Prerenal azotemia or established acute renal failure

In the context of a hypovolemic, hypotensive, or hypoxic insult, having excluded renal or postrenal cause of ARF, several authorities recommend the performance of biochemical investigations to help distinguish between so-called 'prerenal azotemia' (the kidney is underperfused and stressed but still functioning appropriately) and 'acute renal failure' (normal cell function has been lost because of the severity of the insult). These investigations typically include the following measurements:

1. urinary sodium concentration, which is low (< 20 mmol/l) when a functioning kidney is seeking to retain it in an appropriate response to diminished renal perfusion;

2. the fractional excretion of sodium, which is also low (< 1 per cent) for the same reasons;

3. the urinary 'concentration', which is relatively preserved with a high specific gravity (> 1020) and a high urinary osmolality (> 500 mosmol/l), if the normal renal response to hypoperfusion is preserved.

Such measurements have several serious flaws in the ICU setting. They have not been validated in critically ill patients, their specificity and sensitivity are poor, and their implications for treatment are unclear. In the ICU, all resuscitation is typically conducted rapidly, is guided by invasive hemodynamic monitoring, and is aggressively directed toward the restoration of vital organ perfusion. Biochemical evidence pointing to 'prerenal azotemia' should not influence either the degree or the speed of resuscitation. Equally, biochemical evidence suggesting 'established ARF' should certainly not inhibit appropriate and speedy resuscitation and re-establishment or maintenance of an optimal circulating blood volume and cardiac output. In this regard, although the clinical assessment of the patient's volume status is a vital first step in the resuscitation process, it is often inexact. Assessment of skin turgor, moistness of mucous membranes, axillary moistness, orthostatic pressure drop, pulse rate, jugular venous pressure, and estimation of the patient's fluid balance are too imprecise to guide resuscitation in critically ill patients. Invasive hemodynamic monitoring (central venous pressure, arterial pressure, and, in patients with cardiac dysfunction or need for inotropic support, pulmonary artery catheterization) is needed to guide rational resuscitation and is strongly recommended in most patients with oliguric ARF. Conclusions

The syndrome of ARF is frequent in the ICU and its presence is easily confirmed by simple biochemical tests and clinical findings. In the vast majority of cases, ARF is due to a severe prerenal insult. This typically requires no specific investigations but, rather, prompt resuscitation. Occasionally, postrenal or renal causes of ARF need to be considered and either confirmed or excluded by specific tests.

Rarely, ARF can be confused with rapidly progressive or chronic renal failure. Clinical clues and some relatively simple investigations are usually sufficent to clarify the diagnosis.

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