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Erschienen in:
12.09.2016 | Understanding the Disease
Understanding oliguria in the critically ill
Erschienen in: Intensive Care Medicine | Ausgabe 6/2017
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The three determinants of urine output (UO) are glomerular filtration, net tubular reabsorption, and/or the patency of the tubular lumen and the postrenal urinary tract.
1.
Tubular reabsorption
UO is predominantly determined by tubular reabsorption in the distal tubules mediated by vasopressin (ADH), although activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system and changes in hydrostatic and oncotic forces in the peritubular capillaries may also contribute. Non-osmotic stimuli for ADH release such as anxiety, pain, hypoxemia, hypercapnia, nausea, vomiting, postoperative states, and some drugs may induce oliguria without affecting glomerular filtration rate (GFR). Intraoperative oliguria indeed appears a poor predictor of postoperative acute kidney injury (AKI) [1]. In addition, oliguria due to increased tubular reabsorption may also be an adequate physiologic response to a reduction in extracellular volume and renal blood flow (RBF), while maintaining GFR through afferent vasodilation and efferent vasoconstriction.
2.
Glomerular filtration
Oliguria in ICU patients is often the first sign of a decreased GFR (=AKI), although non-oliguric AKI has also been described, especially when nephrotoxicity is implicated. The classical distinction between prerenal and renal AKI is increasingly being questioned and both can probably co-exist in the same patient. However, the concept of mainly functional versus mainly structural (tubular damage) AKI may help clinicians in the management of the patient with oliguria [2]. Oliguria of functional AKI is mainly due to renal hypoperfusion, secondary to hypovolemia or low cardiac output, and increased tubular reabsorption (preserved tubular function). A reduction of renal perfusion pressure below the lower limit of autoregulation or in patients with impaired autoregulation may also result in a reduction of RBF and GFR with oliguria.
“Renal” AKI is characterized by tubular damage mainly resulting from ischemia and inflammation. The mechanisms underlying a decrease of GFR and UO in acute tubular damage are less clear. Depending on the underlying etiology persistent hypoperfusion (direct or via activated tubuloglomerular feedback), altered glomerular hemodynamics, intrarenal shunting, heterogeneity of intrarenal blood flow due to impaired microcirculation and/or tubular obstruction and backleak have been implicated [3]. Some authors have suggested that the reduced GFR (and oliguria) is a protective mechanism to reduce the filtered solute load and thus the required energy for reabsorption.
3.
Obstruction of the urinary tract is another reversible cause of oliguria that, however, is less frequent in ICU patients.