DIP Episode 53 - Comprehensive USMLE Step 1 Renal Review (Session 2 of 3)

Welcome. My name is Divine. This is the 53rd episode of the Divine Intervention Podcast. Today I'm going to be continuing the Reno part of things. This will be the second part of the Reno review. It's going to be three parts already uploaded part one. This will be part two and then there will be part three and that will be the final part. Okay. So first slide says the region of the kidney most susceptible to infarction in the setting of systemic hypotension. This will be the proximal tubule because the proximal tubule is the most metabolically active. Right. Does a lot of stuff. Right. So if there's not enough blood, not enough nutrients, it will die first. Right. The person that consumes the most resources is more susceptible to ischemia if you may. And then if you want to trace the pathway of urine to the outside world, right. So it's like you sort of start with the, we start with the glomerulus, right. You filter urine into like woman space and then it goes to the proximal tubule, goes through the thin descendant limb of the loop of Henley, the thin ascended limb of the loop of Henley, and then the thickest descendant limb of the loop of Henley. And then you form the distal convoluted tubule that contains the macular denser. Remember the macular denser is actually simple columny epithelium. And then you form the distal convoluted tubule, right.

And then you form the principal cell, basically from the collecting ducts that includes the principal cell, the alpha intercollated cell and the bitter intercollated cell. And then you form like the renal k lesis, from the renal pelvis, from the ureters, and then you form the bladder and then bladder to the urethro, and then urethro to the outside world. Okay. And the two types of nephrons, right. We have like the corticometerlerine fronds and the corticone fronds. And the shed anatomical characteristic between the kidneys, ureters, pancreas and ascended descending colon. So go back to your first year of med school. Remember sad bocker? Those are retroperitoneal structures. And then next one is a 50, 53 old male with stage five chronic kidney disease is being considered for renal transplantation. Hally match donor has been found to ensure optimal transplant outcomes. What is the preferred donor kidney, right. So this is the left kidney. Okay. The thing is the left kidney just gives you more room to work with because it has a longer in all things. So you have like more tubing if you may. And then just one real quick thing I want to say is that I was talking about the pathway of urine, right. From the kidneys to the, from the kidneys to the, to the outside world right between the renal pelvis and the ureter. That's a region known as the ureteropelvic junction of ureteropelvic junction. So it's the junction between the renal pelvis and the ureters.

That is actually the most common location where there's like a failure to recalculate which may actually cause like hydronophrosis in a fetus, right. So if you do a newborn ultrasound, you see like hydronophrosis that can arise from a ureteropelvic junction obstruction. So next slide. So 58-year-old female presents with a six-month history of urinary urgency and frequency. She cannot make it to the bathroom in time before she pays on herself. Ure dynamic studies are notable for a post-void residual of 50 cc's or 50 males. So what's going to diagnosis right. So this is obviously urgent continents, right. And this really arises from the Boswad pathophysiology. I want to remember is like the trusser hypermotility, okay, or like the trusser instability. The trusser muscles are just a little too touching, right. So they contract like way too often. So that can cause urgent continents. And classically, these patients have a low post-void residual, okay. Low post-void residual. So basically because they're just peeing so much all the time, there's actually not much left in the bladder, but then you give it a point in time. So the thing is, if you know that your trusser muscles are like a little too touchy, right. You may sort of want to quieten them down, right. But if you understand your aeronomic nervous system, the pharmacology makes perfect sense. The thing is your sympathetic nervous system, if you activate it, that shuts down your tetrosomocells.

Your parasympathetic system, if you block it, that also shuts down your tetrosomocells, right. So you can give most chronic antagonists, right. So like the oxygen in, uh, torteridine, um, d'arphinocene, sulfenocene, and trospium, right. There's a monic for that. It's on the darn toilet. So the on is for oxygen in the, the, the is, um, the torteridine. The darn is like d'arphinocene and sulfenocene. And then the T's for trospium, right. So the team toilet. Alternatively, you can also give a sympathetic agonist like a beta-3 receptor agonist like myra-begrain. So if you watch TV at all, I know that's not a thing that's pretty, that's common amongst my students who are like actually, like, you know, like enjoy your life and watch TV. But if you heard of the drug, my vitric, my vitric is a, it's myra-begrain. It's a beta-3 agonist that's used to treat urgent continents, okay. And the classic exam demographic for urgent continents is a patient that has like multiple sclerosis, okay. So you're just going to keep that at the back of your mind. Now, what would your diagnosis be in a patient with constant urinary dribbling and a post weight residual of 400 mils, okay. If you ever see that, think about more overflow in continents. Overflow in continents is the one that's actually, you're just dripping urine all the time, right. But the post weight residual is usually pretty high.

And the Boswapathophysiology is from like urethral, I mean, sorry, from the trusermosol, like hypomotility. So basically like your bladder cannot sense when it's full. So usually this arises when like again, it cannot happen with MS, it can happen with diabetes. You can sense when the bladder is full. So when the bladder is just over full, it can't take it anymore. You begin to drip urine, okay. So that's why the post weight residual is a little higher than normally in these patients. And the classic demographic again, patients with diabetes. And the way you treat this is, since the trusermosols are quiet in this disorder, you want to give a most granic agonist for this, right. So like Bethany call, or you can give something that can raise your levels of acetylcholine to then encourage those trusermosols to contract. So you can give something like like a new stigmin, right. It's an acetylcholine estrus inhibitor, that boosts your levels of acetylcholine and that will promote the drainage of, promote contraction of the trusermosols. Alternatively, you can also tell the patients to like, catheterize themselves on a fairly regular basis. Okay. And then the last one says a 60-year-old female that loses urine with coffee no sneezing. And it's like, what's the buzzword? What's the diagnosis? How do you screen for this? How do you treat this? Blah blah blah. Okay. So let's talk about this, right. So the thing is this is stressing containers, right.

So like you lose urine with anything that increases in trapdominal pressure like coffee and of sneezing, that's stressing containers. And really the buzzword is, or I guess a pathophysiology is that basically the thing that happens is you have urethral, so not urethra, urethral hypermobility. And the thing that happens is for some reason, you essentially, because on the most circumstances, if you bear down an increase in trapdominal pressure, you transfer that, you transfer that in trapdominal pressure equally to the external urethral's finchter. So that sort of prevents you from like losing urine from the bladder when you increase in trapdominal pressure. But if something bad happens and you're, you're basically like, your urinary tract, like your urethra, so that like falls out of sync with the abdominal cavity when you increase the intrapdominal pressure, that pressure is not transmitting quality to the urethra, okay. And then those people can pee when they increase the intrapdominal pressures. And really the way you treat screen for this is you do something called a q-tip test. You literally insert a q-tip into the urethra and you'll see that it goes I think more than 30 degrees or something like that to show you that there is some kind of urethral hypermobility going on. Again, you screen with a q-tip test and the way you treat this is you can, you do a kigle exercise, that sort of strengthens your levitter in eye muscles, right.

So like there's like ilio-coxigias, there's pubocoxigias, there's puboretales, those are strengthened by kigle exercises. If that doesn't work then you can do like you can insert a pestery, that sort of like is like a plastic that holds everything in the right spot in the pelvis alternatively, and also do something called urethral pexy, that's a surgical procedure. And the most common cause of stress incontinence in men will be like after like surgical like prostate cancer or something like that, okay. So next question, 15 year old male is brought to the ED with a chief complaint of severe headache, phytocinesis notable for blood pressure of 180 over 110, labs are notable for hypochylemia, basically a hyperneutrymia and alkalosis, okay. He recently consumed large amounts of a legume that was brought by a friend from India, right. So what's your diagnosis? Now just to do that, this legume is licorice, okay. So licorice, right. So how does licorice, consuming a ton of licorice explain these findings, right. So the thing is licorice contains an acid known as glyceridic acid, okay. Glyceridic acid inhibits an enzyme known as 11 beta HSD2. So 11 beta HSD2. The four name is like 11 beta hydroxy steroid dehydrogen is 2. The thing is that enzyme converts cortisol to cortisol, right. So on the normal circumstances, many a lot of the cortisol in your body, you make it into cortisol, not a huge deal.

And the reason your body will want to do that is that cortisol has active like agonist activity, admiral or corticoid receptors, cortisol does not. So because I mean we make a ton of cortisol on a fairly regular basis, I mean think about if you're a met student, right. You stress all the time and we're gonna crap ton of cortisol, right. So that cortisol can activate active mineral or corticoid receptors. So the body sort of avoids that by converting it to cortisol with 11 beta HSD2. So the thing is if you consume the ton of licorice, you consume the ton of glyceridic acid, that basically inhibits 11 beta HSD2. So you don't convert cortisol to cortisol. So you have a lot of cortisol sort of persistent. And that cortisol can activate mineral or corticoid receptors and you can basically get like a hyper-adosteronic effect if you made, right. So like you have like hypochylemia because that potassium channel at the principal cell of the collecting doctors, wasting a lot of potassium, you get a hyper-natrimea, right. Because you again, you're basically acting like aosterone. So that inactional of the principal cell work like too well or the sodium chloride sample or the distal-convoluted tubule, tubule will work too well and you're going to absorb a ton of sodium that way, right. So you get a hyper-natrimea and you also be hyper-attensive because you're expanding your blood, your blood volume, okay.

So basically this phenomenon I described is known as the syndrome of apparent mineral or corticoid excess, right. So it's like an apparent excess because you're getting like a hyper-adosterone effect but it's not because you have high levels of a dostor. It's because you have high levels of cortisol, okay. So if you actually measured our dostorone in these people because they're hyper-attensive, you'll down the renal angiotensin-audosterone system so the renal will be low angiotensin one and two-an-audosterone and EDH will all be low, okay. And really the way you can make this diagnosis, you can just basically like take the person's urine, check how much cortisol there is, check how much cortisol there is. The ratio of cortisol to cortisol in the person's urine will be high in a same, okay. In a syndrome of apparent mineral or corticoid excess. And then this could also be a genetic disorder. There's literally people that have genetic deficiencies of 11 beta HSD2. And if you know that you're getting all these symptoms and signs, right, because you're having like too much activation of the mineral or corticoid receptors by cortisol, it makes perfect sense, right. That you should inhibit those mineral or corticoid receptors, right. So you can use an out dostorone receptor antagonist like Spironolactone or a plerenoid, although remember that Spironolactone can cause like a big boobies. Sorry, it can cause kind of comastia, right. So that's the more appropriate term.

So it can cause genicomastia, right. So because remember Spironolactone also has an undue receptor blocking activity, right. So you can give Spironolactone or plerenoid, but give it plerenoid if you want to avoid that the genicomastia that comes with a Spironolactone, okay. And then in con syndrome, right. So con syndrome, it's like an adrenal adenoma, right. It's in the zonal glomerulosa adenocortex, we cannot turn off our duster, right. So your levels of our duster will obviously be high, right. And again, you have all these hyper-out dostorone effects, like hypochylemia, hyperitrenia metabolic alkylosis, blah, blah, blah. But the thing is, you're renein, right. Because of your expanded blood volume and your hypertension, again, your renein will be low, your angiotensin 1 and 2 will be low as well, okay. So in same, you have low levels of renein, angiotensin 1, angiotensin 2, our dostorone and in each, but in con syndrome, because you have like an actual tumor making a ton of our dostorone, your dostor will be high, but because of the negative feedback, your renein, angiotensin 1 and angiotensin 2 will all be low, okay. Very high, you'll know that. And then, if you have better and gyroman syndrome, right. So batter is like taking a low diuretic, gyroman syndrome is like taking a thazide diuretic, basically those things all make you volume down, right. So that will dial up your renein and your tensin adosterone system, right.

So your renein and your tensin 1 and your tensin 2 and our dostorone will all be low, okay. In con syndrome, right. In con syndrome, I already talked about your findings there. If you have renein and larder stenosis, or like fibromoscular dysplasia, right. So that's like a sort of thing, of fibromoscular dysplasia is like younger persons are renein and larder stenosis. You'll basically hypoprefuse your afraid of the tear, right. And if that happens, obviously those active video gg cells, they're secretive, crap ton of renein. So your renein will be high, your angiotensin 1, angiotensin 2 and our dostorone will all be high as well, okay. And if you have a renein secretive tumor, it will be the same thing, right. If renein is high, everything down stream of renein in the renein and your tensin adosterone system will be high as well, okay. So next slide. So calcium balance and chronic kidney disease, right. So we talked about the mechanisms behind all of these already. You have hypocalcemia because you're not making calcium trial because there's no more one alpha hydroxylase, right. So you're not reabsorbing calcium in the and phosphated in the gut, right. So you'll be hypocalcymic. Your phosphate will actually be high, right. Because because you may think about it, you're like, we're divine. But in chronic kidney disease, I'm hypocalcymic, right. So if your hypocalcymic, your pTH should be high, right.

But the thing is, and pTH is appropriately known as the phosphate trash in hormone, right. So you think that your phosphate will be low. But actually that's not the case in chronic kidney disease, right. Because your kidney is the primary excretory organ of phosphate. And if your kidney is not functional, you have no ability to excret phosphate. So you actually hyperphosphatemic if you have chronic kidney disease. So chronic kidney disease will be an example of a cause of a secondary hyperparthyroidism. Okay. And again, I've talked about the pathophysi. And really the way you treat this is you give calcium trial, not calcium dial. You give 125 dihydroxy vitamin D calcium trial. Because if you give calcium dial, it doesn't make any sense because there's no one alpha hydroxy because you have no kidneys to activate that vitamin D. Okay. And the chronic kidney disease, the big thing you want to keep in mind is that your kidneys, again, they are the primary excretory organs of acid. Okay. So if you're not excreting acid appropriately, you will get a metabolic acidosis if you have CKD and that can sort of lead you a weeble. Okay. And then a hemoglobin of it in a patient will get CKD because you're not making Epo already talked about that before. Chess pain worsened with a supination and relief with sitting operating in a patient with CKD. Right. So the thing is if your kidneys are gone, right, you can deal with your your rear problem, right. So your B and will go up.

So you get a uremia. Okay. And the thing is your urea or uremia, if you want to be more renal like I guess, uremia. Basically urea makes it hard for things to degranulate like your pleaklets, right. So you can have a coagulopathy with CKD, right. So you can bleed because your pleaklets just don't work right. So right. So your bleeding time, for example, will be elevated, although your PTPT will be just fine. Okay. Because it's a pure pleaklet problem. If your white cells cannot degranulate, right, you have like an increased risk of recurrent infections, right. So CKD is not good. In fact, infections are really important cause of death in patients with a chronic kidney disease, right. Because again, their immune system cells cannot degranulate, so they cannot deal with infections appropriately. And then uremia can cause pericarditis. That's basically what this patient has like chest pain better when you sit up or when you lie back. That's supination. That happens in the setting of uremia. Uremia can cause something like a kind of a fibrenospheric adicties if you make. And then the most common cause of kidney disease in the US, that's diabetes. Okay. Second most common cause is hypertension. The easy way to remember that is that D comes before H in the alphabet, right. So diabetes is number one. Hypertension is number two.

And again, if a patient has chronic kidney disease and you want to protect the kidneys, remember, I told you that diabetes, if you want to slow down like hyper-filthration injury with that whole intra-glomerular hypertension business, you can take a, you can take an ACE inhibitor, right. So that's the answer to this question. ACE inhibitor and ARB. And then really for chronic kidney disease, there's a bunch of things you do, right. You try to sort of like restrict phosphate in the diet. You can give like a phosphate binder like a sevalammer, right. You give like an ACE inhibitor, right. So that you can slow down kidney damage. You try to supplement vitamin D, right. So that they don't get like a secondary hyperparthyroidism. Okay. And remember again, the kidneys help you excrete potassium, right. So if you have, if you see a patient with CKD having like a white cure, as big T-waves, think about hyper-killine. Okay. And really the way you money severe your remains, you go ahead and just do dialysis. Remember, there's like an AEI OU nomonic for the treatment for the, for people for when dialysis is indicated, right. So there is like for severe acidosis, there is for like a weird electrolyte imbalance, the eyes for like ingestion, right. So let's see, you take like ethylene glycol or something ridiculous, you can sort of dialize that out. And then fluid overload is the O and then the U is a remia, right. So if a person has severe urinia, go ahead and dialize those patients.

And then the next question, right. So PICT waves and rising creatinine, the patient receiving R-chup for some hematologic malignancy, right. So this is a, they have PICT waves, so they have hyper-killine, right. And they have raising creatinine. So let's assume maybe they are beginning to get like some kind of uric nephrapathy, right. So this is something that happens when you think about if you're receiving R-chup, right. You're killing like lymphocytes. And as you're lysing those lymphocytes, right, from a tumor like a lymphoma, right. Remember that you make a lot of nucleotides, right. Because lymphocytes divide a lot, right. So all those like purines, for example, can form uric acid, although the activity of azanthine oxidics, and that can basically cause like a urit nephrapathy, okay. So this is tumor lysis syndrome. And really tumor lysis syndrome, again, arises because all the nucleic acids in your lymphocytes that are in the lymphocytes that are dying from like the killing of the lymphoma or leukemia. All those purines are meeting to uric acid, and then that clogs up your kidneys and you get into trouble. So how could you prevent this, right. One is you could hydrate the patient vigorously, right. Really another thing you could actually do is to give aloe purinol, right. That's a zanthine oxidize inhibitor. Zanthine oxidize helps you convert, basically make uric acid, right.

So if you inhibited the enzyme that helps you make uric acid, like you, by giving aloe purinol fibroxostats, then you can prevent the formation of uric acid, right. And then another thing you can do is if you sort of like think of birds, so birds, they actually have pretty concentrated urine. And if you sort of think about it, with birds having pretty concentrated urine, you should be having like a cropped on a kidney stones. But that doesn't really happen in birds because they have the enzymes known as uricase, okay. Because birds like to conserve water, so they have consented, consented urine, right. So they express uricase, uricase actually helps them break down uric acid to something that's a lot more water soluble known as alantoine, okay. So from acetylchocompanyes have invented uricase analogs if you may, right. So like raspberry case, big lotty case, those can basically turn uric acid to alantoine, okay. And that prevents you from having a uric nephrapathy. And then the nephrotoxicity will be splatting. This is just basically a human question. So splatting can is nephrotoxic. You can prevent that by giving a drug known as amyphostane, it sort of maps up the free radicals that may be observed with us as splatting use, okay. And then the two high-year antibody classes implicated in an ET and already talked about these think about like amino glycosides like gentomysine, you're mysin, amychysine, tubermysine, streptomysine and all that stuff.

And then also your vancomycin, right. Use the treatment merse, covers, gram positives only, right. That can also cause an ETN. And then this one, next one, this is just an association you need to know. 26-year-old female who is through these false problems is found to have large amounts of blood in her fully catheter by the rotating met student, pregnancy was complicated by a broptuoplacente, okay. You'll learn about that in your 30-year and your reproblox of met school. Broptuoplacente basically is like the placenta like falling off the uterus literally. Social across an emergency section, right. And she has a histropropinatal poor prenatal care and deliose of cocaine during pregnancy, actually using cocaine is a big risk factor for a broptuoplacente. So this patient, this is just something you need to know, this is something that is diffuse corticone acrosis. It classically arises on exams in the setting of like an obstetric emergency where you lose a tumor blood and then that causes the acrosis of the renal cortex, okay. So another reason I sort of bring this up is trade or sort of differentiate between diffuse corticone acrosis and renal papillary necrosis. renal papillary necrosis arises on exams in the setting of like chronic end-set use or diabetes which is actually the most common cause of renal papillary necrosis or sickle cell disease, okay. So it presents as like a painless ineturia, in maturia if you may, okay.

Contrast that with again, diffuse corticone acrosis that again presents in the setting of like an obstetric emergency where you lose a crap ton of blood. Okay and the potential pathophysed they believe that it involves like some DIC kind of thin going on and your hemelapse, right. If you have DIC, right, you have a lot of problems, right, like your PTT. Basically all your coagulation markers are all screwed up. Your PTT will be high, your PTT will be high, your bleeding time will be high, right. Your INR will be high, like everything will all be screwed up with the fuses of corticone acrosis because it sort of involves a DIC, DIC-like picture. And then the next question. So given the following clinical presentations, what is the most likely pathonomonic finding on your analysis, right. So first one says we have a 27 year old male smoker, okay, presents with a three week history of hematurian hemoptysis. And then a physical exam is, yeah, physical exam is notable for extensive sinusitis. This is a, this is a, Wagner's, right. So you have like hemoptysis, hematurian, the upper respiratory symptoms, it can be sinusitis, it can actually be an ear problem. So don't be tossed by that in the exam, it can actually, because your ear sort of kind of constitutes your upper respiratory tract, right. So this is Wagner's. You can also see a saddo knows the formity as the upper respiratory tract okay. So that's Wagner's. Remember it's Cianca positive, right.

So because it's a kind of nephrodix syndrome, you'll see ribloxel casts in the urine. And then the next one says we need ear old male, recently started on empathy flossing for type 2 diabetes, presents with a 12-hour history of severe left-sided flung pain. A physical exam is notable for CV tenderness, right. So this is pylon arthritis, right. So you see why blood cell casts. Now 15 year old female with no relevant pass medical history was found three days after she got lost in a desert, right. So this is, this is just a person that's volume down, right. So they will have concentrated urine. So you may find no cast at all, or like higher link casts, okay. Made of a tamwhospala protein. And then 55 year old female with rising creatinine after is even a 30s inhibitor for the treatment of a life threatening so the monolin infection, right. So let's assume they got an amino glycoside, right. So they probably have ETN, right. So you should see the moody brown casts in the urine. Next one says of 45 year old chronic alcoholic is found down on the street by police. His core temperature is 91, creatinine is seven and potassium is six. This is bad news, right. This is ribomyolicis, right. And again, I talked about this earlier. You find urine dips take positive for blood negative for red blood cells, right. So you see like four plus blood, but zero to two red cells per high power field. If you do urine microscopy, that's ribomyolicis.

Next is 44 year old HIV positive male comes to his PCP who complains over three month history of swelling everywhere. Physical exam is notable for generalized anestharka. His serum will be managed too. So this patient has a FSGS, right. So this is an afrodic syndrome. So you may find like fatty casts, like lipid casts in the urine with a multis cross pattern. So that's a micro tying here. Remember, multis cross pattern in your red cells, hopefully that gets you thinking about BZM, okay. BZM, okay. And just real quick, sort of backtrack here, right. So a patient that has HIV has FSGS, right. What's the kind of FSGS they have? They have the collapsing FSGS. That's the one with the worst prognosis is actually pretty common in African-Americans. And then I'll contrast that with the more B91, I guess not B9, but has a better prognosis like the TIP lesion. The TIP lesion is a subclassification of FSGS. It has a more B9, more B9, I guess a better prognosis. Although FSGS in general is bad, but has a better prognosis, okay. And it's more common in Caucasians versus the the collapse in FSGS that's found in African-Americans, but it's primarily found in HIV positive patients. Now, next last question says that when two-year-old female recently started on a dichloroxacillin form a stitis, right. So that's an anti-staff locococopinicillin. Presented at three-day histrava generalized upper body rash, right. So that temperature is 102.1. So this patient has a high fever, has a rash.

I didn't give you the last part of the triad, right. This will be, the last part will be like Eocino fills in the blood, elevated Eocino fills in the blood and urine, right. So this is AIN, acute interstitial nephritis, right. So you'll find Eocino fills, not Eocino phylic cast, you'll find Eocino fills in the urine. Eocino phylic cast, you'll find them in the urine in chronic pylon nephritis. Okay. And then the last question in this series, or I guess second to the last is, it will be the classic USML index refining in a patient with on dialysis with stage 5 CKD. The big thing I would just say is that let me talk about something before I answer that question, right. So in chronic kidney disease, again, you have no one alpha hydroxylates, right. So you're not making active vitamin D. So you do not reabsorb calcium and phosphatine in the gut, right. So your high bulk calcium, if you're high bulk calcium, your PTA2 rice, okay. Your PTA2 rice. And if your PTA2 rice is the phosphate trussion hormone, right. So what should we choose your phosphate? Should it be high or low? I know the answer you're each and you say is no, but it's not. It's high, okay. Because again, your kidneys are your primary phosphate excretine organs, right. So if you have no phosphate, if you have no kidneys, you have no phosphate excretion. So in CKD, secondary hyperparthyroidism, you usually have a hyperphosphatemia, okay. And because your PTA2 is always high, always litgin away at bone, right.

You classically have like bone pain in CKD, right. And the Bosnian looking for an example is subperial still thinning of the bone. It's usually like the bones of the hand, okay. That's like almost pathonomonic for primary hyperparthyroidism that may arise in the setting of a chronic kidney disease. So let's assume a patient has chronic kidney disease and they get a new kidney, okay. They get a new kidney. You basically fix their vitamin D problems, right. So the thing is you may think that, oh, everything sort of returns to normal. That's not always the case, okay. Because the thing is some patients with a history of chronic kidney disease, right. Their parathyroid glands are just used to secretive the crap ton of parathyroid hormone all the time, okay. All the time. So those patients, they may get new kidneys and the parathyroid, they may actually just still keep secretive in a ton of parathyroid hormone, okay. That's something in a tertiary hyperparthyroidism is like the parathyroid glands just don't the same thing for so long. It becomes unresponsive to normal signals. So in tertiary hyperparthyroidism, right. These patients have new kidneys, right. So the PTH is high because the parathyroid gland is again just autonomously secreting a ton of PTH. So their calcium will actually be high, okay, because now they have active vitamin D. Their phosphid will actually be low because it's now appropriately trashed by the new kidneys, okay.

And you have like normal or high levels of active vitamin D, okay. And really the way you treat hypercalcemia in patients that have CKD is you give them like calcium trial, like I mentioned earlier. If a patient has a primary hyperparthyroid, I mean tertiary hyperparthyroidism, you can give them, you can basically remove three and a half of the four parathyroid glands. So you remove three and a half of the four parathyroid glands to treat a tertiary hyperparthyroidism. Okay. Now last question, him obtruses, plus him at terrioplus, your analysis reveal in a red cell cast, plus creatinine of 525-year-old male smoker, right. So I know you're eagent to pick webinars, but please don't. Because this patient doesn't have all respiratory symptoms. So this is webinars, I mean this is a good posture syndrome, okay. Good posture syndrome, basically you make autoantibodies against that pesky type four collagen that I mentioned in the first podcast, right. So you make a auto, actually it was in this podcast, but it was early in this podcast, you make autoantibodies against the type four collagen, like the alpha-3 chain of type four collagen, right. And that's the pathophys behind the good pastures. And really the way you make the diagnosis, you biopsy the kidneys, you do like light microscopy, you do immunofluorescence, you do electro microscopy. And really the money shot here is immunofluorescence, you see a linear pattern along the glomerular basement membrane, okay.

And really this, because you're making an antibody against like a fixed antigen, which is like a glomerular basement membrane, this is actually a kind of type two hypersensitivity reaction, just like an autoimmune hemolytic anemia, if you may. And really the way you treat this, basically use the pathoma prescription steroids and cyclophosphamide, okay. Although you can also try to get rid of those antibodies pretty quickly with plasma ferrisis, that's the hematologic procedure that can help you get rid of the other antibodies. And again, this is a, this is a kind of nephritic syndrome. If you want to be a little more specific, this is a kind of a type one RPG, it's a type one rapidly progressive glomerular variety. So you may actually find chrysancts on light microscopy of the kidneys. So I'm going to stop here. And then we'll have a third and final podcast that covers the rest of the renomaterial. And hopefully you should feel better with the renomaterial for step one. Have a wonderful day and God bless. I'll see you next time. Thank you.

The proximal tubule, because it is the most metabolically active and consumes the most resources.

The ureteropelvic junction (UPJ). Obstruction here can cause hydronephrosis.

Muscarinic antagonists (e.g., Oxybutynin, Solifenacin).

Patients with diabetes mellitus.

The Q-tip moves significantly (e.g., >30 degrees) when pressure is applied, indicating poor support/hypermobility.

$11\beta$-HSD2 (11$\beta$-hydroxy steroid dehydrogenase 2).

Fever, rash, and eosinophilia.

Inhibition of $11\beta$-HSD2 by glycyrrhizic acid leads to cortisol accumulation, causing mineralocorticoid receptor activation.

In CKD, Phosphate is high (hyperphosphatemia). In Tertiary Hyperparathyroidism, Calcium is high, Phosphate is low, and PTH is high due to autonomous secretion.

A linear pattern of IgG deposition along the glomerular basement membrane.

White blood cell (WBC) casts.

Uremia impairs platelet degranulation, leading to an elevated bleeding time, even if the PTT is normal.

Fever, rash, and eosinophilia.

Inhibition of $11\beta$-HSD2 by glycyrrhizic acid leads to cortisol accumulation, causing mineralocorticoid receptor activation.

In CKD, Phosphate is high (hyperphosphatemia). In Tertiary Hyperparathyroidism, Calcium is high, Phosphate is low, and PTH is high due to autonomous secretion.

A linear pattern of IgG deposition along the glomerular basement membrane.

White blood cell (WBC) casts.

Uremia impairs platelet degranulation, leading to an elevated bleeding time, even if the PTT is normal.

Fever, rash, and eosinophilia.