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the prevalence of acute kidney injury (AKI) over the past 15 years due to the increased per-centage of older adults in the popula-tion and increased survival rates with cardiac disease and diabetes mellitus (Talbot, 2008). Up to 50% of AKI cases are thought to develop in the hospital (Armitage & Tomson, 2003). Approximately 5% of hospital patients admitted to medical or surgi-cal floors will have their admission complicated by the development of AKI (Cheung, Ponnusamy, & Anderton, 2008; Talbot, 2008). Research by Barrantes et al. (2009) found that development of AKI in hospitalized patients was associated with a 7-fold increase in likelihood of death, a 4-fold increase in length of stay, and a 4-fold increase in the like-lihood of transfer to a critical care unit than those who did not develop AKI in the hospital. An evaluation of 13 studies comprehensively found that mortality for patients without AKI was 6.9% compared with 31.2% in patients with AKI (Ricci, Cruz, & Ronco, 2007).

These findings indicate that AKI leads to increased risk of mortality of hospitalized patients. Since the preva-lence of AKI is increasing, it is very likely that most healthcare profession-als will encounter patients with AKI. The purpose of this article is to pro-vide education on the pathophysiolo-gy of AKI, aid in identifying risk fac-tors, and discuss current research on treatment options and interventions.

Kristina M. Yaklin

Continuing Nursing Education

Kristina M. Yaklin, BSN, RN, is a Cross-Trained Float Registered Nurse, Owosso Memorial Hospital, and Student in the Doctorate of Nurse Practice, University of Michigan – Flint, Owosso, MI. She may be contacted via e-mail at kryaklin@umflint. edu

Statement of Disclosure: The author reported no actual or potential conflict of interest in relation to this continuing nursing education article.

This offering for 1.3 contact hours is provided by the American Nephrology Nurses’ Association (ANNA).

ANNA is accredited as a provider of continuing nursing education (CNE) by the American Nurses Credentialing Center’s Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP 00910.

Accreditation status does not imply endorsement by ANNA or ANCC of any commercial product. This CNE article meets the Nephrology Nursing Certification Commission’s (NNCC’s) continu-ing nurscontinu-ing education requirements for certification and recertification.

Copyright 2011 American Nephrology Nurses’ Association

Yaklin, K.M. (2011). Acute kidney injury: An overview of pathophysiology and treat-ments. Nephrology Nursing Journal, 38(1), 13-19, 30.

Acute kidney injury, or acute kidney failure, is thought to complicate 5% of hospital admissions (Cheung, Ponnusamy, & Anderton, 2008). Most healthcare providers are likely to encounter patients experiencing acute kidney injury. Nurses and other health-care professionals can play a vital role in identifying patients at risk for acute kidney injury and aid early intervention by identifying decreased kidney function. This article summarizes the current literature on acute kidney injury, including the definition, patho-physiology, risk factors, diagnostic tests, and current treatments and interventions. Goal

To provide an overview of acute kidney injury, its pathophysiology, and treatments. Objectives

1. Define acute kidney injury (AKI).

2. Discuss the pathophysiology, including the three categories of AKI. 3. Identify the risk factors associated with AKI.

4. Describe treatment options for AKI.


AKI is a complex disorder with varying definitions, most including an abrupt decline in kidney function leading to a rise in serum creatinine and/or blood urea nitrogen levels, with or without a decrease in urine output (ADIS International Ltd., 2009, Barrantes et al., 2009, Cheung et al., 2008, Talbot, 2008,). AKI can be classified into three cause categories: pre-renal, intrinsic, and post-renal.

Pre-Renal Kidney Injury

Pre-renal kidney injury is caused by hypoperfusion of the kidneys most commonly caused by volume

deple-tion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and renal artery stenosis (ADIS Inter national Ltd., 2009, Cheung et al., 2008, Talbot, 2008). Some vasoactive med-ications, such as angiotensin-convert-ing enzyme inhibitors, epinephrine, high-dose dopamine, and angiotensin receptor antagonists, can also cause pre-renal kidney injury by producing intrarenal vasoconstriction leading to hypoperfusion of the glomeruli (Cheung et al., 2008; Porth, 2007, Talbot, 2008).

Kidneys usually receive 20% to 25% of the total cardiac output (Porth, 2007). This blood supply is required to


Acute Kidney Injury: An Overview of Pathophysiology and Treatments

remove wastes and manage fluid and electrolyte balance. If the blood flow is reduced, the glomerular filtration rate (GFR) drops, decreasing urine output and filtration, and reabsorp-tion of substances filtered through the glomerulus (Porth, 2007). The glo -merular capillaries are supplied by the afferent arteriole; blood then flows out of the glomerular capillaries via the efferent arteriole. This location between two arterioles maintains the pressure necessary to move fluid through the glomerular capillaries, maintaining the GFR. The afferent and efferent arterioles are innervated by the sympathetic nervous system (SNS) and are sensitive to vasoactive substances. Therefore, kidney blood flow is affected during times of SNS stimulation (for example, shock) and when exposed to vasoactive hor-mones or drugs (Porth, 2007). When kidney blood flow reaches approxi-mately 20% of normal, damage can occur to tubular cells (Porth, 2007). This is further discussed in the next section, Intrinsic Kidney Injury.

Intrinsic Kidney Injury

Intrinsic kidney injury involves structural damage to glomerulus, ves-sels, or kidney tubules, which can often be brought on by prolonged pre-renal causes leading to cell necro-sis by ischemia, or by infectious agents and toxins that result in inflam-mation or injury (ADIS International Ltd., 2009; Cheung et al., 2008; Talbot, 2008). The most common forms of intrinsic kidney injury are acute tubular necrosis (ATN), acute interstitial nephritis (AIN), and con-trast-induced nephropathy (CIN).

Acute tubular necrosis (ATN). ATN is the most common cause of AKI, particularly in hospitalized patients (ADIS International Ltd., 2009; Cheung et al., 2008; Talbot, 2008). ATN typically occurs after an ischemic or toxic ATN event. Ischemic ATN is caused by pro-longed pre-renal azotemia or by sep-sis and toxic ATN is caused by direct tubular damage by nephrotoxins, such as aminoglycosides or radio con-trast agents (Cheung et al., 2008).

Sepsis is the most common cause of ischemic ATN, occurring in up to 50% of critically ill patients (Cheung et al., 2008). Sepsis produces ischemia through systemic vasodilatation lead-ing to intrarenal hypoperfusion. Sepsis also results in toxins that make kidney tubular cells more sensitive to the effects of ischemia (Porth, 2007). Nephrotoxic agents cause kidney injury by combinations of kidney vasoconstriction, direct damage to tubular cells, or intratubular obstruc-tion (Porth, 2007). The kidneys are particularly susceptible to nephrotox-ic injury due to its rnephrotox-ich blood supply, ability to concentrate toxins, and metabolic processes within the kid-ney that can turn substances into toxic metabolites (Porth, 2007).

No matter what the cause, in ATN, the necrotic tubular epithelial cells begin to slough off and lead to tubular obstruction and back-leak of filtrate through the damaged epitheli-um (Cheung et al., 2008). The obstruction also increases pressure on the system, decreasing GFR and con-tributing to afferent arteriole constric-tion via tubuloglomerular feedback, which results in decreased glomerular capillary filtration pressure (Porth, 2007). Tubular injury is frequently reversible if damage is not severe enough to cause cortical necrosis (Porth, 2007).

Clinical progression of ATN typi-cally follows a sequence of three events: initiation, maintenance, and recovery. The initiation phase is char-acterized by an increase in blood urea nitrogen and serum creatinine levels, and a decline in urine output (Cheung et al., 2008). Urine output in ATN can vary from near normal levels to anuria (Cheung et al., 2008). The maintenance phase consists of sus-tained decrease in kidney function. This may last 7 to 21 days, and during this time, kidney support (such as dialysis) may be required (Cheung et al., 2008). The recovery phase is defined by a marked increase in urine output and decline in serum creati-nine and blood urea nitrogen; this is a time of regeneration of tubular epithelial cells (Cheung et al., 2008).

Acute interstitial nephritis (AIN). AIN accounts for 2% to 3% of AKI, with most cases of AIN being caused by exposure to certain nephrotoxic drugs, such as NSAIDs and antibacte-rials (Cheung et al., 2008). This is thought to be an immune reaction and is not dose dependent (Naughton, 2008). AIN is a result of medications binding to antigens in the kidney or acting as antigens deposited in the interstitium, causing an immune reac-tion even though the classic symp-toms of a hypersensitivity reaction may be absent (Naughton, 2008).

Contrast-induced nephropathy (CIN). CIN usually occurs within 12 to 24 hours of a procedure using radiocontrast agents (ADIS Inter -national Ltd., 2009). Risk factors for developing CIN include underlying kidney insufficiency, being older than 70 years, volume depletion, repeated exposures to contrast in a short time frame, and heart failure and/or dia-betes mellitus (Naughton, 2008). Potential ways to prevent CIN include using low-osmolar contrast in the lowest dose possible, avoiding multiple procedures over a 24 to 48-hour time period, hydrating before and after procedures, or administer-ing prophylactic drugs, such as statins, sodium bicarbonate, or N-acetylcys-teine (ADIS International Ltd., 2009; Naughton, 2008). Many potentially preventative measures discussed are still under investigation and have had mixed outcomes in studies, particular-ly the use of prophylactic medica-tions.

Post-Renal Kidney Injury

Post-renal kidney injury is caused by obstruction either from kidney cal-culi, strictures, blood clots, benign prostatic hypertrophy, malignancies, and pregnancy (ADIS International Ltd., 2009; Cheung et al., 2008; Talbot, 2008). Obstructions such as those mentioned cause kidney injury by increasing the pressure within the kidney collecting systems, resulting in a drop in the GFR, decreased water and sodium reabsorption, and phos-phaturia (Talbot, 2008).


occur over the next 24 to 48 hours. Careful monitoring during this period is required to prevent pre-renal injury through volume depletion or fluid overload from too much fluid resusci-tation (ADIS International Ltd., 2009; Cheung et al., 2008; Talbot, 2008).

Risk Factors and Identification Of AKI

Common risk factors for develop-ing AKI include age greater than 60 years, diagnosis of sepsis, diabetes mellitus, heart disease, exposure to multiple nephrotoxic drugs, volume depletion, or underlying kidney insuf-ficiency (Cheung et al., 2008; Naughton, 2008; Talbot, 2008).

There is a higher incidence of AKI in older adults. Anatomical changes that occur in the aging kid-ney include shrinking with loss of parenchymal volume, cortical atro-phy, decreased glomeruli and proxi-mal tubule numbers, thickening of arteries and arterioles that supply kid-neys, and increased glomerulosclero-sis (Cheung et al., 2008). Function -ally, this means the aging kidney has a decrease in kidney blood flow and GFR. The most important functional factor in aging is the decreased GFR. Normal GFR is 120 to 130 mL/ min/1.73m2until about age 30, when

it drops 1 mL/min/year (ADIS International Ltd., 2009). Despite having a decreased GFR, it is impor-tant to remember older adults may have a serum creatinine within nor-mal limits due to loss of muscle mass associated with aging (Cheung et al., 2008). Another factor in older adults making them more susceptible to AKI is their increased vulnerability to hypovolemia due to impaired ability to concentrate urine (Cheung et al., 2008). Older adults are also more likely to have diabetes mellitus and/or heart disease, which are con-tributing factors as well. It is impor-tant to remember that with each addi-tional risk factor present, the risk for AKI goes up (Naughton, 2008).

One of the most commonly used

systems to identify and classify AKI or kidney dysfunction is the Risk, Injury, Failure, Loss, End Stage (RIFLE) classification. Ricci and co-authors (2007) conducted an analysis of research using RIFLE criteria and found it is a useful predictor of rela-tive risk of mortality in hospitalized patients. The RIFLE classification system for AKI is shown in Table 1 (Ricci et al., 2008).

Laboratory and diagnostic tests that aid in the diagnosis of AKI and in the determination of the possible cause are shown in Table 2. Along with the diagnostics, it is important to test and monitor for complications of AKI that may be life-threatening, such as hyperkalemia, pulmonary edema, and metabolic acidosis. Hyper kalemia with serum potassium of greater than 6.5 mmol/L is an emergency due to the risk of cardiac arrhythmias. Patients should be assessed for pulmonary edema by watching for signs of respiratory dis-tress, ascultating the lungs for crackles or other abnormalities through chest X-ray, and monitoring blood gases or oxygen saturation regularly. Meta

-bolic acidosis is also a life-threatening emergency; when blood pH is less than 7.2, systemic vasodilation is pro-duced, and the risk of hyperkalemia and cardiac arrhythmias is increased. If any of the above occur and are unresponsive to medical treatment, the patient should be referred for urgent dialysis (Cheung et al., 2008; Talbot, 2008).

Current Treatment

Nurses can play a vital role in identifying patients who are at risk for AKI and intervening early, possibly preventing life-threatening complica-tions. It is also important for nurses to be aware of the currently suggested treatments and implications for their practice. This knowledge can be used for nurses to advocate on behalf of patients, provide the best care, and be mindful of current research.

Managing Hemodynamics and Fluid Status

Monitoring fluid balance in the patient with AKI is extremely impor-tant. This includes the monitoring of RISK





Glomerular Filtration Rate Criteria Urine Output Criteria

Increased creatinine x 1.5 or GFR decrease greater than 25% Increased creatinine x 2 or GFR decrease greater than 50% Increased creatinine x 3 or GFR decrease greater than 75% or creatinine greater than 4 mg/100mL

Urine output less than 0.5 mL/kg/hour X 6 hours

Urine output less than 0.5 mL/kg/hour X 12 hours

Urine output less than 0.3 mL/kg/hour X 24 hours or Anuria X 12 hours

Persistent loss of kidney function greater than 4 weeks

End stage kidney disease/failure


Acute Kidney Injury: An Overview of Pathophysiology and Treatments

Laboratory Test or Diagnostic Normal Value Abnormal Value Possible Indication

Blood Tests

Serum creatinine Adult women: 0.6 to 1.1 mg/dL Adult men: 0.9 to

1.3 mg/dL

Greater than 1.3 mg/dL Impaired kidney function, chronic nephritis, or obstruction of urinary tract. Dependent upon muscle mass of individual. Gives indication of GFR related to excretion of creatinine by kidneys.

Blood urea nitrogen (BUN) Adults: 6 to 20 mg/dL Elderly (over 60

years): 8 to 23mg/dL

Greater than 23 mg/dL Panic value greater

than 100 mg/dL

Can indicate impaired kidney function caused by CHF, hypovolemia, shock. May also indicate glomerulonephritis or pyelonephritis or urinary tract obstruction.

BUN/creatinine ratio 10:1 to 20:1 Greater than 20:1 Less than 10:1

Increased with elevated creatinine may indicate obstruction of urinary tract or pre-renal azotemia. Decreased ratio with elevated creatinine may indicate rhabdomyolysis. Decreased ratio with decreased BUN may indicate acute tubular necrosis.

Cystatin C Adults: Less than 0.70 mg/mL

Elderly: Less than 0.85 mg/mL

Elevated above stated levels

Not affected by age, lean body mass, infection, or inflammation. Is a more sensitive indicator of kidney function, particularly in the elderly.

Urine Tests

Dipstick Blood: Negative Protein: Negative

Hematuria Protein:+3 to +4

on strip

Blood may indicate glomerulonephritis or rhabdomyolosis. Protein may indicate intrinsic kidney disease or rhabdomyolosis.

Osmolality 24-hour specimen: 300 to 900 mOsm/kg of water Random specimen: 50 to 1200 mOsm/kg of water Urine-to-serum ratio: 1:1 to 3:1

Above or below stated values

Increased in pre-renal azotemia, hypovolemia. Decrease in AKI. Urine to serum osmolality is increased in azotemia, decreased in acute tubular necrosis.

Urine sodium and electrolytes Adult: 40 to 220 mEq/24 hours

Above or below stated level

Low excretion may indicate pre-renal failure. High excretion with low osmolality may indicate acute tubular necrosis.

Diagnostic Tests

Kidney ultrasound Normal size, shape, and structure

Cysts, masses, obstruction of ureters, calculi, or hydronephrosis

Can show intrarenal or postrenal obstructions – potential causes of intrinsic or post-renal kidney injury.

Kidney doppler Equal blood flow to both kidneys, excretion of 50% of radiopharmaceutical agent within 10 minutes.

Deviation from stated normal

Deviation may indicate obstruction,

hypertension, or other acute or chronic kidney injury, such as renovascular disease.

Biopsy Normal tissue composition

Deviation from normal May indicate glomerulonephritis, vasculitis, or malignancy.

Table 2

Laboratory and Diagnostic Tests that Aid in the Diagnosis of AKI and in the Determination of the Possible Cause

Note: AKI = acute kidney injury.


urine output, and wound or nasogas-tric drainage (Sumnall, 2007). It is beneficial to have a Foley catheter inserted in patients with AKI so that urine output can be closely moni-tored. Patients should also be assessed for dependent or peripheral edema, third spacing of fluids, and for signs of pulmonary edema. Since patients with AKI can be intravascularly hypovolemic, it is important to deter-mine accurate fluid status to prevent overload; this monitoring is done through keeping intake and output, or through more invasive means, such as central venous pressure monitoring (Cheung et al., 2008; Talbot, 2008).

The loss of plasma proteins that occurs in AKI can alter the oncotic pressure (a form of osmotic pressure within the vasculature/capillaries that pulls fluid into the capillaries because the plasma proteins cannot cross the capillary wall). This causes fluid to leak out of the capillaries into the tis-sues leading to edema of the lungs and periphery, while the vasculature becomes hypovolemic (Sumnall, 2007). The goal of therapy is to opti-mize hemodynamics. If fluid resusci-tation fails to maintain cardiac output or correct hypotension, inotropic sup-port may be required (Cheung et al., 2008). Fluid overload may be man-aged by diuretics, particularly loop diuretics that inhibit the sodium-potassium-chloride pump in the loop of Henle. Diuretics are thought to reduce the oxygen demands of the cells and reduce susceptibility to ischemia; however, there are scarce data supporting the benefit of their use (Talbot, 2008). Sumnall (2007) suggests that continuous infusions of small amounts of diuretics may be more beneficial than bolus doses. In some cases, dialysis may be required to treat fluid overload.

Nutritional Considerations

When planning for nutritional needs of the patient experiencing AKI, it is important to consider both the severity of AKI and other co-mor-bidities the patient may have and how

that may affect his or her nutritional needs. The purpose of nutritional management is to avoid further stress on the body to control intake of spe-cific nutrients to avoid further dam-age to the kidneys and promote heal-ing (Cotton, 2007). A summary of suggestions of nutritional needs for patients with AKI is shown in Table 3.


The use of pharmacological agents in AKI is a complex process that may require renal dosing and careful selection of medications. Several drugs have been researched and are still being debated as to the benefit of their use in patients with AKI. Those that will be discussed here are dopamine, atrial natiuretic peptide, fenoldopam, and pentoxi-fylline. Diuretics were discussed pre-viously.

Prior to discussing any medica-tions, it is important to once again stress the avoidance or stopping of nephrotoxic medications in the patient with AKI. Naughton (2008) provides a more comprehensive guide of nephrotoxic medications than what is within the scope of this article. Commonly used nephrotoxic

medications include aminoglycoside antibiotics, non-steroidal anti-inflam-matory drugs, and antiretroviral med-ications (Cheung et al., 2008, Naughton, 2008).

Kidney doses of dopamine (0.5 to 3 mcg/kg/min) have been used previ-ously in hopes of limiting kidney injury. At this dose, dopamine dilates both afferent and efferent arterioles and increases kidney blood flow; how-ever, little gain in GFR is experienced (Cheung et al., 2008). Recent research has shown no benefit to the use of dopamine in AKI, with some research showing further harm in older patients; therefore, currently available evidence does not support the routine use of dopamine in treating AKI (Cheung et al., 2008, Talbot, 2008).

Atrial natiuretic peptide (ANP) vasodialates the afferent arteriole and constricts the efferent arteriole increasing GFR (Cheung et al., 2008). The use of this medication is still being researched and is largely inves-tigational. One meta-analysis found that in low doses, ANP reduced the need for dialysis and decreased over-all hospital length of stay. However, in high doses, ANP was associated with more hypotension and cardiac

Severity of AKI Daily Nutritional Suggestions

Mild AKI • 30 to 35 kcal/kg of desirable weight • 0.8 to 1.0 gm protein/kg of desirable weight

• May consider oral supplement if nutritional status is poor or oral intake is inadequate

Moderate AKI • 25 to 35 kcal/kg of edema free weight, limit to 25 kcal/kg if on ventilator

• 0.8 to 1.2 gm protein/kg if not on dialysis, minimum of 1.2 gm protein/kg if on dialysis

• If enteral nutrition use renal formula to avoid excess vitamins A and C

• May consider renal vitamin

Severe AKI • 20 to 25 kcal/kg of edema free weight • 2.0 to 2.5 gm protein/kg

• Early introduction of enteral feedings suggested for ventilat-ed patients to maintain gut integrity

• Parental nutrition should be maximally concentrated to avoid further fluid overload

Note: AKI = acute kidney injury.


Acute Kidney Injury: An Overview of Pathophysiology and Treatments

arrhythmias; there was no difference in mortality between the two groups (Nigwekar, Navaneethan, Parikh, & Hix, 2009). Perhaps in the future, more research may support low-dose ANP for prevention and faster recov-ery time for those at risk for or who have AKI.

Another potentially preventative drug is fenoldopam, which can reduce vascular resistance in the kid-ney and increase kidkid-ney blood flow. Several studies, though small in size, have shown potential prevention of AKI in patients undergoing cardio-vascular procedures who receive fenoldopam (Cheung et al., 2008).

Finally, pentoxifylline, a tumor necrosis factor-a production, has shown results in animal studies in the prevention of further kidney tubular damage from ischemia or reperfusion injury. This has not been widely stud-ied in humans but shows potential for future research (Cheung et al., 2008).

Stem Cell Treatment

Current research is looking into the use of stem cells for regeneration of tubular epithelial cells. It is thought that the kidney has some stem cells within itself contributing to its ability to regenerate after injury; however, a certain number of cells need to remain functional for regeneration to take place (Cheung et al., 2008; Yokoo, Kawamura, & Kobayashi, 2008). Experimental studies have been conducted that show promising results with both hemopoetic and mesenchymal stem cells differentiat-ing into kidney tubular cells; howev-er, more research is needed to sup-port the use in humans (Cheung et al., 2008; Yokoo et al., 2008).

Renal Replacement Therapy

Some guidelines for the initiation of renal replacement therapy (RRT) include hyperkalemia that is unre-sponsive to medical treatment or presents with EKG changes, metabol-ic acidosis with pH less than 7.2, or presentation of uremic encephalopa-thy or pericarditis (Cheung et al., 2008). There is conflicting research regarding when dialysis should be

ini-tiated and what modality or intensity should be utilized (Cheung et al., 2008; Talbot, 2008). Two common modalities of RRT are continuous renal replacement therapy (CRRT) and intermittent hemodialysis (IHD).

CRRT is a 24-hour-a-day, 7-day-a-week process that slowly removes excess fluid and solutes, and corrects electrolyte imbalances associated with AKI (Talbot, 2008). CRRT can be administered at different intensi-ties. Bellomo and colleagues (2009) conducted a study evaluating differ-ent intensities of CRRT and found that higher intensity CRRT did not reduce mortality or rate of depend-ence on dialysis, and the higher inten-sity group had more adverse out-comes. Some advantages to CRRT compared with IHD include increas -ed hemodynamic stability and fluid control, greater effectiveness in man-aging acid/base and electrolyte bal-ance, improved nutritional support and removal of toxins, and the ability to remove inflammatory mediators (Talbot, 2008).

IHD is a process of removing sol-uble substances and water across a semi-permeable membrane outside the body through the process of diffu-sion and trans-membrane pressure (Talbot, 2008). IHD requires a dual venous access device and is done for three to five hours, three to seven times a week. Caution is needed with IHD to prevent hypotension during and after dialysis that may lead to fur-ther kidney damage (Talbot, 2008). Benefits of IHD compared with CRRT include decreased risk of sys-temic bleeding, more time for diag-nostic testing, better control of hyper-kalemia, more cost-effective, and shorter ICU stays (Talbot, 2008).

In summary, there are many fac-tors and much debate about the use of

RRT in AKI. It is suggested that a specialist be consulted to manage AKI patients who may require RRT (Cheung et al., 2008).


AKI is a complex disorder that affects many body systems and car-ries a high mortality rate. Research by Hsu and colleagues (2007) found that community-based incidence of AKI is increasing. It is likely that rates of AKI will continue to increase with time. As healthcare professionals, it will become more important to understand the pathophysiology, treatments, and risk factors for AKI. By the brief understanding of these factors discussed in this article, one might be able to identify, intervene earlier, and possibly prevent serious complications from AKI in a patient who is at risk.


ADIS International, Ltd. (2009). Treat -ment of acute renal failure (ARF) in elderly patients requires early recog-nition and initiation of supportive treatment. Drugs & Therapy Perspec -tives, 25(4), 14-17.

Armitage, A.J., & Tomson, C. (2003). Acute renal failure. Medicine, 31(6), 43-48.

Barrantes, F., Feng, Y., Ivanov, O., Yalamanchili, H.B., Patel, J., Buenafe, X., ... Manthous, C. (2009). Acute kidney injury predicts outcome of non-critically ill patients. Mayo Clinic Proceedings, 84(5), 410-416.

Bellomo, R., Cass, A., Cole, L., Finfer, S., Gallagher, M., Lo, S., ... Su, S.(2009). Intensity of continuous renal-replace-ment therapy in critically ill patients.

The New England Journal of Medicine, 361(17), 1627-1638.

Nephrology Nursing Journal Editorial Board Statements of Disclosure

In accordance with ANCC-COA governing rules Nephrology Nursing Journal Editorial Board statements of disclo-sure are published with each CNE offering. The statements of disclodisclo-sure for this offering are published below. Paula Dutka, MSN, RN, CNN, disclosed that she is a consultant and research coordinator, is on the speaker’s bureau, and has sat on the advisory board for Genentech.

Patricia B. McCarley, MSN, RN, NP, disclosed that she is on the Consultant Presenter Bureau for Amgen, Genzyme, and OrthoBiotech. She is also on the Advisory Board for Amgen, Genzyme, and Roche and is the recipient of unrestricted educational grants from OrthoBiotech and Roche.


Cheung, C.M., Ponnusamy, A., & Anderton, J.G. (2008). Management of acute renal failure in the elderly patient: A clinician’s guide. Drugs & Aging, 25(6), 455-476.

Cotton, A.B. (2007). Medical nutrition ther-apy in acute kidney injury. Nephrology Nursing Journal, 34(4), 444-446. Fischbach, F. (2004). A manual of laboratory

and diagnostic tests (7th ed.). Phila -delphia: Lippincott, Williams & Wilkins.

Hsu, C., McCulloch, C.E., Fan, D., Ordonez, J.D., Chertow, G.M., & Go, A.S. (2007). Community-based inci-dence of acute renal failure. Kidney International, 72, 208-212.

Naughton, C.A. (2008). Drug-induced nephrotoxicity. American Family Physi -cian, 78(6), 743-750.

Nigwekar, S.U., Navaneethan, S.D., Parikh, C.R., & Hix, J.K.(2009) Atrial natriuretic peptide for preventing and treating acute kidney injury. Cochrane Database of Systematic Reviews, 4,

CD006028. DOI:10.1002/14651858. CD006028.pub2.

Porth, C.M. (2007). Renal failure. In C.M. Porth (Ed.), Essentials of pathophysiology: Concepts of altered health (2nd ed., pp. 521-536). Philadelphia: Lippincott, Williams & Wilkins.

Ricci, Z., Cruz, D., & Ronco, C. (2008). The RIFLE criteria and mortality in acute kidney injury: A systematic review. Kidney International, 73, 538-546.

Sumnall, R. (2007). Fluid management and diuretic therapy in acute renal failure.

Nursing in Critical Care, 12(1), 27-33. Talbot, S. (2008). Acute renal failure. In P.

Jevon, B. Ewens, & M. Humphreys (Eds.), Nursing medical emergency patients (pp. 199-229). United King -dom: John Wiley & Sons.

Yokoo, T., Kawamura, T., & Kobayashi, E. (2008). Stem cells for kidney repair: Useful tool for acute renal failure?



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Acute Kidney Injury: An Overview of Pathophysiology and Treatments

Kristina M. Yaklin, BSN, RN

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