Immune reconstitution, glomerulonephritis, and successful treatment with rituximab.

BACKGROUND: Alemtuzumab can induce secondary autoimmunity affecting multiple organs. While kidney involvement is uncommon, it can be associated with devastating forms of glomerulonephritis (GN). CASE PRESENTATION: A 32-year-old African American woman presented with hypertension, proteinuria, and progressive renal failure. Her medical history was remarkable for secondary progressive multiple sclerosis (SPMS). She had received her first induction dose of alemtuzumab 1 year prior to presentation. Upon evaluation, she had scanning speech, multidirectional nystagmus, and mild edema. Her serum creatinine was 2 mg/dL. Urine studies revealed proteinuria and microscopic hematuria. Her serologic tests were positive for c-antineutrophil cytoplasmic antibodies (> 1 : 640). In addition, she was found to have new-onset severe thyroid dysfunction with antibodies against thyroglobulin and thyroid peroxidase. Kidney biopsy was diagnostic for pauci-immune crescentic GN. The patient was treated with methylprednisolone and rituximab with subsequent renal, thyroid, and neurological recovery. CONCLUSION: This is an atypical case of GN following therapy with alemtuzumab. We hypothesize that immune reconstitution may be a potential mechanism. Alemtuzumab is a new treatment for SPMS that can be associated with GN. Practice guidelines should address the management of its renal complications.

A Pregnant Woman Presenting With Progressively Worsening Dyspnea and Pneumothorax.

CASE PRESENTATION: A 29-year-old Ukrainian woman presented to the obstetric clinic at 28 weeks' gestation with pregnancy complicated by intrauterine growth restriction. She reported progressively worsening dyspnea during her pregnancy and was found to have significant hypoxia with an oxygen saturation of 84% on room air prompting admission for further evaluation. Oxygen saturation improved to 92% on 10 L of supplemental oxygen. On further questioning, she was found to have a history significant for pleurodesis as a treatment for recurrent pneumothoraces and nephrectomy for a benign renal mass several years prior while living in Ukraine.

Coagulopathy does not protect against venous thromboembolism in hospitalized patients with chronic liver disease.

BACKGROUND: It is uncertain whether pathologically prolonged international normalized ratio (INR) seen in chronic liver disease (CLD) protects against venous thromboembolism (VTE). Previous studies reported VTE incidence of 0.5% to 1.9% in patients with CLD. We sought to evaluate VTE incidence among hospitalized patients with CLD according to INR levels. METHODS: This was a retrospective cohort study performed at a tertiary university hospital. We included all adult patients admitted with a primary diagnosis of CLD over a 7-year period. The primary outcome was the development of VTE during hospital stay. Patients were divided into quartiles according to their highest admission INR. VTE events and prophylaxis rates were compared among INR quartiles. RESULTS: During the allotted 7-year period, we included 190 patients. Of these, 12 developed VTE events, yielding a VTE incidence of 6.3%. There was no significant difference in the incidence of VTE between INR quartiles. Hospital mortality rates were higher in the higher INR quartiles than in the lower ones (P < .001), but hospital length of stay was not significantly different. Of the patients with documented VTE, one (4.2%) was Child-Pugh stage A, three (4.6%) were stage B, and eight (8.0%) were stage C (P = .602). VTE prophylaxis was not used in 75% of patients. CONCLUSIONS: An elevated INR in the setting of CLD does not appear to protect against the development of hospital-acquired VTE. The notion that "auto-anticoagulation" protects against VTE is unfounded. Use of DVT prophylaxis was extremely low in this population.