Acute kidney injury: an overview of pathophysiology and treatments.
To provide an overview of acute kidney injury, its pathophysiology, and treatments.
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.
There has been an increase in the prevalence of acute kidney injury (AKI) over the past 15 years due to the increased percentage of older adults in the population 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 surgical 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 likelihood 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 prevalence of AKI is increasing, it is very likely that most healthcare professionals will encounter patients with AKI. The purpose of this article is to provide education on the pathophysiology of AKI, aid in identifying risk factors, and discuss current research on treatment options and interventions.
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 depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and renal artery stenosis (ADIS International Ltd., 2009, Cheung et al., 2008, Talbot, 2008). Some vasoactive medications, such as angiotensin-converting 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 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 reabsorption of substances filtered through the glomerulus (Porth, 2007). The glomerular 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 hormones or drugs (Porth, 2007). When kidney blood flow reaches approximately 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, vessels, or kidney tubules, which can often be brought on by prolonged pre-renal causes leading to cell necrosis by ischemia, or by infectious agents and toxins that result in inflammation 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 contrast-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 prolonged pre-renal azotemia or by sepsis and toxic ATN is caused by direct tubular damage by nephrotoxins, such as aminoglycosides or radio contrast 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 leading 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 obstruction (Porth, 2007). The kidneys are particularly susceptible to nephrotoxic injury due to its rich blood supply, ability to concentrate toxins, and metabolic processes within the kidney 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 epithelium (Cheung et al., 2008). The obstruction also increases pressure on the system, decreasing GFR and contributing to afferent arteriole constriction 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 typically follows a sequence of three events: initiation, maintenance, and recovery. The initiation phase is characterized 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 sustained 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 creatinine 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 antibacterials (Cheung et al., 2008). This is thought to be an immune reaction and is not dose dependent (Nanghton, 2008). AIN is a result of medications binding to antigens in the kidney or acting as antigens deposited in the interstitium, causing an immune reaction even though the classic symptoms 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 International 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 diabetes 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 administering prophylactic drugs, such as statins, sodium bicarbonate, or N-acetylcysteine (ADIS International Ltd., 2009; Naughton, 2008). Many potentially preventative measures discussed are still under investigation and have had mixed outcomes in studies, particularly the use of prophylactic medications.
Post-Renal Kidney Injury
Post-renal kidney injury is caused by obstruction either from kidney calculi, 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 phosphaturia (Talbot, 2008).
Following removal or correction of obstruction, profuse diuresis can 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 resuscitation (ADIS International Ltd., 2009; Cheung et al., 2008; Talbot, 2008).
Risk Factors and Identification Of AKI
Common risk factors for developing AKI include age greater than 60 years, diagnosis of sepsis, diabetes mellitus, heart disease, exposure to multiple nephrotoxic drugs, volume depletion, or underlying kidney insufficiency (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 kidney include shrinking with loss of parenchymal volume, cortical atrophy, decreased glomeruli and proximal tubule numbers, thickening of arteries and arterioles that supply kidneys, and increased glomerulosclerosis (Cheung et al., 2008). Functionally, 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/1.73[m.sup.2] until about age 30, when it drops 1 mL/min/year (ADIS International Ltd., 2009). Despite having a decreased GFR, it is important to remember older adults may have a serum creatinine within normal 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 contributing factors as well. It is important to remember that with each additional 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 relative 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. Hyperkalemia 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 distress, ascultating the lungs for crackles or other abnormalities through chest X-ray, and monitoring blood gases or oxygen saturation regularly. Metabolic acidosis is also a life-threatening emergency; when blood pH is less than 7.2, systemic vasodilation is produced, 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).
Nurses can play a vital role in identifying patients who are at risk for AKI and intervening early, possibly preventing life-threatening complications. 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 important. This includes the monitoring of strict intake and output from all sources, such as IV and oral intake, urine output, and wound or nasogastric drainage (Sumnall, 2007). It is beneficial to have a Foley catheter inserted in patients with AKI so that urine output can be closely monitored. 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 determine 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 tissues leading to edema of the lungs and periphery, while the vasculature becomes hypovolemic (Sumnall, 2007). The goal of therapy is to optimize hemodynamics. If fluid resuscitation fails to maintain cardiac output or correct hypotension, inotropic support may be required (Cheung et al., 2008). Fluid overload may be managed by diuretics, particularly loop diuretics that inhibit the sodiumpotassium-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-morbidities 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 specific nutrients to avoid further damage to the kidneys and promote healing (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 pentoxifylline. Diuretics were discussed previously.
Prior to discussing any medications, 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-inflammatory drugs, and antiretroviral medications (Cheung et al., 2008, Naughton, 2008).
Kidney doses of dopamine (0.5 to 3 mcg/kg/min) have been used previously in hopes of limiting kidney injury. At this dose, dopamine dilates both afferent and efferent arterioles and increases kidney blood flow; however, 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 investigational. One meta-analysis found that in low doses, ANP reduced the need for dialysis and decreased overall hospital length of stay. However, in high doses, ANP was associated with more hypotension and cardiac 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 recovery time for those at risk for or who have AKI.
Another potentially preventative drug is fenoldopam, which can reduce vascular resistance in the kidney and increase kidney blood flow. Several studies, though small in size, have shown potential prevention of AKI in patients undergoing cardiovascular 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 studied 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 differentiating into kidney tubular cells; however, more research is needed to support 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 unresponsive to medical treatment or presents with EKG changes, metabolic acidosis with pH less than 7.2, or presentation of uremic encephalopathy or pericarditis (Cheung et al., 2008). There is conflicting research regarding when dialysis should be initiated 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 intensities. Bellomo and colleagues (2009) conducted a study evaluating different intensities of CRRT and found that higher intensity CRRT did not reduce mortality or rate of dependence on dialysis, and the higher intensity group had more adverse outcomes. Some advantages to CRRT compared with IHD include increased hemodynamic stability and fluid control, greater effectiveness in managing acid/base and electrolyte balance, improved nutritional support and removal of toxins, and the ability to remove inflammatory mediators (Talbot, 2008).
IHD is a process of removing soluble substances and water across a semi-permeable membrane outside the body through the process of diffusion 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 further kidney damage (Talbot, 2008). Benefits of IHD compared with CRRT include decreased risk of systemic bleeding, more time for diagnostic testing, better control of hyperkalemia, more cost-effective, and shorter ICU stays (Talbot, 2008).
In summary, there are many factors 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 carries 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.
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Nephrology Nursing Journal Editorial Board Statement of Disclosure
In accordance with ANCC-COA governing rules Nephrology Nursing Journal Editorial Board statements of disclosure are published with each CNE Offering. The statements of disclosure 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.
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Armitage, A.J., & Tomson, C. (2003). Acute renal failure. Medicine, 37(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.
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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 therapy in acute kidney injury. Nephrology Nursing Journal, 34(4), 444-446.
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Hsu, C., McCulloch, C.E., Fan, D., Ordonez, J.D., Chertow, G.M., & Go, A.S. (2007). Community-based incidence of acute renal failure. Kidney International, 72, 208-212.
Naughton, C.A. (2008). Drug-induced nephrotoxicity. American Family Physician, 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 Kingdom: John Wiley & Sons.
Yokoo, T., Kawamura, T., & Kobayashi, E. (2008). Stem cells for kidney repair: Useful tool for acute renal failure? Kidney International, 74, 847-849.
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 email@example.com
Statement of Disclosure: The author reported no actual or potential conflict of interest in relation to this continuing nursing education article.
Table 1 RIFLE Classification System for AKI Glomerular Filtration Rate Urine Output Criteria Criteria RISK Increased creatinine x 1.5 Urine output less than 0.5 or GFR decrease greater mL/kg/hour X 6 hours than 25% INJURY Increased creatinine x 2 Urine output less than 0.5 or GFR decrease greater mL/kg/hour X 12 hours than 50% FAILURE Increased creatinine x 3 Urine output less than or GFR decrease greater 0.3 mL/kg/hour X 24 than 75% or creatinine hours or Anuria X 12 greater than hours 4 mg/100mL LOSS Persistent loss of kidney function greater than 4 weeks ESRD End stage kidney disease/failure Source: Adapted from Ricci et al., 2008. Table 2 Laboratory and Diagnostic Tests that Aid in the Diagnosis of AKI and in the Determination of the Possible Cause Laboratory Test or Diagnostic Normal Value Abnormal Value Blood Tests Serum Adult women: 0.6 to Greater than 1.3 mg/dL creatinine 1.1 mg/dL Adult men: 0.9 to 1.3 mg/dL Blood urea Adults: 6 to 20 mg/dL Greater than 23 mg/dL nitrogen (BUN) Elderly (over 60 Panic value greater years): 8 to than 100 mg/dL 23mg/dL BUN/creatinine 10:1 to 20:1 Greater than 20:1 ratio Less than 10:1 Cystatin C Adults: Less than 0.70 Elevated above stated mg/mL levels Elderly: Less than 0.85 mg/mL Urine Tests Dipstick Blood: Negative Hematuria Protein: Negative Protein:+3 to +4 on strip Osmolality 24-hour specimen: Above or below stated 300 to 900 values mOsm/kg of water Random specimen: 50 to 1200 mOsm/kg of water Urine-to-serum ratio: 1:1 to 3:1 Urine sodium Adult: 40 to 220 Above or below stated and mEq/24 hours level electrolytes Diagnostic Tests Kidney Normal size, shape, Cysts, masses, ultrasound and structure obstruction of ureters, calculi, or hydronephrosis Kidney doppler Equal blood flow to Deviation from stated both kidneys, normal excretion of 50% of radiopharmaceutical agent within 10 minutes. Biopsy Normal tissue Deviation from normal composition Laboratory Test or Diagnostic Possible Indication Blood Tests Serum Impaired kidney function, chronic nephritis, or creatinine obstruction of urinary tract. Dependent upon muscle mass of individual. Gives indication of GFR related to excretion of creatinine by kidneys. Blood urea Can indicate impaired kidney function caused nitrogen (BUN) by CHF, hypovolemia, shock. May also indicate glomerulonephritis or pyelonephritis or urinary tract obstruction. BUN/creatinine Increased with elevated creatinine may ratio 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 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 may indicate glomerulonephritis or rhabdomyolosis. Protein may indicate intrinsic kidney disease or rhabdomyolosis. Osmolality Increased in pre-renal azotemia, hypovolemia. Decrease in AKI. Urine to serum osmolality is increased in azotemia, decreased in acute tubular necrosis. Urine sodium Low excretion may indicate pre-renal failure. and High excretion with low osmolality may electrolytes indicate acute tubular necrosis. Diagnostic Tests Kidney Can show intrarenal or postrenal obstructions ultrasound - potential causes of intrinsic or post-renal kidney injury. Kidney doppler Deviation may indicate obstruction, hypertension, or other acute or chronic kidney injury, such as renovascular disease. Biopsy May indicate glomerulonephritis, vasculitis, or malignancy. Note: AKI = acute kidney injury. Sources: Compiled from Cheung et al., 2008; Fischbach, 2004; Talbot, 2008. Table 3 Summary of Suggestions of Nutritional Needs for Patients with AKI 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 ventilated patients to maintain gut integrity * Parental nutrition should be maximally concentrated to avoid further fluid overload Note: AKI = acute kidney injury. Source: Compiled from Cotton, 2007.
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|Title Annotation:||Continuing Nursing Education|
|Author:||Yaklin, Kristina M.|
|Publication:||Nephrology Nursing Journal|
|Date:||Jan 1, 2011|
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