Life After Renal Fellowship Survey Results

A few months ago we had put a poll up for graduating fellows in Nephrology at our website, Renal Fellow Network and Uremic Frost along with ASN Kidney news Facebook page.

The results of our survey, although subjective and small, were surprising and hence the data was presented at ASN 2010 Denver meeting this year and the publication just published in the current ASN Kidney News 2011 January Edition.
34% of the graduating fellows didn't have a job following completion of training
12% who had a job, were going to do Hospitalist rather than Nephrology Job
What was more surprising is that 18.5% of fellows graduating Nephrology felt that they chose the wrong field!!!!
Few biases: Small survey with only 70-80 responders; mostly from the East coast and the South USA.
Survey has its own biases.
Regardless of the size, the fact that significant numbers were disappointed following completion of fellowship is a big red flag for trainers and programs - perhaps we need to do better in marketing and promoting our field. We need to make it more fun and appealing and perhaps try to help our fellows find a job and career planning. Perhaps, if we polled other specialities we might find similar findings. A larger survey might be needed to confirm this data.
Here is the link to the ASN Kidney News article
http://www.asn-online.org/publications/kidneynews/archives/2011/jan/KN_jan2011.pdf

Bisphosphonate Therapy in CKD and ESRD patients

Bisphosphonate Therapy in CKD and ESRD patients

CONSULT ROUNDS: Amyloidosis vs Light Chain Deposition Disease

Paraproteins can manifest in many ways in the kidney. One that often brings confusion and can look very similar clinically and pathologically is AL amyloidosis and light chain deposition disease.

AL Amyloidosis

Beta pleated sheets

Usually fibrillary proteins( a diameter of 8 to 10 nm and may be up to 1 micrometer in length. They fibrils are randomly arranged and tend to form compact arrays when adjacent to cell membranes)

AL protein mainly lambda type usually seen with plasma cell dyscrasias

5% of the cases present with nephrotic syndrome

Usually older adults

An involve any organ, but the deposits with more clinical relevance are in kidneys, heart and liver. Other frequent locations are skin, tongue, peripheral nerves, gastrointestinal tract, and spleen. 

Renal function effected only in 50% of the patients

In 2/3 of patients there is a monoclonal protein in urine. Bence Jones protein is usually not detected.

Glomeruli are affected in almost all the cases of AA amyloidosis and in less than half of AL amyloidosis. Deposits can be nodular or irregular in mesangium. Congo red positive

No cellular proliferation. In cases with little glomerular involvement diagnosis can be difficult and requires high suspicion to request Congo red and/or electron microscopy.

Amyloid is eosinophilic (pink) with H&E; weakly PAS-positive 

Light Chain Deposition Diseases

It is an infrequent complication of myeloma 

Kappa more than lamda( 4:1) ratio

Renal involvement is the one that dominates the clinical picture. can also see heart, liver, lungs, skin, and endocrine glands.

Non selective proteinuria usually as compared to AL amyloidosis

More chances to be seen with renal dysfunction, often associated with cast nephropathy if also present. 

The most frequent finding in glomeruli is nodular glomerulopathy.

PAS-positive but do not stain with silver stains (unlike nodules in diabetic nephropathy) and they are Congo red and crystal-violet-negative (unlike those in amyloidosis). 

The peritubular deposits are granular and very electron-dense. In glomeruli they are identified in the nodules, mesangium, and subendothelials. vascular disease can be seen as well.

References:

http://www.ncbi.nlm.nih.gov/pubmed/17075231

http://www.ncbi.nlm.nih.gov/pubmed/17699366

The Study of Heart and Renal Protection — SHARP Trial

The Study of Heart and Renal Protection — <em>SHARP Trial</em>

Can Alcohol Consumption be protective post transplant?

One study presented at the recent ASN 2010 at Denver found that alcohol consumption in moderation was indicative of lesser incidence of post transplant diabetes (NODAT). The investigators argue that the belief of interactions with medications might be false and without evidence. Not only did they show that it was a decreased NODAT risk but also decreased risk of death post transplant.  So kind of similar to the general population.  

Check out Renal and Urology news's website for a video on the presenter at ASN 2010

http://www.renalandurologynews.com/moderate-alcohol-use-benefits-renal-transplant-patients/article/191147/

DID YOU KNOW? Extra renal Podocyte like systems?

Besides the kidney, where else does a well designed filtration barrier exist in our body? This area lacks podocytes but produces a filtrate that is also virtually free of plasma proteins.
Its the choroid plexus. The sieving coefficient of the plexus is similar to that of the renal glomerulus. So do patients leak protein in the CSF in proteinuric diseases? In a small cohort study of diabetic patients that protein concentrations where increased in the CSF with diabetes duration.
Hmm!!


Take a look at these references:
http://www.ncbi.nlm.nih.gov/pubmed/21184239
http://www.ncbi.nlm.nih.gov/pubmed/18628631?dopt=Abstract
Image source: Penn state

TOPIC DISCUSSION: Low or negative Anion gap!

 We often encounter positive anion gaps and know very well the causes of + anion gap.

In certain clinical settings,one can also see a low, zero or negative anion gap.
What are the causes that one has to consider in a low anion gap?
If one considers Na, K, Mg, Ca and immunoglobulins (IgG) as + cations and Cl, Bicarb, Phos, IgA and Phos as negative anions then the anion gap is the balance of these substances. Usually normal is 10-12.
So if one increases the + cations or decreases the - anions, you can have a negative or low anion gap.

Hence the causes are obvious
1. Hyperkalemia, Mg and Calcemia
2. elevated paraproteins( igG usually)-- one of the classic causes and whenever you see a low or negative anion gap, think paraproteinemias
3. decreased albumin or phosphorus
4. Lithium( increases the Cationic side)
5. Unmeasured cations like bromide or iodine or triglycerides can also do it
6. Lab error( most common cause)
7. Severe hypernatremia
8. Spurious elevation of HCo3 if cells are not separated from the sera
9. Over estimation of Cl ion

Out of these the ones to cause a negative anion gap more than low anion gap are lab errors, paraproteins, bromide and iodine intoxication.

Something to keep in mind while we walk the wards!
A nice review is here

http://www.ncbi.nlm.nih.gov/pubmed/17699401
http://www.pbfluids.com/2009/08/high-osmolar-gap-and-low-anion-gap.html