Heterotopic mesenteric ossification (HMO) is abnormal bone formation in tissues which usually do not undergo ossification. There are approximately 75 cases reported worldwide. We present two cases of HMO. The first case is that of a 39-year-old man who presented with abdominal pain and a computerized tomography scan of the abdomen and pelvis revealed an apple core lesion resulting in small bowel obstruction. The second case is that of a 36-year-old woman who presented 2 months after undergoing robotic gastric sleeve resection complaining of weakness and emesis. An esophagogram revealed kinking at the distal esophagus. Surgical resection was performed in both, yielding the diagnosis of HMO. There are various theories as to the pathophysiology of HMO, but no clearly defined mechanism has been established. Management should be conservative whenever possible to prevent further ossification with subsequent surgical intervention.
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Background Acute kidney injury (AKI) is a common cause of morbidity and mortality. It mainly targets the renal tubular epithelium with pathological changes, referred to as acute tubular injury. The latter is followed by a regenerative response that is difficult to visualize on routine hematoxylin and eosin (H&E) stains. In this study, we examined the regenerative capacity of renal tubules by correlating vimentin (VIM) immunohistochemical (IHC) expression and pathological findings of AKI and renal tubular regeneration (RTR) on H&E.
Methods We reviewed 23 autopsies performed in the clinical setting of AKI and RTR. VIM expression was scored in the renal cortical tubular epithelium using a statistical cutoff ≥ 3% for high expression and < 3% for low expression.
Results Of the 23 kidney tissues examined, seven (30.4%) had low VIM expression, and 16 (69.6%) had high VIM expression. Kidney tissues with evidence of AKI and RTR had significantly higher VIM expression. Renal peritubular microenvironment features showing regenerative changes on H&E were associated with high VIM expression. In the univariate model, kidney tissues with RTR were 18-fold more likely to have high VIM expression.
Conclusions In conclusion, our findings suggest that VIM could serve as an IHC marker for RTR following AKI. However, correlation with H&E findings remains critical to excluding chronic tubular damage. Collectively, our preliminary results pave the way for future studies including a larger sample size to validate the use of VIM as a reliable biomarker for RTR.
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Morin attenuates sepsis-induced acute kidney injury by regulating inflammatory responses, oxidative stress and tubular regeneration (morin and sepsis-induced acute kidney injury) Aya M. Shehata, Nagui H. Fares, Basma H. Amin, Asmaa A. Mahmoud, Yomna I. Mahmoud Environmental Toxicology and Pharmacology.2024; 111: 104543. CrossRef