Overview Of Acute Kidney Injury - pediagenosis
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Saturday, May 16, 2020

Overview Of Acute Kidney Injury

Overview Of Acute Kidney Injury
Acute kidney injury (AKI) consists of any precipitous decline in renal filtration function, which can occur secondary to disease affecting the renal vasculature, renal parenchyma, or urine collecting system. Such a decline is often first evidenced as an increase in serum creatinine concentration, which may be accompanied by normal urine output, oliguria, or anuria.

Over time, various criteria have been proposed to define what degree of functional impairment constitutes AKI. The Acute Dialysis Quality Initiative (ADQI) created a consensus definition known as the RIFLE criteria, which stratifies patients based on serum creatinine concentration, estimated glomerular filtration rate (GFR), and urine output. A modification of these criteria was subsequently proposed by the Acute Kidney Injury Network (AKIN) since smaller changes in serum creatinine than proposed by the RIFLE criteria can have adverse effects on outcome. The criteria include:
Stage 1 AKI: increase in serum creatinine by 0.3 mg/dL or by 150% to 200%, OR urine output <0.5 mL/kg/hr for 6 hours Stage 2 AKI: increase in serum creatinine by 200% to 300%, OR urine output <0.5 mL/kg/hr for 12 hours
Stage 3 AKI: increase in serum creatinine by >300% or to more than 4.0 mg/dL with an acute increase of greater than 0.5 mL/dL, OR urine output <0.3 mL/kg/hr for 24 hours, anuria for 12 hours or renal replacement therapy
These diagnoses should be applied only if the decline in renal function occurs over a rapid time course (i.e., less than 48 hours). There are several issues that may complicate application of these criteria. First, they require knowledge of the patient’s baseline renal function. Second, serum creatinine concentrations may not be in a steady state in patients with declining renal function. Research efforts into more sensitive biomarkers of renal injury, such as cystatin C and neutrophil gelatinase-associated lipocalin (NGAL), are ongoing but have not yet had a wide impact on clinical practice.

Classification Of Etiologies
The various etiologies responsible for AKI are typically categorized as “prerenal,” “intrarenal,” or “postrenal.” Prerenal. “Prerenal” AKI, the most common kind (60% of cases), reflects a significant reduction in renal perfusion. Mild reductions in renal perfusion do not affect the glomerular filtration rate (GFR) because of compensatory feedback responses, such as activation of the renin-angiotensin system and release of vasodilatory prostaglandins (see Plate 3-18). In the setting of markedly reduced flow, however, these compensatory mechanisms fail, and renal filtration declines. By definition, however, the renal parenchyma remains intact, and normal function can be restored with intravascular fluid repletion.
Common causes of prerenal AKI include excessive diuresis, diarrhea, vomiting, hemorrhage, burns, poor cardiac output (i.e., congestive heart failure, see Plate 4-38), liver failure (i.e., hepatorenal syndrome, see Plate 4-40), and hypercalcemia (due to renal vasocon-striction). In addition, patients with low baseline renal perfusion may experience prerenal AKI if their normal compensatory mechanisms are blocked by either nonsteroidal antiinflammatory drugs (e.g., ibuprofen), which interfere with tubuloglomerular feedback, or inhibitors of the renin-angiotensin system (i.e., angiotensin-converting enzyme [ACE] inhibitors, aldosterone receptor blockers [ARBs]).
Patients with prerenal AKI may exhibit other signs of volume depletion, such as tachycardia, orthostatic hypotension, and dry mucous membranes. In addition, prerenal AKI can be distinguished from other causes by the intense reabsorption of solutes that results from the normal renal response to decreased perfusion. Specifically the fractional excretion of sodium (FENa, see Plate 3-6 for formula) should be low (<1%); the serum blood urea nitrogen (BUN): creatinine ratio may be elevated (i.e., >20:  1), reflecting increased reabsorption of urea; and the urine should be concentrated (> 500 mOsm/kg H2O). Note that FENa values may be invalid among patients who have recently taken diuretics; in this case, the fractional excretion of urea has been proposed as an alternative means of assessing tubular reabsorption because it is generally less than 35% in the prerenal state. Finally, because the renal parenchyma is not damaged, the urine sediment should not contain red blood cells, white blood cells, or other markers of renal inflammation. Hyaline casts, however, may be seen; these occur because low tubular flow rates increase aggregation of Tamm-Horsfall mucoproteins, which are secreted by the distal tubular epithelium.
Once prerenal AKI is suspected, the diagnosis can be confirmed by documenting normalization of renal function upon resuscitation of intravascular volume.
Intrarenal. “Intrarenal” AKI, the second most common kind (35% of cases), reflects direct damage to the renal parenchyma. Acute tubular necrosis (ATN, see Plate 4-3) accounts for nearly 90% of cases and is by far the most common cause. ATN occurs in the setting of either severe renal ischemia or direct toxic damage to the renal tubules by either extrinsic toxins (such as aminoglycosides or radiocontrast agents) or intrinsic toxins (such as myoglobin or hemoglobin). The many other causes of intrarenal AKI include acute or rapidly progressive glomerulonephritis (GN, see Plate 4-14), thrombotic microangiopathy (see Plate 4-32), disseminated intravascular coagulation, malignant hypertension (see Plate 4-44), acute interstitial nephritis (AIN, see Plate 4-28), and post-transplant renal allograft rejection.
Unlike prerenal AKI, intrarenal AKI does not improve in response to an intravenous fluid bolus. In addition, it generally does not produce evidence of increased tubular reabsorption. Thus the FENa is often >2%, the BUN : creatinine ratio is 10 to 15 : 1, and the urine osmolality is 400 mOsm/kg.
Intrarenal AKI may also be distinguished by findings on urine microscopy that indicate glomerular or tubular damage. ATN, for example, is often (but not always) associated with “muddy brown” pigmented granular casts or tubular epithelial cell casts. GN is associated with evidence of glomerular bleeding (dysmorphic red blood cells [RBCs], red blood cell casts; see Plate 4-14 for details). AIN is associated with white blood cell casts, white blood cells, and RBCs. In addition, glomerular and interstitial diseases are often associated with proteinuria, unlike prerenal or postrenal disease.
Finally, several glomerulonephritides cause abnormal complement levels, which are generally not seen in prerenal or postrenal disease unless the patient has other comorbidities. Additional details are available later in this section.
Once intrarenal AKI is suspected, the diagnosis of ATN is often reached based on history and laboratory findings. If a cause other than ATN appears likely, however, and the patient’s renal function is not improving, a renal biopsy is often performed.
Postrenal. “Postrenal” AKI, the least common kind (5% of cases), reflects obstruction to urine flow from both kidneys (or in a solitary kidney). The obstructions must therefore affect the urethra, bladder neck, or both ureters. Such obstructions are often associated with intense flank and groin pain, which results from stretching of the proximal collecting system. Although flank intrinsic renal diseases, referred pain to the groin indicates lower tract inflammation and is more suggestive of obstruction. The patient may offer a history of weak urine stream or incomplete emptying. On examination, an enlarged bladder or prostate (in men) may be palpable. Microscopic analysis of urine may be unremarkable or may reveal RBCs in the case of nephrolithiasis.
Once postrenal AKI is suspected, the patient should undergo further evaluation with radiographic imaging to further characterize the obstruction.

The specific management of these various etiologies is discussed later in this book. Irrespective of the cause, however, clinicians should be cognizant of the common sequelae of severely impaired renal function, such as fluid retention (with subsequent hypertension and edema), hyperkalemia, and metabolic acidosis. Any of these conditions, if not correctable wit medications, may require renal replacement therapy.

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