The kidneys normally receive an abundant blood supply of about 1100 ml/min, or about 20 to 25 percent of the cardiac output. The main purpose of this high blood flow to the kidneys is to provide enough plasma for the high rates of glomerular filtration needed for effective regulation of body fluid volumes and solute concentrations. Therefore, decreased renal blood flow is usually accompanied by decreased GFR and decreased urine output of water and solutes. Consequently, conditions that acutely diminish blood flow to the kidneys usually cause oliguria, which refers to diminished urine output below the level of intake of water and solutes. This condition causes accumulation of water and solutes in the body fluids. If renal blood flow is markedly reduced, total cessation of urine output can occur, a condition referred to as anuria.

As long as renal blood flow does not fall below about 20 to 25 percent of normal, AKI can usually be reversed if the cause of the ischemia is corrected before damage to the renal cells has occurred. Unlike some tissues, the kidney can endure a relatively large reduction in blood flow before actual damage to the renal cells occurs. The reason for this phenomenon is that as renal blood flow is reduced, the GFR and the amount of sodium chloride filtered by the glomeruli (as well as the filtration rate of water and other electrolytes) are reduced. This decreases the amount of sodium chloride that must be reabsorbed by the tubules, which use most of the energy and oxygen consumed by the normal kidney. Therefore, as renal blood flow and GFR fall, the requirement for renal oxygen consumption is also reduced. As the GFR approaches zero, oxygen consumption of the kidney approaches the rate that is required to keep the renal tubular cells alive even when they are not reabsorbing sodium. When blood flow is reduced below this basal requirement, which is usually less than 20 to 25 percent of the normal renal blood flow, the renal cells become hypoxic, and further decreases in renal blood flow, if prolonged, will cause damage or even death of the renal cells, especially the tubular epithelial cells.

If the cause of prerenal AKI is not corrected and ischemia of the kidney persists longer than a few hours, this type of renal failure can evolve into intrarenal AKI, as discussed later. Acute reduction of renal blood flow is a common cause of AKI in hospitalized patients, especially those who have sustained severe injuries. Table 1 shows some of the common causes of decreased renal blood flow and prerenal AKI.

Table1. Some Causes of Prerenal Acute  Kidney Injury

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مواضيع ذات صلة

Vicious Cycle of Chronic Kidney Disease Leading to End-Stage Renal Disease

Intrarenal Acute Kidney Injury Caused by Abnormalities Within the Kidney

kidney Diseases

Diuretics and Their Mechanisms of Action

Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume

Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume

Integrated Responses to Changes in Sodium Intake

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion

Role of Aldosterone in Controlling Renal Excretion

Role of Ang II in Controlling Renal Excretion

Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes

Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance