Acute cardiorenal syndrome is a common complication of acute cardiovascular disease. Studies of acute kidney injury (AKI) to chronic kidney disease (CKD) transition, including patients suffering acute cardiovascular disease, report high rates of CKD development. Therefore, acute cardiorenal syndrome associates with CKD, but no study has established causation. To define this we used a murine cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) model or sham procedure on male mice. CA was induced with potassium chloride while CPR consisted of chest compressions and epinephrine eight minutes later. Two weeks after AKI was induced by CA/CPR, the measured glomerular filtration rate (GFR) was not different from sham. However, after seven weeks the mice developed CKD, recapitulating clinical observations. One day, and one, two, and seven weeks after CA/CPR, the GFR was measured, and renal tissue sections were evaluated for various indices of injury and inflammation. One day after CA/CPR, acute cardiorenal syndrome was indicated by a significant reduction of the mean GFR (649 in sham, vs. 25 mL/min/ 100g in CA/CPR animals), KIM-1 positive tubules, and acute tubular necrosis. Renal inflammation developed, with F4/80 positive and CD3-positive cells infiltrating the kidney one day and one week after CA/CPR, respectively. Although there was functional recovery with normalization of GFR two weeks after CA/CPR, deposition of tubulointerstitial matrix proteins a-smooth muscle actin and fibrillin-1 progressed, along with a significantly reduced mean GFR (623 in sham vs. 409 mL/min/100g in CA/CPR animals), proteinuria, increased tissue transforming growth factor-b, and fibrosis establishing the development of CKD seven weeks after CA/CPR. Thus, murine CA/CPR, a model of acute cardiorenal syndrome, causes an AKI-CKD transition likely due to prolonged renal inflammation.
First-year osteopathic students may have comparable amounts of research experience as allopathic medical students. Although these findings are limited to 2 campuses of 1 osteopathic medical school, they suggest that first-year osteopathic medical students are highly motivated to participate in research while in medical school.
Spondyloarthritis presents in various and occasionally unusual ways that imitates other diseases. Without forthcoming risk factors, such atypical presentation may elude diagnosis for months. The case presented here of a child, aged 4 years, who is negative for human leukocyte antigen B27 (HLA-B27) and with no family history of HLA-B27 related disease, who developed torticollis with neck pain and lymphadenopathy, highlights the necessity of continually evaluating a diagnosis, especially when treatment fails to produce expected results. Painful torticollis in a child with adenopathy often is infectious in nature or potentially due to Griesel syndrome when persistent. Chronic arthritis of the cervical spine may enter the differential diagnosis when torticollis is persistent, and early recognition and aggressive treatment is necessary to prevent permanent functional impairment.
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