Sweet hydrothorax: A PD complication

Acute hydrothorax is an uncommon but a well-recognized complication of peritoneal dialysis. No single test is definitive for diagnosis. Diagnosis becomes a challenge.

Peritoneal dialysis-(PD) related hydrothorax was first reported in 1967 by Edward and Unger in JAMA( see attached). Transudative pleural effusion develops, more commonly involving the right side, and usually occurs immediately after starting PD or a few days later. The patients may remain asymptomatic or have sudden dyspnea, decrease in ultrafiltration, or pleuritic chest pain.

How do we diagnose it?

Presence of high pleural-fluid glucose concentration.

Pleural fluid concentration of glucose >300mg/dl might be diagnostic.

Others have hypothesized that, given dynamic movement of dialysate, an absolute glucose-concentration level cannot be used to diagnose PD-related hydrothorax. The pleural fluid-to-serum glucose concentration gradient of greater than 2.77 mmol/L (50 mg/dl) was proposed as the cut-off to diagnose the condition.

In general, any pleural-fluid glucose concentration greater than serum is considered to be highly supportive of PD-related hydrothorax.

Imaging:

1.Radionuclide scan (for example, Tc-99 m DTPA) is associated with sensitivity of 40% to 50%.
2.The methylene blue test has been used where its injected and dye is traced from the peritoneum to the pleura. In one study showed no sensitivity and is associated with a risk of chemical peritonitis.

Some case report examples in literature

http://www.pdiconnect.com/content/27/3/296.full.pdf

http://www.sciencedirect.com/science/article/pii/S1755001708001103

Check out this powershow that reviews the management of this entity.

CASE BASED DEBATES SESSION AT ASN 2013

This year ASN is doing a Fellows In Training( FIT) Bowl again and we shall be doing a mystery case based debate with two fellow teams.
Case based debates are a fun challenging debate sessions that we have invented at our institution that has been a monthly event at our fellowship. Fellows get a brief discussion of a case and then have to choose tests from the power point slide on the left( sample example) and get closer to the diagnosis. Each tests comes with positive and negative points and can get you closer or far from the diagnosis. Costs and what the tests entails have to be known. Finally, the team with the most points reads the kidney biopsy findings. A pathologist will then discuss the case.
This is going to be held on Nov 8th 2013 from 2-4PM at Rm B311 hosted by myself and Dr Hitesh H Shah. Following case debate, there is going to be fellows jeopardy competition.
All fellows in training should try to attend as this will be a fun event.

Quick Chemotherapy toxicity quiz flashcards using quizlet.com

A glomerular disease simple flashcard using quizlet.com

Harvard Macy Digital Citizen 2013 course

As I am teaching in and attending the Harvard Macy course on Digital Citizen this year, I am live blogging and tweeting some sessions. Check out the live tweet summaries and blogs on eAJKD.org

Promoting Palliative care in ESRD

A recent article in CJASN promotes 5 policies that are essential to provide good palliative care in ESRD.

1. Universal screening for palliative care(PC) needs:  How can this be done? Questionnaires and screening tools. One such example is the surprise question tool.

2. Incorporate PC measures in ESRD QIP: The advance care planning and documentation of code status can be a start. What has been done thus far has not touched PC.

3. Train the nephrology workforce to deliver PC: This is the most essential piece. With the current fellowship structure, is this possible? Are the faculty in major academic centers even comfortable? Lot of work to be done in this area. A recent study showed that PC experience of renal fellows is very poor.

4. Payment reform for PC services: Incentive always works

5. Fund PC research: Hope this will also happen as well.

The last two policies will only work when big health systems and medical schools promote the science of palliative care. It's about time sub specialists train in PC irrespective of their specialty- cardiology, GI, heme/onc, critical care or renal.

TOPIC DISCUSSION: Renal biopsy findings in Diabetics

A recent study looked at patients who had diabetes and had a biopsy at Columbia Univ path registry.
They wanted to see what other findings are seen besides diabetes. Most of these patients had atleast 10 years of diabetes. Prior reports have suggested IgA and Membranous GN as the most common non diabetic findings in these patients.

1. 37% had Diabetic nephropathy
2. 36% had non diabetic renal disease alone
3. 27% had diabetic neph and another disease
4. In the non diabetic renal disease alone:- FSGS , HTN, ATN, IgA neph, membranous GN, Anca disease comprised most of the diagnosis in that order of frequency.
5. ATN was the surprise finding that had not been reported prior reports.

Interesting and useful data. This is probably lower than expected as most that get a biopsy had a clue for an alternate illness in the kidney. The ones that don't get a biopsy also might have dual disease states that often get missed.

http://www.ncbi.nlm.nih.gov/pubmed/23886566

ANIO-ASN Dinner evite

The American Nephrologists of Indian Origin (ANIO) invite you to join
us for a reception and dinner at the American Society of Nephrology
Meeting 2013 in Atlanta.

Date:  11/8/2013 at the Peachtree special events and conference center

200 Peachtree Street, Suite 206, Atlanta, GA 30303
7:00 pm  onwards

RSVP  at  anio.asn@gmail.com to attend.

www.an-io.com

Clinical Case Answers and Summary 75

What is the mechanism of injury of carfilzomib induced renal injury?

Carfilzomib (Kyprolis, Onyx) is a next-generation epoxyketone proteasome inhibitor that is approved for the treatment of relapsed refractory multiple myeloma. The phase 2 trial  that initially raised interest in this agent was a single-arm study of patients with refractory multiple myeloma who received carfilzomib 20 mg/m2 intravenously twice weekly for 3 weeks in cycle 1 and  then 27 mg/m2 for subsequent cycles. Increased serum creatinine was the most frequently reported renal adverse event, affecting 25% of the 266 patients in this study.

Case report and discussions with experts suggests its more likely to be a pre-renal insult. Glomerular disease is less likely the cause of the renal toxicity. In a patient who has multiple myeloma with renal involvement, nephrotoxicity caused by the disease can be hard to distinguish from nephrotoxicity caused by an agent. 

Non renal causes of microalbuminuria

Non renal causes of Microalbuminuria

Fever
Infection
Non specific Inflammation
Prolonged elevation in blood pressure
Hyperglycemia
Hypercholesterolemia
Exercise

Courtesy of Dr George Bakris.

ROADMAP: Did we forget to use this map?

Microalbuminuria is an early predictor of diabetic nephropathy and premature cardiovascular disease( so we think). Some people might argue its a word that needs to be taken away from the medical dictionary. In 2011, NEJM published the ROADMAP trial.  They wanted to show if the use of ARB would delay the onset of microalbuminuria or albuminuria in patients with Type 2 DM. In a randomized trial, over 4000 patients were either in olmesartan arm or placebo for close to 3 years. The primary outcome was the time to the first onset of microalbuminuria. 

Interesting results:
1. The target blood pressure (<130/80 mm Hg) was achieved in nearly 80% of the patients taking olmesartan and 71% taking placebo; 
2. Microalbuminuria developed in 8.2% of the patients in the olmesartan group  and 9.8% in the placebo group 
3. The serum creatinine level doubled in 1% of the patients in each group. 
4. Greater number had fatal cardiovascular events in the treatment arm — 15 patients (0.7%) as compared with 3 patients in the placebo arm (0.1%) (P=0.01), a difference that was attributable in part to a higher rate of death from cardiovascular causes.

This is striking. Causes:- was it hyperkalemia? was it lower blood pressure than we think should be for DMII. This was reviewed by FDA as well. Other renal blogs had mentioned this trial as well.

IN THE NEWS: Conservative management in CKD, and no dialysis

A recent study published in a non nephrology journal highlights a critical point that is often missed by nephrologists. Although there is data coming out from prior studies that conservative management might be better for certain groups of patients then offering dialysis, more studies need to confirm this. This study is a retrospective observational study that looked at conservative management vs offering dialysis.

Some key points

1. The renal replacement therapy group survived for longer when survival was taken from the time estimated glomerular filtration rate at different GFRs.
2. When factors influencing survival were stratified for both groups independently, renal replacement therapy failed to show a survival advantage over conservative management, in patients older than 80 years or with a World Health Organization performance score of 3 or more. 

3. Acute hospitalizations were more in the RRT arm

4.Seventy-six percent of the conservative management group accessed community palliative care services compared to 0% of renal replacement therapy patients ( THIS is a striking number).

I would urge all to read the renal physician associations statements regarding palliative care in nephrology.

http://onlinelibrary.wiley.com/doi/10.1111/nep.12064/abstract
ASN had a series of videos on this topic as well.
Finally, a nice blog post on GeriPal on this topic on HD patients.

Image source: www.gloryhpc.com

CONSULT ROUNDS: Hemophagocytic syndrome and the kidney?

What is hemophagocytic syndrome? and what do nephrologists have to do with it?

Its a dysregulation and  inappropriate activation of the immune system.  Its infiltration of non malignant macrophages and phagocytosis of blood cells. 
Key features: fevers, hepatosplenomegaly, pancytopenia, low fibrinogen levels, LFTS dysfunction, seizures, hypertriglyceridemia. and multi organ failure with AKI

Primary cause: immune dysregulation
Secondary causes: autoimmune such as Stills disease, SLE.  Infections such as EBV. Herpes, PB19, HIV.etc and malignancy such as T and B leukemias/lymphomas. 

Renal manifestations:

ATN and interstitial disease( being most common on autopsy findings), macrophage infiltration, intra renal hemaphagocytosis
Collapsing FSGS( most common glomerular disease), MCD, FSGS 
TMA, and intravascular lymphoma

Treatment:

Chemotherapy usually etoposide based
IVIG
Rituximab

EBV disease- think this syndrome as well if above features are present.

What do nephrologists have to do with it?- recognize it when appropriate as AKI and proteinuria is not uncommon with this entity. 


References:
http://www.ncbi.nlm.nih.gov/pubmed/12813287
http://211.144.68.84:9998/91keshi/Public/File/19/5-6/pdf/nrneph.2009.73.pdf
http://www.ncbi.nlm.nih.gov/pubmed/16557222

Consult Rounds: Why does infusion of normal saline cause metabolic acidosis?

Why does infusion of normal saline cause metabolic acidosis?

       

This should be an easy answer but when you review the literature, the literature is all over the place( literally!!).Collection of responses I received when I asked few experts in the field:

1. “ The bicarbonate ions are diluted by the isotonic fluid, and acidosis occurs as a result.”

            
            2. “The fall in serum bicarbonate is due to the expansion of the extracellular fluid volume                                   with large IV fluids”

3.  The "strong ion difference" (SID) helps explain this that in order to maintain electroneutrality. Since there is diluting fluid, water must dissociate, providing excess protons which leads to metabolic acidosis. “- via the stewart method of acid base

4.  “Usually 60% of the filtered bicarbonate load is reabsorbed in euvolemia. When extracellular volume is low the proximal tubular absorption is increased, maybe to 80%,due to changes in oncotic pressure and hydrostatic pressure of peri tubular capillaries and glomerulus.  This results in increased reabsorption in setting of volume depletion.  When extracellular volume is increased then proximal tubular absorption of bicarbonate is decreased, thus an acidosis.”

5. “ The ph of normal saline is 5.5, won't that also lead to dissociation and use of Hco3 and cause an acidic environment”

            
6. “Nacl is a weak acid so despite the low ph it will not change systemic ph.”

            
7. “The PCT reabsorbs 80 to 90 % of filtered HCO3. When micropuncture needle is not inserted in the terminal PCT, just the last accessible PCT that can be seen on the cortical surface. When Walker et  al micro-disceted the entire PCT, the reabsorption was close to 90% of filtrate, which prevents bicarbonaturia and percipitation of CaHPO4 in the deepest bend of the LOH, as this would cause  obstructive nephron damage and kidney stone disease among our ancestors and we would not be alive.

            
8.  “With a pH of isotonic saline of 5.5, there are far too few H+ added to cause metabolic                           acidosis if infusion volumes are less than 50 L/day.”

Take your pick! 

References:

http://www.ncbi.nlm.nih.gov/pubmed/19533091

http://m.anesthesia-analgesia.org/content/103/1/144.full