ABSTRACT
Oxalate nephropathy is a rare pathology that can be difficult to diagnose. It results from calcium oxalate crystals that are deposited in the renal interstitium or renal tubules. Once the deposition ensues, a multitude of complications can occur, including renal failure. One etiology for oxalate nephropathy is a lack of biliary acid. The diagnosis of oxalate nephropathy is typically based on visualization of oxalate crystals in the renal tubules on biopsy, and treatment based on the etiology can range from simple removal of the offending agent or a change in diet to liver/kidney transplant in the setting of primary hyperoxaluria. This report discusses a case of severe oxalate nephropathy related to long-term cholecystostomy tube placement resulting in a deficiency of biliary acid.
ABSTRACT
Statin-induced necrotizing myositis is a rare subtype of idiopathic inflammatory myopathies due to the production of an antibody to the 200/100 kDA protein complex which was subsequently found to be directed against 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Similar to other auto-immune necrotizing myopathies, the disease is characterized by proximal muscle weakness, significant serum creatine kinase elevations, and histological evidence of necrosis of myocytes. However, there is often little to no infiltration of inflammatory cells noted on muscle biopsy. As the name implies, this subtype of idiopathic inflammatory myopathy is provoked by statin use which may be a helpful finding during the history-taking process when developing a differential diagnosis. Below, we discuss a case of a 52-year-old female with delayed-onset immune-mediated necrotizing myopathy secondary to statin use.
ABSTRACT
We present a case report of a patient with symptomatic bilateral severe axillary artery stenosis who underwent drug-coated balloon angioplasty. A 59-year-old female with a past medical history of peripheral artery disease presented with bilateral upper extremity claudication on exertion and episodes of syncope. Peripheral angiography showed significant bilateral upper extremity peripheral artery disease (PAD) including bilateral severe axillary artery stenosis. The patient underwent endovascular management with drug-coated balloon angioplasty of the axillary artery bilaterally. Symptoms completely resolved and the patient continues to be on follow-up. Arterial duplex studies on both upper extremities showed no evidence of high-grade stenosis six years after intervention. Drug coated balloon angioplasty can be a successful modality of endovascular management for patients with symptomatic severe axillary artery stenosis. However, more randomized controlled data is required before making any conclusion.
ABSTRACT
[This corrects the article DOI: 10.7759/cureus.22893.].
ABSTRACT
We present a case report of a patient presenting with subarachnoid hemorrhage whose electrocardiogram (ECG) mimicked non-ST-elevation myocardial infarction. A 36-year-old male with a past medical history of resistant hypertension, previous severe acute respiratory syndrome coronavirus 2 infection, and alcohol abuse presented to the hospital after cardiac arrest. He was taken to the catheterization lab upon arrival and was found to have an unremarkable coronary angiogram. After angiography, computerized tomography (CT) head was performed revealing an acute, large-volume, subarachnoid hemorrhage. Subsequent CT angiogram of the head confirmed this with source noted to be a ruptured aneurysm of the anterior communicating artery. ST depression on ECG has been reported in patients who have suffered a subarachnoid hemorrhage. Although the most common etiology of cardiac arrest is an acute coronary syndrome, other etiologies based on a patient's past medical history need to remain in the differential. Recognition of ECG changes may lead to earlier diagnosis and decreased mortality in subarachnoid patients.
