Complex Autonomic Dysfunction and IgA Nephropathy Following Chlamydia Infection: A Diagnostic Challenge
Rhea Verma1, Gurleen Kaur2, Andrea Synowiec2
1Drexel University College of Medicine, 2Allegheny Health Network
Background:
Autonomic dysfunction arises from dysregulation of the autonomic nervous system, which governs vital functions like cardiovascular stability, gastrointestinal motility, and thermoregulation. Symptoms include orthostatic hypotension, gastroparesis, and cardiac arrhythmias. Conditions like Guillain-Barré syndrome (GBS) and autoimmune small fiber neuropathy are known causes, with autonomic involvement in up to 65% of GBS cases.
Results:
A previously healthy 25-year-old male presented with hematuria and urinary issues, diagnosed with Chlamydia trachomatis and treated with antibiotics. Three weeks later, he developed a burning foot sensation, orthostatic hypotension, gastroparesis, urinary retention, and constipation. Orthostatic vitals showed a systolic blood pressure drop from 134 mmHg supine to 74 mmHg standing. Cranial nerves, motor, and sensory exams were intact, with reflexes 2+ throughout. Imaging of the neuro-axis was normal. Heavy metal screen, porphyria, and dysautonomia workup were negative for AChR, ANNA-1, CRMP-5-IgG, CASPR2-IgG, and LGI1-IgG antibodies. Electromyography (EMG) showed a low amplitude motor response in the peroneal nerve without demyelinating polyneuropathy. Lumbar puncture revealed elevated protein (62 mg/dL) without pleocytosis. Renal biopsy, performed due to abnormal 24-hour urine protein collection, confirmed IgA nephropathy. The patient was treated with IVIG and high-dose steroids, leading to mild symptom improvement.
Conclusions:
This case highlights the complexities of diagnosing autonomic dysfunction. Autonomic GBS was considered, but due to lack of areflexia and normal EMG findings, Acute Sensory and Autonomic Neuronopathy (ASANN) was more likely. ASANN features acute sensory loss and autonomic dysfunction, affecting urinary, cardiovascular, and gastrointestinal systems. ASANN is rarely reported, with limited cases since its 1980 description. Although immunomodulatory therapies can slow progression, treatment response is limited.
In this patient, co-occurrence of IgA nephropathy and ASANN was likely the result of post-infectious immune dysregulation. Although there are no previous reports of co-occurrence of the two auto-immune disorders, Chlamydia Trachomatis is known to cause autoimmunity via molecular mimicry mechanisms.
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