Highlights from the
43rd annual American Society of Nephrology
Meetings in Denver,
CO



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SHARP Trial: The Study of Heart and Renal
Protection
Presenters: Not available
click here

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Lupus Nephritis Presenters: Dr. Brad
H. Rovin, Dr. Frederic A.Houssiau, Dr. Gabriel Contreras, Dr.
Gerald B Appel Blogger: Lakshmi Turlapati, MD (East Carolina
University – Brody School of Medicine) This was great review of
lupus Nephritis especially focusing on management strategies. They
discussed the Euro Lupus study of the low dose vs. high dose
Cyclophosphamide
. The low dose Cytoxan may be a good
option for certain groups of patients. They also discussed the
ALMS trial and use of Cellcept especially
in certain populations. Rituximab is a third line drug for lupus
and its efficacy needs to be closely evaluated. It should be
reserved for refractory cases of lupus resistant to other lines of
therapy.
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State of the Art
Topics
Vascular
access
Presenters: Dr. Arif Asif, Dr. Aris Q
Urbanes, Dr. Bharat Sachdeva, Dr. Alexander S Yevzlin. Blogger:
Lakshmi Turlapati, MD (East Carolina University – Brody School of
Medicine) This was a good review of the Fistula first initiative.
The presenters stressed that though it must be tried to evaluate
for fistula placement in dialysis patients, it may not be the best
option for all. Decision to place fistula vs. graft must be
individualized.
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Forefronts in Hyponatremia Presenters:
Dr. Biff Palmer and Dr. Richard H Sterns Blogger: Lakshmi
Turlapati, MD (East Carolina University – Brody School of Medicine)
This was an excellent talk on diagnosis and management of
hyponatremia. It was a case based discussion. Dr. Sterns stressed
on the rate of correction of sodium in both acute and chronic
hyponatremia. Interesting was the use of ddAVP to slow the correction of hyponatremia
if needed
in selective cases.
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Infections in Kidney transplant Recipients: Emerging
Challenges
Presenters: Dr. Michael Green, Dr,
Michael Ison, Dr. Camille Kotton, Dr. Shirish Huprikar Blogger:
Lakshmi Turlapati, MD (East Carolina University – Brody School of
Medicine) This was a very good lecture on the infections in renal
transplant recipients. It was stressed that all CKD patients should be vaccinated
whenever possible so that their antibody titers are
protective by the time of transplant. Dr. Huprikar talked about
Candida arteritis in transplant recipients and importance of
checking preservation fluid cultures.
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A
new frontier: implementation of bundled payments for ESRD
care
Presenter: Information not available Blogger:
Raeesa Mirza, MD (East Carolina University – Brody School of
Medicine) This was a panel discussion regarding what bundling means
for us going forward These were the key messages:

  1. Protocols are going to play an even greater
    role in management of ESRD patients than ever before
  2. This is a great opportunity for us to be even more
    efficient in our patient care by promoting more home therapies:
    recent research shows that most patients would prefer home therapy
    if offered
  3. There is concern about oral-only
    medication in 2014 and what that will mean for patient co-pays
    (will likely increase)
  4. For dialysis centers
    who have low numbers of incident patiients, there may be more to
    lose from the per patient payment, as there is significant
    reimbursement given for the newly initiating hemodialysis
    patient


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Plenary
Address
Glomerular Damage
leading to IFTA? How?
Presenter: Wilhelm Kriz, MD
Blogger: Kenar Jhaveri, MD (North Shore – LIJ/Hofstra University
Medical Center) A nice plenary session at ASN 2010 by Dr. Wilhelm
Kriz discussed the ways glomerular damage leads to Tubular
interstitial damage? Two theories exist:
  1. Leak
    theory and loss of albumin and other proteins can be damaging to
    the tubules
    • Data
      on this theory not that
      great
  2. As
    glomruli get damaged, eventually the damage gets closer to glomuler
    tubular juunction and that leads to spreading of misdirected
    filtrate and cell proliferation and that leads to intra tubular
    obstruction and degeneration of tubules
    • Leads to IFTA in glomerular
      disease…

Interesting concepts and worth exploring more on this…

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Plenary
Address
Is fibrosis
harmful? In the intact nephron?
Presenter: Wilhelm
Kriz, MD Blogger: Kenar Jhaveri, MD (North Shore – LIJ/Hofstra
University Medical Center) At the plenary session at ASN 2010, Dr.
Kriz discussed about fibrosis and is that really harmful to the
intact nephron. Studies showed that it is not — at least in the
early stages. The key points are:
  1. Progressive
    renal failure is based on the progressive loss of nephrons and they
    all loose nephrons independently
  2. Fibrosis is
    an advanced stage that has an autonomous drestruction of so far
    unaffected nephron remains an open question


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Drugs in Osteoporosis and CKD
Presenter: Orson Moe, MD Blogger: Kenar Jhaveri, MD (North Shore -
LIJ/Hofstra University Medical Center) Take home points:
Anti reabsorptive agents
  1. Kill
    osteoclasts
  2. Bisphosphanates: work fast, blasts
    slow down and increase bone quantity but turnover is reduced (so
    not a good option for someone with Adynamic bone disease). Usually
    contraindicated in GFR more fractures
  3. HRT/SERM: inhibit osteoclast proliferation and function,
    again leading to low turnover
  4. Calcitonin:
    doesn’t completely kill osteoclast, the balance of blasts is
    maintained. Not widely used though
  5. Anti-RANKL
    M AB: data on CKD lacking and transplant no
    experience

Take home points:
Osteo-anabolic agents

  1. Pth: pulse pth,
    data on CKD not very strong
  2. Strontium, IGF-1
    and others in pipeline
  3. Best agents in CKD:
    Calcicum, Vitamin D, Exercise and dietary acid
    lowering


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Is
it Osteoporosis or CKD-BMD?
Presenter: Miller
Brent, MD Blogger: Kenar Jhaveri, MD (North Shore – LIJ/Hofstra
University Medical Center) Take home points:

  1. Fractures in CKD can be caused by CKD-BMD and
    osteoporosis
  2. Clinical risk factors in CKD:
    chronic heparin use, hypoganadism, steroid exposure, increase
    prolactin, poor nutrition, Vitamin D def, secondary pth
  3. KDIQO guidelines for osteoporosis in CKD-BMD
    • Stage 1-3 low bone mass or
      fracture noticed, more likely osteoporosis related than
      CKD-BMD
    • Stage 4-5 bone biopsy might be
      necessary to differentiate
  4. If bone specific Alk Phos is elevated, you can rule out
    osteoporosis, and adynamic bone disease as long Paget and
    malignancy has been ruled out
  5. An elevated Pth
    ( 6 normal) excludes adynamic bone disease
  6. A
    normal alkaline phosphatase, and normal to low pth cannot rule out
    adynamic bone disease
  7. Gold standard would be
    Bone biopsy
  8. Is osteoporosis and CKD-BMD
    overalap, or is osteoporosis a part of CKD-BMD or is CKD-BMD a type
    of osteoporosis is not clear?



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Steroid related Osteoporosis
Presenter: Mary Leonard , MD Blogger: Kenar Jhaveri, MD (North
Shore – LIJ/Hofstra University Medical Center) Take Home
Points:
  1. Steroid induced osteoporosis
    is 2nd most common cause of osteoporosis
  2. Steroids uncouple bone formation and
    reabsorption
  3. They increase osteoclast
    apoptosis
  4. Besides other known risk factors,
    kidney associated risk factors are microalbuminuria and
    proteinuria, medications like CNI
  5. Vitamin D is
    albumin bound and in nephritic syndrome, there is Vitamin D loss.
    Usually in NS, the 250H levels are low, this is temporary as pth
    levels don’t really rise as much based on studies compared to true
    Vitamin D deficiency
  6. FRAX program
    online
    is a good tool to assess risk for fractures. Age,
    gender, BMI, prior fracture, smoking and other factors are all
    entertained
  7. Recent ACR 2010 guidelines say
    that Steroid induced osteoporosis can be divided into three
    categories based on FRAX scores, <10% low risk, 10-20% is
    mod risk and rest high risk
  8. Bisphosphanates
    work best for steroid induced osteoporosis. Data on Forteo is new
    and can be better than bisphosphanates


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AKI
and Crush Injuries
Presenter: Dr. VanHolder Blogger:
Maria E. de Ferris, MD MPH PhD (University of North Carolina -
Chapel Hill)
  1. Crush Victims following major
    natural disasters die of Rhabdomyolysis, the
    2nd cause of death after direct
    trauma
  2. Shift of K+ out
    of the muscle
  3. No nephrologists have training
    or guidelines

Solution:
Consensus by MD’s of various disciplines who have helped in
disasters for the last 10 years and a text will published in 2011
…these were written for other providers
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Katrina aftermath Presenter: Andrew
Cohen, MD Blogger: Maria E. de Ferris, MD MPH PhD (University of
North Carolina – Chapel Hill)
  1. Dialysis
    Facilities: all free-standing facilities closed and almost all ESRD
    patients were displaced
  2. 148 deaths within 3
    months
  3. Attrition of Nephrology workforce (even
    2 year later) was a consequence
  4. Patients who
    missed dialysis treatments were more likely to have
    hospitalizations, complications (infections of
    fistulas/catheters)
  5. Excess mortality was noted
    in the early 180 days but then a reduction was noted, so the 12
    months afterwards were no different than in previous years. Risk
    factors for mortality were age at Rx initiation, Medicaid coverage,
    White race, non-ambulatory and HD patients

Take home message: Emergency preparedness
education needs to be implemented in dialysis units.

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ANCA
Conditions and Anti-Lamp 2-Ab-induced GN
Presenters:
Information not available Blogger: Maria E. de Ferris, MD MPH PhD
(University of North Carolina – Chapel Hill)
Background: In healthy humans with gram (-)
organisms, LAMP 2 is intimately involved in infections. Molecular
mimicry has been demonstrated. These AB co-exist with PR-3 and MPO
Antibodies, but unknown why. Results: The
results of the human experiments in the USA cohort of the GDCN
(Glomerular Disease Collaborative Network)
do not confirm the animal studies from the Viena Group.
Take home point: Should we routinely screen
for LAM-2 AB? Not yet
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Plenary
Address
New Insights,
Surprises and Lessons about the Pathogenesis of Cystic Fibrosis
Pigs
Presenters: Michael Welsh, MD Blogger: Maria E.
de Ferris, MD MPH PhD (University of North Carolina – Chapel Hill)
Cystic Fibrosis (CF) is an autosomal recessive condition affecting
many organs. Using a pig model the discussant drew many parallels
to the human presentation of this condition including micro-colon,
pancreatic and airway changes. Many hypotheses for the pathogenesis
of CF have been generated based on the inflammatory changes
occurring in this condition. The pathogenesis of inflammatory
changes overtime are still unknown in many way and novel therapies
are needed.
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The
Podocyte and VEGF
Presenters: Susan Quaggin, MD
Blogger: Kenar Jhaveri,
MD
(North Shore – LIJ/Hofstra University Medical Center)

  1. Local VEGF is important for glomerular
    development
  2. VEGF and VEGF R-2 signal against
    the flow of urine
  3. Modulation of VEGF is
    important
  4. When you remove VEGF in mice, you
    get TMA , but when you remove the VEGF-R , no TMA
  5. If all VEGF-R2 receptors are removed from entire body
    endothelial cells, showed TMA in all of the kidney. The liver
    showed endothelial damage and nodular liver as
    well


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The
Kidney in Liver Disease
Presenters: Garcia-Tsao, MD
and Enver Aklin, MD Blogger: Kenar Jhaveri, MD
(North Shore – LIJ/Hofstra University Medical Center) Take
home points:
  1. Pre liver transplant
    creatinine affects even post transplant survival of patient (based
    on data)
  2. Patients with Crt >1.0
    pre-transplant do worse post transplant
  3. Why is
    the serum crt low in cirrhosis (falsely): Decreased synthesis,
    malnutrition, less muscle mass, hyperbilirubenemia, and
    dilutational
  4. AKI can be divided in pre renal,
    renal and post renal causes in cirrhosis
  5. Pre
    renal causes are GI bleed, diarrhea usually due to lactulose, and
    hepatorenal syndrome (HRS)
  6. HRS is not volume
    responsive
  7. Intre renal causes are ATN and
    GNs
  8. Post renal are rare
  9. 20% of patients with cirrhosis in hospital have kidney
    injury (19% is AKI and 1% is CKD). 68% of all are pre-renal. Of all
    pre-renal most are volume responsive.
  10. In a
    study comparing pre-renal (diarrhea and GI bleed) causes and HRS,
    HRS has the lowest Na, lowest Mean arterial pressure and highest
    mortality
  11. Two things that make HRS worseà
    worse splanchnic vasodilation and worse decrease in effective blood
    volume
  12. HRS-1 is AKI, HRS-2 is usually a
    chronic renal injury. HRS -1 is a diagnosis of exclusion. 20% of
    AKI in cirrhosis, usually followed by infection and kidney is
    really not injured.
  13. Diagnosis includes
    stopping all volume depleting agents first , looking for infection,
    giving IV Albumin 1g/kg qd or bid and if still no response in 48
    hours, then check a CVP to see if volume replete and renal us, if
    all normal, then HRS Is diagnosed
  14. There is no
    data or studies on using bladder pressure in cirrhotics to date to
    discuss intra abdominal HTN

Key
Points about dual Liver and Kidney Transplantation:

  1. After the introduction of MELD scoring system,
    the crt was in that and that led to increase number of combined
    liver and kidney transplants from 2% to 6%
  2. Who
    gets combined: ESRD with Cirrhosis, ESLD with 8 weeks on HD, ESLD +
    biopsy proven >30% IFTA and >30%
    glomerulosclerosis
  3. After Introduction of MELD,
    the outcomes of Liver and kidney combined were worse, not
    donor-related, perhaps recipient-related as they were sicker. Now
    if MELD > 23, they do worse and surgeons think twice before
    a combined liver kidney
  4. A biopsy proven way of
    deciding if you want to do a kidney and liver was suggested.
    Interestingly they found that the most common biopsy finding was GN
    and DM being top, followed by MPGN, FSGS and IgA
    nephropathy
  5. >30% had biopsy
    complications, especially INR > 1.5
  6. Interesting GN found after liver transplant alone; some
    sort of nodular GN, as it looks like DM nephropathy but they don’t
    have DM and never develop it

***Note: Click here for
additional teaching resources regarding dual-organ
transplantation
.

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The
VEGF and Diabetic Nephropathy
Presenter: Fuad
Ziyadeh, MD Blogger: Kenar Jhaveri,
MD
(North Shore – LIJ/Hofstra University Medical Center)
Take home points:
  1. Glucose,
    glycosalation, ROS, TGF B and Ang II all increase VEGF –A ( in
    podocyte) and lead to proteinuria.
  2. Two new
    players that might be interesting are Notch 1 and Mir 93 in this
    concept
  3. Two mechanisms of albuminuria are
    paracrine and autocrine effects

    • Paracrine meaning effecting
      the receptor of the VEGF
    • Autocrine meaning
      affect the VEGF directly
  4. Paracrine: increase glucose, ROS and ang II lead to
    endothelial NOS and VEGF expression and then vascular
    injury
  5. Autocrine effects: a decrease in
    nephrin and nephrin is in the podocytes hence leading to an
    autocrine effect
  6. A recent paper showed that VEGF was
    activated in many human GNs
  7. Early in DM – you
    get increase VEGF, later on there is loss of podocytes and hence a
    decrease in VEGF. So using VEGF inhibitors can lead to bad outcomes
    as well and sclerosis.



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Clinical Nephrology
Conference
Therapeutic
Apheresis: The Kidneys and Beyond
Moderators: Emaad
Abdel-Rahman, MD, PhD and Michele Mokrzycki, MD Blogger: Melanie
Hames, DO (East Carolina University – Brody School of Medicine)
Presentations in this conference include:

  1. Overview of Conventional Therapeutic Apheresis
    by David Ward,
    MD
  2. The Kinetics of removing large
    molecules: Implications for the rationale prescription of plasma
    exchange by Andre Kaplan, MD
  3. Pheresis for TTP
    by Timothy Bunchman, MD
  4. Pheresis for
    vasculitis by Rasheed
    Balogun, MD

Dr. Ward
gave a comprehensive overview of Apheresis including the history,
methodology, anticoagulation, replacement fluid types, clinical
indications, ASFA indication categories, and then some
specific examples of therapy for various disorders. Dr. Kaplan
spoke and the kinetics of molecule removal . Though Dr. Bunchman
provided a disclaimer of being jet-lagged and also a pediatric
rather than adult nephrologist, he gave a nice review on
Plasmapheresis for TTP. Dr. Balogun gave an enthusiastic review of
Plasmapheresis for Vasculitis. Some points
I) Why Should I Care?

Specialties performing CPT 36514:

  1. Pathology 40%
  2. Nephrology
    40.1%
  3. HemOnc 6.6%
  4. IM
    4.5%
  5. Neuro 3.4%
  6. Rheum
    1.3%
  7. Other 2.29%

So you might think HemOnc is mostly
running apheresis programs, but they really are not. II) Only 40% of fellowship programs
have nephrologists managing apheresis and training fellows in
apheresis in this fashion; need to do better III) Most common substance being removed with
plasmapheresis is IgG (146,000 daltons)

  1. Only 25-30% of IgG is intravascular
  2. Half-life of IgG is 22 days (except for IgG3 which is 7
    days)

IV) IgM is
much larger ~970,000 daltons

  1. 90%
    of IgM stays intravascular
  2. Half-life of IgM is
    5 days

V) ASFA
clinical practice guidelines
used to come out in the
Journal of Clinical Apheresis every 7 years, but after 2007
publication, it will now be published every 3 years. Click here
VI)
TTP

  1. familial patients who have an
    ADAMTS-13 deficiency should respond to plasma infusions rather than
    plasmapheresis
  2. For idiopathic TTP,
    plasmapheresis has taken mortality from 90% to
    <10-20%
  3. For TTP, no difference in
    replacement with FFP vs cryoprecipitate (not sure if Dr. Bunchman
    really meant cryo-poor FFP)
  4. More recently:
    Balduini et al Ann Hematol 2010: maybe higher dose steroids are
    better in conjunction with TTP to achieve a remission
    rate

VII) Disease
states in Neurology

  1. Acute
    Guillain-Barre syndrome and CIDP, but also more rare conditions
    including meuromyelitis optica and Stiff-person syndrome
  2. Remember the key study reported by the Guillain Barre Trial group proving that
    TPE and IVIG have equivalent efficacy and if combined do not add
    benefit. At that time, IVIG was “cost-effective” – $26.00/gram; now
    it’s much more expensive. IVIG may be more convenient than
    TPE

VIII) Myeloma
cast nephropathy is controversial

  1. data from MERIT will be coming out next year
    looking at the benefit of plasmapheresis in
    myeloma

IX) Dr.
Ward had a chart for overview of when to use pheresis in
GN:

  1. ANCA – yes
  2. Anti-GBM – yes (but maybe not if the Creatinine >
    6mg/dL because the kidneys aren’t coming back)
  3. Membranous nephropathy – slowly develops and
    immunosuppressive therapy suffices without need for
    plasmapheresis

X)
Role of TPE in anti-GBM (or Goodpasture’s) disease

  1. Rapid decline in anti-GBM Ab titers
  2. Lower Creatinine levels
  3. Fewer
    patients progressing to renal failure
  4. Decreases mortality from 85 to 40%

XI) 2 key trials for anti-GBM (or
Goodpasture’s) disease and TPE

  1. Johnson JP, Moore J, Austin HA, et al. Therapy
    of antiglomerular basement membrane antibody disease: analysis of
    prognostic significance of clinical, pathologic and treatment
    factors Medicine (Baltimore) 1985;64:219-227
  2. Levy et al
    • Cr < 6, 100% patient
      survival and 95% renal survival at 1 year
    • Cr
      > 6, 83% patient survival and 82% renal survival at 1
      year
    • Dialysis dependent –65% patient survival
      and only 8% renal survival at 1
      year

XII) ANCA+ and pauci immune on pathology – can
be:

  1. No systemic vasculitis (ANCA
    GN)
  2. Systemic vasculitis but no asthma and no
    granulomas – microscopic polyangiitis
  3. Systemic
    vasculitis and granulomas but no asthma –Wegener’s
    granulomatosis
  4. Systemic vasculitis with asthma
    and granulomas – Churg strauss

XIII) Good evidence now that ANCA is
pathogenic

  1. Charles Jennette, MD:
    JCI 2002 (with MPO knockout
    mice)
  2. Increase in ANCA titer precedes relapse,
    decline in titer with remission

XIV) Treatment outcomes:

  1. Natural history: mean survival 5 mos, 1 yr
    survival 20%
  2. Steroid only era: mean survival
    increased to 12 mos
  3. Early 70’s: 1971 Fauci and
    others added cyclophosphamide to prednisone and got 5 yr survival
    to 87%
  4. Treatment choices: Block production of
    ANCA (immunosuppression including agents such as rituximab) or
    remove it (TPE)

XV) Nice diagrams here in Paul Bacon’s NEJM perspective in 2005:
XVI) EUVAS formed early 1990s to investigate
diagnostic role of ANCA, to standardize ANCA assay, to launch
trials (1995) which aimed to compare established therapies of
vasculitis and assess the role of lymphocyte depleting
therapies.

  1. 1st wave of trials = 4
    trials: NORAM, CYCAZAREM, MEPEX and SOLUTION
  2. 2nd wave of trials = 3 trials: CYCLOPS, IMPROVE, and
    REMAIN

XVII) MEPEX
in 1st wave: published by Jayne et al randomized ANCA+ RPGN with cr
>6 to get IV Solumedrol alone or IV Solumedrol + TPE of dose
60mg/kg x 7 treatments (max PE volume 4L)

  1. At 12 months, no difference in
    survival
  2. if you took only the patients who
    survived, and then looked at those free of dialysis, the group with
    TPE much more likely to be off dialysis
  3. MEPEX
    did not address alveolar hemorrhage, mild-mod renal disease,
    mononeuritis, or other clinical problems

XVIII) Study that looked at Plasmapheresis therapy for Diffuse Alveolar
Hemorrhage (DAH) in patients with small vessel
vasculitis

  1. Goal: to
    study the role of PLEX (plasma exchange) in treating DAH associated
    with AASV (ANCA-associated small vessel vasculitis)
  2. None had anti-GBM disease or Goodpasture’s; all but one
    was ANCA +
  3. All 20 patients had resolution of
    DAH. Number of PLEX treatments was between 4 and 9, with a mean of
    6 PLEX treatments
  4. 1 died from PE 16 days after
    resolution of DAH
  5. Conclusion: patients who
    presented with hemoptysis and pulmonary infiltrate caused by DAH
    would benefit from PLEX and immunosuppressive
    therapy

XIX) New
from EUVAS: new trial, PEXIVAS started randomizing patients this
past summer

  1. The purpose of PEXIVAS is to determine
    whether plasma exchange as well as immunosuppressive therapy are
    effective in reducing death and end-stage renal disease (ESRD).
  2. The trial will also study whether a reduced
    cumulative dosing regimen of glucocorticoids is as effective as a
    standard disease regimen.

    • Hypothesis: Addition of PLEX
      in severe AAV increases the time to develop ESRD or
      death
    • Multicenter, multinational trial, goal
      to enroll 500
    • 50% will get oral or IV
      cyclophosphamide followed by azathioprine or rituximab
    • The test pts (50% of the patients) will get adjunctive
      plasma exchange
    • Follow to ESRD or
      death

XX) Q and A from Dr. Ward’s 1st
session:
Timing of rituximab and TPE – Dr. Ward: used
to say 3-4 days, others say they have done studies and rituximab is
bound to its CD20 ligand so quickly that TPE the next day is ok.

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Careers in Nephrology Presenter: Not
available Blogger: Iti Yadav, MD (North Shore – LIJ University
Medical Center) 1. Academic Nephrology provides the following:

a. Job Security, b. Diversity, c. lifestyle
advantages (division of labor), d. opportunities for
multidisciplinary interventional studies (e.g. CKD-CVD), e.
opportunity to be part of translational research team, f. reward of
teaching endeavors in Clinical Nephrology, g. integration of care
of CKD patients with PCP’s through the PCMH (Patient centered
medical health) concept.

2. Elaborating on the
patient centered medical health concept: There is a need for
outcomes research related to new reimbursement strategies,. In
addition, chronic kidney disease will be one of the major chronic
diseases to serve as a model for the PCMH concept and the
Nephrologist as a PCMH-N (Neighbor). These efforts attempt to lay
the ground work for coordinated care of CKD patients by attempting
to do the following:

a. better collaboration for
consultation, b. information exchange and evidence based decision
making, c. PCP’s to continue to manage CKD due to HTN and DM while
nephrologists manage specific glomerular diseases, d. Nephrologists
developing systems for PCP’s to ensure early detection of
CKD

3. Guidelines for a job in academic
nephrology:

a. have a plan for the next five
years b. negotiate your contract c. ask about promotion guidelines
d. apply for grants; this is the best way at securing dedicated
research time e. have more than one mentor f. don’t move too
quickly into leadership roles g. don’t take up assignments that
others will not!


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