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Antiphospholipid syndrome (APLS) is an autoimmune condition which commonly manifests as an arterial or venous thrombosis affecting medium to large vessels, with the presence of antiphospholipid antibodies. APLS can be a primary disease by itself, or secondary to other autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). Catastrophic APLS is a rare but a fatal sequelae of APLS, affecting up to three or more organs, and progresses rapidly with a high mortality rate. We report a case of catastrophic APLS in a young woman with underlying SLE who presented to us with multiple cranial nerve palsies due to bilateral pontine infarct, and eventually developed deep vein thrombosis and pulmonary embolism during the course of the illness. She was treated with high dose corticosteroids and intravenous cyclophosphamide with biochemical improvement. In this case report, we would like to highlight the fact that our patient had bilateral pontine infarcts as the initial presentation, with no inciting events and  antiphospholipid antibodies were negative during the acute illness.

Thrombotic thrombocytopenic purpura is a rare but life threatening medical condition. Early recognition and treatment of thrombotic thrombocytopenic purpura is important especially in patients who do not present with the classic pentad to reduce the high mortality. Herein, we describe a case of a patient who does not fulfil the classic pentad features thrombotic thrombocytopenic purpura that was induced by dengue fever. The patients' initial full blood picture did not have all the typical features of microangiopathic haemolytic anaemia but there were fragmented red blood cells. However, even a small number of fragmented red blood cells in the peripheral blood should alert physicians of the possible diagnosis of thrombotic thrombocytopenic purpura together with other symptoms. Furthermore, signs and symptoms of thrombotic thrombocytopenic purpura and dengue fever can overlap such as fever, thrombocytopenia, neurological deficit mimicking dengue encephalopathy and dengue induced acute kidney injury.

Managing primary or even secondary glomerulonephritis remains a challenge to many nephrologists. In primary focal segmental glomerulosclerosis (FSGS) with heavy proteinuria, renin aldosterone system blockade and high dose of oral prednisolone is the mainstay of treatment. Other immunosuppressive medications like Cyclophosphamide, Cyclosporine A and Mycophenolate Mofetil (MMF) are warranted if a complete remission is not achieved.  We illustrate a case of 21 year old gentleman with primary FSGS that was difficult to achieve remission despite on high dose steroid and oral Cyclophosphamide. He was also not responsive to a combination of MMF and Cyclosporine A (CSA) and even throughout the therapy he developed significant steroid and CSA toxicity. He presented to our center with severe nephrotic syndrome and acute kidney injury requiring acute haemodialysis. Despite re-challenged him again on high dose prednisolone, total of 2.4g of intravenous Cyclophosphamide, and MMF, he failed to achieve remission. He was subsequently given intravenous Rituximab 500mg/weekly for 4 doses and able to attained remission for 1 year. He relapsed again and a second course of Rituximab 500mg/weekly for 6 doses were given to attain remission. This case demonstrates the difficulty in managing refractory steroid dependent FSGS and we found that Rituximab is proven beneficial in this case to induce remission.