included rolling and lifting weights on an exercise ball. After returning home he became nauseated, diaphoretic, weak, and experienced excruciating left flank pain followed by an episode of watery diarrhea. His symptoms worsened and he presented to the emergency room the following morning. Physical examination at that time revealed a well-nourished man in marked distress secondary to intractable pain. There was significant tenderness to minimal palpation and percussion in his lower left quadrant and over his left costovertebral angle region. An initial computerized tomography (CT) of the abdomen showed an insignificant left renal cyst. Laboratory evaluation was significant for leukocytosis with a left shift, mild normocytic anemia, slightly elevated creatinine and CPK, and urine which showed pyuria but was sterile. Overnight he experienced fever and worsening pain with apparent peritoneal signs. The next morning a chest x-ray was done which showed no evidence of pneumonia. CT of the abdomen was repeated. In view of the patient's declining condition, this subsequent CT was read as a possible abscess. Aspiration of the renal abscess grew Streptococcus pneumoniae, as did all blood cultures. Predisposing factors for pneumococcal bacteremia were excluded. He recovered fully after a two-week course of ceftriaxone and four weeks of levofloxacin. IMPLICATIONS/DISCUSSION: Streptococcus pneumoniae is a very uncommon pathogen in renal abscesses. Extrapulmonary pneumococcal infection is most often metastatic from the lung. No respiratory disease was noted in our patient. Only two published cases of Streptococcus pneumoniae renal abscesses have been reported. These will be discussed, one in full detail. The etiology of our patient's Streptococcus pneumoniae continues to be a mystery. Two hypotheses will be presented. LEARNING OBJECTIVES: Often uncommon diseases present initially in the primary care setting, and appropriate referral and diagnosis are essential. The following case illustrates an unusual skin condition seen in a primary care setting in order to expand the generalist physician's differential diagnosis of dermatologic conditions associated with renal failure. CASE INFORMATION: The patient is a 36-year-old woman with a history of type I diabetes complicated by renal failure for which she underwent a kidney-pancreas transplant ten years ago. Her transplanted kidney remained functional until three months prior to presentation, at which time hemodialysis (HD) was initiated. Within one month of starting HD, she developed thickening and hardening of the skin on her left hand, which rapidly expanded to involve the entire left arm, and the right hand and arm. Within two months, the feet, lower legs, buttocks, and areas of the back had areas of skin hardening. The face, abdomen, and chest were spared. These areas of skin hardening were associated with minimal overlying skin changes, but she developed burning paresthesias during this time for which she was treated with oxcarbazepine. A skin biopsy confirmed the diagnosis of nephrogenic sclerosing dermopathy (NSD), with the findings of increased numbers of dermal spindle cells and thick collagen bundles in the reticular dermis. IMPLICATIONS/DISCUSSION: NSD was first described in September 2000 in a case series of 14 patients with a fibrotic skin condition resembling scleromyxedema. Each patient had a history of renal failure and 12 of the patients were receiving HD at the time of diagnosis. Patients displayed skin thickening and hardening with overlying brawny skin discoloration, which was localized to the torso and limbs with sparing of the face. Several patients complained of painful paresthesias beginning with the onset of skin hardening. In each case, the skin condition has been progressive with no known effective therapy. The etiology of NSD is unclear, but infectious agents or toxic agents (toxins in the dialysate, endogenous toxins not cleared by dialysis) have been proposed. Resolution of the skin lesions occurred in one case when HD was stopped following resolution of acute tubular necrosis. Through accurate referral and diagnosis of patients, more can be learned about the etiology, prevention, and treatment of NSD. Early recognition of NSD may allow early referral for transplantation to prevent progression of disease on HD, although there is not definitive evidence to date that NSD regresses following transplantation. A 58 year old Mexican man presented with progressive shortness of breath and a dry cough for over 1 month. Review of systems was positive for dyspnea on exertion, three pillow orthopnea, and an eight pound weight loss. His past history is noncontributory, and he uses no medication, tobacco or alcohol. On physical exam breath sounds were decreased with bilateral rales 1/2 way up. He was tachycardic with a loud P2, a jugular venous pressure of 10cm and 2+ edema to the shins. Chest x-ray showed bilateral pleural effusions; right greater than left. Echocardiogram revealed an ejection fraction of 70% with pulmonary hypertension. Laboratories were significant for a normocytic anemia with low iron, TIBC and reticulocyte count; ESR 116; urinalysis with trace protein and 20 red cells; and negative serologies for hepatitis B/C, HIV, and coccidiodes. CT chest was negative for pulmonary embolism and infiltrate. Diagnostic thoracentesis removed 200cc of hazy fluid with pH 7.48, 1250 white cells (81% lymphocytes) and cultures negative for bacteria, fungi and acid fast bacilli (AFB). Cytology was negative for malignant cells. Rapid reaccumulation later prompted removal of another 1L of fluid. A tuberculin skin test was 8 mm but sputum AFBs were negative. Further work-up revealed a positive ANA (1:2560 titer) and strongly positive anti-Smith antibody with negative anti-dsDNA and ANCA. He was diagnosed with SLE and started on prednisone 40 mg daily with resolution of the effusion and improvement in pulmonary hypertension. IMPLICATIONS/DISCUSSION: Pleural effusion is the initial manifestation in 1%, and pleurisy in 3%, of SLE patients, more often in those with late-onset (after age 50). Lupus pleuritis usually presents as pleuritic chest pain with fever, cough and dyspnea but rarely with massive effusions. Pleural symptoms may precede other manifestations of SLE by months or years, particularly in men. To diagnose pleural effusions caused by lupus pleuritis, one must rule out other causes including pulmonary embolism, congestive heart failure, infections (i.e. parapneumonic or tuberculous), and malignancy. Effusion ANA titer detection is a very sensitive but nonspecific test while anti-DNA antibodies or LE cells in the pleural fluid are diagnostic but not very sensitive. Treatment includes NSAIDs for mild cases and systemic corticosteroids for more severe cases. Early diagnosis and prompt treatment can greatly decrease morbidity from this disease. year old man presents with complaints of progressive leg swelling, erythema, 30 lb weight loss, and severe bilateral hip pain over 3 months. He initially noted several fluid filled blisters and pedal edema that spontaneously resolved. Over the next several weeks he described progressive bilateral hip pain requiring the use of crutches for ambulation. The month prior to admission the patient was bed bound secondary to pain. He denied other constitutional symptoms. Of note, he had eliminated fruits and vegetables from his diet 3 years ago. The patient had emigrated from Ethiopia 35 years ago. Physical exam revealed poor dentition, a perifollicular petechial rash of his lower extremities, hyperpigmentation of his upper thighs and bilateral lower extremitity edema. MRI was significant for lower extremity soft tissue edema and osteoporotic femoral heads with abnormal marrow signal. Laboratory values were notable for a normocytic anemia, normal coagulation panel, and electrolyte panel and a Vitamin C level of <0.12 mg/dL. Punch biopsy of the petechial lesions demonstrated perifollicular hemorrhage and corkscrew hair follicles. Vitamin C supplemenation 1000mg per day was initiated with resolution of symptoms over several weeks. Repeat MRI of his LE noted resolution of soft tissue edema and improving osteoporosis. IMPLICATIONS/DISCUSSION: Symptoms of scurvy have been described as early as 1500 BC by the ancient Egyptians. In contemporary history, epidemics have been described in the Renaissance era, when sailors were frequently affected, and during the 19th century, by those who experienced the Great Potato Famine, American Civil War armies, and the California Gold Rush communities. A cofactor and strong reducing agent, vitamin C is crucial to numerous biochemical pathways including collagen synthesis, norepinephrine synthesis, prostaglandin synthesis, and antioxidant function. Collagen synthesis disruption in particular leads to the clinical syndrome of scurvy including ecchymoses, bleeding gums, petechiae, and arthralgias. Other signs and symptoms include muscle pain, microcytic anemia, decreased wound healing, mood disturbances, and anorexia. While scurvy occurs rarely in the US, typically it is seen in elderly or alcoholic patients and those with diets devoid of fruits and vegetables. Sudden cardiac death has been reported in these patients however, morbidity and mortality largely occurs as a result of hemorrhage which can occur in any organ. Skin biopsy findings of perifollicular hemorrhage and follicle corkscrewing are pathopneumonic for the disorder. Symptoms typically improve over days to weeks with the addition of Vitamin C to the diet. Prognosis is excellent with timely diagnosis and treatment.