formers. This study gives further evidence of THP’s role in kidney stonepathogenesis.

ug THP/mg Creatinine SEM p-valueMale Control 48.4 6.5 _

Male Patient 23.9 1.8 0.0016

Female Control 40.6 2.7 _

Female Patient 30.2 3.9 0.0180

Sialic Acid nmol/mg THP SEM p-value

Male Control 114.4 4.5 _

Male Patient 78.3 4.3 3.2E-07

Female Control 95.8 2.8 _

Female Patient 72.4 6.5 0.0005

Monosaccharides nmol/mg THP SEM p-value

Male Control 725 19 _

Male Patient 602 25 0.0003

Female Control 715 17 _

Female Patient 568 42 0.0006

Source of Funding: UC San Diego Academic Senate Grant

2307P38 MAPKINASE SIGNAL TRANSDUCTION PATHWAY: APOTENTIAL THERAPEUTIC TARGET IN OXALATENEPHROTOXICITY

Sweaty Koul, Douglas Lim, Joshua Steffan, Mintu Pal, Hari Koul*,Aurora, CO

INTRODUCTION AND OBJECTIVES: Nephrolithiasis is amulti-factorial disease, with hyperoxaluria being a contributing factor insub-groups of the patients. The molecular events that trigger crystaldeposition are not completely understood. Previous studies in our labdemonstrated that oxalate induced activation of p38 Mitogen ActivatedProtein Kinase (p38MAP kinase) in renal epithelial cells in a tissueculture and in an animal model of hyperoxaluria in vivo. Present studiesevaluated the effects of inhibition of p38 MAP kinase on the effects ofoxalate in renal cells.

METHODS: For these studies HK2 cells, a line of human renalepithelial cells were exposed to oxalate alone or in combination with ap38 MAP kinase inhibitor SB203580 and cell functions and geneexpression were monitored. In parallel experiments hyperoxaluria wasinduced in male Wistar rats by addition supplementing 0.7% ethyleneglycol in drinking water. Where indicated, SB203580 in DMSO wasadministered via i.p injections. At various time points urine and renaltissues were collected. Tissues were fixed and subjected to HN&Estaining and or immuno-histochmical or immunofluorescence assaysfor visualization of morphological changes and NF-KB (p65) expres-sion.

RESULTS: Oxalate exposure to HK2 cells was associated within morphological changes and increased IL-6 expression and NFKBactivation. Hyperoxaluria in experimental animals resulted in increasedrenal tubular damage/dysfunction and crystal deposition/retention. In-hibition of p38MAP kinase decreased oxalate induced IL-6 expressionand inhibited oxalate induced NFKB activation. We also observed thattreatment of hyperoxaluric animals by p38 MAP kinase inhibitor de-creased hyperoxaluria induced NF-KB activation and decreased ox-alate induced renal tubular damage as well as crystal retention.

CONCLUSIONS: Inhibition of p38 MAP kinase decreasesnephrotoxic action of oxalate in part by blocking NFKB and tubular celldamage. These results suggest that p38 MAP kinase might serve as anattractive target to decrease oxalate nephrotoxicity and perhaps crystalretention and nephrolithiasis.

Source of Funding: National Institutes of Health (NIH-RO1-DK-54084) (HKK) and Chair commitment-the Department ofSurgery Academic Enrichment Funds (HKK).

Transplantation & Vascular Surgery: RenalTransplantation, Renal Vascular Surgery (II)

Podium Session 39

Wednesday, May 8, 2013 10:30 AM-12:30 PM

2308WHAT SHOULD THE ROLE OF A DIAGNOSIS OF PROSTATECANCER BE ON LISTING ESRD PATIENTS FOR RENALTRANSPLANTATION?

Lara Martinez*, Puneet Sindhwani, Oklahoma City, OK; Sean Elliott,Oluwakayode Adejoro, Minneapolis, MN; Joel Slaton,Oklahoma City, OK

INTRODUCTION AND OBJECTIVES: A diagnosis of cancerincluding prostate cancer amongst patients with end stage renal dis-ease (ESRD) can result in delays of up to two or more years in listingpatients for renal transplantation due to concerns relating cancer pro-gression under immunosuppressive drug regimens. There are currentlyno specific UNOS requirements for incorporation of a diagnosis ofcancer into decision making with final decisions being made on a localinstitutional level. To answer the question what role a diagnosis shouldplay in listing patient for a renal transplant, we examined outcomesamong two populations a) patients with ESRD who develop prostatecancer and b) patients with a transplant and who are immunosup-pressed who also have prostate cancer.

METHODS: We interrogated the SEER-Medicare Databasefrom the years 1992-2007 to identify these two patient populations. Forpatients with ESRD and prostate cancer, we compared the competingrisks of ESRD-related vs prostate-cancer related morbidity and mortal-ity. From the second group, we compared the cancer specific survivaland overall survival amongst those patients with a renal transplant andimmunosuppression and the general prostate cancer population. Theimpact of prostate cancer related risk factors in particular stage andgrade were examined in both populations.

RESULTS: Among patients with ESRD diagnosed with prostatecancer (n� 8692), patients were far more likely to die from ESRD-related cardiovascular events even among those with high grade dis-ease. From 1992-2007, 184,723 were diagnosed with nonmetastaticprostate cancer. Among patients who have a renal transplant and areimmunosuppressed (n�455), 70% had low grade prostate cancer and30% had high grade prostate cancer. Only 20% had undergone aprostatectomy. While the standard risk factors (high grade and highstage) did predict for a poor outcome, the presence of a renal transplanthad no impact on either overall or cancer-specific survival.

CONCLUSIONS: Patients with ESRD and prostate cancerwere far more likely to die from ESRD related complications comparedto prostate cancer regardless of prostate cancer related risk factors.Immusuppresion added no additional risk of mortality to renal trans-plant patients with prostate cancer regardless of risk factors. Weconclude that prostate cancer should not serve as a hindrance to listingpatients with ESRD for renal transplantation.

Source of Funding: None

2309COMPETITIVE MARKET ANALYSIS OF TRANSPLANT CENTERSAND DISCREPANCY OF PATIENT ACCESS TO KIDNEYTRANSPLANTATION

Patricia Cho*, Christopher Cutie, Evgeniy Kreydin, Dicken Ko,Boston, MA

INTRODUCTION AND OBJECTIVES: There are over 250 U.S.kidney transplant programs grouped geographically by adjacent statesinto 11 organ donation regions to promote sharing of deceased donorkidneys. Over the past ten years, the number of transplant programshas increased while donor supply remains stable. As each program

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mandates growth in volume confined by the current allocation scheme,larger waiting lists draw more organs for the individual center. Wehypothesize that highly competitive regions will approve and wait-listmore end-stage kidney disease (ESRD) candidates for transplant de-spite consistent incidence and prevalence of ESRD nationwide.

METHODS: The most recent data was obtained from all trans-plant centers. Data reviewed included listing data, market saturation,market share, organs transplanted, and ESRD prevalence. Herfindahl-Hirschman Index (HHI) was used to measure the size of firms inrelation to the industry to determine amount of competition.

RESULTS: Each state was classified into one of three groups,defined as: HHI�1000 � competitive, HHI 1000-1800 � moderatecompetition, and HHI�1800 as highly concentrated. The percentage ofall ESRD patients listed in competitive, moderate, and highly concen-trated regions was found to be 19.73%, 17.02%, and 13.75% respec-tively. The ESRD listing difference between competitive versus highly-concentrated is significant (p�0.05).

CONCLUSIONS: When there is strong competition without adominant center, the entire state will list more patients for transplant inan attempt to drive up their own market share. Despite a governmentmandate to ensure equitable access, our analysis suggests a discrep-ancy in access for medical care in ESRD patient which may be drivenby financial factors of competition.

Source of Funding: None

2310KIDNEY DONOR RADIATION EXPOSURE PRIOR TOTRANSPLANTATION

David Culpepper*, Caroline Wallner, Gene Huang,Steven Engebretsen, Gaudencio Olgin, Don Arnold II, Jason Smith,D. Duane Baldwin, Loma Linda, CA

INTRODUCTION AND OBJECTIVES: During the evaluation ofpotential kidney donors, every effort is made to protect these patientsfrom experiencing unnecessary harm. Thus it is important for donorsurgeons to understand the potential risks and radiation dosagesassociated with donor imaging studies. The purpose of this study is tocharacterize living donor radiation exposure.

METHODS: A retrospective review of 363 donor nephrectomypatients evaluated over a 12-year period was performed. By protocol,each donor received a chest x-ray, nuclear renal scan, and 3-phase CTof the abdomen. Female patients greater than 40 years of age receivedscreening mammograms. Patients with a smoking history underwentCT of the chest. Estimated effective dose (EED) was calculated for CTby multiplying the dose-length product (DLP) by standard conversionfactors. EED for nuclear renal scans, mammograms, and chest x-rayswere calculated using published values. Image modality with total EEDand EED averages with yearly time points were correlated usingPearson’s correlation.

RESULTS: Of the 363 donors, complete radiation parametersincluding DLP were available in 154 patients. Mean total effective dosewas 29.4 mSv (SD 13.4), with 83.7% of exposure resulting from3-phase CT of the abdomen (Table 1). A subset of donors evaluated(42.7%) received � 30 mSv, while 4.8% received � 50 mSv. Averageradiation exposure decreased by 30.4% in the latest 6 years of thestudy period (correlation � -0.90) with changes in imaging protocol.

CONCLUSIONS: Renal donors are exposed to significant lev-els of ionizing radiation with a mean that approaches the maximumoccupational radiation exposure for nuclear workers of 30 mSv. Knowl-edge of the radiation exposure received by donors may allow transplantcenters to more accurately counsel donors regarding risk and tailorimaging protocols to maximize patient safety.

Source of Funding: None

2311RECIPIENT GRAFT FAILURE OR DEATH IMPACT ON LIVINGKIDNEY DONOR QUALITY OF LIFE BASED UPON THE LIVINGORGAN DONOR NETWORK DATABASE

Justin Watson*, Norfolk, VA; Martha Behnke, Richmond, VA;Michael Fabrizio, Virginia Beach, VA; Thomas McCune, Norfolk, VA

INTRODUCTION AND OBJECTIVES: There is a paucity ofprospective long term data on living kidney donor long term quality oflife (QOL) outcomes. The Living Organ Donor Network (LODN) data-base follows donors longitudinally and when cross-referenced withUnited Network for Organ Sharing (UNOS) data, can be used to assessthe effect of recipient graft failure and death on donor QOL.

METHODS: The SF-36 was sent to donors 6 months afterdonation and yearly thereafter. Recipient outcomes were determinedfrom the UNOS database. Included were all donors who donatedbefore 12/31/10 and returned at least 2 QOL surveys. Of 2,204 donorsconsented, 311 were associated with a functioning graft and livingrecipient, 54 were associated with a non-functioning graft, 34 wereassociated with recipient death. The results were analyzed by Stu-dent’s t-test.

RESULTS: Initial QOL scores were not different between do-nors whose recipients are alive with graft function, and those whoserecipients later died (88.9 vs 89.6, p � 0.8). For donors whose recipientdied, QOL in the year subsequent to recipient death was an average of6 points lower than the initial QOL (89.6 vs 83.6, p � 0.04). 24 donorsreturned surveys an average of 2.9 years after their recipient’s death.Final QOL score averaged 4.1 points higher than right after recipientdeath (87.7). This improvement did not reach significance (p � 0.11),but is also not significantly lower than the original QOL. For 51 donors,the recipient’s graft failed more than 6 months after transplant. Theirinitial QOL was lower than the donors whose recipients are still alivewith graft function (88.9 vs. 84.8, p�0.02) and donors whose recipientsdied �6 months post-donation (89.4 vs 84.8, p � 0.07). Eight recipientshad graft failure within 6 months of transplant, and the QOL responsesfor their donors was 77.9 (n.s.). Forty donors returned surveys in theyear subsequent to their recipient’s graft failure and their QOL scoreswere unchanged (86.4 vs 84.4, p � 0.54). 19 of these donors returnedfuture surveys and their final QOL scores were slightly, but not signif-icantly, lower than at time of recipient graft failure (84.4 vs 81.7, p �0.53).

CONCLUSIONS: Donor QOL was negatively impacted by thedeath of their recipient, with an average 6-point drop in the year

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