Core principles of renal physiology and pathophysiology in critical illness

The kidney is responsible for regulating several key physiologic functions in critically ill patients, including solute and water balance, acid-base homeostasis, and local and systemic hemodynamics. Each kidney contains approximately 1 million functional units called nephrons. Within the nephron, blood is filtered across a capillary structure called the glomerulus. Specialized cells form tubules that control the reabsorption and secretion of solutes and water from the glomerular filtrate. The rate of glomerular filtration is determined by a combination of renal blood flow and the relative hydrostatic and oncotic pressures in the glomerular capillaries and in the region between the glomerulus and tubules (Bowman space). Critical illness may disrupt the autoregulatory mechanisms that control renal blood flow or the various functions of the tubular cells. The kidney is highly susceptible to such alterations in glomerular perfusion and tubular function, which manifest as an abrupt reduction in glomerular filtration rate, or “acute kidney injury.” Acute kidney injury is common in the intensive care setting and may be accompanied by life-threatening disturbances in electrolyte concentrations, extracellular volume, or acid-base status. Although the pathophysiology of acute kidney injury is incompletely understood, it manifests as structural and/or functional damage to tubular epithelial cells, vascular endothelial cells, and cellular metabolism. Recovery is variable and dependent on patient- and disease-related factors. Maladaptive repair processes promote persistent inflammation and fibrosis that may culminate in the development of acute and chronic kidney diseases.