What nursing measures are included in the plan of care for a client with acute renal failure?

Join NURSING.com to watch the full lesson now.

Join NURSING.com to watch the full lesson now.

Join NURSING.com to watch the full lesson now.

Learning Outcome

1. List the causes of renal failure

2. Describe the presentation of renal failure

3. Summarize the treatment of renal failure

4. Recall the role of the nurse in managing patients with renal failure

5. Emphasize the role of initial nursing care in the detection of AKI

6. Understand the importance of monitoring biochemistry as advised by the consultant

Acute kidney injury (AKI), formerly known as acute renal failure (ARF), denotes a sudden and often reversible reduction in kidney function, as measured by glomerular filtration rate (GFR).[1][2][3] There is no clear definition of AKI. Several different criteria have been used in research studies, such as RIFLE, AKIN (Acute Kidney Injury Network), or KDIGO (Kidney Disease: Improving Global Outcomes) criteria. However, KDIGO is the most recent and most commonly used. According to KDIGO, AKI is the presence of any of the following:

1. Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more) within 48 hours

2. Increase in serum creatinine to 1.5 times or more baseline, within the prior 7 days

3. Urine volume less than  0.5 mL/kg/h for at least 6 hours

Nursing Diagnosis

• Decreased or no urine output

The etiology of AKI has always been traditionally divided into three categories: pre-renal, renal, and post-renal. Each of these categories has several different causes associated with them.[4][5]

Pre-renal includes any reduced blood flow to the kidney. This may be part of systemic hypoperfusion resulting from hypovolemia or hypotension or might be due to selective hypoperfusion to the kidneys, such as those resulting from renal artery stenosis, aortic dissection.

Renal includes acute tubular necrosis, which can result from several different causes. Prolonged renal ischemia, sepsis, and nephrotoxins being the most common ones. It is worthwhile mentioning that pre-renal injury can convert into a renal injury if the exposure to the offending factor is prolonged enough to cause cellular damage.

Post-renal mainly includes obstructive causes, which lead to congestion of the filtration system and thus eventually lead to shutting down the kidneys. The most common ones being renal/ureteral calculi, tumors, or any urethral obstruction. Another noteworthy fact is that a unilateral obstruction may not always present as AKI, especially if the obstruction is gradual such as a tumor, because a normal working contralateral kidney may be able to compensate for the function of the affected kidney. Therefore, the most common etiology of post-renal AKI is bladder outlet obstruction.

AKI is commonly seen in patients admitted to the hospital. It is often an important factor that contributes to the decision to hospitalize for other conditions, if not being the sole reason for hospitalization. AKI is one of the most clinically impactful diseases since it affects patient management greatly regarding the treatment options for their primary disease. Most drugs or procedures that use contrast media may need to delay due to co-existent AKI. Most of the drugs are renally excreted, and dosages might need to be adjusted to account for the reduced renal function. Sometimes, it may even necessitate frequent monitoring of drug levels, for example, Vancomycin. AKI is thus an important contributor to longer hospital stays and patient morbidity.[6][7][8]

The history and physical exam should focus on determining the etiology of AKI and the timeline of progression. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. The physician needs to look for inciting events such as diarrhea, nausea, vomiting, which may have caused volume loss, or any over-the-counter drugs such as NSAIDs or other nephrotoxins. One of the important signs to look for on a physical exam is orthostatic vital signs since they are an important clue for hypovolemia and, in an appropriate clinical context, would guide treatment. History and physical are essential in AKI because, more often than not, labs are unable to provide a clear answer as to the etiology of AKI.

All patients presenting with AKI warrant a basic lab panel, including a basic metabolic panel. Sometimes, urine electrolytes can be helpful in suggesting an etiology of the AKI. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. Urine sediment examination can also provide important clues as to the etiology, such as muddy brown casts seen in acute tubular necrosis. [9][10]

There are markers of tubular function that can be calculated to help distinguish an etiology like the fractional excretion of sodium and urea, urine osmolality, but the sensitivity of all these markers is very poor, and they are affected by many drugs very commonly used in clinical practice such as diuretics. Therefore, no single marker can be reliably used in isolation to distinguish pre-renal from renal causes of AKI, which is a common misconception in clinical practice.

Except for post-renal AKI, most cases overlap between pre-renal and acute tubular necrosis type of AKI.[11][12] The best way to determine if the AKI is pre-renal or not is a fluid challenge. If the clinical scenario doesn't contradict it, all patients with acute renal dysfunction should receive a fluid challenge. They require close monitoring of urine output and renal function. If the renal function improves with fluid, that is the best indicator of a pre-Renal AKI. Acute tubular necrosis is very slow to recover and can take weeks to months for complete recovery of renal function. It may not normalize at all sometimes. Another important thing to consider for these patients is to avoid any further insult to the kidneys, such as nephrotoxic drugs. Any and all medications need to be renally dosed once a patient develops AKI. Sometimes, AKI may need short-term renal replacement therapy until the kidney function recovers. This is seen especially in the oliguric phase of acute tubular necrosis, where the patient is prone to develop multiple electrolyte and acid-base abnormalities as well as fluid overload.[13]

Nursing Management

• Monitor vitals including urine output

• Weigh patient daily to determine fluid retention

• Assess heart and lung sounds

• Monitor mental status changes and level of consciousness

• Assess periorbital and dependent edema

• Review chest x-ray and laboratory parameters (BUN and creatinine)

• Insert a Foley catheter to monitor ins and outs

• Administer diuretics as prescribed

• Monitor blood pressure and treat accordingly

• Check levels of potassium and if high, treat as clinician orders

• Encourage a low sodium diet, limit foods with high potassium like bananas, oranges, and tomatoes

• Keep head of bed elevated

When To Seek Help

• Extreme nausea and vomiting

• Unresponsive or sudden change in mental status

Outcome Identification

• Normalization of BUN and creatinine

• Healthy body weight with no dependent edema

• Alert and normal mental status

Monitoring

• BUN and creatinine levels

• Patient skin for dryness and itching

• Check eyes and feet for dependent edema

• Listen for rales and look for signs of respiratory distress

• Read ECG to ensure that the T wave has no large peaks (a sign of hyperkalemia)

AKI does have significant morbidity and mortality. Today, the aim is to try and prevent the condition in the first place by employing a multidisciplinary team approach. All healthcare workers must be aware of the condition and its causes. The pharmacist should ensure that the patient is on no nephrotoxic medications at the first signs of creatinine elevation. The nurse should ensure that the patient is well hydrated prior to any contrast study and can produce adequate urine. For those who develop AKI, the nurse should educate the patient on agents to avoid worsening the renal injury. Plus, close follow-up with a nephrologist is highly recommended. Finally, the patient should have a dietary consult because salt and fluid restriction is vital when managing AKI. Similarly, the patient should avoid a high potassium diet when there is renal dysfunction. Because AKI induces a catabolic state, the patient should be encouraged to eat at least 1800 calories per day.[14][15][16] [Level 5]

Outcomes

The outcomes for patients with AKI depend on the cause of the renal dysfunction, the presence of any underlying kidney disease, and the duration of the renal dysfunction. In the past, it was widely believed that AKI was fully reversible in all patients. Studies now show that in patients with a low eGFR, not only is there a higher risk of progressing to end-stage renal disease, but it also increases the mortality rate. In addition, AKI can also worsen the quality of life compared to the general population. Individuals who have a sudden increase in creatinine usually tend to have the worst prognosis. Today, in-hospital mortality for patients with AKI varies between 30-50%, especially when dialysis is required. Negative prognostic factors include:

• Advanced age

• Oliguria

• Use of vasopressors

• Multiorgan dysfunction

• Need for blood transfusions

• Hypotension

Over the long term, at least 12% to 15% of patients with AKI may require permanent dialysis. Mortality is increased in patients with high APACHE lll score, advanced age, and persistent creatinine elevation.[17][18] [Level 5]

Health Teaching and Health Promotion

• Eat a healthy low sodium diet, avoiding bananas, oranges, and tomatoes

• Avoid medications like NSAIDs

• Educate patient on renal failure and potential treatments

• Get blood work regularly to ensure that BUN, creatinine, and potassium levels are within the normal range

Risk Management

• Refer patient to a nephrologist if urine output is low, potassium is high and BUN/Creatinine levels are high

• If there is a change in mental status, the clinician should be notified.

Discharge Planning

• Take medications as prescribed

• If short of breath or not passing urine, return to the emergency department.

Mild AKI can often be managed outpatient. More often than not, AKI is a co-existent problem for hospitalized patients and usually is appropriate for these patients to be on the general medical floor unless they also have an electrolyte imbalance or significant volume overload, in which case, they may require a higher level of care. The most important issues to realize for clinicians dealing with AKI are adjusting the dose of any medications these patients are taking and avoiding nephrotoxic medications as much as possible. The other important thing to consider is an appropriate fluid challenge whenever possible.

Review Questions

1.

Muroya Y, He X, Fan L, Wang S, Xu R, Fan F, Roman RJ. Enhanced renal ischemia-reperfusion injury in aging and diabetes. Am J Physiol Renal Physiol. 2018 Dec 01;315(6):F1843-F1854. [PMC free article: PMC6336981] [PubMed: 30207168]

Palevsky PM. Endpoints for Clinical Trials of Acute Kidney Injury. Nephron. 2018;140(2):111-115. [PubMed: 30205392]

Zuber K, Davis J. The ABCs of chronic kidney disease. JAAPA. 2018 Oct;31(10):17-25. [PubMed: 30204617]

Moresco RN, Bochi GV, Stein CS, De Carvalho JAM, Cembranel BM, Bollick YS. Urinary kidney injury molecule-1 in renal disease. Clin Chim Acta. 2018 Dec;487:15-21. [PubMed: 30201372]

Crabbs TA. Acute Kidney Injury (AKI)-The Toxicologic Pathologist's Constant Companion. Toxicol Pathol. 2018 Dec;46(8):918-919. [PubMed: 30189797]

Winther-Jensen M, Kjaergaard J, Lassen JF, Køber L, Torp-Pedersen C, Hansen SM, Lippert F, Kragholm K, Christensen EF, Hassager C. Use of renal replacement therapy after out-of-hospital cardiac arrest in Denmark 2005-2013. Scand Cardiovasc J. 2018 Oct;52(5):238-243. [PubMed: 30182752]

Park S, Lee S, Lee A, Paek JH, Chin HJ, Na KY, Chae DW, Kim S. Awareness, incidence and clinical significance of acute kidney injury after non-general anesthesia: A retrospective cohort study. Medicine (Baltimore). 2018 Aug;97(35):e12014. [PMC free article: PMC6392954] [PubMed: 30170408]

Kirkley MJ, Boohaker L, Griffin R, Soranno DE, Gien J, Askenazi D, Gist KM., Neonatal Kidney Collaborative (NKC). Acute kidney injury in neonatal encephalopathy: an evaluation of the AWAKEN database. Pediatr Nephrol. 2019 Jan;34(1):169-176. [PMC free article: PMC6986688] [PubMed: 30155763]

Sanguankeo A, Upala S. Limitations of Fractional Excretion of Urea in Clinical Practice. Hepatology. 2019 Mar;69(3):1357. [PubMed: 30180288]

Brkovic V, Milinkovic M, Kravljaca M, Lausevic M, Basta-Jovanovic G, Marković-Lipkovski J, Naumovic R. Does the pathohistological pattern of renal biopsy change during time? Pathol Res Pract. 2018 Oct;214(10):1632-1637. [PubMed: 30139556]

Abdelsalam M, Elnagar SSE, Mohamed AH, Tawfik M, Sayed Ahmed N. Community Acquired Acute Kidney Injury in Mansoura Nephrology Dialysis Unit: One Year Prospective Observational Study. Nephron. 2018;140(3):185-193. [PubMed: 30205406]

Azzalini L, Vilca LM, Lombardo F, Poletti E, Laricchia A, Beneduce A, Maccagni D, Demir OM, Slavich M, Giannini F, Carlino M, Margonato A, Cappelletti A, Colombo A. Incidence of contrast-induced acute kidney injury in a large cohort of all-comers undergoing percutaneous coronary intervention: Comparison of five contrast media. Int J Cardiol. 2018 Dec 15;273:69-73. [PubMed: 30196995]

Cahn A, Melzer-Cohen C, Pollack R, Chodick G, Shalev V. Acute renal outcomes with sodium-glucose co-transporter-2 inhibitors: Real-world data analysis. Diabetes Obes Metab. 2019 Feb;21(2):340-348. [PubMed: 30207040]

Hobson C, Lysak N, Huber M, Scali S, Bihorac A. Epidemiology, outcomes, and management of acute kidney injury in the vascular surgery patient. J Vasc Surg. 2018 Sep;68(3):916-928. [PMC free article: PMC6236681] [PubMed: 30146038]

Doi K, Nishida O, Shigematsu T, Sadahiro T, Itami N, Iseki K, Yuzawa Y, Okada H, Koya D, Kiyomoto H, Shibagaki Y, Matsuda K, Kato A, Hayashi T, Ogawa T, Tsukamoto T, Noiri E, Negi S, Kamei K, Kitayama H, Kashihara N, Moriyama T, Terada Y., Japanese Clinical Practice Guideline for Acute Kidney Injury 2016 Committee. The Japanese Clinical Practice Guideline for acute kidney injury 2016. J Intensive Care. 2018;6:48. [PMC free article: PMC6088399] [PubMed: 30123509]

Sarin SK, Choudhury A. Management of acute-on-chronic liver failure: an algorithmic approach. Hepatol Int. 2018 Sep;12(5):402-416. [PubMed: 30116993]

Huang ST, Ke TY, Chuang YW, Lin CL, Kao CH. Renal complications and subsequent mortality in acute critically ill patients without pre-existing renal disease. CMAJ. 2018 Sep 10;190(36):E1070-E1080. [PMC free article: PMC6131084] [PubMed: 30201614]

Helgason D, Long TE, Helgadottir S, Palsson R, Sigurdsson GH, Gudbjartsson T, Indridason OS, Gudmundsdottir IJ, Sigurdsson MI. Acute kidney injury following coronary angiography: a nationwide study of incidence, risk factors and long-term outcomes. J Nephrol. 2018 Oct;31(5):721-730. [PubMed: 30187381]