Reactions 1267 - 29 Aug 2009

with intratubular calcium phosphate deposits in tworecipients from the same donor prompted us to carefully★ SPotassium phosphate review the clinical course of the donor during her terminalillness. It became evident that prolonged and substantiveAcute phosphate nephropathy (first report) in anadministration of intravenous phosphorus had led to a rise inorgan donor and two transplant recipients:serum phosphorus from 0.9 to 6.2 mg/dL over 72 h and a3 case reports serum creatinine that rose to 1.7 mg/dL consistent with acuteAcute phosphate nephropathy (APN) was identified in tubular injury."two male renal transplant recipients. Both men’sAgrawal N, et al. Unrecognized acute phosphate nephropathy in a kidney donortransplants had been donated by a 30-year-old woman,with consequent poor allograft outcome: case report. American Journal ofwho had received potassium phosphate for Transplantation 9: 1685-1689, No. 7, Jul 2009 - USA 801150174

hypophosphataemia; APN was retrospectively confirmedin the donor. » Editorial comment: A search of AdisBase, Medline and

The woman, whose history included type 1 DM, was Embase did not reveal any previous case reports ofnephropathy associated with potassium phosphate. Thehospitalised with diabetic ketoacidosis and volumeWHO ADR database contained no reports of nephropathydepletion, and started receiving IV potassium phosphate onassociated with mono- or dibasic potassium phosphate.hospital day 1 (total dose 120 mmol over about 48 hours).

Her serum phosphorus level had improved to 3.9 mg/dL at60 hours after admission, and the potassium phosphateinfusion was discontinued. She was pronounced braindead on hospital day 5; at that time, she had serumcalcium, phosphorus and creatinine levels of 5.8 mg/dL,6.2 mg/dL and 1.4 mg/dL, respectively. Her serumphosphorus and creatinine levels had both been 0.9 mg/dL29 hours after admission. Postprocurement kidneybiopsies, evaluated at a different institution, revealedadequate glomeruli, and normal arteries, arterioles andtubules; both kidneys were transplanted. However,intratubular calcium phosphate deposits wereretrospectively identified.

The first renal transplant recipient was a 65-year-oldman. Post-transplant immunosuppression comprisedprednisone, mycophenolate mofetil (MMF) and tacrolimus.After transplantation, his serum creatinine level only slowlyimproved, reaching 2.9 mg/dL by day 10. A renal biopsy7 days later revealed acute tubular injury and diffuseintratubular microcrystal deposits, consistent with calciumphosphate crystals; a BK virus stain was negative. His graftfunction continued to decline slowly and, 3.5 months post-transplant, a second biopsy showed persistent tubularcalcium phosphate deposits and interstitial inflammation;on this occasion, a BK virus stain was positive and he had aviral load of 69 500 copies/mL. Tacrolimus was decreased,MMF was withdrawn and he started receiving leflunomidewith good virological response. However, his renalfunction continued to deteriorate and haemodialysisbecame necessary about 6 months post-transplant. Hesubsequently required transplant nephrectomy and waslisted for a second transplant. Biopsy of the explantedspecimen revealed diffuse and persistent tubular calciumphosphate deposits, but no evidence of BK virus.

The second recipient, a 52-year-old man, experienceddelayed graft function post-transplant and required renalreplacement therapy for 8 days; post-transplantimmunosuppression comprised prednisone, MMF andtacrolimus. A kidney biopsy on post-transplant day 15showed numerous intratubular calcium phosphatedeposits but no viral changes or signs of rejection; a repeatbiopsy on day 40 showed the same findings. His renal graftfunction continued to be impaired, and a third biopsy wasperformed 3 months post-transplant. Crystal depositspersisted, but on this occasion, BK virus nephropathy wasalso evident (viral load 871 832 copies/mL). MMF waswithdrawn, his tacrolimus dose was decreased, andleflunomide and cidofovir were initiated. At 5 months post-transplant, biopsy findings were negative for BK virus, butcontinued to show calcium phosphate deposits. Heremained largely asymptomatic at 17 months post-transplant.

Author comment: "We believe that the two patientsreported here received kidneys from a deceased donor inwhom APN developed. The persistence of poor graft function

1

Reactions 29 Aug 2009 No. 12670114-9954/10/1267-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved