CLINICAL CASE 19, ANSWER AND SUMMARY

Which of the following is associated with MPGN pattern of injury?

Hepatitis B and C	21 (87%)
Celiac Sprue	4 (16%)
Systemic Lupus	11 (45%)
MGUS	5 (20%)
Chronic TMA	10 (41%)
Paraproteinemias	10 (41%)
Sickle Cell Disease	8 (33%)
Parvovirus B19 infection	1 (4%)

Nice work! Since in this question you could choose multiple answers, most of you got major causes of MPGN pattern of injury.  Besides parvovirus B19( classically collapsing FSGS), rest all of the above diseases cause a MPGN pattern of injury or have been documented cases of MPGN with the diseases.
I think a good article for everyone to read is H.Renke's Kidney International Forum from many years ago.
Whenever you see double contouring and MPGN pattern of injury, THINK OF secondary causes and rule it out before you call it IDIOPATHIC.
The classic four categories that you want to make sure you don't miss are:
Immune complex disease( your MPGN I, II and III and all your autoimmune disease such as SLE)
Chronic Infections( Hep virus,Cryo, malaria, endocarditis)

Chronic Thrombotic Microangiopathies( APLAS, Chronic HUS/TTP, radiation nephropathy, bone marrow transplant nephropathy, sickle cell)
Paraprotein deposition diseases  ( includes MGUS)

References:
http://www.ncbi.nlm.nih.gov/pubmed/7723253

IN THE NEWS- HYPOMAGNESEMIA AND PPI?

Two recent papers in AJKD describe two independent observations of proton pump inhibitor induced hypomagnesemia. We have seen a lot of AIN from PPI as a class of drugs and perhaps the most common cause of AIN now.  But their association with low mg levels is new.
The first paper in AJKD describes 4 cases of long term PPI induced hypomagnesemia, hypokalemia, hypocalcemia and all were on different PPI, so a class effect.
Although only four cases, they couldn't say for sure if it is dose related or time related but seems more like a long term being on PPI effect. The low K and Ca might be a low Mg related effect. Low K from the ROMK effect and low Ca from an PTH related effect of low Mg.
The mechanism of why PPIs cause low Mg is not described in detail but thought about. One reason could be decreased colon transport of Mg which is mediated via the TRPM channels.  Its possible that the PH changes from PPI alter the TRPMs. Fe Mg was low in all cases 0.8-1% suggesting the kidney is doing the right thing.
Prior case reports and the second paper clearly show that its more of a GI loss of Mg due to a Ph effect rather than a mg wasting syndrome seen with perhaps CNI and post transplant patients.

Check it out
http://www.ncbi.nlm.nih.gov/pubmed/20493607
http://www.ncbi.nlm.nih.gov/pubmed/20189276
http://www.ncbi.nlm.nih.gov/pubmed/19920278

JOB MARKET for RENAL FELLOWS

Take a look at the recent Renal Business Today. on Getting creative in a tight job market.
This article highlights a very important issue that the job market in Nephrology is tight and is getting tighter perhaps. Based on the FREIDA 104/324 fellows didn't have a job this May 2010. Compared to 2008, there is a 50% increase in fellows pursuing extra fellowships.
We did a recent survey and found similar numbers, based on some preliminary data, 20% of graduating fellows don't have a job and 20% felt they made a wrong decision by choosing nephrology.
This article suggests 8 ways for getting a job: Fellowship, faculty position at your institution, part time positions, locums, less optimal practice( fast turnover), hospitalist, startup practice( the hardest), reconsider re location( not an option for many).
These are all options that we all think about but there is nothing creative about it. Its a tough market out there.
As a community we need to attract more people into nephrology and perhaps organizations such as ASN and NKF might have to help out for job positions more for our graduating fellows( visa issues, costs of visa issues, relocation costs)-- not all of us can afford this!
Nephrology as a field might be in jeopardy if we don't do anything about this!

Nephron Power: NYSN Fellows Boot camp

Nephron Power: NYSN Fellows Boot camp

NYSN Fellows Boot camp

The New York Society of Nephrology has set up a nice boot camp, or a Nephrology 101 crash course for the new fellows that are starting now. This is an excellent line up of lectures that will last all day and prepare all fellows for a work filled but fun filled year!

The topics are:

Assessing Patients with Kidney Disease

Definitions and Differential Diagnosis

Hypertensive urgencies and emergencies

Medical issues in the transplant patient

Introduction to Glomerular Diseases and Kidney Biopsy

Treatment of Acute acidosis

Hyperkalemia

Hyper and Hyponatremia

CKD:Classification, Management

Principles of hemodialysis

Hemodialysis access

Management of Intoxications

Principles and Practices of Dialysis: CRRT

Principles and Practices of Dialysis: Peritoneal Dialysis

Check out the syllabus and the website at the http://www.nysn-online.org/

TOPIC DISCUSSION: captopril and stones?

Did you know that our friend captopril, an ace inhibitor can help treat cysteine stones as well? 
Captopril actually has a sulfhydrly group and captopril-cystein disulfide bond is more soluble than cysteine. The dose suggested is usually 75mg to 150mg/day. It might be a good choice for a patient with HTN and cysteine stones as well.




http://www.ncbi.nlm.nih.gov/pubmed/19582183
http://www.ncbi.nlm.nih.gov/pubmed/8488818
http://www.ncbi.nlm.nih.gov/pubmed/2820331

Topic Discussion: D-Lactate vs D-lactic acid

Do we ever wonder when we give lactate ringers and use lactate in our PD fluids.. what happens to that? Lactate comes in 2 forms the D- and L+ isomers and LR contains both of them.  Humans lack D lactate dehydrogenase. Its only 10% of what we can do with L lactate.  This ultimately gets metabolized to base and as a result we can use it as an effective medium for PD as well. The PD fluid is both a mix of D and L lacatate. 
This keeps the sugar from carmelizing.  When you give someone LR or lactate, do you get lactic acidosis-D?
Well lactate is a base and not the acid so it should not and hence we don't see it causing it. LR is a widely used fluid and lactate in PD fluid is also widely used. Accumulation of D lactic acid will cause an anion gap if that would happen. The lactate( base ) is not usually associated with this problem.


Where do you see D lactic acidosis?  It can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or other cause of the short bowel syndrome. This is due to overgrowth of gram positive anerobes and relatively low glucose delivery to the colon.


Think of this diagnosis when there is elevated anion gap, normal lactate, negative ketones, considered in the patient presenting with an increased serum anion gap, normal serum concentrations of lactate, negative ketones, and history of short gut syndrome or bypass as stated above.  

Ref:

http://www.ncbi.nlm.nih.gov/sites/pubmed
http://www.ncbi.nlm.nih.gov/pubmed/9175054
http://www.ncbi.nlm.nih.gov/pubmed/3713944