Chronic kidney disease (CKD) is a progressive disease that affects millions of adults every year. Major risk factors include diabetes, hypertension, and obesity, which affect millions of adults worldwide. CKD is characterized by cellular injury followed by permanent loss of functional nephrons. As injured cells die and nephrons become sclerotic, remaining healthy nephrons attempt to compensate by undergoing various structural, molecular, and functional changes. While these changes are designed to maintain appropriate renal function, they may lead to additional cellular injury and progression of disease. As CKD progresses and filtration decreases, the ability to eliminate metabolic wastes and environmental toxicants declines. The inability to eliminate environmental toxicants such as arsenic, cadmium, and mercury may contribute to cellular injury and enhance the progression of CKD. The present review describes major molecular alterations that contribute to the pathogenesis of CKD and the effects of arsenic, cadmium, and mercury on the progression of CKD.

Background: Every year, more than 795,000 people in the United States have a stroke, and each year about 140,000 Americans die from strokes. Although there is abundant information on the epidemiology, risk factors, pathophysiology, and many clinical features of strokes, there is a lack of specific numerical quantitation on the neuroanatomical distribution of strokes.

Acinetobacter baumannii has emerged as a pan-resistant superbug causing fatal infections in vulnerable patients. This report is the case of an immunosuppressed transplant patient with a fatal pneumonia due to pan-resistant Acinetobacter baumannii. Alternative therapy for resistant Acinetobacter infection is currently the subject of intense interest and research. This report illustrates the features of this type of emerging infectious disease and reviews some of the novel approaches to treatment.

Autops Case Rep, vol.11, e2021311, 2021

In a rural mountainous region on a Friday, a 78-year-old man was seen in his physician’s office for leg edema and diagnosed with new onset atrial fibrillation. He was discharged home to start medications for atrial fibrillation and heart failure. He was hospitalized the next day with septic shock due to pneumococcal pneumonia. The new onset of atrial fibrillation requires a trigger acting on a vulnerable substrate. These triggers include acute conditions such as alcohol intoxication, myocardial infarction and pulmonary embolism. Pneumonia may act as a trigger causing the new onset of atrial fibrillation.