What’s going on, guys. My name is Brad and welcome to nursing.com. And in today’s video, what we’re going to discuss is chronic kidney disease. We’re going to discuss some of the pathophysiology behind chronic kidney disease, some of the signs and symptoms, as well as how we’re going to treat patients suffering from it. Let’s dive in. 

So regarding the pathophysiology of chronic kidney disease, the way that I like to think about it is, essentially, the kidneys are the filters of the body, right? They’re directly responsible for filtering out all the nitrogenous waste products that would otherwise accumulate within our body. It filters it out and then we end up peeing it out in the form of a waste product. So the way that I think about it here is kind of like this little fish tank, right? Think about the filter on a fish tank. Okay. What would happen if you didn’t change that filter out for months and months and months, right? Crud, gunk is going to accumulate within that filter, blocking that filter off and preventing it from being able to do its job of filtering. As a result, what is going to occur, right, no filtration. We’re going to end up seeing algae, mold, crud accumulate on the sides of this fish tank. Think about the kidneys in the same way as that filter, as these filters slowly degrade over time, our body’s ability to filter out these waste is decreased. 

So what are some things that can affect the filters of our body that can lead to chronic kidney disease? Well, one would be hypertension. If you’ve not seen our video on hypertension, I highly recommend you at least check out the pathophysiology regarding it. But, think about hypertension as prolonging narrowing of the arteries, that renal artery that feeds the kidneys, all of that nice freshly oxygenated blood, as we have prolonged hypertension, prolonged narrowing of that renal artery, what we’re looking at as a result is prolonged hypoperfusion. Okay? That’s the biggest takeaway. We have prolonged hypoperfusion of that kidney. As we, over years and years and years, we reduce the amount of blood that’s being fed to that kidney. The kidney itself is going to begin to fail. 

Diabetes is another one, right? Diabetes. So I’d like to think about it like this glass of sweet tea over here. If you’re from the south, if you’re like me, maybe this will resonate with you. We drink sweet tea in the south, right? What would happen? In diabetes we know diabetes is lack of insulin production, therefore resulting in hyperglycemia. What would occur, if you had too much sugar in your blood? Well, think about the glass of sweet tea, for example. If you poured more, and more, and more sugar into a glass of sweet tea and stirred it up, the more you pour in the more viscous and thick that sweet tea is going to get. Same concept with diabetes, right, way too much glucose in the blood resulting in thicker blood. And if our blood is thicker, if it’s more viscous, then it is much more difficult to perfuse these kidneys with that thicker blood. It’s just a lot more difficult. So as a result, the kidneys don’t get the blood flow that it needs. And we end up having renal failure. 

The next would be glomerulonephritis, right? You would have to go back to the anatomy of the kidneys, but remember that there’s actually something called a glomerular filtration apparatus, right? That is actually where blood flows in and the initial filtration process begins within that nephron, the cell of the kidney. We can actually have inflammation of that glomerular filtration apparatus, right? If you have inflammation of the filter, then think about it as you get inflammation, all of these little areas where fluid, where blood could pass through, all of these areas are going to get a lot more narrow. And as a result, filtration will be impaired. And of course, also like with most diseases, chronic kidney disease is also hereditary. 

So what are some assessment findings that we’re going to see or things that we’re going to look for in patients with chronic kidney disease? Well, a few lab values that we’re definitely going to want to take note of would be our BUN and creatinine. That’s the first thing. This is one of the classic markers of renal function, right? Creatinine being a by-product, a waste product, that our kidneys would normally filter out. So, you should think, if our kidneys, if our filter is failing, then this waste product is only going to go up and up and up. So we could see increasing creatinine in patients with chronic kidney disease. They may also live with an increased baseline creatinine, as opposed to others, kind of like how patients with COPD live with a chronically higher CO2, same thing with chronic kidney disease, chronically higher creatinine levels. 

GFR, glomerular filtration rate. So the way that we think about this is that glomerular filtration apparatus that we spoke about with glomerulonephritis, we actually have a GFR rate. It’s the actual rate at which we are able to filter out blood through our kidney. That’s exactly what the GFR is. That’s how you should think about it. And whenever we look at chronic kidney disease, it’s kind of broken up into five stages and it’s pretty much, you’re looking at the GFR to classify whether you’re in chronic kidney disease, stage 1, 2, 3, et cetera. And the way that you classify it is, if you’re in chronic kidney disease, stage one, you basically have a GFR greater than 90. Chronic kidney disease stage two, you’re looking at 60 to 90 for your GFR. Three, you’re looking at 30 to 60. Four, 15 to 30. And if you’re in chronic kidney disease, stage five, the last stage, you have a GFR less than 15. That’s how it’s broken down. 

Urine output.  You’re going to see a decrease in urine output in patients who have had chronically hypoperfused kidneys, right? For a long period of time, blood is not gotten to those kidneys, therefore, the kidneys are now failing. As a result that filter is breaking down and we’re not able to, not only not able to filter out products, but we’re also not able to filter out fluid. So fluid is going to back up. It’s not going to be put out of the body. So decreased urine output.

Increased fluid volume overload. As you’re not able to filter out that fluid, it backs up. We start seeing that in the form of fluid overload, edema, for instance. Azotemia, as you have continual increased a build up of nitrogenous waste products in the body, you start to see it in the form of azotemia.  Lethargy. Also anemia. Remember that the kidney is where erythropoiesis begins the release of EPO (erythropoietin). If you do not have this, one of the stimulating factors necessary for erythropoiesis or the building of red blood cells, than anemia is going to result. 

Now, some things that we’re going to educate our patient on, avoiding NSAIDs.  NSAIDs, other nephrotoxic medications, right? Making sure that we’re educating our patients on avoiding things that are going to only cause further damage to those filters. Okay. Renal diet. Again, making sure that their dietary adherence is in line with what the nephrologist is recommending that they take in. Medication adherence, of course, that’s a no-brainer. And as we’re monitoring daily weights, reporting any excessive weight gain, again, just to see how good or poor these kidneys may be doing as well as how is the patient tolerating dialysis if they’re a dialysis patient.

So summarizing some key points from chronic kidney disease, it’s important to remember that the entire idea is that the kidneys are the filters of the body and in chronic kidney disease, what we see is over time, a gradual breakdown in this filter’s ability to filter out toxins, as well as fluid. Remembering that the causes of chronic kidney disease all revolve around the idea that what we have are chronically hypoperfused kidneys, whether it’s due to hypertension, you know, constriction of that renal artery over time feeding into that kidney or diabetes with more viscous blood, or maybe inflammation of the actual glomerular filtration apparatus itself. Remembering that all of the assessment findings that we’re going to see are directly reflective of that breakdown in the filter, right: increase in our waste products, blood urea nitrogen (BUN), creatinine, and we’re going to be seeing a decrease in the rate at which that glomerulus can actually filter blood, we’re going to see a decrease in urine output as well. And our therapeutic management, knowing that our patients may be on dialysis, knowing that they may get erythropoietin, replacing electrolytes, et cetera, and the patient education that we just discussed.

Guys, that was chronic kidney disease. I hope that you take this information forward with you, and I hope that it helps you crush those exams. Now guys go out there and be your best selves today. And as always, happy nursing.