Aires, I

Carvalho, F

Mesquita, I

Nolasco, F

Viana, H

Repositório do Centro Hospitalar de Lisboa Central, EPE

CMYKP84     CLINICAL PRESENTATIONA 73-year-old man, with end-stage renal failure secondary to ADPKD was transplanted with a deceased allograft kidney in 1996.Between 1996 and 2004, he was immunosup-pressed with cyclosporine, azathioprine (AZA) and prednisone (PDN). In 2004, after the diagnosis of squamous-cell carcinoma of the lip, the immunosup-pression was changed to sirolimus (SRL) and AZA. Since 2010, after sepsis with pulmonary origin, he was in monotherapy with SRL.  Along these years, the serum creatinine increased slightly from 1.2 to 1.8 mg/dl.A diagnosis of adenocarcinoma in the right upper pulmonary lobe was made, in September 2013, and the patient underwent a right upper lobectomy in November 2013. The serum creatinine was 1.9 mg/dl at discharge after surgery. At this time, the siro-limus was switch to tacrolimus.An allograft kidney biopsy was done 75 days after surgery, due to creatinine increase (1.9 to 3.2 mg/dl), with a proteinuria of 50 mg/dl. The following figures demonstrate the main morphological aspects of the biopsy. HISTOLOGICAL DIAGNOSISThe paraffin-embedded fragment shows kidney cortical with a total of six glomeruli and several medium-sized arteries. The frozen fragment shows four glomeruli and the search of C4d in peritubular capillaries by immunofluorescence is negative.Acute allograft kidney dysfunction 18 years after transplantationHelena Viana, Isabel Mesquita, Inês Aires, Fernanda Carvalho, Fernando NolascoNephrology Department, Hospital Curry Cabral, Centro Hospitalar de Lisboa Central. Lisboa, PortugalNEPHROPATHOLOGY QUIZPort J Nephrol Hypert 2014; 28(1): 84-86Advance Access publication 20 March 2014Figure 2Masson trichrome green, x200.Figure 1Periodic acid-Schiff, x100.Nefro - 28-1 - MIOLO.indd   84 28/03/2014   16:26:29Port J Nephrol Hypert 2014; 28(1): 84-86    85CMYKPFigure 1 reveals a kidney with profound altera-tions; an area of interstitial fibrosis with intense inflammatory infiltration and tubular atrophy stands next to a tubular necrosis area.Figure 2 presents the acute tubular necrosis area in higher magnification; one ischemic glomerulus is visible.In Figure 3, we can see that the acute tubular necrosis is very severe; almost all the tubular basal membranes are denuded of epithelial tubular cells.Figure 4 shows two glomeruli with pseudo-cystic appearance; the capillaries tufts are severely retracted to the vascular pole. The medium-sized artery pres-ents a reduction of vascular lumen diameter.In Figure 5, we can see two medium-sized arteries with biconvex, needle-shaped clefts. The vascular lumens are occluded; the clefts are surrounded by fibrous intimal hyperplasia.In Figure 6, the cleft is surrounded by eosinophilic material and fibro-oedematous intimal hyperplasia.In summary, optical microscopy demonstrates: 3 globally sclerosed glomeruli in areas of interstitial fibrous/tubular atrophy and chronic inflammatory infiltrate; occluded medium-sized arteries surrounded Figure 3Masson trichrome green, x400.Figure 4Masson trichrome green, x400.Figure 5Masson trichrome green, x200.Figure 6Masson trichrome green, x400.Nefro - 28-1 - MIOLO.indd   85 28/03/2014   16:26:2986    Port J Nephrol Hypert 2014; 28(1): 84-86CMYKPby severely ischemic, medium-sized arteries and acute tubular necrosis. The histological diagnosis was athe-roembolic nephropathy. COMPLEMENTARY EXAMINATIONSerum analysis reveals a low C3 with normal C4, without eosinophilia.  DISCUSSIONAtheroembolic disease in kidney allograft is a rarely reported disease; between 0.2% and 1% cas-es1-3 of all biopsies. Until the end of 2012, we report-ed 0.21% cases of all biopsies4 belonging to two patients from our department. In the last year, ath-eroembolic disease was diagnosis in the first 10 days after transplantation (early form) in one patient and 18 years after transplantation (late form) in this same patient.The late form of the disease in stable allograft kidney is usually associated with the same risk fac-tors and systemic manifestations as the general populations. The atherosclerothic plaques are dis-rupted by direct lesion (angiography or surgery) or by drugs (anticoagulant and thrombolytic agents). Our patient underwent a major surgical procedure and take anticoagulants for prophylaxis of pulmonary thromboembolism in the post-operative period. The pathognomonic features5 are the biconvex, needle shaped clefts. The clefts are the “ghosts” of choles-terol crystals that are dissolved by the xylol used during routine preparation of paraffin-embedded biopsy. In this biopsy, we can see an early phase of endothelial reaction to cholesterol crystals (Fig. 6) and a later phase (Fig. 5). The fibrous intimal hyperplasia results in arteries occlusion and isch-aemia of the surrounding tissue. CLINICO-ANATOMICAL DIAGNOSIS Atheroembolic disease in allograft kidney. TREATMENT AND EVOLUTIONThe patient was treated with 500 mg IV of methyl-prednisolone in 3 consecutive days; tacrolimus was switched to sirolimus and low-dose aspirin was initiated. Serum creatinine rapidly decreased to 1.9 mg/dl.Conflict of interest statement: None declared.References 1. Lai CK, Randhawa PS. Cholesterol embolization in renal allografts: a clinicopathologic study of 12 cases. Am J Surg Pathol 2007;31(4):536-545 2. Ripple M, Charney D, Nadasdy T. Cholesterol embolization in renal allografts. Trans-plantation 2000;69(10):2221–2225 3. Modi KS, Rao VK. Atheroembolic Renal Disease. J Am Soc Nephrol 2001;12(8):1781–1787 4. Viana H, Ferreira C, Carvalho F, et al.. Atheroembolic renal disease as a cause of allograft primary non–function. Port J Nephrol Hypert 2013; 27(1): 61-67 5. Kassirer JP. Atheroembolic renal disease. N Engl J Med 1969;280(15):812-818Correspondence to: Drª Helena VianaDepartment of Nephrology, Hospital Curry CabralRua da Beneficência, nº 8, 1069-166Lisboa, PortugalE-mail: viana.helena@gmail.comHelena Viana, Isabel Mesquita, Inês Aires, Fernanda Carvalho, Fernando NolascoNefro - 28-1 - MIOLO.indd   86 28/03/2014   16:26:30

Acute Allograft Kidney Dysfunction 18 Years After Transplantation

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