A 67-year-old woman is hospitalized due to worsening abdominal pain. The patient has long-standing end-stage renal disease from diabetic nephropathy for which she undergoes hemodialysis 3 times a week. Temperature is 37 C (98.6 F), blood pressure is 159/79 mm Hg, pulse is 97/min, and respirations are 16/min. Abdominal examination shows high-pitched bowel sounds and mild distension without rebound tenderness. Laboratory results show elevated blood urea nitrogen and creatinine. Noncontrast CT scan of the abdomen shows a small bowel obstruction. The patient also has the findings demonstrated by the arrows in the abdominal CT scan below: Which of the following most likely contributed to the observed findings?

Question

A 67-year-old woman is hospitalized due to worsening abdominal pain.  The patient has long-standing end-stage renal disease from diabetic nephropathy for which she undergoes hemodialysis 3 times a week.  Temperature is 37 C (98.6 F), blood pressure is 159/79 mm Hg, pulse is 97/min, and respirations are 16/min.  Abdominal examination shows high-pitched bowel sounds and mild distension without rebound tenderness.  Laboratory results show elevated blood urea nitrogen and creatinine.  Noncontrast CT scan of the abdomen shows a small bowel obstruction.  The patient also has the findings demonstrated by the arrows in the abdominal CT scan below:  Which of the following most likely contributed to the observed findings?

Quizplus · Accepted Answer

This patient with end-stage renal disease (due to diabetic nephropathy) and worsening abdominal pain (due to small bowel obstruction) has extensive vascular calcifications (VCs) noted on abdominal CT scan. Under normal conditions, calcification inhibitors expressed by smooth muscle cells prevent the formation of calcifications. VCs occur when metabolic insults (eg, electrolyte abnormalities, dyslipidemia, oxidative stress, uremia) cause smooth muscle cells in the arterial media to differentiate into osteoblast-like cells (ie, osteogenic differentiation), resulting in active deposition of calcium salts within the vessels. Excessive VCs occur frequently in patients with chronic kidney disease, especially those on dialysis, because they are predisposed to developing these calcifications through the following mechanisms: Electrolyte abnormalities: Hyperphosphatemia (decreased filtration and excretion of phosphorus) and/or hypercalcemia (typically iatrogenic due to the administration of calcium products as phosphate binders) promote calcification by stimulating osteogenic differentiation (Choices C and D). Chronic inflammation: Inflammation, due to uremia and/or hyperlipidemia, suppresses the expression of calcification inhibitors in smooth muscle cells and damages vascular endothelial cells, providing a nidus for calcification. In addition, mineralization is proinflammatory and reinforces the cycle of inflammation within vessel walls. Atherosclerosis: In addition to its proinflammatory effects, lipid deposition in the vessel wall results in the formation of atherosclerotic lesions that can also become calcified and contribute to the calcific burden. VCs are thought to contribute to increased cardiovascular risk and mortality but are often an incidental finding. (Choice A) Magnesium inhibits extraosseous calcification, putting those with hypomagnesemia at increased risk for VCs. Hypermagnesemia would have a protective effect, making VCs less likely. (Choice E) Diabetes mellitus is associated with a significantly increased risk for atherosclerosis and subsequent atherosclerotic calcification. However, hypoglycemia does not increase the risk for VCs. Educational objective: Vascular calcifications occur more commonly in patients with chronic kidney disease due to electrolyte abnormalities (eg, hyperphosphatemia, hypercalcemia) and chronic inflammation (secondary to atherosclerosis and/or uremia). These changes promote calcification and suppress calcification inhibitors, which can result in extensive vascular calcifications. __________ References: Vascular calcification: from pathophysiology to biomarkers. (http://www.ncbi.nlm.nih.gov/pubmed/25236333)

A 67-Year-Old Woman Is Hospitalized Due to Worsening Abdominal Pain