RESUMO
Uremic neuropathy (UN) is a sensorimotor polyneuropathy typically affecting the lower extremities due to length-dependent demyelination and axonal degeneration. Hemodialysis (HD) and peritoneal dialysis (PD) are the two widely used modalities for treating end-stage renal disease (ESRD) patients. Today, with the understanding of solute and water kinetics, PD is considered equivalent to in-center HD. Chronic inflammatory demyelinating polyneuropathy (CIDP) manifests as symmetric, motor-predominant neuropathy that results in both proximal and distal muscle weakness. It is treatable with immune modulatory therapies. Here, we present a series of three patients who developed CIDP following the initiation of PD. Patient A: 39-year-old male with ESRD secondary to renal dysplasia presented with new onset neuropathy four months after starting PD. Patient B: 30-year-old male with ESRD secondary to IgA nephropathy presented with a history of numbness in his feet gradually progressing to his legs 12 months after initiating PD. Patient C: 56-year-old female with ESRD and uncontrolled diabetes mellitus presented with progressive muscle weakness four months after initiating PD. These three patients were all on continuous cycling PD. They were followed at three different dialysis units and were initiated on CCPD at different times. All of these patients were found to have CIDP on electromyography. Patients A and B were treated with IV immunoglobulin (IVIG) and improved, while patient C received plasmapheresis and improved. It has been recognized that PD solution is not physiological and may lead to activation of the host immune system triggering an autoimmune demyelinating process. Immunologic pathogenesis is not clearly understood. Macrophage activation and cytokines may play a role in the demyelination process. With the recent initiative to increase the use of PD, more studies are warranted to understand this uncommon complication.
RESUMO
Pericardial disease is a rare complication after renal transplantation. We present a patient who developed high-output cardiac failure from a large arteriovenous (AV) fistula with recurrent pericardial effusion resulting in a constrictive hemodynamic pattern that was revealed during cardiac catheterization. Pericardiectomy was considered for recurrent effusive pericarditis, but per cardiac surgery recommendations, closure of the AV fistula dramatically cured the patient's heart failure, and no recurrence of pericardial effusion was seen during follow-up almost a year later.
Assuntos
Fístula , Insuficiência Cardíaca , Transplante de Rim , Derrame Pericárdico , Pericardite Constritiva , Fístula/complicações , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/etiologia , Humanos , Transplante de Rim/efeitos adversos , Derrame Pericárdico/diagnóstico , Derrame Pericárdico/etiologia , Pericardite Constritiva/diagnóstico , Pericardite Constritiva/etiologia , Pericardite Constritiva/cirurgiaRESUMO
Gout is a common inflammatory arthritis that has a high prevalence worldwide. It is characterized by monosodium urate deposition, usually affecting the joints and soft tissue of the lower extremities. Urate deposition in the axial skeleton resulting in spinal gout is rare. However, it seems to be more prevalent than usually thought, largely because it is underdiagnosed. Imaging findings are, for the most part, nonspecific and often mimic infectious etiologies. Definitive diagnosis requires pathological examination. Thus, it can be easily missed. We present a 41-year-old male with a seven-year history of untreated gout who came in with severe back pain, fevers, and radiculopathy. He was initially diagnosed with vertebral osteomyelitis. However, after a biopsy, spinal gout was confirmed. Spinal gout can be misdiagnosed as vertebral osteomyelitis given the similarities in presentation and imaging findings. This case report highlights the importance of keeping spinal gout as a differential of vertebral osteomyelitis, especially in patients with long-standing or uncontrolled gout with tophi.