Which pathology may result in acute kidney injury (aki) from a prerenal etiology?

Diagnosis

Table 3 summarizes useful clinical features, urinary findings, and confirmatory tests in the differential diagnosis of AKI.

BACKGROUND AND DEFINITION

Acute renal failure [ARF] is the sudden development of renal insufficiency that leads to retention of nitrogenous waste [urea nitrogen and creatinine] in the body. Despite consensus regarding this broad definition, there are diverse opinions as to the degree of elevation of serum creatinine sufficient to ascribe a diagnosis of ARF.1–4 These differences in diagnostic criteria, as well as in the populations under study, have led to variances in reported frequency, causes, and outcomes of ARF. In an effort to arrive at a more standard definition of ARF, some recent studies have emphasized the RIFLE criteria.5–8 These criteria refer to various elements in the developmental pathway of ARF including risk [R], injury [I], failure [F], loss [L], and end stage [E] and are based on both the magnitude of rise in the serum creatinine concentration and the urine output. The RIFLE criteria for the diagnosis of ARF are depicted in Table 56-1. Although further validation of the RIFLE criteria is necessary, these criteria can serve as a reasonable starting point for a more uniform approach to the clinical aspects of ARF. Clearly, better criteria for the uniform definition of ARF are necessary.

Although the precise definition of ARF may remain arguable, experts generally agree on several aspects of contemporary ARF. First, ARF occurs with significant frequency, especially in the hospital and in the intensive care unit [ICU] setting.1–9 Second, multiple pathophysiologic pathways and clinical events lead to an identical syndrome of ARF.1–9 Third, timely delineation of the cause of ARF is paramount in designing appropriate therapy.10–13 Fourth, even when modest in degree, ARF is associated with significant morbidity and mortality.10,14,15 Fifth, ARF is one of the few causes of complete organ failure that is potentially totally reversible.1–9 Finally, some studies indicate that a significant percentage of cases of ARF are preventable.10–13 The high frequency of occurrence, multiple causes, associated morbidity and mortality, and potential reversibility demand an organized approach to ARF. In this chapter we review the incidence, pathogenesis, clinical manifestations, management, and outcome of ARF, especially as it relates to critically ill patients. An overview of contemporary ICU-associated ARF is depicted in Table 56-2.

Definition of Acute Kidney Injury

Acute kidney injury [AKI] is a heterogeneous syndrome defined by rapid [hours to days] decline in the glomerular filtration rate [GFR], resulting in the retention of metabolic waste products, including urea and creatinine, and dysregulation of fluid, electrolyte, and acid-base homeostasis.1 Although often considered a discrete syndrome, AKI represents a broad constellation of pathophysiologic processes of varied severity and cause. These include decreases in the GFR as the result of hemodynamic perturbations that disrupt normal renal perfusion without causing parenchymal injury, partial or complete obstruction to urinary flow, and a range of processes with characteristic patterns of glomerular, interstitial, tubular, or vascular parenchymal injury. AKI occurs in a heterogeneous patient population—genetics, age, kidney functional status, accompanying comorbidities—and the cause is often multifactorial.

The termacute kidney injury has largely supplanted the older terminology of acute renal failure [ARF]. This change reflects recognition of serious shortcomings with the older terminology. Acute renal failure suggested a dichotomous relationship between normal kidney function and overt organ failure; in contrast, AKI captures the growing body of data associating small to moderate acute and transient decrements in kidney function with serious, adverse outcomes. Although the AKI terminology does emphasize the graded aspect of acute kidney disease, it should be recognized that this terminology is also imperfect. The terminjury can be construed to imply the presence of parenchymal organ damage, which may be absent in a variety of settings associated with an acute decline in kidney function, such as early obstructive disease and prerenal azotemia associated with volume depletion. Although the termacute kidney dysfunction might better characterize the entire spectrum of the syndrome, AKI is the term that has been adopted by consensus and is now increasingly used in the medical literature.2,3 In this chapter, AKI will be used to describe the entire spectrum of the syndrome. Although, in clinical practice, the termacute tubular necrosis [ATN] is often used synonymously with AKI, these terms should not be used interchangeably. Although ATN is the most common form of intrinsic AKI, particularly in critically ill patients, it represents only one of multiple forms of AKI. In addition, there may be a lack of concordance between the clinical syndrome and the classic histopathologic findings of ATN.4,5

Decreased urine output is a cardinal [although not universal] manifestation of AKI, and patients are often classified based on urine flow rates as nonoliguric [urine output >400 mL/day], oliguric [urine output 20:1 in prerenal disease.

In oliguric patients, FENa < 1% usually suggests prerenal ARF whereas FENa > 2% usually suggests intrinsic renal disease.

The approach to renal failure should include determination of [a] chronicity, [b] patient comorbidities, [c] whether there has been a recent vascular intervention, [d] whether the patient has received intravenous contrast or other nephrotoxic medications, and [e] volume status.

General management principles of ARF include [a] institution of a “renal” diet, [b] adjusting dosages of all medications metabolized or excreted by the kidneys, [c] discontinuing nephrotoxins or substituting non‐nephrotoxic alternatives [if possible], [d] monitoring fluid status, and [e] monitoring and treating complications of ARF [such as hyperkalemia, hyponatremia, and hyperphosphatemia].

Prompt treatment of renal obstruction can lead to complete recovery of renal function. Post‐obstructive diuresis [4–20 L/day], which sometimes occurs following correction of bilateral urinary obstruction, can lead to hypovolemia, hypokalemia, and hypomagnesemia.

Diuretics do not reduce mortality or the need for dialysis in ARF patients.

Low‐dose intravenous dopamine [1–3 μg/kg/min] does not reduce mortality or promote recovery of renal function in patients with ARF.

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7.07.1.2 Definitions

AKI is a group of syndromes characterized by a sudden and sustained decrease in the excretion of nitrogenous waste products that is not readily reversed by correction of inciting factors and it is associated with histological changes in the kidney. Generally, AKI is diagnosed after a clear increase in serum creatinine over hours or days, often well after a significant decline in glomerular filtration rate [GFR] has occurred. Changes in serum creatinine and urine output can occur in the normal response to intravascular volume depletion and decreased renal blood flow. Thus, changes in serum creatinine and/or urine output do not always define renal pathology, and more specific biomarkers are needed. Studies of AKI have employed changes in creatinine, changes in estimated GFR, urine output, and/or the provision of dialysis to define AKI. In general, there are no uniform criteria for dialysis for studies that used dialysis to define AKI. The heterogeneity of AKI definitions, the diverse patient populations studied, and differences in the severity of renal injury examined have complicated comparisons. More recently, the RIFLE [risk, injury, failure, loss, end-stage renal disease [ESRD]] criteria for AKI were proposed by the Acute Dialysis Quality Initiative [ADQI] group [Bellomo et al. 2004]. Definitions and classifications of severity of AKI are given in Table 1. These consensus criteria have proven to be useful and are associated with both mortality and length of hospital stay. In a retrospective study, Hoste and coworkers [2006] reported AKI according to RIFLE criteria in 67% of ICU admissions; AKI class F [failure] was associated with 26.3% mortality, class I [injury] with 11.4% mortality, and class R [risk] with 8.8% mortality [vs 5.5% in the absence of AKI]. Given that small changes in renal function affect outcome, the Acute Kidney Injury Network [AKIN] proposed a modification of the RIFLE criteria. These modifications [Mehta et al. 2007] are also given in Table 1. The criterion of increase in creatinine of 0.3 mg dl−1 was proposed in response to data showing that mild declines in renal function are associated with increased mortality [Lassnigg et al. 2008]. In addition, AKIN proposed that increases in creatinine occur within 48 h, that criteria be applied after volume status optimization, and that urinary tract obstruction be excluded before the use of anuria to diagnose AKI. As such, the AKIN criteria have been shown to be predictive of mortality [Barrantes, Tian, Vazquez et al. 2008]. Interestingly, Zappitelli et al. [2008] reported markedly different estimates of AKI incidence in hospitalized children using different accepted definitions of AKI.

Table 1. Definitions of acute kidney injury [AKI]

Azotemia refers to increases in blood urea nitrogen [BUN] and usually indicates decreased clearance of nitrogenous waste products or renal failure. With normal kidney function, however, BUN can increase in the presence of gastrointestinal bleeding, steroid administration, a catabolic state, or the infusion of amino acids [usually in the form of parenteral nutrition] Increases in serum creatinine [independent of renal function] can occur with increased creatinine release from muscle or decreased tubular secretion [i.e., due to cimetidine or trimethaprim]. In addition, acetoacetate, cephalosporins, flucytosine, methanol, and isopropyl alcohol can interfere with the standard laboratory [Jaffe] reaction used to determine creatinine.

GFR is the rate at which plasma crosses from glomerular capillaries to the urinary space, and inulin clearance is the standard for estimating GFR or renal excretory function as insulin secretion/reabsorption after filtration is minimal. At this time, renal function is generally estimated from serum creatinine, 24 h creatinine clearance, abbreviated modification of diet in renal disease [MDRD] [Levey et al. 1999], or Cockcroft–Gault equations [Cockcroft and Gault 1976] [Table 2]. A significant limitation of these estimates is the assumption of a steady state or stable renal function.

Table 2. Estimates of renal function

The relationship between creatinine and GFR is not linear [Figure 1]. A normal or near-normal GFR may decrease significantly [i.e., by 50%] before a clear increase in creatinine is observed. As GFR decreases, tubular creatinine secretion may also increase. Conversely, in chronic kidney disease [CKD], a relatively large change in serum creatinine can occur with relatively small changes in GFR.

Oliguria generally refers to a urine output of 500 mOsm/kg, urine sodium [UNa] is