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    Metabolic alkalosis is a widespread acid-base disturbance, especially in hospitalized patients. It is characterized by the primary elevation of serum bicarbonate and arterial pH, along with a compensatory increase in Pco2 consequent to adaptive hypoventilation. The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid. The loss of acid may be via the gastrointestinal tract or the kidney, whereas the sources of excess alkali may be via oral or parenteral alkali intake.

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    Cortical necrosis commonly manifests clinically as a rapid loss of glomerular filtration rate, often with oliguria, granular casts, and low-level proteinuria. Cortical necrosis may occur at any age. Causes include complications of vascular anastomosis in the transplanted kidney. In the native kidney, it occurs after thrombosis of interlobular or larger arteries, massive cholesterol emboli, septic abortion, or other catastrophic obstetrical complications (including eclampsia), and in the neonate, it occurs as complications of sepsis and placental hemorrhage.

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    Eric Ryan, MD Eric Ryan recently completed fellowship and is joining the nephrology faculty at Oregon Health and Science University. He has an early career interest in medical education, critical c…

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    • #AJKDBlog Commentary by Eric Ryan, Vanderlene Liu Kung, and @r_avasare: Challenging the Concept of “Benign” Microscopic Hematuria: How Far Do We Go? https://t.co/KNAujECOuo @OHSUNephrology Article by Yoo Jin Um et al: https://t.co/60FxR55vuf https://t.co/cTiCLxy6XU