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New Developments in the

Management of Kidney

Transplant Patients







Christine E. Chamberlain, Pharm.D., BCPS

Clinical Center Pharmacy Department

10/23/01

End Stage Renal Disease

 Options for patients with renal disease:

– Peritoneal dialysis

– Hemodialysis

– Kidney transplantation

 Living Donor (related and unrelated)



 Cadaveric Donor



 Approximately 222,000 patients were receiving

hemodialysis (1999 US Renal Data System Report)

 Only 9000 cadaveric kidney transplants performed in 1999

 Approximately 4000 living donor transplantations per year

 In the year 2000, more than 45,000 patients receiving

dialysis were awaiting cadaveric kidney transplantation



Am J Kidney Dis 1999;34(Suppl 1)

Cause of End Stage Renal Disease

Among New Patients on

Hemodialysis in 1997



Diabetic

nephropathy

18% Hypertension

3%

38% Glomerulo-

13% nephritis

Cystic Kidney

28% Dz

Other





Am J Kidney Dis 1999;34(Suppl1)

Factors Determining

Transplantation Outcomes

 Type of donor (cadaveric vs. living)

 Matching and sensitization

– HLA match (0 antigen mismatch > 6 antigen mismatch)

– Negative crossmatch

 Racial Differences

 Recipient Age

 Donor Age

 Other Factors (delayed graft function, cold ischemia time,

acute rejection, chronic rejection, years on dialysis,

diseases leading to ESRD)

History of Kidney Transplantation

1950’s

 First successful kidney transplant

 Total body irradiation for immunosuppression

 Steroids

1960’s

 Azathioprine

1970’s

 Polyclonal anitbodies – anti-lymphocyte globulin (now

Atgam, Thymoglobulin)

1980’s

 Cyclosporine (Sandimmune ), “triple drug therapy”

 Monoclonal antibody, OKT3 (Orthoclone ) in 1985

Basics of Immunosuppression

 Immune system distinguishes self from non-self

 Antigen: anything that can trigger an immune

response

 B-cell (lymphocyte) – secretes antibodies, presents

antigen to T-cell

 T-cell (lymphocyte), secretes cytokines (ex. IL-2),

directs and regulates immune responses, also

attacks infected, cancerous or foreign cells

Basics of Immunosuppression

 Cytokines are chemical messengers – bind to

target cells, encourage cell growth, trigger cell

activity, direct cell traffic, destroy target cells, and

activate phagocytes (“cell eaters”)

 IL-2 activates T-cells and causes proliferation

 T-cell surface markers (CD3, CD25, CD52 and T-

cell receptor) CD=cluster of differentiation of T-

cells

T- Lymphocyte Activation

Three signals involved in T-cell activation

Calcineurin is activated and induces

cytokine genes and T-cell activation genes

IL-2 binds to IL-2 receptor which in turn

activates Target of Rapamycin (TOR) and

promotes T-cell proliferation

De novo synthesis of purines is necessary

for B and T cell proliferation

Management of a Transplant

Recipient

 Induction Therapy: administer medications that

provide marked suppression prior to and during

the first week post transplantation, some agents

can also block B-cell mediated rejection

 Maintenance Therapy: administer

immunosuppressive agents continuously to

prevent acute rejection

 Administer medications to induce Tolerance?

What is Tolerance?



Immunologic unresponsiveness by the

recipient to the kidney graft in the absence of

maintenance immunosuppression.

Goals of Transplant Research

 Prevent rejection and kidney graft loss

 Reduce the amount of immunosuppression

– Decrease side effects

– Decrease toxicity and long term effects

 Enhance long term patient and graft survival

 Provide reasonable cost effective therapy

 Improve patient adherence and quality of life

 Induce Tolerance (no long term medications, reduces

adverse effects, improves quality of life)

Immunosuppressant Discoveries

1990-2000

Tacrolimus (Prograf)

Mycophenolate Mofetil (Cellcept )

Basiliximab (Simulect )

Cyclosporine Microemulsion (Neoral )

Daclizumab (Zenapax )

Rabbit Antithymocyte globulin (Thymoglobulin )

Sirolimus (Rapamune )

How are we doing?

One Year Survival Rate Percentage

Living vs. Cadaveric



100

90

80

70

60

50 Prior to 1988

40

1988-1996

30

20

10

0

Living CAD

Modes of Action of Currently

Available Immunosuppressants

 Calcineurin inhibitors  Target of Rapamycin inhibitor

– Cyclosporine – Sirolimus

 Polyclonal antibodies (bind

– Tacrolimus several CD’s)

 Purine synthesis inhibitors – Thymoglobulin 

– Azathioprine – Atgam 



– Mycophenolate mofetil  Monoclonal Antibodies

– Blocks Il-2 receptor

 Nonspecific  Daclizumab

– prednisone  Basilixmab

– OKT3 (anti-CD3)

Graft Half-life in Years

40

35

30

25

20 Half-life prior to

1988

15

Half-life 1988-1996

10

5 censored half-life

prior to 1988

0

Living CAD censored half-life

1988-1996

Trends in Immunosuppression



Steroid sparing regimens, and steroid

avoidance

Reducing calcineurin inhibitor dose after

critical post transplant period

Calcineurin inhibitor avoidance

Single drug regimens

Agents on the Horizon



 Campath 1H (anti-CD52) – lymphocyte and

monocyte depleting agent

 Deoxyspergualin – blocks maturation of T and B

cells

 Everolimus – TOR inhibitor like sirolimus

 FTY-720 – reversible depletion of lymphocytes

from peripheral blood (migration to spleen)

 CTLA4-Ig – blocks T-cell activation

Other New Developments in

Kidney Transplantation

 Laparoscopic kidney donation

– Advantages: less post operative pain, shorter hospital

stay, minimal scarring

– Disadvantages: impaired early graft function, graft loss

or damage, longer operative time

 Improved surgical techniques and storage of the

kidney graft

 New antibiotics to treat and prevent opportunistic

infections (new antifungals, oral ganciclovir and

valganciclovir)

Current Trials at NIH

 Sirolimus Monotherapy to Optimize Activation

Induced Cell Death (AICD) in Renal Transplants

Following Lymphocyte Depletion Induction with

Thymoglobulin

 Tolerance Induction Following Human Renal

Transplantation Using Treatment with a

Humanized Monoclonal Antibody Against CD52

Campath1-H

 Renal Allotransplantation for the Treatment of

End Stage Renal Disease in the Setting of Human

Immunodeficiency Virus (HIV) Infection

Role of the Transplant Pharmacist

 Disease state management

– Hypertension

– Diabetes Mellitus

– Osteoporosis

– Hyperlipidemia

– Electrolyte abnormalities

 Patient understanding and adherence to the drug

regimen

 Pharmacokinetic drug level monitoring

 Drug interactions (esp. with immunosuppressants)

 Adverse drug reaction monitoring

Kidney Transplant

 View a kidney transplant at:

– www.vesalius.com

– Click on clinical folios

– Click on abdomen

– Click on kidney transplant


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