Acute Kidney Injury: Inpatient Management and Treatment

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Introduction   

Acute Kidney Injuries (AKI) are common in hospitalized patients. Studies have shown that acute kidney injuries make up 7% of hospital admissions and 30% of ICU admissions [1]. Acute kidney injuries have been shown to correlate with hospitalized mortality and an increased length in the hospital stay for the patient [2]. These in turn can cause an increase in healthcare costs [2].

In 2020, the rate of hospitalizations due to AKI’s were lower than in 2019 {3]. However, patients with AKI’s requiring dialysis were higher in 2020 than the previous year [3]. The rate of mortality has decreased in patients with AKI’s over the past several years, but it is still high and varies on the severity of the AKI [2].

According to these statistics, acute kidney injuries have serious implications for patients, and it is important for nurses to be aware of the signs, symptoms, and complications of this condition. Patients that experience an acute kidney injury are at risk for developing chronic kidney disease [2]. This course is designed to increase knowledge of this condition to better care for our patients and provide our patients with accurate education.

What is an Acute Kidney Injury?

The term Acute Kidney Injury refers to the decrease in renal function that is measured by the glomerular filtration rate (GFR) [1]. This condition used to be referred to as acute renal failure [1]. The diagnosis of an acute kidney injury is based on meeting specific criteria.

The Kidney Disease Improving Global Outcomes group developed and published criteria for diagnosing acute kidney injuries [2].

• A serum creatinine level increase to at least 0.3mg/dL in 48hours
• Serum creatinine level 1.5 times higher than the baseline, which was taken within the past 7 days,
• A decrease of urine output that is less than 0.5ml/kg/hr. for 6 hours [1] [2].

The patient must meet at least one criterion for the diagnosis of acute kidney injury. The creatinine and blood urea nitrogen (BUN) may be within normal limits at the onset of the kidney injury [1]. The decrease in urine output may be the first sign of acute kidney injury [1].

Epidemiology 

Acute kidney injury is a very common condition. Studies have shown that in the United States, 1% of all hospital admissions have an acute kidney injury [1]. This condition can impact the management and treatment of the patient. Diagnostic tests that use contrast dye are often delayed because the dye can cause damage to the kidneys [1].  

A significant number of medications are excreted through the kidneys, so if the kidneys are not functioning normally the metabolism of the drug will be reduced. The doses of drugs may need to be altered or kidney function labs may need to be monitored closely.

Pathophysiology/ Etiology 

Pathophysiology and etiology go hand in hand as the pathophysiology of the acute kidney injury can be determined by the cause. There are three types of acute kidney injuries, which can determine the pathophysiology of the condition.  

Pre-Renal – caused by lack of perfusion to the kidney. The decreased perfusion can be attributed to hypovolemia or hypotension [1]. The decreased perfusion can also be due to selective hypoperfusion from an aortic dissection or renal artery stenosis [1]. With prerenal acute kidney injuries, the glomerular and tubular function stays within normal limits [1].  

Some examples of this form can be renal vasoconstriction due to NSAID use or iodinated contrast [1]. Also decreased cardiac function from congested heart failure or acute myocardial infarction can cause this form of acute kidney injuries [2]. Anesthesia and surgical operations can increase vascular resistance which can cause prerenal acute kidney injuries. 

Intrinsic – affects the glomerular tubular functions [1]. The injury of the glomerulus or tubular injury release vasoconstrictors from renal pathways [1]. Sepsis and prolonged renal ischemia are common causes.  

Medications such as vancomycin and aminoglycosides can cause acute tubular necrosis [1]. Acute tubular necrosis has been shown to be the most common cause of acute kidney injuries in a patient who is hospitalized [1].  

Glomerulonephritis can be caused by autoimmune diseases such as systemic lupus erythematous [1]. Interstitial nephritis can be caused by medications such as NSAIDS, diuretics, and proton pump inhibitors [1] [2].

The process of acute kidney injuries due to acute tubular necrosis is broken down into four phases [4] [5].  

The phases walk through what is happening at a cellular level during the injury [4]: 

1. Initiation phase – blood flow is reduced to the kidney which causes a reduction in ATP accessibility [4]. There is structural damage to the cell which leads into the next phase and the inflammatory process [4]. 
2. Extension phase consists of the inflammatory process and hypoxia [4]. The effects are in the medullary part of the kidney [4]. The changes reduce the glomerular filtration rate and release chemokines and cytokines [4]. For intervention it is important to counteract the inflammatory process at this phase [4]. 
3. Maintenance phase – cell repair begins. The blood vessels begin the process of restoring normal structure [4].  
4. Recovery phase – organ function improves [4]. The extent of the normal function related to the cellular activity during the injury [4]. 

Post Renal – caused by obstruction that affects the filtration system [1]. Blood clots, renal calculi, and tumors are common causes of obstructions [1]. If the obstruction is one-sided it may not show as an acute kidney injury because the normal functioning kidney may compensate for the impaired kidney. [1] 

Because kidneys are highly sensitive, acute kidney injuries are usually caused by other systemic causes such as septic shock, cardiogenic shock, post-major surgical intervention and hypovolemia [2].

Case Study: A 55-year-old female presents to the emergency department with lower back pain, nausea, and vomiting. Pt has a past medical history of type II diabetes, hypertension, and anxiety. Pt reports decrease urine output in the last day. Urinalysis reveals red blood cells present in the urine. Renal ultrasound shows right renal calculi. Creatinine level of 2.9mg/dL and BUN 20mg/dL.  

• In this case study, what form of AKI is the patient most likely to have? 

• Which risk factors for acute kidney injuries does the patient have?

Case Study: A 4-year-old male presents to the pediatric emergency department, brought in by mom for lethargy, vomiting, and decreased urine output. Mom reports the patient has had vomiting and diarrhea for 3 days and is refusing to eat or drink. The mom states the patient voided once in the last 12 hours and it was dark amber in color. Creatinine level of 2.1mg/dL and BUN 22mg/dL. 

• What form of AKI could this patient most likely be experiencing? 

• What would be the first action to treat this acute kidney injury? 

• Are there any other diagnostic tests that should be performed? 

Clinical Signs and Symptoms 

The signs and symptoms of acute kidney injuries are dependent on the cause and the severity of the injury [6]. A patient with a mild acute kidney injury may be asymptomatic [6].  

Patients with a more severe acute kidney injury may experience peripheral or periorbital edema, shortness of breath, oliguria, confusion, nausea and vomiting, and back pain [6].  

Seizures can develop in severe cases [6].  

There are four phases of acute kidney injuries: 

1. Onset Phase: This phase includes the initial injury which causes decreased renal perfusion. [6]. Some of these causes can include dehydration, infection, or blood loss. [6] The renal tissue oxygenation has decreased by 25% and the urine output has decreased to less than 0.5ml/kg/hr. The phase varies from hours or up to days [6].  
2. Oliguric Phase: Oliguria occurs within 1 to 7 days of the initial renal injury [6]. This phase may last around 10 to 14 days or in some severe instances up to months [6]. The longer the duration of this phase is related to the lessened chance for recovery of renal function [6]. Some cases patients do not experience oliguria [6]. Fluid overload is seen in this phase.  
3. Diuretic Phase: The urine output increases in the phase to around 1 to 3 liters [6]. Due to increased loss of fluid hypovolemia and hypotension may be a side effect of this phase [6]. This phase can last 1 to 3 weeks [6]. Electrolytes, BUN, and creatinine usually start to be within normal limits [6]  
4. Recovery Phase: This phase is when kidney function starts to improve and the GFR may increase while the BUN and creatinine return to normal limits [6]. This phase can take up to a year for a patient to recover [6]. In some severe cases the patient is unable to recover, and the condition leads to end stage renal disease (ESRD) [6]. This can depend on the patient’s comorbidities and response to the treatment [6].

Diagnostic Testing 

When diagnosing acute kidney injuries history and physical play a center role. Obtaining the history from the patient about events that took place prior to the hospitalization is key to developing a treatment plan. If the patient experienced diarrhea or vomiting the provider needs to focus on fluid resuscitation [1]. A medication history should be obtained to identify if the patient is on any medications that can be nephrotoxic.  

Lab tests can be useful in diagnosing and well as indicating the etiology of acute kidney injury. The serum creatinine often takes a couple of days to increase after the initial kidney injury so this cannot be used as an early diagnostic tool [2]. The urine output can be used to identify an acute kidney injury however it can be difficult to assess without using a urinary catheter [2].  

A complete blood count can be used to determine if infection or anemia is present [6]. A urinalysis can be used in diagnosing acute kidney injuries as this can help determine the type. Urine brown in color and sediment may indicate acute tubular necrosis [6]. White blood cells may indicate pyelonephritis [6]. Red blood cells in the urine may be due to glomerular nephritis [6].  

Imaging studies can be used in diagnosing acute kidney injuries. Renal ultrasounds can determine if there is an obstruction [6]. A CT scan without contrast can identify nephrolithiasis or urolithiasis [1].  

A renal biopsy may be warranted if the patient’s kidney function is rapidly decreasing without knowledge of the cause [1]. A biopsy can be used if the patient’s kidney function has not normalized for a prolonged period [6].

Inpatient treatment 

The treatment of acute kidney injury can be dependent on the form of the injury. Commonly fluid resuscitation is the first line of treatment for an acute kidney injury unless it is contraindicated for the patient [1].  

The urine and kidney function should be closely monitored [1]. If the kidney function improves after fluid, it is most likely the result of a prerenal acute kidney injury [1]. Patients with acute tubular necrosis their kidney function does not rapidly improve after fluid and can take up to months to improve [1].  

Diuretics may be required if the patient is fluid overloaded with acute tubular necrosis [1]. Nephrotoxic drugs should be stopped, and other medications should be renally dosed [1]. 20- 40% of acute kidney injuries have been attributed to nephrotoxic drugs as the cause [2]. This number has been said to increase to 60% in patients with advanced age [2].  

Dietary changes are also a part of management of acute kidney injuries [1]. Reduction of phosphorus and potassium in the diet is necessary [1].  

The type of fluid that is given during fluid resuscitation has been up for debate. Both crystalloids and colloids are used during fluid resuscitation [2]. Common crystalloids are saline, lactated ringers, and PlasmaLyte [2]. Colloids can be albumin and starches [2].  

A study was done that investigated patients that received colloids and they were less likely to need vasopressors, mechanical ventilation, and a decrease in mortality [2]. When albumin is given for fluid resuscitation it requires less volume than crystalloids [2].  

Renal replacement therapy in the intensive care unit may be necessary in patients with severe acute kidney injuries [2]. Continuous RRT (CRRT) is a common type of renal support given to patients with acute kidney injuries [2]. RRT can have adverse effects on the patient such as infection due to the dialysis catheter, risk of thrombosis, and risk of hemorrhage [7]. Studies have shown that the intensity of the RRT can slow the recovery process from acute kidney injuries [7].  

Nursing management of a patient with acute kidney injury can include monitoring urine output and vitals. Also, when performing a physical assessment, the heart and lungs should be auscultated [8].  

Mental status should be monitored and level of consciousness [8]. Monitor for any signs of periorbital and dependent edema [8]. The head of the bed should be elevated [8].

Patient Education 

Acute kidney injuries require follow-up and education to complete the recovery process. As nurses we must provide our patients with education so they can make decisions about their healthcare and to improve their recovery process. Education can cut down on readmissions and healthcare costs.  

Dietary education should be included in patient education. Patients should be encouraged to avoid tomatoes, oranges, and bananas and to follow a low sodium diet [8]. Smoking should be discouraged [8].  

Certain medications like NSAIDs should be avoided. Follow-up is necessary with their provider and repeat lab work such as creatinine, BUN, and electrolytes [8].

Conclusion

An acute kidney injury is a common condition that can produce lasting effects for a patient. Acute kidney injuries can make managing other conditions more difficult. Diagnosing an AKI should include a history and physical, kidney function tests, as well as clinical symptoms.

Early recognition of acute kidney injuries can prevent long term damage. As healthcare providers it is important to identify the signs and symptoms of acute kidney injuries to provide early interventions for our patients.

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