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Pregled bibliografske jedinice broj: 486934

End-stage kidney disease after mushroom poisoning and abo-incompatible liver transplantation


Mrzljak, Anna; Knotek, Mladen; Guštin, Denis; Sabljar-Matovinović Mirjana; Kocman, Branislav; Ljubanović, Danica; Gašparov, Slavko
End-stage kidney disease after mushroom poisoning and abo-incompatible liver transplantation // Nephrology, 15 (2010), 6; 660-661 doi:10.1111/j.1440-1797.2010.01277.x (međunarodna recenzija, pismo, znanstveni)


Naslov
End-stage kidney disease after mushroom poisoning and abo-incompatible liver transplantation

Autori
Mrzljak, Anna ; Knotek, Mladen ; Guštin, Denis ; Sabljar-Matovinović Mirjana ; Kocman, Branislav ; Ljubanović, Danica ; Gašparov, Slavko

Izvornik
Nephrology (1320-5358) 15 (2010), 6; 660-661

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pismo, znanstveni

Ključne riječi
End-stage kidney disease; Amanita phalloides; liver transplantation

Sažetak
Acute liver and kidney injury after mushroom poisoning are associated with high patient mortality. Acute kidney injury following mushroom poisoning is a frequent complication, but the progression to chronic end-stage kidney failure (ESKF) occurs rarely. We describe a case of acute kidney injury following Amanita falloides poisoning in a patient without preexistent kidney diseases with developement of ESKF. Three days after ingestion of A. phalloides, a 52 years old female presented with acute liver and kidney failure. Her past medical history was uneventful, and 1 month prior her liver and kidney functions were normal. Her laboratory values on admission included: AST 6347 U/L, ALT 6140 U/L, PV< 10 sec, ammonia 347 μmol/L, BUN 19 mmol/L, creatinine 227 μmol/L ; urinalysis was unremarkable. Treatment included intravenous penicillin G, red cell transfusion and continuous veno-venous haemofiltration (CVVH). She was listed for urgent liver transplantation (LT), and because of an incompatible blood group donor (A+), the patient (O+) was preconditioned with plasma exchange (PE) with AB+ plasma to reduce isohemaglutinin titer to <1:16. LT was performed with immunosuppression induction with anti-thymocyte immunoglobulin with tacrolimus, mycophenolate mofetil, and prednisone maintenance. On postoperative day (POD) 5 she was treated for Aspergillus fumigatus cultured from bronchial specimen with voriconazole and caspofungin. On POD 24 a mild acute cellular rejection was diagnosed, which resolved after corticosteroid pulses. Because of persistent kidney failure CVVH was continued during post- transplant period. On POD 64 renal biopsy demonstrated normal morphology of glomeruli and blood vessels with diffuse loss of brush border and vacuolization of tubular epithelial cells with moderate interstitial edema and patchy mononuclear interstitial inflammation. Mild focal interstitial fibrosis and tubular atrophy was noted. Immunofluorescence was negative. The final diagnosis was acute tubular injury with mild interstitial fibrosis and tubular atrophy. Three years after LT her liver function has been stable but renal function did not recover and she was maintained on intermittent haemodialysis. The toxicity of Amanita phalloides is related to amatoxin which inhibits RNA polymerase II within enterocytes, hepatocytes and proximal renal tubular cells. A progressive liver injury may lead to acute liver failure with mortality rate between 10% to 20%. Kidney injury following intoxication with Amanita manifests as acute tubular necrosis. It usually resolves after resolution of liver injury and in exceptional cases may lead to ESKD. There are no experimental models of amanita- induced acute kidney injury to address its pathophysiology. Contributory factors to renal injury may be preexisting kidney disease, hypovolemia and nephrotoxic drugs. No preexistent kidney disease was identified in our patient and, except for a tacrolimus she was not receiving other nephrotoxic drugs. However, it is unlikely that only exposure to tacrolimus, although it may be contributory, was predominantly responsible for development and maintenance of prolonged oliguric acute kidney injury with eventual chronic end- stage kidney disease. Similarly, hepatorenal syndrome should have resolved with successful liver transplantation. With pathohistologic finding of only mild acute tubular injury and mild chronic changes, recovery of renal function should be expected. We speculate that amatoxins alone or in the combination with medications were responsible for irreversible kidney damage. A successful liver transplantation may have unmasked potential of amanita intoxication to lead to CKD.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti



POVEZANOST RADA


Projekt / tema
044-0000000-3356 - Imunološki nadzor u bolesnika s transplantiranim solidnim organom (Mladen Knotek, )
108-1081873-1891 - Prognostička vrijednost FOXP1 i FOXP3 u B limfoproliferativnim bolestima (Slavko Gašparov, )
108-1081873-1893 - Prognostički faktori, dijagnostika i terapija hemoblastoza (Branimir Jakšić, )

Ustanove
Klinička bolnica "Merkur",
Medicinski fakultet, Zagreb

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


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