Reading between the (guide)lines—the KDIGO practice guideline on acute kidney injury in the individual patient

Abstract

The KDIGO guidelines for acute kidney injury (AKI) are designed to assist health-care providers around the world in managing patients with AKI. Clinical guidelines are intended to help the clinician make an informed decision based on review of the currently available evidence. Due to the generic nature of guidelines, it is sometimes difficult to translate a guideline for a particular individual patient who may have specific clinical circumstances. To illustrate this point, we have discussed the interpretation of the KDIGO guideline in patients who have subtleties in their clinical presentation, which may make treatment decisions less than straightforward.

Difficulties in diagnosing acute kidney injury post liver transplantation using serum creatinine based diagnostic criteria

“…Changes in serum creatinine are now used to define acute kidney injury. As such, although small changes in serum creatinine are linked to adverse outcomes, changes in serum creatinine concentration can be influenced by changes in hydration status [54] , and in particular for the patient with cirrhosis a falling serum bilirubin post liver transplant can lead to an apparent increase in serum creatinine, simply due to loss of interference with the colorimetric assay, and secondly due to changes in intra-renal perfusion associated with immunphyllins, without necessarily implying acute kidney injury. As serum creatinine is likely to remain the routine clinical marker of kidney function, additional biomarkers are required to help differentiate between assay interference and reversible changes in renal function on one hand and acute kidney injury on the other.…”

Reduction of Tubular Flow Rate as a Mechanism of Oliguria in the Early Phase of Endotoxemia Revealed by Intravital Imaging

“…31,32 Less is known, however, about the mechanisms underlying oliguria, despite it being a diagnostic criterion of AKI in several guidelines (e.g., AKIN, RIFLE, and KDIGO). [15][16][17] To our knowledge, this study is the first to show that (1) LPS signaling through a TLR4-dependent mechanism is associated with reduced intraproximal tubular urine flow rate and (2) the dilation of LPScontaining tubules in response to fluid resuscitation may distinguish urine flow rate responders and nonresponders during early phases of endotoxemia in mice. Inasmuch as the tubular flow rate was reduced when BP or GFR was maintained, hypotension or reduction in GFR was likely not the primary factor initiating oliguria.…”

“…[15][16][17] The reduction in urine output is thought to depend on GFR reductions in septic kidneys induced by hypoperfusion and/or intravascular depletion. Maintaining hemodynamics by fluid resuscitation and treatment with additional vasoactive agents, however, frequently fails to restore urine output.…”

Renal Failure and Heart Surgery

“…What we do have is a general consensus that volume depletion and congestive heart failure (CHF) symptoms should be addressed and corrected as part of the management of AKI [22]. [12,40]. Increases specified are defined as increases from baseline serum creatinine (i.e.…”

“…A consensus definition of AKI was proposed by the Acute Dialysis Quality Initiative (ADQI), which introduced the RIFLE (RiskInjury-Failure-Loss-End Stage Renal Disease) criteria [11]. These criteria have since been modified by the Acute Kidney Injury Network (AKIN), which specifies a timeframe of 48 hours within which AKI occurs,along withthree classifications describing increases in serum creatinine relative to baseline [12] (Table 1). In most patients after cardiac surgery, serum creatinine will increase only by 0.1-0.2mg/dL.…”