Acute Kidney Injury following Cardiac Surgery

Acute Kidney Injury following Cardiac Surgery

Bryan Romito (University of Texas Southwestern Medical Center, USA) and Joseph Meltzer (David Geffen School of Medicine at UCLA, USA)
Copyright: © 2015 |Pages: 30
DOI: 10.4018/978-1-4666-8603-8.ch017
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Abstract

The primary goal of this chapter is to provide the reader with an overview of basic renal physiology and function and to review the identification, pathogenesis, and treatment of acute kidney injury following cardiac surgery. Particular focus will be directed toward the diagnostic criteria for acute kidney injury, short- and long-term impacts on patient outcomes, role of novel biomarkers, mechanisms of acute renal injury, general management principles, preventative strategies, and the influence of anesthetic and surgical techniques on its development. The content of this chapter will serve to underscore a particularly harmful but likely underappreciated problem affecting patients in the cardiothoracic critical care setting.
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Renal Anatomy And Physiology

The Nephron

The kidney has a number of important physiologic functions including balancing electrolytes to maintain cardiovascular stability and prevention of dysrhythmias; preserving volume status through the regulation of salt and water; maintaining pH by regulating acid-base status for the appropriate functioning of medications, enzymes, and cells; eliminating drug metabolites and toxins; and production of renin, erythropoietin, and calcitriol.

The nephron is the functional unit of the kidney, and each kidney contains approximately 1 million nephrons. The proximal end of the nephron consists of Bowman’s capsule surrounding a glomerulus, a network of capillaries supplied by an afferent arteriole and drained by an efferent arteriole. Collectively, this unit is known as the renal corpuscle. The basement membranes of the glomerular endothelial cells form a filter that prevents charged molecules, large proteins, and cells from entering the nephron while allowing ions, amino acids, and water to freely pass. Fluid is initially absorbed from the glomerulus into Bowman’s capsule and then subsequently flows through the proximal tubule, loop of Henle, distal tubule, and finally to the collecting duct (see Figure 1). In the proximal tubule, as sodium and water are reabsorbed, organic anions and cations are secreted. Other molecules and ions transported here include glucose, proteins, amino acids, bicarbonate, chloride, potassium, magnesium, calcium, and lactate. Next fluid travels to the loop of Henle where it becomes concentrated, creating a gradient that allows for additional fluid reabsorption via osmosis further down the nephron. Also in the loop of Henle, sodium, chloride, potassium, calcium, and magnesium are reabsorbed. The initial segment of the distal tubule, called the macula densa, functions primarily to monitor the chloride concentration of the passing fluid. Based on this concentration, the macula densa alters afferent arteriolar tone and renin release to regulate changes in the glomerular filtration rate (GFR). The distal tubule also reabsorbs and secretes electrolytes and regulates acid-base status by adjusting the fluid’s hydrogen ion and bicarbonate concentration. Finally as the fluid enters the collecting duct, the concentration gradient created by the loop of Henle allows for further water reabsorption and the formation of hypertonic urine (Loutzenhiser, Griffin, Williamson, & Bidani, 2006).

Figure 1.

Structure of the nephron.

Adapted with permission from: Melican, K., Sandoval, R. M., Kader, A., Josefsson, L., Tanner, G. A., Molitoris, B. A., & Richter-Dahlfors, A. (2011). Uropathogenic Escherichia coli P and Type 1 Fimbriae Act in Synergy in a Living Host to Facilitate Renal Colonization Leading to Nephron Obstruction. PLoS Pathogens, 7(2), e1001298.

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