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Comparison of the 4 biomarkers scores at various thresholds in low and high viremia levels between patients with minimal/mild (F0â 1) and moderate-severe (F2â 4) fibrosis. (DOCX 18 kb)

Sensitivity, specificity, positive and negative likelihood ratios of the four biomarkers at different cut-off values in identifying significant fibrosis (F2â 4) in the overall cohort (n = 366) of patients. (DOCX 16 kb)

The incidence of renal cell carcinoma (RCC) in renal allograft in transplant recipients is 0.22–0.25%. De novo clear cell, papillary, and chromophobe RCCs and RCCs with sarcomatoid differentiation originating in renal allograft have been reported. Routine surveillance for graft tumours is not routinely practiced and these tumours are commonly asymptomatic and incidentally discovered. We describe a case of incidental, eosinophilic chromophobe RCC in a 31-year-old, long-term renal transplant male recipient, who presented with acute gastroenteritis 11 years after transplantation. The graft was nonfunctional at the time of presentation. Abdominal ultrasound and computed tomography scan demonstrated 1.8 cm well-defined, round enhancing lesion, confined to the renal allograft and suspicious for malignancy. Pathological examination of graft nephrectomy specimen showed gross, histopathological, and immunohistochemical features of eosinophilic chromophobe RCC. Fifty-five months after surgery, the patient was alive and free of malignancy. To the best of our knowledge, only five chromophobe RCCs originating in a renal allograft were previously described in English literature. We suggest that chromophobe RCC should be considered in the differential diagnosis of renal allograft mass, including eosinophilic tumours, and emphasise the importance of periodic screening of renal allograft in all renal transplant recipients.

Light chain deposition disease (LCDD) is a rare illness with, as yet, no clear evidence-based guidelines for its treatment. To the best of our knowledge, LCDD has not been previously reported from Saudi Arabia. We present in this report, a 38-year-old Saudi male who presented with clinical features suggestive of hypertensive nephropathy but kidney biopsy later revealed the diagnosis of LCDD. His serum creatinine at presentation was 297 μmol/L which came down to 194 μmol/L on treatment with Bortezomib, Cyclophosphamide and Dexamethasone. His 24-hour protein excretion at presentation was 6 g/L which also came down to less than 1 g/day. He was later placed on Cyclophosphamide, Thalidomide, and Dexamethasone regimen because of persistent high titres of serum free light chains. He went into remission with undetectable serum free light chains and remained so for three years at the time of writing this report. We conclude that LCDD, though rare, does occur in Saudi population. The treatment of LCDD is challenging but the use of Bortezomib, a proteosome inhibitor, is promising. However, suboptimal response may require further treatment with other therapeutic options such as chemotherapy with alkylating agents or high-dose Melphalan with autologous stem cell transplant.

A 29-year-old man developed chronic allograft nephropathy 63 months after renal transplantation. He became symptomatic with advanced chronic graft failure; his immunosuppressive medications were reduced and he was commenced on haemodialysis. Two months following the withdrawal of immunosuppression, he presented with abdominal pain, haematuria, and a marked drop in haemoglobin. The patient was taken to the operating room, where the renal allograft was found to be ruptured, and graft nephrectomy was subsequently performed. Histological examination of the graft specimen showed severe haemorrhagic acute vascular cellular rejection in a background of marked chronic allograft vasculopathy. Immunostaining for C4d showed diffuse, strong, linear circumferential staining of the peritubular capillaries, indicating a concurrent antibody-mediated rejection. We report herein an unusual case of spontaneous renal allograft rupture that occurred long time after transplantation due to severe acute rejection following cessation of immunosuppressive medications for advanced chronic allograft failure. To the best of our knowledge, the time interval between transplantation and the rupture of this allograft is the longest of those reported in the literature.

Congenital diaphragmatic hernia is a common congenital anomaly of uncertain etiology. Its association with multiple congenital anomalies in various organs is well recognized and antenatal radiological evidence of congenital diaphragmatic hernia warrants thorough evaluation to detect other anomalies, some of which can be life threatening. Rarely, heterotopic hepatic tissue is identified in the hernia, a rare pathological finding, exhibiting more than one macroscopic and microscopic characteristics, and always associated with cardiac congenital anomalies. Herein, we report a case of left-sided microscopic heterotopic hepatic tissue in a congenital diaphragmatic hernia in an infant with multiple cardiac congenital anomalies, but with preserved pericardium.

Although systemic amyloidosis of amyloid-associated protein (AA) type (secondary or reactive amyloidosis) frequently involves the liver, it rarely causes clinically apparent liver disease. Mild elevation of alkaline phosphatase and hepatomegaly are the most common biochemical and clinical findings, respectively. We report a case of systemic amyloidosis of AA type, which clinically presented as subacute hepatic failure and resulted in a fatal clinical course in a 69-year-old man. To the best of our knowledge, this is the fifth case of hepatic amyloidosis of AA type that clinically presented as fatal subacute hepatic failure, an unusual clinical presentation for hepatic involvement by systemic AA-type amyloid.