Acute Kidney Injury (AKI): Complete NCLEX Review

Welcome to The Explainer, where we break down complex topics to help you absolutely crush your exams. Today, we are diving deep into acute kidney injury, or AKI, and trust me, this is a high-yield topic you are guaranteed to see on your NCLEX. To confidently answer a critical thinking question like this, you have to have the essentials mastered. So, let's get right into it. We're going to build a rock-solid foundation on AKI, so you can handle anything and everything the NCLEX decides to throw at you. Okay, let's start with the absolute fundamentals. What exactly is AKI? And you know it's just as important to know what it isn't because the NCLEX just loves to test you on the key differences between acute and chronic conditions. The two words you absolutely have to burn into your memory here are abrupt and reversible. This is not a slow decline, not at all. It is a sudden crisis. But the good news is, with the right moves, we can often restore that kidney function. Now, this slide right here perfectly lays out the contrast you need to know. On the left, you've got AKI. It's a sudden crisis, but it's often something we can fix. On the right, you have chronic kidney disease, or CKD, which is that slow, gradual, irreversible decline over a long period of time. The NCLEX will 100% expect you to know this distinction inside and out. Understanding these three categories is so, so crucial, because the cause is what dictates your nursing priorities. Think of it this way: Prerenal is a perfusion problem, not enough blood getting to the kidney. Intrarenal is direct damage inside the kidney. And postrenal is a plumbing problem, after the kidney. So now let's see how all this science actually translates to the bedside. This is where we connect the "why" to what you're actually going to see and assess in your patient. You have got to be able to tell which phase your patient is in. In the oligaric phase, urine output is super low, so the patient is basically drowning in fluid and holding on to way too much potassium. But then, in the diuretic phase, the floodgates just open. The risk completely flips to dehydration and losing too much potassium. Your priorities have to change on a dime. Okay, this table? This is pure gold for your NCLEX prep. Seriously, memorize it. Creatinine and BUN are up because the filters are clogged. Potassium is high because it can't get out. Sodium looks low, but it's really just diluted by all that extra fluid. And notice that low pH? That's your signal for metabolic acidosis, another huge complication. So you've gathered all this assessment data. What are you going to do next? This is the most important part, putting together your nursing action plan. These are your four pillars of care. You are watching that fluid balance like a hawk with daily weights. You are on high alert for any cardiac issues from that high potassium. You're controlling their diet to prevent even more electrolyte problems. And because of that low sodium, you are protecting that patient from having a seizure. Okay, listen up. If you only remember two things from this whole explainer, please make it these next two life-threatening complications. These are absolute high-priority, must-know topics for the NCLEX. I really can't stress this enough. High potassium, or hyperkalemia, is the most immediate threat to your patient's life because it can literally stop their heart. It can cause fatal cardiac dysrhythmias, which makes it your absolute number one priority to monitor and manage. And this slide right here shows you exactly why your patient has to be on a cardiac monitor. Those peaked T waves, that's the classic early warning sign on an ECG that potassium levels are dangerously high. And yep, this is the answer to that question from the very beginning. And here's what you do about it. K-exalate pulls potassium out through the gut. IV insulin, which you give with glucose to prevent hypoglycemia, temporarily shoves potassium back into the cells. And calcium gluconate. Now this one doesn't lower potassium, but it stabilizes the heart muscle to prevent those deadly dysrhythmias. You have to know all of these for your exam. The second major complication is metabolic acidosis. When the kidneys fail, they just can't get rid of acid waste products, so the body's pH drops down to really dangerous levels. So when you see a patient breathing really deep and fast, don't just think it's a respiratory issue. This is Kussmaul's breathing. The body is desperately trying to compensate for all that metabolic acid by blowing off carbon dioxide, which is an acid, through the lungs. It is a critical assessment finding. Alright, you have absorbed a ton of information. Let's put it to the test with a quick review to really make sure these concepts are locked in for good. Come on, think about it. What vital hormone do the kidneys produce that's related to our blood? Exactly! The kidneys make erythropoietin, which is the hormone that tells the bone marrow to make red blood cells. So when the kidneys get injured, production drops and the patient becomes anemic. Remember, this is the phase where the risk totally flips on its head. What happens when you lose a massive amount of fluid? Here is the key takeaway. A high urine output is not automatically a sign of recovery. It can signal massive fluid and electrolyte loss, which can lead to hypovolemic shock and dangerous hypokalemia. Vigilant constant monitoring is absolutely essential. Go back to that lab values slide in your mind. Which two electrolytes were dangerously high because the kidneys couldn't get rid of them? Excellent! Potassium and phosphorus are the two big ones you have to restrict in the diet to prevent a toxic buildup. This is a fundamental nursing responsibility and a very common NCLICS topic. And really, this is what it all comes down to. It's not about just knowing facts for a test. It's about using that knowledge to think critically when you're at the bedside, to anticipate problems before they even happen, and to provide safe, proactive care.