Helena Viana

Morphologic patterns and treatment of transplant glomerulopathy: A retrospective analysis

Transplant glomerulopathy is mainly due to chronic antibody‐mediated rejection and actually represents a major cause of long‐term allograft failure. The lack of effective treatment remains a serious problem in transplantation. A retrospective and uni‐center study was performed in 48 kidney allograft recipients with transplant glomerulopathy between January 2010 and December 2015. Median time for diagnosis was 7.1 (3.6‐11.8) years post‐transplant. Light microscopy showed severity of transplant glomerulopathy in the majority of patients (cg1=10.4%; cg2=20.8%; cg3=68.8%). Moderate microvascular inflammation was present in 56.3% (g+ptc≥2), and almost half of recipients (51.1%) were C4d positive in immunofluorescence. Female gender (P=.001), age (P=.043), renal dysfunction (P=.002), acute rejection episodes (P=.026), and anti‐HLA class II antibodies (P=.004) were associated with kidney allograft failure. Treatment of transplant glomerulopathy was performed in 67.6% of patients. The histologic and laboratory features that led to a therapeutic intervention were score ptc (P=.021), C4d (P=.03), and the presence of anti‐HLA antibodies (P=.029), whereas score ah (P=.005) was associated with conservative measure. The overall cumulative kidney allograft survival at 10 years was 75%. Treatment of transplant glomerulopathy was ineffective to improve long‐term kidney allograft survival.

Cavernous Sinus Thrombosis in a Patient with Nephrotic Syndrome

Nephrotic syndrome (NS) is a glomerular disease characterized by altered permeability of the glomerular capillary wall to macromolecules. This results in heavy proteinuria, hypoalbuminemia, hypercholesterolemia, lipiduria, and edema. This clinical and laboratory syndrome is a life-threatening disease, and is associated with several complications, not only related to the disease itself, but also related to its treatment. Disease-associated complications include acute kidney injury, chronic kidney disease, cardiovascular disease, negative nitrogen balance, infections, endocrine disorders, and hypercoagulability. Venous and arterial thromboembolism is a significant complication of NS, occurring in approximately 27% of the patients [1]. This represents an 800% increase relatively to the general population [1, 2]. The pathophysiology of thrombogenesis in NS is not fully understood, and seems to be multifactorial [3], depending on the etiology (particularly frequent in membranous nephropathy), serum albumin level (most likely when\2 g/dl), previous episodes, and genetic predisposition [1, 2, 4]. These patients are at an increased risk of deep vein thrombosis (DVP), renal vein thrombosis (RVP), and pulmonary embolism (PE). Cerebral venous thrombosis (CVT) is infrequent, being primarily reported in children [1, 2]. The authors report a case of a 45-year-old white female patient admitted with NS and multiple venous thrombosis.

Specificity and Sensitivity of Screening for Anti-HLA Antibodies in Kidney Allograft Dysfunction

BACKGROUND Prospective testing for posttransplant circulating anti-HLA antibodies seems to be a critical noninvasive tool, but confirmatory data are lacking. MATERIALS AND METHODS Over the last 3 years, peritubular capillary (PTC) C4d deposition was prospectively sought by an immunofluorescence technique applied to frozen tissue in biopsies obtained for allograft dysfunction. Screening for circulating anti-HLA class I/II alloantibodies (AlloAb) by the flow cytometric test was performed simultaneously. RESULTS We evaluated 132 sets of biopsies and simultaneous serum samples. PTC C4d deposition was demonstrated in 15.9% (21/132) of biopsies. Circulating anti-HLA I/II AlloAb were detected in 25% (33/132) of serum samples. Employing receiver-operator characteristic (ROC) curves for all C4d-positive biopsies, screening for AlloAb showed a global specificity of 82% and sensitivity of 61.9%. When this analysis was restricted to biopsies obtained in the first month posttransplantation, the sensitivity increased to 81.8%, but the specificity decreased to 76.9%. After the first month posttransplantation, we observed sensitivity of 40.0% and a specificity of 86.4%. In the first month posttransplantation, all patients with a diagnosis of acute antibody-mediated rejection displayed circulating anti-HLA class I/II, but not always at the same time as the C4d-positive biopsy. CONCLUSIONS In the first month posttransplantation, prospective monitoring of anti-HLA antibodies may be useful. The high sensitivity allows the identification of patients at risk, affording an earlier diagnosis of antibody-mediated rejection. After the first month, the test can be used to evaluate allograft dysfunction episodes, since positivity is highly suggestive of an antibody-mediated process.