Article:
Beyond the cholinergic crisis: non-oliguric acute kidney injury in organophosphate poisoning

creativeworkseries.issnOnline ISSN: 2676-1424; Print ISSN: 2676-1319
dc.contributor.authorShah, Laliteshwar
dc.contributor.authorDahal, Rashmi
dc.contributor.authorDahal, Sagar
dc.contributor.authorShrestha, Suman
dc.contributor.authorKarki, Kamala
dc.contributor.authorAcharya, Sulav
dc.creator.affiliationDepartment of Critical Care Unit, Nepal Medical College and Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu https://orcid.org/0009-0003-4442-6898
dc.creator.affiliationDepartment of Internal Medicine, Nepal Medical College Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu
dc.creator.affiliationDepartment of Critical Care Unit, Nepal Medical College and Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu
dc.creator.affiliationDepartment of Critical Care Unit, Nepal Medical College and Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu
dc.creator.affiliationDepartment of Critical Care Unit, Nepal Medical College and Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu
dc.creator.affiliationDepartment of Critical Care Unit, Nepal Medical College and Teaching Hospital, Attarkhel, Gokarneshwor-8, Kathmandu
dc.date.accessioned2026-09-30T07:32:13Z
dc.date.available2026-09-30T07:32:13Z
dc.date.issued2026
dc.description.abstractAbstract: Organophosphate (OP) poisoning is a common toxicological emergency, primarily presenting with cholinergic manifestations. Acute kidney injury (AKI) is an uncommon but clinically important complication of OP poisoning, usually attributed to secondary factors such as hypotension, dehydration, rhabdomyolysis, or sepsis. However, intrinsic renal injury may occur even in the absence of these classical risk factors. We report a case of a 24-year-old male who developed non-oliguric acute kidney injury following intentional ingestion of an organophosphate compound containing chlorpyrifos 50.0% and cypermethrin 5.0%. The patient presented with features of cholinergic excess and markedly reduced plasma cholinesterase levels. He remained hemodynamically stable during hospitalization without persistent hypotension or need for renal replacement therapy. Laboratory investigations showed a transient rise in serum creatinine, peaking on the second day and returning to baseline with supportive management. Serum creatine kinase levels were normal, and urine output was preserved throughout the hospital stay. This case suggests the possibility of intrinsic tubular injury as a mechanism of AKI in organophosphate poisoning. Routine monitoring of renal function may help in early detection of renal involvement even in clinically stable patients. Awareness of non-oliguric AKI as a potential complication of organophosphate toxicity is important for timely supportive management.
dc.identifier.doihttps://doi.org/10.3126/nmcj.v28i1.92189
dc.identifier.urihttps://hdl.handle.net/20.500.14572/7933
dc.language.isoen_US
dc.publisherNepal Medical College Pvt. Ltd.
dc.subjectAcute kidney injury
dc.subjectCholinesterase inhibition
dc.subjectNon-oliguric AKI
dc.subjectOrganophosphate poisoning
dc.subjectTubular toxicity
dc.titleBeyond the cholinergic crisis: non-oliguric acute kidney injury in organophosphate poisoning
dc.typeArticle
dspace.entity.typePublication
local.article.typeCase Report
oaire.citation.endPage85
oaire.citation.startPage81
relation.isJournalIssueOfPublication251426f6-5314-4bf5-a4df-69ddabdb49fc
relation.isJournalIssueOfPublication.latestForDiscovery251426f6-5314-4bf5-a4df-69ddabdb49fc
relation.isJournalOfPublication865934c8-5e95-468c-8ca6-7bb2529e4064

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