To pee or not to pee…lets talk acute kidney injury

Acute kidney injury (AKI), formerly called, acute renal failure, is common among hospitalized patients. AKI is defined as a rapid decline in renal function with resulting disruption in regulation of volume, electrolytes, and build up of nitrogenous waste products. In class, you may learn about the KDIGO (Kidney Disease: Improving Global Outcomes) criteria for defining AKI: including an increased creatinine and decreased UOP (<0.5 mL/kg/hr).

So, we know what it is, but how do we get there and why is it important? I think a brief discussion of the main functions of the kidney would fit well here. The kidneys are composed of many different structures, but one structure makes it all happen: the nephron. Each kidney has about a million nephrons, each of which contain a glomerulus, and renal tubules. The glomerulus is a network of twisted capillaries that performs filtration of the blood. The tubules are responsible for reabsorption and secretion. So basically, stuff like glucose, amino acids, electrolytes, and metabolites are passed back and forth between the glomerulus and the tubules until blood composition is just how the body needs it. What’s left over after these processes is secreted in the form of urine. Fun fact, we only excrete about 1% of filtered fluid as urine…and we excrete between 1-2 L of urine per day!

Ok, let’s talk causes of AKI. All underlying causes are classified as either pre-renal, intra-renal, or post-renal causes. Pre-renal causes for AKI include diseases/ disorders that lead to decreased renal perfusion; think CHF and hypovolemia which decrease cardiac output. Sepsis, and other conditions which cause widespread vasodilation also reduce renal perfusion leading to pre-renal AKI. Also, hepato-renal syndrome (HRS) is a condition seen in patients with advanced liver disease. When the liver fails, toxins build up within the blood that cause splanchnic vasodilation and reactive renal vasoconstriction, thus decreasing blood flow to the kidneys.

Next are the intrarenal causes. Intrarenal AKI occurs when there is damage to the actual renal parenchyma; in other words the glomerulus, interstitium, or tubules are damaged. Among intra-renal causes, the most common is called acute tubular necrosis (ATN) and this happens when there is death of actual renal tubular cells. Nephrotoxic drugs like Vancomycin, amino-glycosides, and contrast dye are the most common culprits here. Glomerulonephritis, inflammation of the glomerulus, is another cause of intra-renal AKI. There are also drugs that can cause intra-renal AKI including beta-lactams and proton pump inhibitors. Also, think about renal artery obstruction and DIC which cause micro-emboli that can lead to renal infarction.

Finally, post-renal causes of AKI occur due to issues with urine outflow. Post- renal causes include BPH which obstructs outflow through the urethra. Also, think about a foley catheter that may be kinked or obstructed, preventing outflow of urine. Typically, post-renal causes are the easiest to resolve.

Whew, that was a lot! So now that we know what acute kidney injury is, what causes it, and the pathophysiology behind it, what are we going to do for these patients? Well, it depends on what stage of AKI they are in. The three stages of AKI are initiation (basically no damage has been done), oliguric (low UOP, high BUN/Cre), and polyuric (high UOP, > 2L per day).

During the oliguric phase, urine output is less than 400 mL/day and BUN and creatinine are increasing daily. By the way, BUN represents the amount of urea in the blood and is a bi-product of protein breakdown. Urea is reabsorbed by the renal tubules as needed to regulate urine/ serum osmolality, so BUN levels can fluctuate. Creatinine is a product of muscle breakdown and remains constant as long as muscle mass remains fairly constant; making it a better indicator of renal function. The BEST indicator of renal function, however, is the glomerular filtration rate (GFR), which reflects the amount of fluid filtered by the kidneys each minute. The GFR will be decreased during the oliguric phase. So, in addition to keeping an eye on these lab levels, our nursing care will center around preventing complications from fluid volume overload, electrolyte imbalances, uremia and metabolic acidosis. *Daily weights are the gold standard for monitoring fluid volume status. Additional critical assessments include lung sounds, respiratory rate/ effort, and O2 saturation due to the risk for pulmonary edema. The nurse will also assess for peripheral edema, blood pressure, and Is and Os. Fluid restrictions will be implemented during this stage.

The patient is also at high risk for hyperkalemia due to decreased excretion. The most dangerous potential complication associated with hyperkalemia is cardiac dysrhythmias so the nurse will monitor for a prolonged PR interval, wide QRS, and tall, peaked T waves. Medications include Ca+ gluconate which protects the heart from dysrhythmias associated with elevated potassium levels. Kayexalate removes K+ from circulation via the stool and IV insulin forces K+ back into the cells. It’s also important to implement a renal diet: low K+, low Na+, low Phos+, and low protein. This means saying no to the morning OJ, bananas, and potatoes. Hyperphosphatemia and hypocalcemia can develop due to the inability to excrete phosphorus. Calcium has an inverse relationship with phosphorus so it will be low as a result. Remember that calcium calms, so manifestations of hypocalcemia include dysrhythmias, tetany, and laryngospasms. Medications include phosphate binders (PhosLo) and Cholecalciferol (Vitamin D3). Vitamin D synthesis is reduced in AKI further contributing to hypocalcemia.

Uremia occurs due to toxic buildup of urea within the blood and causes mental status changes that require frequent neuro checks to ensure patient safety. Urea also irritates the pericardium and can cause pericarditis and interferes with clotting leading to excessive bleeding.

Metabolic acidosis results from the kidneys’ inability to produce HCO3 and excrete H+. Monitoring the patient’s ABGs and neuro status are key.

Finally, uremia places renal patients at really high risk for infection, so strict hand-washing cannot be overemphasized. Closely monitor the patient’s body temperature and WBC for early signs of potential infection. If infection develops, it will need to be treated promptly with antibiotics as infection is THE most common complication among patients with AKI.

That was A LOT! Remember that the oliguric stage can last a couple weeks before the patient moves into the polyuric stage. During this stage, the nurse’s focus will be on preventing complications from volume depletion and hypokalemia. This stage happens because glomerular filtration is improving, but there is still residual tubular damage preventing reabsorption. It may be a while before BUN and Cre begin to decrease as well.

I hope you have found this post helpful as you prepare for your renal exam. Don’t forget to browse around the site for other helpful resources and follow us on IG, Facebook, and Youtube. New resources added weekly!