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2/22/24, 2:39 PM Realizeit for Student Introduction Acute kidney injury (AKI) is a rapid loss of renal function due to damage to the kidneys. Depending on the duration and severity of AKI, a wide range of potentially lifethreatening metabolic complications can occur, including metabolic acidosis as...

2/22/24, 2:39 PM Realizeit for Student Introduction Acute kidney injury (AKI) is a rapid loss of renal function due to damage to the kidneys. Depending on the duration and severity of AKI, a wide range of potentially lifethreatening metabolic complications can occur, including metabolic acidosis as well as fluid and electrolyte imbalances. Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased kidney injury with the goal of minimizing long-term loss of renal function. AKI is a problem seen in patients who are hospitalized and those in outpatient settings. Pathophysiology Although the pathogenesis of AKI and oliguria is not always known, many times there is a specific underlying cause. Some of the factors may be reversible if identified and treated promptly, before kidney function is impaired. This is true of the following conditions that reduce blood flow to the kidney and impair kidney function: hypovolemia; hypotension; reduced cardiac output and heart failure; obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; and bilateral obstruction of the renal arteries or veins. If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine levels, oliguria, and other signs may be reversed. Although renal stones are not a common cause of AKI, some recurrent types may increase the risk of AKI. Some hereditary stone diseases, primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury may cause repeated bouts of obstruction as well as crystal-specific damage to tubular epithelial cells and interstitial renal cells (Odom, 2017). Classifications of Acute Kidney Injury The term acute kidney injury has replaced the term acute renal failure because it better describes this syndrome, in both those who require RRT and also in those patients who experience minor changes in renal function. Classification criteria for AKI include assessment of three grades of severity and two outcome-level classifications. This 5https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 1/7 2/22/24, 2:39 PM Realizeit for Student point system is known as the RIFLE classification system. RIFLE stands for risk, injury, failure, loss, and ESKD (Bellomo et al., 2004). Risk, injury, and failure are considered grades of AKI severity, whereas loss and ESKD are considered outcomes of loss that require some form of RRT, at least temporarily (Bellomo et al., 2004). Table 48-2 lists the classification criteria for the RIFLE system for AKI (Bellomo et al., 2004). This classification system is used by health care professionals to identify kidney injury and improve patient outcomes. A diagnosis of AKI results in significantly longer hospital stays, has an increased mortality rate, and is a major risk factor for the development of CKD (Medel-Herrero, Mitchell, & Moyce, 2019). Categories of Acute Kidney Injury The major categories of AKI are prerenal (hypoperfusion of kidney), intrarenal (actual damage to kidney tissue), and postrenal (obstruction to urine flow). Prerenal AKI, which occurs in 60% to 70% of cases, is the result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and obstruction of renal vessels, ultimately leading to a decrease in the GFR (Odom, 2017). Intrarenal or intrinsic AKI is the result of actual parenchymal damage to the glomeruli or kidney tubules. Acute tubular necrosis (ATN), or AKI in which there is damage to the kidney tubules, is the most common type of intrinsic AKI. Characteristics of ATN are intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate and decreased urine flow through the tubule), vasoconstriction, and changes in glomerular permeability. These processes result in a decrease of GFR, progressive azotemia, and fluid and electrolyte imbalances. CKD, diabetes, heart failure, hypertension, and cirrhosis can contribute to ATN. Postrenal AKI usually results from obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hyperplasia, malignancies, and pregnancy. Pressure rises in the kidney tubules, and eventually the GFR decreases. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 2/7 2/22/24, 2:39 PM Realizeit for Student Phases of Acute Kidney Injury There are four phases of AKI: initiation, oliguria, diuresis, and recovery. The initiation period begins with the initial insult and ends when oliguria develops. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, phosphorus, and the intracellular cations [potassium and magnesium]). The minimum amount of urine needed to rid the body of normal metabolic waste products is approximately 400 mL in 24 hours or 0.5 mL/kg/h over 6 hours. In this phase, uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. Laboratory values stabilize and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal, since the filtration of urea and creatinine has not yet commenced. Because uremic symptoms may still be present, the need for expert medical and nursing management continues. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 3/7 2/22/24, 2:39 PM Realizeit for Student The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase and an elevated serum BUN and creatinine will be noted. The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patient’s normal level. Although a permanent 1% to 3% reduction in the GFR may occur, it is not clinically significant. However, in those patients with preexisting CKD, an episode of AKI may necessitate beginning CRRT. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 4/7 2/22/24, 2:39 PM Realizeit for Student https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 5/7 2/22/24, 2:39 PM Realizeit for Student Some patients have decreased renal function with increasing nitrogen retention but actually excrete normal amounts of urine (1 to 2 L/day). This is the nonoliguric form of kidney injury and occurs predominantly after exposure of the patient to nephrotoxic agents (any substance or medication that damages kidney tissue), burns and traumatic injury. Clinical Manifestations Almost every system of the body is affected with failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic. Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures. Assessment and Diagnostic Findings Assessment of the patient with AKI includes evaluation for changes in the urine, diagnostic tests that evaluate the kidney contour, and a variety of laboratory values. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 6/7 2/22/24, 2:39 PM Realizeit for Student In AKI, urine output varies from scanty to a normal volume, hematuria may be present, and the urine has a low specific gravity (compared with a normal value of 1.010 to 1.025). One of the earliest manifestations of tubular damage is the inability to concentrate the urine (Odom, 2017). Patients with prerenal azotemia have a decreased amount of sodium in the urine (less than 20 mEq/L) and normal urinary sediment. Patients with intrarenal azotemia usually have increased urinary sodium levels greater than 40 mEq/L with urinary casts and other cellular debris. Ultrasonography is a critical component of the evaluation of patients with kidney disease. A renal sonogram or a noncontrast CT scan may show evidence of anatomic changes. The BUN level increases steadily at a rate that depends on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake. Serum creatinine levels are useful in monitoring kidney function and disease progression and increase with glomerular damage. With a decline in the GFR, oliguria, and anuria, patients are at high risk for hyperkalemia. Protein catabolism results in the release of cellular potassium into the body fluids, causing severe hyperkalemia (high serum potassium levels). Hyperkalemia may lead to cardiac arrhythmias, such as ventricular tachycardia and cardiac arrest. Sources of potassium include normal tissue catabolism, dietary intake, blood in the GI tract, or blood transfusion and other sources (e.g., IV infusions, potassium penicillin, and extracellular shift in response to metabolic acidosis). Progressive metabolic acidosis occurs in kidney disease because patients cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by decreased serum carbon dioxide (CO2) and pH levels. Blood phosphorus concentrations may increase; calcium levels may be low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for the elevated blood phosphate levels. Anemia is another common laboratory finding in AKI, as a result of reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan, and blood loss from the GI tract. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zYjdcLReD0xWqoW33TqQEI8BS%2f7OmZzvGp21HqGixm2HQ… 7/7