Risk and prevention of acute renal failure in critical illness

This has not appeared in the past papers. However, the great Competencies document makes mention of it. Thus, if an SAQ ever came up on this topic, it might ask the candidates to "Discuss the features which identify patients at risk of developing ARF, and discuss some of the therapies that may have prophylactic benefits." Or perhaps "Discuss the influence of ARF on the morbidity and mortality of ICU patients",  which sounds like some sort of creative writing task. Question 29 from the first paper of 2005 has some vague relationship with prevention of ARF, but it is in context of AAA repair, and more closely related to rhabdomyolysis and contrast-induced nephropathy.

Patient population at risk of developing acute renal failure in the ICU:

A famous and widely cited study by De Mendonça et al (2000) contains within it tables of comparison, which relate the risk factors for developing acute renal failure in the ICU, as well as risk factors for developing all kinds of other organ failure once renal failure is already established. These tables look something like this:

In addition to these, one can also add

• Cardiac surgery patients
• Survivors of cardiac arrest
• Patients with pre-existing renal failure

Influence of acute renal failure on ICU outcome

"It makes everything worse" is a fairly accurate summary of what happens with acute renal failure in the ICU. Mandelbaum et al (2011) applied AKIN criteria to categorise 14,524 hospitalised (not necessarily ICU) patients and found the following raw mortality rates:

• No ARF: 6.2%
• AKI 1: 13.9%
• AKI 2: 16.4%
• AKI 3: 33.8%

In case you are wondering, the urine output part of the AKIN criteria was a better predictor of mortality than creatinine. However you categorise it, AKI basically doubles your risk of dying in hospital. This was redemonstrated among a cohort of ICU patients by Peters et al (2018), except the raw numbers were obviously higher (14% vs 34% for the group without sepsis, or 40% vs 22% with sepsis). 

Why does it kill so? That people die with renal failure, rather than of renal failure, is probably a trite platitude.  Hoste & Kellum (2004) challenged it in their editorial by thoroughly describing all the lethal things it does to ICU patients. In brief summary:

• Uraemic toxicity produces delirium, which is itself a risk factor independently associated with increased ICU and hospital mortality.
• Volume overload produces all manner of organ system complications, and a positive fluid balance is a known risk factor for worse outcomes in sepsis, abdominal surgery, trauma, cardiac failure, and so forth.
• Acidosis is probably associated with decreased survival; or at least we suspect that sustained acidosis is harmful on some level, because it has negative physiological effects (eg. on the cardiovascular system).
• Altered immune function is thought to be more related to chronic rather than acute renal failure.  There is still some evidence of neutrophil dysfunction and a pro-inflammatory state in ARF, which is mainly coming out of animal data.
• Electrolyte derangement is certainly enought to kill you, mainly by arrhythmia (hyperkalemia), though theoretically all manner of lifethreatening electrolyte disturbances could develop
• Drug error and drug dose accumulation contribute to morbidity, for example by extending the duration of ICU stay and ventilation
• Added instrumentation increases ICU morbidity by increasing the number of invasive procedues (vas cath, circuit connection and disconnection), giving rise to an increased risk of bloodstream infections, vascular access complications, embolic phenomena, clots, and so forth.

Prevention of acute renal failure in the ICU

There is a good, reasonably recent (2017) reference for this subject matter. Michael Joannidis et al performed a thorough literature search and generated a list of recommendations, graded by the strength of the evidence.

There are several general strategies which can be employed.

In addition to these, there are specific protective strategies which are helpful in specific conditions, for example in the case of contrast-induced nephropathy. The specific strategies are discussed in greater detail in other sections; this brief summary will only mention them in passing.

Generic strategies to prevent renal failure

The strategies suggested by OH's Manual:

• Maintain a haemoglobin over 70
• Rapidly ensure intravascular volume is adequate
• Achieve satisfactory haemodynamic parameters (eg. a MAP of 70mmHg in most people)

Additional strategies suggested by other sources

• Avoid using chloride-rich fluids (Bellomo et al, 2012)
• Avoid using hydroxyethyl starch

Specific strategies to prevent renal failure in specific at-risk groups

• In chronically hypertensive septic patients, aim for a higher MAP (eg. 75-80mmg), according to Asfar et al (2014)
• To prevent contrast-induced nephropathy, use a range of effective strategies (discussed elsewhere)
• In pre-op cardiothoracic patients at risk of AKI, consider fenoldopam (Landoni et al, 2007)

Strategies which we know to be ineffective:

• Diuretics in the prevention or management of renal failure
• Low-dose dopamine
• Natriuretic peptides