Abstract
Urine output often is used as a marker of acute kidney injury but also to guide fluid resuscitation in critically ill patients. Although decrease of urine output may be associated to a decrease of glomerular filtration rate due to decrease of renal blood flow or renal perfusion pressure, neurohormonal factors and functional changes may influence diuresis and natriuresis in critically ill patients. The purpose of this review is to discuss the mechanisms of diuresis regulation, which may help to interpret the urine output in critically ill patients and the appropriate treatment to be initiated in case of changes in urine output.
Highlights
Acute renal failure or acute kidney injury (AKI) is defined by an acute decline of glomerular filtration rate (GFR)
The decrease of glomerular filtration rate and urine output in response to a decrease of renal blood flow is classically referred as pre-renal azotemia, which can evolve into structural damage if renal hypoperfusion persists
Urine output often is used as a marker of AKI and to guide fluid resuscitation in critically ill patients
Summary
Acute renal failure or acute kidney injury (AKI) is defined by an acute decline of glomerular filtration rate (GFR). Infusion of norepinephrine in septic patients titrated to increase MAP from 65 to 75 mmHg was associated with a decrease of renal Doppler resistive index, suggesting an increase in renal vascular conductance [42], confirming the experimental data These results are in accordance with physiological animals studies that showed that norepinephrine and vasopressin can induce, in septic states, an increase of renal blood flow through a combined increase of renal perfusion pressure (i.e., prerenal mechanism) and an increase of renal vascular conductance (i.e., intrarenal mechanism) [38,43]. In other words, increasing renal perfusion pressure can increase urine output and natriuresis independently of changes in total renal blood flow and GFR These discrepancies could, in part, be due to the effect of neurohormonal regulation of vascular tone between the afferent and efferent glomerular arterioles (Figure 2). Because the descending vasa recta provide blood flow to the medulla emerge from efferent arterioles of juxtamedullary glomerules, these data suggest that changes in resistance in the GFR regulation
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