I'm here. Good morning. I think I finally got it. Sorry about the delay. So good morning everyone.
So today we're going to talk about the renal and urine system. So right here is just your list of objectives you guys can read. It's just describing the impact of renal function on blood pressure, evaluate the presentation of CKD, AKI, neurogenic, PCI, and reduction in odor-active blood. So right here is just like directly from your book. It's a picture of the anatomy of the renal system with the kidneys, the uterus.
ringing pelvis, the bladder. Basically, it's just anatomy. If you think about it, if you see where kidneys are located, that's why a lot of times when infants have nephritis and they have that flank pain is because of where the kidneys are located. The upper pole of the urine is the 12th thoracic vertebra. Lower pole is the third lumbar vertebra.
Like I said, the lower part of your back is why they have that flank pain when they have infection. And just note that the right kidney is slightly lower than the left. This is just another picture of the anatomy of the actual kidney.
And I'll just stray from you both. Okay, so getting into the anatomy, the nephron. The nephron of the kidney is basically the brain of the kidneys.
That's basically where all your concentration happens. It dilutes the fluids and everything. So everything that happens with the kidneys happens in the nephron section.
It contains subunits the renal corpuscle proximal covalent tubule, lupus henli, dental covalent tubula, and the collecting ducts. And as you can see it's approximately 1.2 million nephrons per kidney so a lot of blood flow, a lot of pressure is going through. So right here is just another picture of the nephrons. It's just the parts of the nephron. You have the cortical nephron and the juxtamum medullary nephron, which is basically where everything pretty much happens within the nephron.
So this is just a slide that basically tells you what different parts of the nephrons do at the proximal covalent tubule is where you have every absorption. reabsorption of ions, water, nutrients, remove toxins, and adjust filtrate pH within a glomerulus portion, building small cell use from the blood. As you can see as you go down an ascending loop of Henle, but you have reabsorption of sodium and chloride, and distal tubules, selective secretion, and absorbs different ions and maintains blood pH and electrolyte balance, collecting ducts.
reabsorbs solutes and water from filtrate and when you get to the descending loop of Henle allows water to pass from the filtrate into the interstitial fluid. You notice when you get into Reno everything in Reno is about a pressure gradient. It's either like the unkind pressure gradient where basically fluid just shifts back and forward.
If you remember way back in anatomy when y'all took it, you have the solvents and the solutes that basically just want to be like a net zero basically. If I'm 50 here I'm 25 here. I want it both to be even. So that's how the fluid shifts back and forth with the immune system. So right here is a picture of the glomerula.
As you can see, aferinaterials deliver blood to the glomerulus. Aferinaterials blood flow exits the glomerulus, which delivers blood to the peritubular capillaries responsible for regulating glomerular blood flow. As you can see, the glomerulus sits within the Bowman's capsule, which supports glomerular capillaries, helps to regulate the capillary blood flow once it goes into the capsule. So here's another picture of the anatomy of the peritubular capillaries and advanced rectus. The peritubular capillaries surround the renal tubules and the cortex, which arise from the ethereonaterials.
The peritubular capillaries are involved in a reabsorption of water, electrolytes, and nutrients. So that's where a lot of your filtration and dilution happens. As you can see, the vas rectus is located within the medulla.
The vas rectus also maintains osmotic gradient within the medulla, which is essential once again for concentrating the urine. That's basically the exchange of salt and water. This complete capillary network supports the kidneys ability to filter blood.
reabsorb necessary substances and concentrate urine. Um renal blood flow you can see a lot of blood goes through the kidneys. The kidneys get at least um a thousand to twelve hundred milligrams of blood per minute that's a ton of blood. Everything goes through the kidneys.
That's how when you see these patients in the hospital when something's happening the first thing is that urine output drops off because all the blood flow goes through the kidneys. 20 to 25% of this in the cardiac output. 20% of the blood is filtered at the glomerulus level. And 80% flows through the peritubule capillary.
You have the gas exchange. I'm so respiratory. But you have the exchange of your sodium and your chloride that creates that concentrated fluid or diluted fluid.
The glomerular filtration rate. is the rate that the plasma is filtered over a period of time through the glomerulus of fluid and solutes into the Bowman space from the glomerular capillaries. Majority of glomerular blood is reabsorbed. Once again, the glomerular filtrate, it goes through three layers of the glomerular membrane to make urine.
The glomerular filtrate is strictly formulated by the blood pressure, a drop in renal blood flow, creates a drop in urine output, the mechanism to maintain adequate perfusion, and you have your auto-regulation or your glomerular feedback, and we will talk about that later. But basically, your blood pressure control, your renal blood flow, because it's blood pressure high, it affects it. If it's too low, it affects your renal blood. So auto-regulation. Like I said, GFR is directly related to the blood flow slash blood pressure.
a drop in a blood pressure or increase, a drop in a blood pressure, increase, increase resistance, increase resistance, decrease blood flow to the kidneys, causing a drop in the urine output. So basically what happens if you have a drop in your blood pressure, you have an increase in resistance, like some type of obstruction or something, but then a kidney level, the kidney function, basically you will get a drop in your urine output. So the kidneys regulate blood flow, you need auto-regulation. Basically, it's a system pressure, 80 to 180, which is your immunitarian pressure, which is why in ICU we always look at the maps.
We want the map, we want the map. When compared to, like if you work in a neuro ICU, everything neuro is systolic because systolic perfuses the brain. Everywhere else, the body, the maps is what perfuses the brain. So that's what you, not the brain, the body.
So if your map is greater than 65, then you should know your body's getting perfused. So the system, if the pressure is between 80 and 180, it's maintained, the body is able to respond to arterial pressure changes and sodium chloride changes in the distal tube of fluid. This in turn produces a constant blood flow and GFR.
So that's what we want. We want a constant blood flow. We want a constant GFR. We don't want those to go up and down.
Increase in systemic pressure will cause the afferent arterioles to contract to produce a constant blood flow and vice versa if it's a low blood pressure. So basically, if your systemic pressure increases, the aphid and arterioles know to contract so we don't have that influx of blood flow going to the kidneys to keep that constant GFR. So that's just the auto-regulation mechanism of the vessels.
Wait, can you repeat that? So if your blood pressure is high, too high, because the whole goal is to have a constant blood flow and a constant GFR. So if the blood pressure shoots up really, really high, the body then says, the apherinaterials then say, well, let me contract a little bit so I don't get that influx of blood flow.
Does that make sense? So you don't have an influx of blood flow to the kidneys because it wants that constant pressure. And that's an auto-regulation feedback mechanism.
But then a tubular glomerular feedback mechanism. It involves the macular densa cells and includes the renin-secreted and juxtaglomerular cells. When the systematic blood pressure increases, the GFR then increases and causes sodium concentration. and cause an increase in sodium concentration, which causes the atherin arterioles to constrict to maintain normal blood pressure.
So same thing. If the blood pressure increases within ejection glomerular feedback, you have also caused the increase in sodium concentration, which causes the atherin arterioles once again to constrict, so you don't have that influx of blood to the kidneys once again. Does that make sense?
Okay. I know it's a lot because there's a lot of like pressure regulation and sodium and water. Big words. Huh?
Big words. We make them up. That's fair.
So just some questions. Which arteriole takes blood out of the glomerular? The glomerular.
Right. And which arterioles bring blood? back to the glomerulus.
And if your patient has a blood pressure of 80 over 40, what urinary changes would you expect to see? A decrease. Right.
And where are your glomerulus located? A glomerulus. A located.
Right. All right. So going back into regulation again.
I just question. So for your patient has a blood pressure of 80 over 40. So then the vessels that we just talked about would dilate to get the blood in. Well, if it's this though, the body can't regulate.
So that's why you have a drop of the urinary output. One is like 80 over 40. Like this is a map, probably something like that. The body can't regulate anything.
So that's why you have the drop in the urinary output because it can't regulate it. Does that make sense? They're not contracting or dilating because the blood pressure is too low.
Like that is not happening because the blood pressure is too low. That happens when you have that 80 to 180. Okay. Got it.
That makes sense. Yes. Yes. Yes. Thank you.
So once again, we get into regulation. A lot of this is innervated by the sympathetic nerve fibers. Once again, going back to patho, sympathetic is your fight or flight nerve fibers that are stimulated via the carotid sinuses and the baroreceptors, which increase, which release catecholamines. What it does is stimulate vasoconstriction, occurs, which decrease blood flow, GFR, increases sodium and water absorption to increase the blood pressure. So this is on the blood pressure side.
This is what the body is doing to increase your blood pressure if you have a low blood pressure. And this is to help increase that renal blood flow, which helps make the GFR constant. And let's see, basal constriction of the apian arterioles in response to a decline in renal blood flow of GFR, increased reabsorption of sodium in water to increase the blood pressure. So this is the body trying to increase that blood pressure to increase the float to the kidneys so that we don't have that drop in urinal.
Parasympathetic. is very minimal when it comes to regulation. It basically helps conserve energy and maintain a stable body function. It's not your fight or flight. It's sympathetic.
It's your fight or flight when your blood pressure gets too low or too high, but basically two of them. So hormonal regulation, we have three different types. You have the renin, antidiuretic hormones, and endostrum. Basically, the hormonal regulation is the renal system response to blood pressure changes.
And I will get into the different ones when I move on the slides. But renin is basically an enzyme formed in arterioles within a juxtaglomerular apparatus. It responds to the decline in the low blood pressure in atheronaterioles, low concentration of sodium chloride in the distal convolume tubules, sympathetic stimulation. of the ducts of glomerular beta-androgenic receptors and proxaglandin release. So this is all the things that the renin responds to.
Antidiuretic hormone is secreted in the posterior pituitary, is important for the concentration of urine, affects the distal tubule collecting ducts, and watery absorption of permeability. Nidastrone is secreted by the adrenal cortex. stimulate sodium reabsorption, and increase potassium hydrogen excretion, but we're going to talk about that in a second. We'll go to the next slide.
So the RENIN basically stabilization of the blood pressure. The RANS is, I remember back when you went into the angiotensin 1, angiotensin 2. So basically, when it is released, angiotensin 1 is converted to angiotensin 2, which then in turn stimulates secretion of aldosterone, causes vasoconstriction, and stimulates antidiuretic and thirst. So basically, it makes you thirsty. It can trickle to raise your blood pressure.
The RANS stabilization of the blood pressure, maintenance of fluid volume. And it also increases arterial blood pressure, like I said, with the re-enflux of the sodium, nasal constriction, aldosterone, and the antithyroidic. So all these things happens within the rest to increase your blood pressure. So this happens when you have a low blood pressure. This is the body trying to raise the blood pressure, which, once again, to try to increase that blood flow to the kidney so we don't have a drop in the urine output.
Neutrogenic peptides causes vasodilation, increases sodium and water excretion, which in turn decrease your blood pressure. So this hormonal regulation dumps in when the blood pressure is too high because once again the blood pressure is too high you don't want too much blood flow going to the kidneys because you want that constant blood flow in GFR. So the neutrogenic I'm saying this wrong I'm sorry. Peptides is basically vasodilation. It increases sodium and water secretions, lowers the blood pressure, protects from fluid overload.
Renin and aldosterone is inhibited. It causes the vasodilation of the aferinaterials. It's vasoconstriction of the aferinaterials, which increase urine production.
The nephron's main function is urine production. And right here, I have listed all the functions that the nephron is going to do to produce the urine. So basically, filtering of plasma, reabsorption of secretion and substance.
It creates the ultrafiltration, which is a protein-free fluid. It regulates filtrate to maintain blood volume, electrolytes, and a pH. Once you get into the glomerular membrane, it is permeable to sodium. chloride, potassium, creatine, urine, and glucose, which means it allows those electrolytes to go back and forth.
Fluor release from the glomerulus to the proximal convolume tubules. The glomerular membrane is impermeable to proteins and large-coli substances. That basically means proteins and large-coli substances cannot filter through the glomerular membrane.
allows for, like I said, the dilution and concentration of urine. It allows certain electrolytes to move across, back, and forth to create that concentration and dilution. Factors influencing glomerular filtration, volume of filter fluid, as you can see, 180 liters per day, one or two liters of urine per day.
So we should at least be one or two liters of urine per day. Other factors that can influence glomerular filtration is urinary obstruction, which causes an increase in hydrostatic pressure at the Bowman space, which decreases your GFR. A reduction in plasma protein decreases glomerular capillary onchonic pressure, which increases your GFR, influence glomerular filtration, and excessive loss of fluid.
The increased glomerular capillary onchonic pressure decreases your GFR also. It's all of these just a list of factors that influence the glomerular filtration. So the loop of Henle and distal convolume tubules, basically what happens here, that's where you see that filtration of your water and your sodium chloride to create concentration and dilution. As you can see, I want to point to it back here. As you can see on the, you guys right, the number starts off at 300 and goes all the way down to 1200. Then as you see, it comes back up on the left.
It's more diluted and more of a hypoosmotic. So basically, water comes out all the way down to at least 1200. And then once water comes out, sodium comes in on the other side. And that, like I said, creates the gradient to create the filtration and dilution to create the urine out. So water first. Water comes out first because as you can see it's like 300, 400, 600, 800, 1200. So water is coming out first.
Then once you get to the side. the sodium the um i'm sorry water comes out sodium going in and then once you get to this side the um you just have water left so that's why the number is like 1200 700 400 200 100. does that make sense okay so water out sodium process over water comes out sodium crosses over as we go down it goes up and then right here you have the sodium out and it's just all water this is all diluted We've got passion, we've got determination. That's good.
We've got passion and determination. Let's see next. Okay. Um, that's basically...
So you think you know Wix? Do you really? I'm not even gonna... Um...
So that's basically the anatomy and how the kidneys function. So basically the whole function of kidneys is to produce urine, filter out your electrolytes and maintain a normal pH. And it does that by pressure regulation and by the regulation of electrolytes across the loop of Henle. Watch that video again.
Okay. So this is just some disease processes that we're going to now. So you have a urinary tract obstruction. which can be complete or partial.
You have structural versus functional. Structural is proximal to the, I'm sorry. Oh, I'm sorry. Once you have obstruction proximal, it would be dilated, which causes an increase of infection.
So basically, if you have obstruction proximal to that, everything is going to dilate, but you have an increase of infection because It's so dilated. Severity is determined by location, the ureter or the kidneys are involved, the duration of the blockage, or the nature of the obstruction. And like I said, you can have complete or partial obstruction. Upper urinary tract obstruction is the blockage. causes abdominal inflammation or scarring.
Compression can cause a stricture or can be congenital. Your lower urinary tract obstructions can either be nutrigenic or obstruction can present anywhere within a urinary tract system. It can cause an increase in hydrostatic pressure causing a decline in GFR which then causes scarring.
And as you can see, tubular function is dependent upon the GFR. Once again, severity depends upon time and degree of the obstruction. Prolonged obstruction affects glomerular and tubular function.
Effects of obstruction, if obstruction is not relieved within seven days, The distal tubules are damaged by fibrosis or collagen deposits. Within 14 days, distal and proximal covalent tubules are affected. If it's not fixed within 28 days, you have glomeruli damage, cortex, and medulla reduction in size. Tubular damage results in inability to concentrate the urine, increases urine volume to fight reduced renal function. and you have a loss of water and electrolytes which can cause a metabolic acidosis or dehydration.
As you can see if a patient have obstruction number one you want to diagnose it early, number two you want to treat it early. And this is another slide with the effects of obstruction. Partial obstruction without presence of infection impairs the ability to concentrate the urine, reabsorption of bicarb, excretion of ammonia, and affects the acid-base balance.
a unilateral obstruction results in tropophrase or paper function. Diuresis can occur once obstruction is relieved. So then you will have a loss of large amount of fluid rapidly and electrolyte disturbance can happen.
So if the patient have obstruction and we're fixed it, then it will have like this massive diuresis phenomenon that will happen. And at that moment, that's when you really want to be mindfully electrolyzed because you can start losing potassium and everything. because of the diet reasons.
The ability to recover. So depending upon the severity and the duration of the obstruction, whether it's partial or complete, you also have a complication. It can be infection. You can have infection complication also because of the obstruction.
Irreversible damage is if vasculature is obstructed within four weeks, partial recovery, possible ability within 56 to 69 days, complete recovery if reversible maybe may take at least four months before your kidneys have complete recovery. So, lower urinary tract obstruction and structural causes can be the prostate, urethral, pelvic organ, prolapse, tumors, infection, or just injury or cancer. Can be functional, meaning neurogenic causes.
Can be a combination of factors. Structural obstruction, increased force of the discero. contraction, which increases urgency.
Afferent nerves affected if persistent, weakened partial muscles, which is a loss of stress and elasticity, underactive bladder, which causes urinary retention and lack of sensation. So basically, if obstruction presents, the bladder wall loses its elasticity and urinary retention occurs, which causes impaired renal functions. UTIs and incontinence. Overactive bladder is categorized by urgency and frequency, urge incontinence, possible absence of UTI or neurological disorder.
Involuntary contractions can be caused due to age, lack of estrogen, trauma of medications. Reduce bladder outlet resistance, incontinence with sneezing. Then you have the overactive bladder. If you sneeze, sometimes patients kind of pee on themselves a little bit. Increase bladder outlet resistance.
They don't have complete emptying and they have hazard. Neurogenic bladder is bladder dysfunction. Can be sensory or motor. involves the upper motor neuron versus it can be upper or lower motor neuron involvement. Upper motor neuron is hyperreflexia, which is overactive bladder.
Or you can have lost neuromuscular coordination. Sacral peripheral nerves that are affected can cause underactive hypotonic or atonic flaccid bladder. Nephrolithiasis. Known as kidney stones, arena calculi, risk factors is patient's age, sex, race, food intake, histories of UTI, hypertension, any type of metabolic syndrome, or diabetes.
Usually it's unilateral. I just mentioned all the risk factors can be classified by mineral makeup, which is calcium, oxalate, phosphate, struvite, or uric acid. Stone formation is supersaturation of salt, precipitation of the salts, crystallization and growth, lack of stone inhibitors. If the urine is alkaline urine, which means pH greater than 7.0, increase the risk of calcium phosphate. Acid urine, pH less than 5, increase the risk of uric acid.
And potassium citrate is a stone inhibiting stone growth. it inhibits stone growth. Urinary tract infections, UTI is the inflammation of the urinary epithelium caused by bacteria from gut flora. Four primary types, we got cystitis, painful bladder syndrome, interstitial cystitis, acute chronic pyelonephritis. Cystitis is mild.
hyper, hyperemic, I'm sorry I'm saying all these words wrong, hemorrhagic, supportive, alterative, gangrenous. E. coli is the most common bacteria you will see in UTIs.
You can have staph, kepsiella, glutamonus, but E. coli is the most prominent bacteria you see within a patient that has a UTI. Basically, it's also an infection.
Golden tough flame is her response, can produce edema, can increase stress receptors. Painful bladder syndrome slash interstitial cystitis, defined as an unpleasant sensation, meaning pain, pressure, discomfort, located on a suprapubic urethral vulva, vaginal or rectum areas. Symptoms can be six weeks or longer.
It will be an absence of infection, more common among female patients. Cause is typically unknown. can be an autoimmune inflammatory response.
So basically having to have bladder inflammation which turn into fibrosis which goes and reduces the bladder volume characterized by hemorrhagic ulcer. Hyaluronephritis is an ascending infection of the urethral, uterus, renal pelvis, and the Most common factor is a visceral urethral reflux, can be unilateral or bilateral. Most common organisms is E. coli, polis, or pseudomonas.
Alkalines the urine, primarily affects the tubules, can be chronic or recurrent, produces scarring and impaired ability to concentrate the urine. So when they have the pilot, that's when a patient's complaining of back pain. When it, um. develop the nephritis, the pyelonephritis.
Acute kidney is acute onset of a rapid decline in urinary function. Can be mild or severe. Can be reversible or irreversible.
Can worsen renal function to the kind of kidney disease or end-stage renal. Depending on the severity, dialysis may be required, may not be required. The patient will be oliguria, which is basically less than 400 mils of urine within 24 hours, and accumulation of nitrous waste products. Acute kidney injury, you have classification criteria. The initial onset is typically a hyperperfusion state.
Something happens when a patient has a hyperperfusion state. Extension continues. I'm sorry. So yeah, so acute kidney injury is basically when you have a hyperperfusion state. This thing here is just the stages of the acute kidney injury.
As you can see, stage one, you have an increase of the creatinine by 1.5 of the patient's baseline or the GFR decreases by 25%. That's, I'm sorry, that's patients at risk. Injury is when you have an increase of the creatinine times two of the patient's baseline or the GFR. rated in 50 percent when you get into renal failure you have an increase of creatinine times three or the gfr decreases by 75 percent when you get into loss you have persistent acute renal failure complete loss of renal function so rated in four weeks and then you have an end stage range so basically if somebody has acute kidney injury if that is not fixed they definitely can advance into end stage renal if um management isn't able to stop the progression of the kidney signs. Acute kidney injury causes depletion of fluid volume, a decrease in blood flow to the kidneys, or it can be a toxic injury, meaning medications, infections, or something autoimmune.
You have different classifications. You have pre-renal, intrinsic, and post-renal. Prerenal is the most common cause of acute kidney injury, which is basically decreased filtration pressure leading to increased delivery of oxygen causing ischemia and necrosis to the kidneys. Intrarenal acute kidney is acute tubular necrosis, which is a result of prerenal, which basically is a nephrotoxic acute tubular necrosis, which basically comes from medication, antibiotics, heavy metal.
Every metal is a patient-developed rhabdo. This is like when a patient is on vancomycin, they have vancomycin toxicity. That's why you monitor your vancomycin levels. Can also be caused by vascular disease, meaning vasculitis or malignant hypertension, maybe acute glomerulonephritis or interstitial disease, medications or infections. 40 to 50 percent is post-surgical because sometimes when in the OR they have these episodes of hypertension basically where you have a lack of perfusion to the kidneys can cause the ATN.
Also pathophysiology, it can be inflammatory response, vasoconstriction, necrosis of the proximal tubules and microvascular changes and obstruction. Osphrenal AKI can develop from tumors, BPH, nephronyglada, urethral obstruction. The patient will present with allegoria, like we said earlier, is 400 cc of urine output within a 24-hour period. Primary causes, altering of blood flow, impaired ability to auto-regulate, basal constriction or ischemia. Other causes can be a tubular obstruction, which causes sloughing.
of tubular cells due to necrosis, cast, edema, or ischemia. You can have a tubular back leak, which increase probability due to ischemia. So also, um, before what occurs in the injury, you have the initial phase where you basically have the hyperperfusion, um, event that happens. The maintenance phase, patient will then develop low urine output.
output, CM creatinine and BUN will increase. Once you get into the recovery phase, the renal function improves. Unable to concentrate the urine.
Patient may be urinating a lot, but not adequately clean. Like I said, once they get into recovery phase, they will do this diuresis, but they're not actually cleaning the urine and diluting the urine. So you want to monitor fluid status and your natural light balance.
The patient at that moment in recovery phase may become dehydrated during this phase. because of that massive diarrhea that happens. Chronic kidney disease factors that advance kidney disease is protein, urine, and angiotensin II activities.
You have five different stages. You have stage one, which you have normal kidneys, functions, no symptoms. CFR is greater than 90. Stage two.
You have mild kidney damage. GFR is between 60 and 89. Stage three, moderate damage. GFR is between 30 and 59. That's when you actually see symptoms start to begin once the patient develops CKD3.
CKD4, severe damage. GFR is 15 to 29. CKD5, that's when you have end-stage renal disease, complete kidney failure. That's when a patient basically needs dialysis.
So moving forward to chronic kidney disease, it's evidence of structural or functional abnormalities of kidneys for three months or longer. Chronic kidney disease can cause albureal presence of sediment in the urine, tubular disorders resulting in electrolyte or other abnormalities. Patients can have an abnormal kidney biopsy, abnormal imaging studies, myelitis kidney transplant, and GFR.
Less than 60. Patients develop a significant reduction in the number of functioning nephron. Mechanisms are damaged depending on the etiology. Initially, the patient is able to compensate, but as you can see, as they progress, they will not be able to compensate anymore.
The location of disease can be tubular, which causes difficulty concentrating the urine. can cause renal tubular acidosis or sodium wasting. It can also be within a vascular glomerul, which causes hematuria or proteinuria and eventually progresses to loss of ability to concentrate or dilate urine. So once a patient develops chronic kidney disease, a whole cascade of events can happen.
They have abnormalities within fluid balance, which can cause edema, shortness of breath. We have acid-base imbalance, which basically a patient could develop a metabolic acidosis. We have electrolyte imbalances, patients with TKD that can develop hyperkalemia, hyperglycemia, cardiovascular damage, hypertension, patients at higher risk for cardiovascular disease than the general population. Also can cause bone and mineral metabolism, vitamin D deficiency, hypokalemia, hyperphosphatemia. Secondary hyperthyroidism on a nutrition level can cause hypoalbumin, low albumin, dyslipidemia.
In a hematological level, patient can develop anemia. Hypercoagulable disorders are impaired platelet function. As you can see, once a patient progresses into chronic kidney disease, it basically affects every system of the body. You have the immune system, patient can become immunosuppressed, can have chronic inflammatory state.
Within a neurological system, patient can develop neuropathy, altered sense of taste, memory issues, sleep disorders, restless leg syndrome. Within a gastrointestinal system, patients can have anorexia, nausea, vomiting, and prone to ulceration. Within the endocrine system, patient can develop hypothyroidism. decreased libido um amenorrhea and integumentary they could develop itching and dry skin um like i said you can continue i had a question after oh this is the last oh but like i said once the patient um progressed to chronic kidney disease it affects like every system in the body um the big thing is you try to you try to prevent it but sometimes you just can't depend on the patient and how compliant they are and i think that is it um so you know for labs i know we didn't talk about it they there's like a difference like they'll have like african-american filtration versus like regular do they still i guess test for that or there's a difference between black people's gfr rate it's more like age related okay if you're older you allow like a higher gf um gfr if you're old it's more like age related you Okay, because I feel like I recently had labs and they still had that on there. So I think, I don't know.
Yes, there is some reference labs. There's lots of literature not supporting the difference anymore. It's going to take time before that science catches up.
But age-related changes to your GFR is the greatest issue you want to focus on when you think about populations. Can I add something? They just recently took that out for transplants because African Americans, they tend to have a higher GFR according to the labs. And so it makes it seem like they weren't eligible for transplant. So they just took that out in the past year or two for eligibility for kidney transplant.
Yeah. It just shows that they have it, but really their GFR wasn't really higher. But lifestyle.
You know what I mean? They had like, we were higher. No, ethnicities.
I didn't, what I work at, they don't have that. It's just. Okay.
I get my labs done a lot and I've always seen it and I just remember hearing, like, they're trying to get rid of that because there was really nothing. Yeah, it's all eating. Supporting it. And that's crazy that the transplant, like, that was affecting that. So that means, you know, they weren't getting their kidneys.
Yeah. 15 minute break. like has she seen it because she just works with like a different like you're in