMT). Genetic polymorphisms of the gene coding for this enzyme are common in the general population (~ 10% are heterozygotes causing low enzyme activity and ~ 0.3% cause complete lack enzyme activity). Testing for the enzyme activity is recommended prior to treatment with azathioprine or any thiopurines in children. However, it is not consistently tested for in adult patients who are immunosuppressed with azathioprine for inflammatory bowel disease, organ transplantation or rheumatologic conditions. Genotypic (testing for polymorphisms in the TPMT gene) and phenotypic (measuring levels of substrates and products of the enzyme in RBCs) testing for TPMT are commercially available but the concordance between them is not 100%.

The following are the metabolites that are tested for in the phenotypic testing:
6- Mercaptopurine – (Ref: 3.0- 6.6) nmol/ml/hr
6- Methylmercaptopurine riboside – (Ref: 5.04 – 9.57) nmol/ml/hr
6- Methylthioguanine riboside – (Ref: 2.7 – 5.8) nmol/ml/hr

Phenotypic testing performed within 30-90 days after a blood transfusion can result in inaccurate interpretation of the results because of donor RBCs influencing the test results. Moreover ethnicity, type of disease, concurrent drug treatment, red cell kinetics and transfusions should be taken into account while interpreting the results of TPMT enzyme activity. Single nucleotide polymorphisms (SNPs) account for the major TPMT low activity variant forms. Four TPMT alleles, TPMT*2, *3A, *3B, and *3C, account for over 90% of inactivating polymorphisms.
The approximate commercial cost is ~ $200 for phenotyping and ~$450 for genotyping. Clinical Pharmacogenetic Implementation Consortium (CPIC) has developed an evidence-based guideline on how to adjust thiopurine doses based on TPMT activity.
Posted by Karthikeyan Venkatachalam
Transplant Fellow
Washington University School of Medicine
St Louis

Wednesday, January 10, 2018

#KIDNEYcon Registration is Open


When- April 6-7, 2018
Where- Little Rock, Arkansas 

Who should attend- Internal Medicine Residents, Pediatric Residents, Adult and Pediatric Fellows, Attending Nephrologists 

Travel Grants- Available to Adult and Pediatric Residents and Fellows (DUE DATE Feb 16th) 

REGISTER HERE

Director- John Arthur, MD, PhD
Professor and Chief of Nephrology
University of Arkansas for Medical Sciences

Co-Director- Shree Sharma, MD
Nephropathologist
Arkana Laboratories, Little Rock, AR

Education Director- Matthew A. Sparks, MD
Assistant Professor and Associate Program Director
Duke University

KIDNEYcon is an annual conference (this is the 3rd year) designed to provide updates in the latest advances in kidney care in a hands-on collaborative format. A key component of KIDNEYcon's mission is to build enthusiasm for the field of nephrology among residents and fellows. We also aim to facilitate collaborative research projects among participants of the conference. The conference is a platform for nephrologists and medicine trainees to interact with experts from across the nation and learn about and discuss recent advancements in the diagnosis and treatment of kidney disease. The conference consists of half day workshops targeted primarily to medicine residents, nephrology fellows and early stage nephrologists and a Saturday scientific and clinical conference with broader applicability.

The FULL AGENDA

KIDNEYcon 2018 will feature 7 interactive hands-on workshops

Attendees will be able to attend 2 workshops (one Friday morning and the other Saturday morning) from the list below

  • The Kidney Biopsy Academy 
  • Vascular Ultrasound for Assessment of Volume Status Workshop 
  • Interventional Nephrology Workshop* only Saturday 
  • NephroTalk Communication Skills Workshop 
  • Acid/Base Fluids and Electrolytes Workshop 
  • Kidney Pathology Workshop 
  • Physician Scientist Workshop- How do I get there from here?* only Friday 
The Friday afternoon session will feature the Nephrology Education Summit at the Clinton Library. Attendees will have the opportunity to tour the library before the Summit. Five speakers representing a wide range of topics spanning from medical student education to fellow education will be presented. This will be followed by a talk from Jeff Amerine focusing on how others can effectively implement educational initiatives at their own institution using LEAN Canvas model.


Friday afternoon will feature a trainee Jeopardy competition and a keynote address discussing the physician scientist pathway.

The Saturday afternoon session will sessions on AKI and Liver Disease and kidney stones "Rocks Rock Little Rock"


Attendees are invited to stay on Sunday to discuss research collaborations in nephrology.
One of the first duties of the physician is to educate the masses — Sir William Osler 
Please consider coming to Little Rock. I am really excited about this years conference and our goal is to break the mold of the traditional conference. You will leave KIDNEYcon with more confidence and knowledge.

Matt Sparks

Tuesday, January 2, 2018

Acute Oxalate Nephropathy

Acute oxalate nephropathy is a rare but well described cause of acute kidney injury (AKI) leading to acute tubular necrosis due to the deposition of calcium oxalate crystals within the tubules.
Acute oxalate nephropathy can occur in both primary and secondary hyperoxaluria.
  • Primary hyperoxaluria is a group of autosomal recessively inherited enzymatic deļ¬ciencies that lead to the increased urinary excretion of oxalate. 
  • Secondary hyperoxaluria can occur due to increased dietary oxalate intake, increased absorption of oxalate from the bowel (also known as enteric hyperoxaluria), and increased production of oxalate. 
This mechanism of enteric hyperoxaluria is manifested in several ways, including with orlistat therapy, Roux-en-Y gastric bypass surgery, celiac disease, and Crohn's disease. Increased production of oxalate is mainly due to increased levels of oxalate precursors, more commonly glyoxylate, which is associated with ethylene glycol ingestion, and less commonly ascorbic acid. Oxalate nephropathy has also been seen in association with large quantities of iced tea consumption and most recently with "green smoothy cleanse".

Let's review a typical clinical scenario.

A young patient with history of alcoholic abuse who arrived to the emergency department with seizures, AKI (creatinine of 35 mg/dL, normal baseline), high anion gap metabolic acidosis, high osmolal gap (20 mOsm/l), oliguria, neurological signs and who strongly denied any drugs-of-abuse or suicidal toxic ingestion. The toxicological serum and urine examination did not show any evidence of toxic substances. No alcohol was noted on breath. The measurement of ethylene glycol serum level was not available. No family history of diabetes or any kidney diseases. Because of accompanying seizures, the patient was admitted to the ICU and treated with CRRT. Radiographic imaging demonstrated posterior reversible encephalopathy syndrome (PRES). A kidney biopsy was performed and showed the presence of several calcium oxalate monohydrate crystals mainly within tubular lumens consistent with acute oxalate nephropathy (Figure above). Eventually, the patient confirmed ingestion of small quantities of car antifreeze solution.

Ethylene glycol is a common component of automotive radiator antifreeze solution and is sometimes used as a substitute for ethanol. It can be ingested voluntarily, accidentally, or consumed in a suicidal or homicidal attempt. Ethylene glycol ingestion can lead to AKI from tubular deposition of oxalate crystals and can also cause neurological damage and death.

The diagnosis of ethylene glycol intoxication is based on a history of ingestion, clinical examination, high anion gap metabolic acidosis, high osmolal gap, and a measured serum level of ethylene glycol. However, it is often times difficult to ascertain an exact time frame of ingestion or have 100% certainty of consumption. Often times ethylene glycol levels are unknown as well. In this case kidney biopsy is essential in making the correct diagnosis. Therefore, a high index of suspicion for this disorder should be maintained in the presence of unexplained metabolic acidosis, hyperosmolality, unexplained AKI, and neurologic dysfunction.

Francesca Cianciotta
Nephrology Resident
University of Bari
Italy