RESUMO
A 77-year-old man presented with fever and back pain. Computed tomography revealed a distal arch aneurysm. Bacteroides fragilis was found in a blood culture, and we diagnosed a thoracic infected aneurysm. Because of the rapid enlargement of the aneurysm and his frailty, a TEVAR procedure was urgently performed. He left the hospital after antibiotic treatment with meropenem. However, he was re-hospitalized due to recurrence of the infection. The infection was well-controlled by treatment with intravenous meropenem, and the subsequent oral administration of metronidazole (MNZ). He was re-hospitalized again 7 weeks after discharge due to unsteady gait and articulatory disorder. MNZ-induced encephalopathy (MIE) was diagnosed because FLAIR brain magnetic resonance imaging revealed an area of high signal intensity in the bilateral basal dentate nuclei. These symptoms improved after MNZ was changed to AMPC/CVA. Fifteen months later, the patient was doing well and had no recurrence of the infection. We performed TEVAR for a patient with a thoracic aneurysm infected by B. fragilis. The recurrence of the infection was controlled by adequate antibiotic therapy, which included the administration of MNZ. However, patients who are treated with MNZ should be carefully observed to detect the development of neurological signs, as MNZ may induce encephalopathy. The early detection and withdrawal of metronidazole is important for the improvement of MIE.
RESUMO
Although the pathogenesis of idiopathic focal segmental glomerulosclerosis (FSGS) may be heterogeneous, autosomal dominant and recessive forms of FSGS are recognized. Recently, mutations in alpha-actinin 4 (ACTN4) and podocin genes were reported in patients with such familial FSGS. However, whether mutations in ACTN4 and podocin genes are associated with sporadic FSGS has not been determined. In the present study, we clarified the relation between mutations in ACTN4 and podocin genes and sporadic FSGS. We analyzed these reported mutations in ACTN4 and podocin in five patients with chronic renal failure due to therapy-resistant FSGS by direct sequencing of polymerase chain reaction products of ACTN4 and podocin. We found a C to T transition at nucleotide 465 in the ACTN4 gene in all of patients, and a T to C transition at nucleotide 954 in exon eight of podocin gene in two of five patients, resulting in no amino acid substitutions. Other mutations were not found in ACTN4 and podocin genes. Our findings suggest that sporadic FSGS is a heterogeneous disease, since ACTN4 and podocin genes are not found in our patients with sporadic FSGS.
