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Received Mar 23; Accepted May This article has been cited by other articles in PMC. 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. 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.
In this line, urine output often is used as a marker of AKI but also to guide fluid resuscitation in critically ill patients. However, both the contribution of renal hypoperfusion to AKI and the genuine definition of pre-renal and intra-renal azotemia have been challenged by several authors [ 3 - 5 ].
The recent international consensus conference on acute renal failure therefore recommended the term "acute kidney insufficiency" rather than "acute kidney injury" in the light of paucity of evidence of a relation between tissue damage and organ failure in human AKI [ 6 ]. The purpose of this review is to discuss the mechanism of diuresis regulation and the interpretation of urine output in critically ill patients in the light of clinical and physiological studies.
Why should we wonder about oliguria and AKI? There is accumulating evidence that critically ill patients developing AKI have an increase relative risk of death. Occurrence of AKI is a marker of severity of the underlying acute illness but also appears as an independent factor associated with mortality in unselected critically ill patients [ 7 ], in sepsis [ 8 ], pneumonia [ 9 ], or cardiac surgery [ 10 ].
The mechanistic pathways of such an association remain elusive, with intrication of inflammation, metabolism, and apoptotic phenomena. Remote organs damage has been suggested in several experimental studies [ 1112 ].
Ischemic-induced AKI has been found to induce myocardial apoptosis [ 13 ], to activate lung inflammatory and apoptotic pathways, and to increase lung water permeability [ 14 ]. Surprisingly, even a small increase of serum creatinine after cardiac surgery or transient i.
Although fluid resuscitation and optimization of renal perfusion pressure are central to the prevention and treatment of AKI, excessive fluid resuscitation may be harmful in some critically ill patients.
First, aggressive fluid resuscitation, although increasing renal blood flow, can be ineffective in restoring renal microvascular oxygenation due to hemodilution with no increase in blood-oxygen carriage capacities [ 18 ].
Second, positive fluid balance can deteriorate cell oxygenation and prolong mechanical ventilation [ 19 ]. Finally, fluid overload may lead to central venous congestion and decrease of renal perfusion pressure [ 20 ], which will promote the development of AKI in patients with acute heart failure [ 21 ] or sepsis [ 22 ].
The type of fluid used also can have a role with "renal toxicity" associated with the use of colloids. Urine output and definition of acute kidney injury In clinical research, more than 30 definitions of acute renal failure have been used before the release of the RIFLE criteria by the Acute Dialysis Quality Initiative group in [ 23 ].
The first merit of this classification was to introduce a standard and simple definition of AKI for clinical research purposes but also to stratify the severity of AKI based on serum creatinine level, creatinine clearance, or urine output.
A part from the change in nomenclature Risk, Injury, and Failure were replaced by stage 1, 2, and 3, the categories Loss and Endstage disappearedan absolute increase of serum creatinine of 0.
Finally, the AKIN criteria should be applied "after following adequate resuscitation when applicable" with the purpose of excluding patients with pure renal pre-azotemia.
The introduction of the RIFLE and AKIN definitions were a crucial step forward in the development of clinical research and have since been widely accepted by the medical community. Using these classifications, a patient with decrease of urine output will be classified as "AKI.
This would be the case if decreased urine output is not associated with a decline of creatinine clearance.
Although severe acute renal failure with oliguria or anuria has been reported to be associated with a worse outcome compared with patients with preserved urine output, the use of urine output as a criterion to classify AKI severity may be misleading. One can conclude that patients classified according to the urine output criterion only might be less severe than those classified according to the combination of creatinine and urine output [ 25 ].
On the other hand, severe tubular dysfunction can lead to increased urine output despite low GFR. Urine output therefore seems to be a nonspecific and poor parameter for classifying of AKI in critically ill patients.
Because the length of the afferent and efferent arterioles in the glomerular capillary network is relatively short and the resistance is low, the glomerular capillary hydraulic pressure remains rather constant along the capillaries, whereas the oncotic pressure along the capillary increases in relation with filtration.
Therefore, the limiting factors of GFR are the renal plasma flow and the plasma protein concentration. A higher renal plasma flow will induce a reduction in filtration fraction i.
Conversely, when the renal plasma flow is reduced, the glomerular filtration rate decreases but with an increase in the filtration fraction. Therefore, the oncotic pressure becomes the limiting factor of glomerular filtration [ 26 ].
In this line, the natriuresis and diuresis response to crystalloids infusion are in part mediated by the changes of intraglomerular oncotic forces following plasma protein dilution [ 2728 ], an effect that is not observed after hyperoncotic colloids administration.Influence of Fluid Intake on Urine Formation Name: Miriam Rivera Instructor: Renee Faulcon Date: Predictions Urine output will be highest during water loading Urine osmolarity will be highest during water loading Plasma osmolarity increases with dehydration Urine Analysis Lab Report Essay Urine Analysis Lab.
Assessing hydration status and measuring fluid balance can ensure optimal hydration Subscribe for full online access and get An archive of around 6, peer-reviewed clinical articles.
Influence of Fluid Intake on Urine Formation Laboratory Report Essay Sample. 1. Urine output will be highest during: water loading. 2. Urine osmolality will be lowest during: dehydration. Fluid intake and urine output Essay Sample. Aim: To find out if there is a relationship between fluid intake and urine output, by measuring my daily fluid intakes and urine outputs.
Urine output will be highest during: water loading 2. Urine osmolality will be lowest during: dehydration 3. Influence Of Fluid Intake On Urine Formation Laboratory Report. Filed Under: Essays Tagged With: drink. 2 pages, words The Essay on Industry Average Ratio Company Influence of Fluid Intake on Urine Formation Essay Sample.
1. State whether dehydration results in production of a concentrated or dilute urine.