Nephrotic syndrome associated with Guillain-Barré syndrome and Sjögren syndrome: a case report and literature review

Rationale: The coexistence of Guillain-Barré syndrome (GBS) and minimal change disease (MCD) is extremely rare. GBS is an autoimmune-mediated peripheral neuropathy that can occasionally be associated with renal complications such as nephrotic syndrome (NS). This case discusses a patient diagnosed with both GBS and MCD, as well as Sjögren syndrome kidney injury, focusing on the potential pathogenesis of these conditions and the role of autoantibodies in their development and treatment outcomes. Patient concerns: A young female patient presented with progressively worsening muscle weakness, sensory abnormalities, and edema. Further investigations revealed NS, characterized by proteinuria and hypoalbuminemia. While the neurological symptoms improved initially, the renal manifestations persisted, raising concerns about ongoing kidney damage. In addition, the patient was also found to have Sjögren syndrome kidney injury, along with positive perinuclear antineutrophil cytoplasmic antibody and antinuclear antibody, suggesting an autoimmune-mediated process contributing to the co-occurrence of these conditions. Diagnoses: GBS was diagnosed based on characteristic ascending paralysis and demyelination, as evidenced by nerve conduction studies. The diagnosis of MCD was supported by the patient's clinical presentation of NS and kidney biopsy findings. The presence of clinical features such as dry mouth and dry eyes, coupled with positive anti-SSA/Ro52 and anti-Sjögren syndrome antigen B antibodies, pointed to Sjögren syndrome. Kidney biopsy results strongly suggested that kidney damage was likely due to Sjögren syndrome. Interventions: The patient was started on immunosuppressive therapy, including prednisone and cyclophosphamide, to address both the autoimmune neuropathy and renal issues. In addition, intravenous immunoglobulin was administered to treat the GBS. Supportive therapies, such as diuretics and albumin infusions, were used to manage edema and protein loss associated with NS. Outcomes: The patient showed significant improvement in neurological symptoms, including enhanced muscle strength and reduced sensory deficits. Proteinuria decreased, and renal function gradually stabilized. Lessons: This case illustrates the rare coexistence of GBS, MCD, and Sjögren syndrome kidney injury in a single patient. Autoimmune markers played a pivotal role in the pathogenesis of these diseases. Immunosuppressive therapy and intravenous immunoglobulin were essential in treating both neurological and renal complications. Further research is needed to deepen our understanding of the overlap of autoimmune diseases and to optimize treatment strategies for such complex cases.