A female juvenile green turtle (Chelonia mydas), found alive in Guanabara Bay, Rio de Janeiro, Brazil, was weak, dehydrated and cachectic, with a healed fracture in the caudal portion of the carapace. Despite supportive treatment, the animal died after 9 days. At necropsy the main lesions were pallor of visceral organs, arthritis and deposits of whitish granular material in the wall of large arteries and the trachea. Histopathological analysis revealed mild to severe deposition of crystals, consistent with calcium oxalate, in both kidneys and the spleen, heart, small intestine, pancreas, thymus and salt gland, as well as bacterial meningitis, septic arthritis, spirorchidiasis and a fibropapilloma on the nictitating membrane. The main pathological findings were suggestive of septic shock, mainly due to the bacterial meningitis and septic arthritis, with systemic oxalosis and spirorchidiasis as contributing lesions. Although renal oxalosis has been described in green turtles as an incidental finding, presumably due to ingestion of oxalate-containing plants, this turtle had an unusual systemic deposition of oxalate crystals.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jcpa.2022.12.004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Unveiling primary Hyperoxaluria type 1: a fortuitous discovery through bone marrow biopsy.
Oxf Med Case Reports
October 2024
Pathology Department, Ibn Sina Hospital, Rabat, Morocco.
Article Synopsis
- A 46-year-old woman with chronic kidney issues and kidney stones was diagnosed with primary hyperoxaluria type 1 (PH1) through a bone marrow biopsy.
- Genetic testing revealed a specific mutation (p.Ile244Thr) in the AGXT gene, which is linked to the disorder.
- The paper emphasizes the need for early diagnosis of kidney stone issues, especially in families with a history of the condition, to avoid severe kidney damage and systemic complications.
Efficient and safe in vivo treatment of primary hyperoxaluria type 1 via LNP-CRISPR-Cas9-mediated glycolate oxidase disruption.
Mol Ther
January 2025
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai 200241, China; Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China; YolTech Therapeutics, Shanghai 201109, China. Electronic address:
Article Synopsis
- Primary hyperoxaluria type 1 (PH1) is a severe genetic disorder caused by AGXT gene mutations, leading to dangerous oxalate buildup, kidney damage, and renal failure.
- Current therapies like siRNA and CRISPR-Cas9 have limitations, including the need for repeated treatments and safety issues.
- The study introduces lipid nanoparticles (LNPs) for CRISPR-Cas9 delivery, effectively targeting the Hao1 gene, which decreased oxalate levels in mice with PH1, showing efficacy and long-lasting effects without significant side effects, indicating a safer treatment option for PH1.
Late-onset retinal oxalosis in primary hyperoxaluria type 2.
Am J Ophthalmol Case Rep
December 2024
Department of Ophthalmology and Visual Sciences, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA, 52242, USA.
Purpose: To report a previously undescribed case of late-onset vision loss due to retinal oxalosis in a patient with primary hyperoxaluria type 2 (PH2).
Observations: An 82-year-old female with a history of biopsy-proven oxalate nephropathy developed vision loss 8 months after end stage kidney disease. She developed progressive retinal ischemia secondary to crystal deposition.
Mutation Characteristics of Primary Hyperoxaluria in the Chinese Population and Current International Diagnosis and Treatment Status.
Kidney Dis (Basel)
August 2024
Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Background: Primary hyperoxaluria (PH) is a rare autosomal recessive disorder, mainly due to the increase in endogenous oxalate production, causing a series of clinical features such as kidney stones, nephrocalcinosis, progressive impairment of renal function, and systemic oxalosis. There are three common genetic causes of glycolate metabolism anomalies. Among them, PH type 1 is the most prevalent and severe type, and early end-stage renal failure often occurs.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!