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He was put on hemodialysis support. Three months later, he received deceased kidney transplant and immunosuppression included prednisolone, tacrolimus and mycophenolate mofetil. The postoperative course was unremarkable. His serum creatinine remained stable (at ?120 ?mol/L) without any significant proteinuria. His serum cholesterol was 5 mmol/L and triglyceride was 1.8 mmol/L. He suffered an episode of acute kidney injury with serum creatinine reaching 201 ?mol/L during follow-up at 18-months post-transplant. There was neither fever nor Selleck SCH772984 urinary symptoms. Renal graft biopsy was performed and light microscopy revealed marked interstitial inflammation consisting of a large amount of polymorphs which were also noted within the tubular lumens (Figure?1B). All these features were suggestive of infective etiology. A course of ceftriaxone was given and the serum creatinine gradually returned to baseline. He continued to have regular follow-ups in our clinic with unremarkable course. However, subsequent review of his native kidney biopsy specimen showed that in addition to features of FGN, components of LPG which were characterized by some vacuolated and stringy materials inside the dilated capillary lumens (Figure?1C) were also seen. These materials were weakly eosinophilic, weakly periodic acid�CSchiff (PAS) positive and stained pale blue under Chromotrope-Aniline Blue (CAB) stain. On electron microscopy, these intraluminal materials contained fine granular material with small lipid vacuoles, consistent with lipoprotein thrombi (Figure?1D). These features Amrinone were not present in the graft biopsy specimen obtained 18 months after transplant. Mutational analysis of the apolipoprotein (APOE) gene by polymerase chain reaction and direct DNA sequencing revealed an E3/E3 genotype and a heterozygous mutation c.480_488del, which is predicted to result in deletion of Leu-Arg-Lys at codons 162�C164 (reference sequences ""type"":""entrez-nucleotide"",""attrs"":""text"":""NM_000041.2"",""term_id"":""48762938"",""term_text"":""NM_000041.2""NM_000041.2 and ""type"":""entrez-protein"",""attrs"":""text"":""NP_000032.1"",""term_id"":""4557325"",""term_text"":""NP_000032.1""NP_000032.1). selleck screening library This is a known mutation called APOE Tokyo causing LPG [11]. A familial genetic study on his son at 18 years of age showed that he also carries the same mutation, though there was no biochemical evidence of proteinuria or renal disease at the time of testing. His maintenance immunosuppressive regimen remained prednisolone, tacrolimus and mycophenolate mofetil while he was also put on diltiazem and lisinopril for blood pressure control. After >10 years post-transplant, his latest serum biochemistry and other laboratory examination revealed no significant abnormality. These included serum creatinine 125 ?mol/L, serum albumin 42 g/L, total cholesterol 4.8 mmol/L, triglyceride 1.2 mmol/L and 24-h urinary protein excretion