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Increased cerebrospinal fluid pressure and nephrotic syndrome: A case report and literature review
To analyze how nephrotic syndrome (NS) correlates to increased intracranial pressure (ICP), and to present a case of an adult patient whose initial manifestation of NS was cephalalgia, with the later identification of raised ICP. Data were retrospectively retrieved from the patient’s record, and a l...
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Published in: | Clinical neurology and neurosurgery 2023-02, Vol.225, p.107567-107567, Article 107567 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | To analyze how nephrotic syndrome (NS) correlates to increased intracranial pressure (ICP), and to present a case of an adult patient whose initial manifestation of NS was cephalalgia, with the later identification of raised ICP.
Data were retrospectively retrieved from the patient’s record, and a literature search with the keywords “nephrotic syndrome”, “intracranial hypertension” and “headache” was conducted in PubMed and Embase.
This is a rare description of co-occurrence of NS and raised ICP in a 48-year-old man, in which ICP normalizes after NS remits. There is no known cause for the raised ICP of our patient. Ten reports (n = 13) of concomitant occurrence of increased ICP and NS were described in the literature, both in children and adults. Cerebral venous thrombosis (CVT) was the most likely underlying cause for the majority of them. For one patient, the underlying cause was meningoencephalitis. Finally, in one case, the cause is unknown, but CVT was not discarded.
The early suspicion of elevated ICP is warranted in patients with new-onset headache and NS. It is possible that NS could both directly and indirectly lead to increased ICP through yet unknown mechanisms, although this direct causal relationship cannot be currently established.
•The early suspicion of elevated ICP is warranted in patients with new-onset headache and NS.•It is possible that NS could both directly and indirectly lead to increased ICP through yet unknown mechanisms.•However, this direct causal relationship cannot be currently established.•We could hypothesize that the hyperaldosteronism originated from the RAAS system led to the increased ICP of our patient.•Notwithstanding, it would be too speculative to try to disseminate any possible pathophysiological connections at this moment. |
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ISSN: | 0303-8467 1872-6968 |
DOI: | 10.1016/j.clineuro.2022.107567 |