C1q nephropathy is a rare glomerular disease with characteristic mesangial C1q deposition noted on immunofluorescence microscopy. It is histologically defined and poorly understood. Light microscopic features are heterogeneous and comprise minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and proliferative glomerulonephritis. Clinical presentation is also diverse, and ranges from asymptomatic hematuria or proteinuria to frank nephritic or nephrotic syndrome in both children and adults. Hypertension and renal insufficiency at the time of diagnosis are common findings. Optimal treatment is not clear and is usually guided by the underlying light microscopic lesion. Corticosteroids are the mainstay of treatment, with immunosuppressive agents reserved for steroid resistant cases. The presence of nephrotic syndrome and FSGS appear to predict adverse outcomes as opposed to favorable outcomes in those with MCD. Further research is needed to establish C1q nephropathy as a universally recognized distinct clinical entity. In this paper, we discuss the current understanding of pathogenesis, histopathology, clinical features, therapeutic options, and outcomes of C1q nephropathy.

Anticoagulation carries a tremendous therapeutic advantage in reducing morbidity and mortality with venous thromboembolism and atrial fibrillation. For over six decades, traditional anticoagulants like low molecular weight heparin and vitamin K antagonists like warfarin have been used to achieve therapeutic anticoagulation. In the past decade, multiple new direct oral anticoagulants have emerged and been approved for clinical use. Since their introduction, direct oral anticoagulants have changed the landscape of anticoagulants. With increasing indications and use in various patients, they have become the mainstay of treatment in venous thromboembolic diseases. The safety profile of direct oral anticoagulants is better or at least similar to warfarin, but several recent reports are focusing on spontaneous hemorrhages with direct oral anticoagulants. This narrative review aims to summarize the incidence of spontaneous hemorrhage in patients treated with direct oral anticoagulants and also offers practical management strategies for clinicians when patients receiving direct oral anticoagulants present with bleeding complications.

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DesCripTionA 69-year-old woman on apixaban for 4 years due to her atrial fibrillation presented with severe left lower abdominal pain. She was discharged from the hospital 4 days prior after treatment for influenza and had finished a course of oseltamivir. She did not receive any heparin products and was continued on apixaban during that admission. A few hours before presentation, she reported coughing severely with sudden onset of excruciating abdominal pain. She denied trauma or injury to the abdomen. On exam, she was alert, normotensive and tachycardic, with significant left lower quadrant tenderness in the abdomen. Laboratory results were significant for decreased haemoglobin from 15.2 to 12.9 g/ dL. CT of the abdomen showed acute left inferior rectus abdominis muscle haematoma (7.5 cm), along with stable and unchanged left adnexal cystic lesion (figure 1). Apixaban was discontinued, and the patient was closely monitored in the hospital with supportive care. Her haemoglobin remained stable and her pain improved. Repeat CT showed stable rectus sheath haematoma. She was asked to withhold apixaban for 1 week and was discharged to follow-up with her primary care physician to restart it.About one in six emergency department visits for adverse drug events is due to bleeding in patients taking anticoagulant medications, and direct oral anticoagulants (DOAC) account for 10% of these events.1 Only four cases of DOAC-associated rectus sheath haematoma have been reported, two associated with apixaban and two with rivaroxaban.2 Rectus sheath haematoma is a rare but serious complication associated with significant morbidity and occasional mortality. It is the result of bleeding into the rectus sheath from damage to the superior or inferior epigastric arteries. Common risk factors and causes of rectus sheath haematoma include anticoagulation, blunt or penetrating trauma, pregnancy, female gender, older age, hypertension, medical conditions such as collagen vascular disorders, and increased abdominal pressure from straining or severe coughing.2 Ultrasound is the initial test of choice, but CT of the abdomen will help to identify the origin, location and extent of bleeding. Management of rectus sheath haematoma depends on several factors such as the severity and size of the haematoma, the haemodynamic status of the patient and the extent of anticoagulation. Treatment includes usual supportive measures, including interventional source control when indicated.2 No guidelines exist to direct the timing of anticoagulation resumption in patients with spontaneous rectus sheath haematomas. The requirement for anticoagulation should be weighed against the risk of rebleeding once the haematoma is stable. For severe DOAC-related bleeding, prothrombin complex concentrate and recombinant activated factor VII have been recommended.1 Current research focuses on antidotes to neutralise the anticoagulant activity of DOACs, including both direct thrombin inhibitors and direct factor Xa (FXa) inhibitors. Idarucizumab is licensed for the rapid...