Plasma cell-rich acute rejection with monoclonal gammopathy in a renal transplant recipient.

Plasma cell infiltration into a renal allograft comprises a spectrum of lesions from acute rejection to posttransplant lymphoproliferative disease. We report an unusual case of plasma cell infiltration into a renal allograft with monoclonal gammopathy. A 42-year-old woman was admitted because of graft dysfunction after noncompliance with immunosuppressive therapy for 5 months. A graft biopsy showed acute T-cell-mediated rejection and massive plasma cell infiltration. Despite initial treatment with steroids and antithymocyte globulin, there was persistence of graft dysfunction, monoclonal gammopathy, and plasma cell infiltration. Subsequent treatment with bortezomib improved graft function and caused the monoclonal gammopathy to resolve. Immunohistochemical evaluation of markers of B cells (CD20 and CD138) and the ratio of kappa-to-lambda light chain (15:1) showed that infiltrating cells were plasma cells producing kappa light chain. This suggested that plasma cell-rich acute rejection with monoclonal gammopathy in this patient might have been in an early stage of kappa light chain-producing posttransplant lymphoproliferative disease confined to the renal allograft, and that bortezomib may be effective in treating a patient with this condition.

De novo glomerulitis associated with graft-versus-host disease after allogeneic hematopoietic stem cell transplantation: A single-center experience.

BACKGROUND: Nephrotic syndrome (NS) and proteinuria are uncommon, often unrecognized manifestations of graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation (HSCT). Only a few isolated case reports and case series involving smaller number of patients who developed NS after HSCT have been published. METHODS: We reviewed the renal histopathological examination findings and clinical records of 15 patients who developed proteinuria after HSCT at Seoul and Yeouido St. Mary's Hospital (Seoul, Korea). We also measured the anti-PLA2R antibodies (M-type phospholipase A2 receptor) in the serum samples from the seven patients at the time of renal biopsy. RESULTS: All patients had GVHD. The most common indication for biopsy was proteinuria (>1 g/day), with nine patients having nephrotic range proteinuria. The most common histopathological finding was membranous nephropathy (MN; n = 12). Other findings were membranoproliferative glomerulonephritis, C1q nephropathy, and diabetic nephropathy. Eleven patients were treated with immunosuppressive agents, and three patients were treated only with angiotensin II receptor blocker. The overall response rate, including complete remission (urinary protein level <0.3 g/day) and partial remission (urinary protein level = 0.31-3.4 g/day), was 73%. The mean follow-up period was 26 months, and none of the patients developed end-stage renal disease. All of the seven patients with MN had negative findings for anti-PLA2R antibodies, measured using an enzyme-linked immunosorbent assay kit. CONCLUSION: In this study the findings of 15 renal biopsies were analyzed and to our knowledge this is the largest clinicopathological study of GVHD-related biopsy-proven nephropathy. Approximately 80% of the patients were MN and 73% responded either partially or completely to immunosuppressive treatment. Currently, there is an increase in the incidence of GVHD-mediated renal disease, and therefore, renal biopsy is essential for diagnosing the nephropathy and preventing the progression of renal disease.

Clinical usefulness of kidney biopsy in liver transplant recipients with renal impairment.

BACKGROUND: Chronic kidney disease is a common complication after liver transplantation. In this study, we analyzed the results of kidney biopsy in liver transplantation recipients with renal impairment. METHODS: Between 1999 and 2012, 544 liver transplants were performed at our hospital. We retrospectively analyzed the clinical and histological data of 10 liver transplantation recipients referred for kidney biopsy. RESULTS: The biopsies were performed at a median of 24.5 months (range, 3-73 months) after liver transplantation. The serum creatinine level was 1.81±0.5 mg/dL at the time of kidney biopsy. There were no immediate complications. The most common diagnosis was glomerulonephritis (GN), such as immunoglobulin A nephropathy (n=4), mesangial proliferative GN (n=1), focal proliferative GN (n=1), and membranous GN (n=1). Typical calcineurin inhibitor (CNI)-induced nephrotoxicity was detected in three cases (30%). Chronic tissue changes such as glomerulosclerosis, interstitial fibrosis, and tubular atrophy were present in 90%, 80%, and 80% of cases, respectively, and mesangial proliferation was detected in 40% of cases. We began treatment for renal impairment based on the result of kidney biopsy; for example, angiotensin-receptor blockers or steroids were prescribed for GN, and the CNI dose was reduced for CNI nephrotoxicity. As a result, eight of 10 patients showed improvement in glomerular filtration rate, but two progressed to end-stage renal disease. CONCLUSION: Kidney biopsy is a safe and effective method for determining the cause of renal impairment after liver transplantation. Management of patients based on the result of kidney biopsy may improve renal outcomes.

Stent fracture at the proximal shaft of the left main stem.

Stent fracture is likely to be caused due to mechanical stress at the hinge point or kinking movement at the point of aneurysm formation with stent malapposition. To our knowledge, this is the first published report of stent fracture at the proximal shaft of the left main stem in a patient with acute myocardial infarction.