This report describes a rare central nervous system complication in a patient with anti-glomerular basement membrane (anti-GBM) disease. A 53-year-old woman presented with fever and headache and rapidly developed acute kidney injury with markedly elevated anti-GBM antibody titers. Renal biopsy confirmed the diagnosis. Despite conventional therapy, renal function deteriorated and the patient required dialysis. During the hospital course she experienced a generalized seizure and was found to have an intracranial subarachnoid hemorrhage (SAH) that was later complicated by a subacute cerebral infarction. Intensive multidisciplinary treatment was continued, antibody titers declined, and the patient did not sustain persistent neurological deficits, although renal function did not recover.
The patient initially presented with systemic symptoms of fever and headache. Laboratory evaluation demonstrated acute kidney injury and markedly elevated circulating anti-GBM antibodies. A renal biopsy provided histopathological confirmation of anti-GBM disease. The clinical picture was consistent with rapidly progressive glomerulonephritis associated with anti-GBM autoantibodies.
Renal biopsy findings confirmed anti-GBM disease; the abstract does not provide detailed histological descriptions beyond confirmation. Serologically, anti-GBM antibody titers were described as markedly elevated at presentation. Despite immunomodulatory efforts, renal function continued to decline, culminating in dialysis dependence.
Initial therapy included therapeutic plasma exchange and high-dose corticosteroids, which represent standard initial management approaches for anti-GBM disease aimed at removing circulating autoantibody and suppressing inflammation. The patient’s renal function nevertheless deteriorated, and she became dialysis-dependent. Because the response to conventional therapy was insufficient to control serology, rituximab was added to the treatment regimen to achieve serological control.
During the clinical course the patient developed a generalized seizure. Subsequent evaluation led to the diagnosis of intracranial subarachnoid hemorrhage (SAH). Later in the hospitalization a subacute cerebral infarction occurred. The sequence—seizure, SAH, then cerebral infarction—is described in the case, and represents an uncommon pattern of central nervous system involvement in anti-GBM disease.
Cerebral angiography was performed and revealed no aneurysms or vascular malformations to account for the SAH. The authors note that the patient’s blood pressure had remained stable prior to the neurological event, suggesting that hypertensive crisis was not an obvious precipitant. The abstract does not include specific imaging study names or detailed radiographic descriptions beyond the angiographic exclusion of aneurysm and vascular malformation.
Following the neurologic events, the treatment approach remained intensive and included continued plasma exchange, corticosteroids, and rituximab, together with strict blood pressure control. With these measures, the patient recovered without neurological sequelae. Anti-GBM antibody titers gradually declined after intensified therapy, but renal recovery did not occur and the patient remained dialysis-dependent.
Central nervous system involvement in anti-GBM disease is described as exceedingly uncommon in the abstract. Intracranial subarachnoid hemorrhage has rarely been reported in association with anti-GBM disease, making this case notable. The authors present the case alongside a literature review; however, the abstract does not give the detailed results or scope of that review. The case highlights the need for clinicians to monitor neurological status carefully in patients with anti-GBM disease, particularly when atypical neurological symptoms such as seizure or severe headache arise.
This case report documents a rare occurrence of intracranial SAH followed by cerebral infarction in a patient with serologically and histologically confirmed anti-GBM disease. Despite an initially poor renal trajectory leading to dialysis dependence, intensified immunomodulatory therapy including plasma exchange and rituximab led to a decline in antibody titers and an absence of persistent neurological deficits. The report underscores the rarity of CNS hemorrhagic complications in anti-GBM disease and the importance of prompt neurological assessment and aggressive multidisciplinary management when such complications occur.
Note: The abstract is the sole source for this summary. Detailed imaging descriptions, timelines, quantitative antibody titers, dosing regimens, and the literature review findings are not reported in the abstract and would require consultation of the full article and its references for additional specifics.