Bradycardia Following Oral Corticosteroid Use: Case Report and Literature Review

Introduction: Corticosteroids are used in various clinical conditions that include many immune-mediated inflammatory diseases. Different side effects were described including cardiac arrhythmias. Most of those arrhythmias were in the form of bradycardia which usually occurs with high intravenous steroid doses. More significant arrhythmias and cardiac arrest were also described. In this report we describe a case of bradycardia that developed after the use of oral corticosteroids.Case report: We report a case of bradycardia that developed in a 14 year-old male after receiving oral prednisone. The patient had steroid- sensitive nephrotic syndrome and presented with anasarca that started to develop few days prior to hospitalization. He had no underlying heart disease. Vitals was normal. Investigations confirmed a new nephrotic relapse. Oral prednisone 80 mg / day divided into three doses was started. Albumin infusions were initially given with intravenous furosemide to control the edema. Seven days after hospitalization, he developed bradycardia with a pulse rate of 50-60 per minute, which was less than 50% of the baseline heart rate. He didn’t develop significant symptoms and he had no other apparent corticosteroids side effects. Cardiac evaluation and echocardiography were normal. Electrocardiogram revealed only sinus bradycardia.The bradycardia recovered after decreasing the dose of steroids to 60 mg PO every other day and he was discharged in stable condition a few days later.Conclusion: Cardiac arrhythmias may develop with all forms of steroids including oral prednisone. Bradyarrhythmias can occur even with standard doses of oral prednisone

Systemic Lupus Erythematosus with Severe Nephritis That Mimicked Henoch-Schoenlein Purpura

Introduction: Systemic lupus erythematosus (SLE) belongs to a family of related autoimmune rheumatic disorders that are capable of affecting multiple organs, and they are all associated with a variety of autoantibodies. Henoch Schoenlein purpura (HSP) is a sort of systemic vasculitis that is not associated with auto-antibodies and can affect different organs including the kidneys. Case report: A 12 year-old girl presented with abdominal pain, low grade fever, swollen and tender feet and left hand, skin rash on the lower extremities, and high blood pressure. Initial laboratory tests revealed severe proteinuria, microscopic hematuria and low C3 level. Renal biopsy showed diffuse proliferative glomerulonephritis with IgA, fibrinogen and C3 deposits. The case was accordingly diagnosed as HSP with severe IgA nephropathy. Treatment was started with mycophenolate mofetil (MMF) and pulse methylprednisolone followed by prednisolone. The patient improved and treatment was discontinued after 5.5 months. One month after withdrawal of her medications, the patient presented again with serositis and recurrent proteinuria. Both antinuclear antibodies (ANA) and anti dsDNA were positive. At this point she was diagnosed to have SLE disease and immunosuppressive treatment was restarted. Following this, symptoms disappeared, proteinuria regressed and anti-dsDNA titer dropped. Conclusion: This case presented with features of HSP and was later-on diagnosed to have SLE. This kind of clinical overlapping has not been reported in the literature to the best of our knowledge.Keywords: Henoch-Schoenlein Purpura; Nephritis; Systemic Lupus Erythematosu

Identification of a Locus on the X Chromosome Linked to Familial Membranous Nephropathy

INTRODUCTION: Membranous nephropathy (MN) is the most common cause of nephrotic syndrome (NS) in adults and is a leading cause of end-stage renal disease due to glomerulonephritis. Primary MN has a strong male predominance, accounting for approximately 65% of cases; yet, currently associated genetic loci are all located on autosomes. Previous reports of familial MN have suggested the existence of a potential X-linked susceptibility locus. Identification of such risk locus may provide clues to the etiology of MN. METHODS: We identified 3 families with 8 members affected by primary MN. Genotyping was performed using single-nucleotide polymorphism microarrays, and serum was sent for anti-phospholipase A2 receptor (PLA2R) antibody testing. All affected members were male and connected through the maternal line, consistent with X-linked inheritance. Genome-wide multipoint parametric linkage analysis using a model of X-linked recessive inheritance was conducted, and genetic risk scores (GRSs) based on known MN-associated variants were determined. RESULTS: Anti-PLA2R testing was negative in all affected family members. Linkage analysis revealed a significant logarithm of the odds score (3.260) on the short arm of the X chromosome at a locus of approximately 11 megabases (Mb). Haplotype reconstruction further uncovered a shared haplotype spanning 2 Mb present in all affected individuals from the 3 families. GRSs in familial MN were significantly lower than in anti-PLA2R–associated MN and were not different from controls. CONCLUSIONS: Our study identifies linkage of familial membranous nephropathy to chromosome Xp11.3-11.22. Family members affected with MN have a significantly lower GRS than individuals with anti-PLA2R–associated MN, suggesting that X-linked familial MN represents a separate etiologic entity