RESUMEN
Idiopathic membranous nephropathy also known as primary membranous nephropathy (PMN) is a common cause of nephrotic syndrome often seen in nondiabetic adults worldwide, rising as high as 40% in adults over the age of 60. Most PMN is mediated by antibodies to the M-type phospholipase A2 receptor (anti-PLA2R) in nearly 70%-80% of individuals. Thrombospondin type 1 domain-containing 7A (THSD7A) accounts for 1%-5% of individuals with PMN. In these individuals, malignancies have a varying incidence of 6%-25%. We present a case of idiopathic membranous nephropathy with anti-PLA2R negative and THSD7A positive with an underlying metastatic neuroendocrine carcinoma. Our goal is to highlight the importance of cancer screening in individuals with THSD7A-positive PMN. In addition, although nonspecific, a negative anion gap may be an indicator of an underlying malignancy.
RESUMEN
We report a case of a 54-year-old immunocompetent female with cervical spine discitis and osteomyelitis secondary to Nocardia nova. Nocardia nova is overall an exceedingly rare cause of infectious diseases. In this case, the patient was admitted for neck and right shoulder pain. One year prior, she had lumbar osteomyelitis (L4-L5) that required laminectomy. Cultures at that time grew Staphylococcus schleiferi and she was treated with cefazolin for six weeks. Six months later she presented with cervical spine (C4-C5) discitis/osteomyelitis. She underwent surgical laminectomy, biopsy and culture, which grew Nocardia nova. The patient was treated with intravenous amikacin and then transitioned to trimethoprim-sulfamethoxazole for a total of twelve months. Other case reports of spinal osteomyelitis secondary to nocardia describe treatment with antibiotics, surgical debridement plus or minus arthrodesis with favorable outcome in improving pain and functionality at 3 years.1 In our case, the patient completed the course of antibiotics and 6 months later, imaging of the cervical spine showed mild height loss at C4 and C5, however no significant acute changes in the cervical spine, epidural or prevertebral soft tissue collections. She continues with chronic neck pain but repeated MRI of the cervical spine at 2 years shows no evidence of osteomyelitis or soft tissue edema.
RESUMEN
Nitrous oxide is clinically used as an inhaled anesthetic in surgical and dental procedures. It is also used as an inhaled recreational drug and can be incredibly addictive. It tends to irreversibly oxidize cobalamin (Vitamin B12), rendering it inactive as a coenzyme in the production of methionine. Methionine is required in myelin sheath phospholipid production, and thus overuse of this anesthetic can affect myelin formation. Furthermore, other substrates that require this coenzyme (such as methylmalonate and propionate) accumulate and get incorporated in the myelin sheath, resulting in subacute combined degeneration of the spinal cord. We present a case of a young, avid hunter with a history of polysubstance use to include inhaled nitrous-oxide abuse, prior cocaine use, current marijuana use, and tobacco abuse, who presented with ascending paresthesias without appreciable motor dysfunction. Initial labs showed isolated macrocytosis without anemia in the setting of low vitamin B12 levels. Relevant studies showed elevated methylmalonic acid, normal anti-parietal cell, and anti-intrinsic factor antibodies. Heavy metals screens were negative for high levels of lead, iron, copper, or zinc. Cervical spine MRI demonstrated dorsal cord signal abnormalities without enhancement, in a pattern consistent with vitamin B12 deficiency. The patient was diagnosed with subacute combined degenerative disease secondary to depleted vitamin B12 as a result of recreational inhaled nitrous-oxide abuse. After cessation of nitrous oxide abuse, in addition to three months of B12 replacement, he reported complete resolution of symptoms.
RESUMEN
Stimulant laxatives are a common class of laxatives that is abused by patients with eating disorders. We present a case of a 30-year-old female who presented with dyspnea, peripheral edema and weight gain who had been chronically using laxatives. Her symptoms were consistent with rebound edema caused by sodium and free water shifts with abrupt cessation of excessive stimulant laxative use. This case highlights the use of furosemide as the mainstay treatment for rebound edema and weight gain.