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Biochemistry of the Urinary System — Transcript

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0:01in today's lecture we'll be talking
0:03about the biochemistry of the urinary
0:06system there are several objectives in
0:10this lecture today so basically we'll be
0:13talking first about the basic renal
0:15function and morphology and we'll follow
0:17up with talking specifically about what
0:20the function of the kidneys are so the
0:23first function is excretory in nature
0:25the second function of the kidney is for
0:28homeostasis the third would be in
0:31doctrinal and a fifth will be metabolic
0:33I'll be talking about specific aspects
0:36for these four functions in the
0:39subsequent sections of the lecture so
0:43going into part one what's the renal
0:45function and how does it look
0:47morphologically so basically you
0:50probably have received a little bit
0:52about the rental morphology from your
0:55anatomy lecture
0:57well basically here we'll be looking
0:58closely about the nephron so right here
1:01in the kidneys we've got small
1:03functional units which we give the term
1:06nephron for each nephron is composed of
1:11essential parts such as their rental
1:13corpuscular and we've got the renal
1:16tubules we've got two types of tumors
1:18actually we've got one proximal
1:22convoluted tubule convoluted because it
1:25looks so messy and just looks like a
1:28twist twist a little thing and then you
1:31go down like a loop which is what we
1:33call a loop of Henle and we go up and
1:36that's the proximal convoluted tubule
1:39the nephron ends with one distal
1:42collecting duct and we'll be looking at
1:45the structure of each and talking about
1:47how these structures affect the
1:49formation of urine so going into renal
1:53function so basically each nephron
1:55carries out all the kidneys jobs the
1:59first job is for excreting stuff for
2:02getting rid of stuff from our body this
2:04includes water and also perhaps
2:07byproducts or metabolisms such as urea
2:10and creatinine and it also includes
2:12homeostasis
2:13specifically how the kidneys regulate
2:16acid-base balance as well as electrolyte
2:19balance the third function is in
2:21doctrinal and we look at how the chemist
2:23synthesizes hormones such as the renin
2:26or the vitamin D activated form hormones
2:29the erythropoietin Homan as well also
2:33what it does metabolically so how is the
2:36in keenly involved in amino acid as well
2:38as carbohydrate metabolism so let's look
2:42into the first function of the kidney
2:44which is the excretory function of the
2:46kidney now we've looked at this
2:49structure before but this nicer diagram
2:51form the biochem atlas shows us more
2:54specifically what each structure is
2:57responsible for so as you can see this
2:59is the rental corpus kill it's got a
3:03part called the Bowman's capsule and the
3:05glomerulus and basically inside the
3:08glomerulus is where all the filtration
3:11happens we'll talk about filtration
3:13later but basically this is responsible
3:15for ultra filtration and in the proximal
3:19convoluted tubules as well as a distal
3:24Proctor convoluted tubules it's their
3:26more responsible for resorption this
3:29this also applies for the hen Leslie
3:31although this the steps of Kim your
3:34information can occur all throughout the
3:36kidneys we're looking at where it is
3:39concentrated at and secretion of course
3:42occurs more in the distal parts and also
3:45in the collecting duct okay so we talked
3:48about you heard me talk about ultra
3:49filtration absorption secretion so what
3:51exactly are they so those are the three
3:54steps of urine formation the first steps
3:57as I said is ultra filtration second is
4:00reabsorption and third is secretion and
4:03in ultra filtration as I mentioned
4:06before it occurs primarily in the gloomy
4:09rely and blood plasma here is filtrated
4:14so all the blood that goes in the kidney
4:16will be filtrated to produce primary
4:19primary urine all blood here is an
4:22overstatement basically what is filtered
4:24is most of the
4:26Kosmic content but they will be
4:28reabsorbed so the kidneys will take back
4:31what we still need in the proximal
4:34convoluted tubule the renal filtrate
4:36undergoes reabsorption in which most 99%
4:40molecules and compounds are absorbed
4:42back from the filtrate so that's a lot
4:44of compounds going back into the rental
4:46filtrate and the third step is secretion
4:49and this occurs in the distal convoluted
4:52tubules mostly and also the collecting
4:54duct
4:55the filtrates will be added with more
4:58compounds that could be compounds from
5:00drug metabolisms etc and it will finally
5:04be excreted as the final urine so this
5:07is the final step in which the pee is
5:09made okay so let's talk a bit about
5:13ultra filtration now this step is non
5:17selective in nature that's a very
5:19important aspect of the step because it
5:21just allows all compounds basically with
5:24a size of less or smaller than 65 mm can
5:29pass through the glomeruli so if it's
5:31smaller than 65 please go through the
5:34glomeruli it is not specific at all and
5:37basically ultra filtration can be
5:40measured by a terminology that we call
5:43glomerular limit rule Marilla filtration
5:46rate which marks the body's ability to
5:48excrete products so in order to know how
5:52well a body our bodies are able to
5:56excrete product then we have to choose
5:58the product that we want to measure so
6:01basically we choose the product what is
6:03the urine concentration of a product
6:05that we want to measure and what is the
6:07plasma concentration of that product and
6:10we times it by the volume basically that
6:11gives us a reflection of how well the
6:14kidney is actually excreting the
6:16products and and one product that can
6:19use those often used as a marker is
6:22creatinine and we'll talk about why
6:25creatinine is often chosen as a marker
6:27for filtration and this is basically the
6:31same formula applied for creatinine
6:34which reflects the glomerular filtration
6:36rate so when we find an abnormal
6:39Goomer lemare Ola filtration rate or GFR
6:42what does that indicate well it means
6:45that the kidney is actually losing or
6:47being disturbed in function so it's a
6:49really good clinical sort of marker for
6:53knowing whether or not a patient's
6:54kidneys are functioning well or not the
6:58second step is which occurs mostly in
7:01the proximal convoluted tubule is
7:03reabsorption as you know basically the
7:06first step was not specific kit
7:08everything gets thrown into the rental
7:10filtrate in this step it is much more
7:12specific because the kidney actually
7:14chooses which compounds it is taking
7:17back and this actually applies for most
7:20of the compounds approximately 99% of
7:23the compounds are reabsorbed back into
7:25the kidneys now how are they reabsorbed
7:29into the kidneys well there are a couple
7:31of mechanisms for that the first is
7:34active transport and then there's
7:35passive transport osmosis and Pinus
7:38cytosis I'm sure you've heard of these
7:40mechanisms before but let's do a little
7:41review when we talk about active
7:43transport and transportation of a
7:45compound in the membrane is basically
7:47occurring actively which means it's
7:49using energy and this is used for
7:52compounds such as glucose amino acids
7:54lactate ketone bodies calcium sodium and
7:57potassium
7:58now passive transport occurs without the
8:01use of energy and this usually occurs in
8:04case of negative ions that are following
8:06the the movements and transport of
8:10positive ions okay the third mechanism
8:12is osmosis as you know osmosis is really
8:16useful water movement and Pinal
8:18psychosis is the last mechanisms that a
8:21kidney often utilizes and it's mostly
8:23for transporting really big heavy
8:25proteins now let's look a little at how
8:28water is reabsorbed so we know the
8:31picture of what exactly occurs in
8:32reabsorption so as we've talked about
8:35before
8:37what are we absorption occurs passively
8:40through the process of osmosis and in
8:42the case of watery absorption there's a
8:45specific hormone that's responsible for
8:47that and that is ADH which is also
8:51called antidiuretic home
8:53and when we hope have a lot of ADH then
8:57what happens more water is reabsorbed
9:00there is actually a specific condition
9:03in which a person will lack ADH and this
9:07is called diabetes insipidus when a
9:10person is deficient in ADH and what
9:12happens the person is unable to reabsorb
9:15water effectively in other words the
9:18person will throw out a lot of water
9:20will be excreting out of water up to 30
9:24liters per day now that makes it really
9:28interesting because now we know that is
9:31affected by a couple of other things
9:33like hormones and what you can see here
9:37are a couple of other examples in
9:39addition to ADH of what hormones can
9:42actually affect kidney reabsorption and
9:45these include parathyroid hormone
9:47aldosterone and an P with parathyroid
9:50hormone what this affects is uptake or
9:53increase in calcium in calcium
9:56reabsorption whilst a dosterone
9:59increases sodium reabsorption and on the
10:03other hand
10:04it increases potassium excretion
10:08so when we have a lot of aldosterone a
10:10lot of nature's are a little sodium's is
10:13retaken back into the body and more
10:16potassium is excreted out of the body so
10:20it works oppositely and then finally we
10:23have lost hormone which is a and P which
10:26is called atrial natriuretic peptide
10:28which works opposite to aldosterone in
10:31terms of its effective sodium what it
10:34does is reduces the reabsorption of
10:36sodium and now we're going to the last
10:39step which is secretion which occurs
10:41mostly in the distal convoluted tubules
10:43as well as a collecting duct and what
10:45here happens here is that the filtrate
10:47that we received from the reabsorption
10:48step will be added with more substances
10:52as needed such as maybe drug compounds
10:54and metabolites and finally once it's
10:57all done it will then be excreted as the
11:00final urine and this nice little table
11:03here shows us what a normal urine looks
11:06like
11:07how much do we have to produce each day
11:09what the color is we all know what the
11:12color of urine is but it should ideally
11:14be clear and not cloudy and what the
11:17specific gravity is which means how much
11:20stuff basically is dissolved in the
11:23urine and then we've got the pH which
11:26ranges between four point six to eight
11:28and we've got composition of urine and
11:31also what nitrogenous waste or metabolic
11:35products are present in the urine sorry
11:40so what is a normal urine composed of
11:44exactly so some references divide this
11:47into basically inorganic compounds and
11:51organic compounds and here we'll follow
11:53suit I'm talking about inorganic
11:56compounds about KT ins and any anions so
12:00we've got examples of cations are sodium
12:03potassium calcium magnesium and ammonium
12:07and whilst anions include chloride
12:09sulfate and phosphate and what we need
12:13to know here really is if you look at
12:15these picture or mountains you can see
12:18exactly how much is produced in the
12:21urine each day as you can see the
12:23biggest mountain here is chloride
12:24meaning that the body excretes chloride
12:27most this is followed closely with
12:29sodium so you can see chloride in
12:32chloride excreted in from the bodies
12:34about 120 to 240 million miles per day
12:38while sodium is about 100 to 150 so yes
12:42so these two are the biggest compounds
12:44in organic compounds that we excrete a
12:47day so please feel free to look at the
12:50normal values and we've got organic
12:52compounds and this include physiologic
12:55compounds as well as metabolic waste
12:57products
12:58so basically metabolic waste products
12:59such as urea uric acid and creatinine
13:02are the products that we make as the end
13:06product of metabolism so when we do
13:08metabolism when the body does the
13:10metabolism sometimes it makes waste and
13:13end products and these include the
13:15important ones in the urine are urea
13:17uric acid and creatinine
13:19and there's other compounds that we
13:21found day to day in the urine such as
13:23glucose ketone bodies and protein as you
13:26can see here the point is that these
13:28compounds are normally present but
13:30they're present under a certain value
13:32which you can see here now we're going
13:36to talk about the metabolic waste
13:38products one by one just because they're
13:40really important so the first metabolic
13:42product we'll talk about is urea and
13:44urea as we may have you may have heard
13:47before is the end product of amino acid
13:50metabolism and synthesis of urea occurs
13:53in the liver and he aims to convert
13:55toxic end products of protein metabolism
13:59such as ammonia into a non toxic product
14:02if you recall amino acid metabolism you
14:04know that during the breakdown of amino
14:08acid it first undergoes transamination
14:11into alpha and then it go undergoes
14:13Deoxys it of deamination and finally and
14:17loot will and in this step will be
14:19creating what we call ammonia and
14:22ammonia is not allowed to go to the
14:24bloodstream which means we have to find
14:26a way somehow to convert it into
14:28something less toxic in this case
14:30ammonia goes into the urea cycle and is
14:33turned into urea and urea is then
14:36allowed to exit the liver go into the
14:40bloodstream it doesn't is not toxic in
14:42normal amounts go into the kidneys to be
14:44filtered and then be excreted in the
14:47urine so that's how basically we get rid
14:50of amino acids from the body because
14:53urea excretion is highly affected by
14:56diet and also by the capability of the
14:59kidney at that stage to excrete and
15:02filter urea then basically we can't
15:05really use it as a reflection of the
15:07glomerular filtration rate because then
15:10when this will be affected a lot by the
15:12patient's diet makes it less reliable
15:15doesn't it
15:16now patients with kidney failure often
15:18struggle to excrete urea so in these
15:20patients we find a condition called
15:22uremia because the Burien is basically
15:25just piling in the blood and not being
15:29excreted right the sec
15:32metabolic waste that we'll talk about is
15:34uric acid uric acid is the end product
15:37of Puran catabolism so purine is one of
15:40the types of nucleotides if you recall
15:42and one thing that we need to know about
15:44new york acid is that it does not really
15:46dissolve in water so let's go back to
15:49what purines are so we know where their
15:52nucleotides and there's two types
15:53appearance at an Olson and Gwen Olson as
15:56shown here in the nice figure from
15:58Harper's biochem so basically what it
16:02doesn't matter what type of purine it is
16:04in the end it will be converted into
16:06santen now sorry
16:09Stanton will be converted into uric acid
16:11through an essential enzyme that we call
16:14certain oxidase and amount of uric acid
16:18that is excreted is affected by diet as
16:22well and hence just like urea it is not
16:25a reliable marker for measuring GFR so
16:31in urine because as we as I've said
16:34before it doesn't really dissolve in
16:35water so in your in uric acid will
16:38precipitate into crystals if it you know
16:41there's too much of it so what happens
16:42it can consequently it can also turn
16:45into kidney stones so increased plasma
16:48your levels or hyperuricemia and urine
16:51uric acid levels often occur and we can
16:54see this lot in people with high purine
16:57diets the third metabolic waste product
17:01the final one that we'll talk about is
17:03creatinine so creatinine is the end
17:05product of muscle energy metabolism so
17:08basically in the muscle they use
17:11creatinine
17:11as a source of energy and the cycle
17:15between creatinine cran phosphate
17:17actually creates an end product or waste
17:19product that we know as creatinine and
17:21creatinine can go right into the kidneys
17:24and get excreted now because unlike uric
17:28acid and urea the amount of creatinine
17:31that we excrete is relatively constant
17:33towards muscle mass then it can be used
17:36as reliable marker for measuring GFR so
17:40we've looked at the normal you're in
17:41competition we know how it's supposed to
17:43look
17:44we know how what it's supposed to
17:46have inside now we'll look at examples
17:48of what can go wrong so what isn't what
17:52we call an abnormal your in composition
17:53so here we'll talk a little bit about
17:55these terms so there's glycosuria
17:58proteinuria hematuria ketonuria and
18:02bacteria from the name you can already
18:04predict what can be inside the urine
18:06that's in too high in amounts so
18:08glycosuria is basically too much sugar
18:12in the urine and as you can predict it
18:15often occurs in patients with diabetes
18:17and secondly proteinuria is basically
18:21too much protein in the urine and this
18:23can sometimes indicate an increase in
18:26glomeruli permeability so what exactly
18:29is the meril eye permeability well
18:32basically it's the capability of the
18:35glomeruli to filter oh so in a normal
18:39kidney as you can recall only substances
18:42less then 65 to adult UM's can pass but
18:46when there are conditions causing the
18:48mirror-like permeability to increase
18:50proteins larger than that or anything
18:53larger than that can actually pass so
18:56that is what and this can be autoimmune
18:59in nature or it could be an infection so
19:01that's all the different things that
19:03proteinuria can indicate and third term
19:06is hematuria basically mean blood too
19:09much blood in the urine and it can also
19:11be caused by glomerular permeability so
19:13once in a row so if normally an
19:16erythrocyte cannot really pass through a
19:18glimmer of light this time it can
19:21because of some reason maybe an
19:24infection or something autoimmune and it
19:26can also indicate urinary tract
19:28infection or kidney stones basically
19:31there's stones
19:32sitting in the rental tracks and just
19:34scraping and injuring and making a lot
19:37of blood
19:37and then there's ketonuria which is
19:39basically a lot of ketone bodies in the
19:41urine and it means when we have ketones
19:45in the urine at to higher level that it
19:48means that the body is using too much
19:49fats and proteins as energy sources
19:52we're not really well which means the
19:54body is not really using carbohydrate
19:56whether intentionally or
19:58intentionally and this can be
20:00unintentionally in cases of diabetes
20:03mellitus and if it's intentional it's
20:05usually in the case of proteins on a
20:07high-protein diet or could be on a
20:09ketogenic diet something like that and
20:11then there's also bacterial rap but
20:13bacteria which means too much bacteria
20:16in urine and it's also accompanied by
20:18leukocytosis look white sorry white
20:21blood cells and it usually indicates a
20:24UTI or urinary tract infection now so
20:28what's the consequence of having to an
20:31abnormal urine for too long basically oh
20:33well one it consequence is rental
20:35calculi and renal calculi or kidney
20:38stones are formed from the precipitation
20:41of excess minerals in the urine so the
20:45main so we we looked about you know the
20:47normal composition of organic and
20:49inorganic compounds so this is what
20:52happens when they are normal for too
20:55long so the main course is renal calculi
20:58in the clinic is calcium but it can also
21:01occur with the precipitation of other
21:03compounds such as uric acid and
21:05basically the risk factors include
21:07consuming these cause causative factors
21:11too much so for example you take too
21:13much calcium supplements always you eat
21:15a diet high in puron and if it's
21:18accompanied with a behavior such as not
21:21drinking enough water then that is a
21:24very big predisposition to renal calculi
21:27now formation usually begins in the
21:29reynold pelvis area but will create
21:31colicky pain once there enters the
21:33ureter okay so let's get to the third
21:37function of the kidney sorry the second
21:39function of the kidney which is
21:41homeostatic function yeah okay so the
21:48kidneys hold an important role in
21:50maintaining acid-base balance let's talk
21:53about first the Rennell regulation of
21:55acid-base balance so there's two aspects
21:57of hemostasis by the kidney there's
21:59acid-base balance and also electrolyte
22:02balance with acid-base balance when we
22:05compare it to the respiratory mechanism
22:07of acid-base balance the kidney
22:09mechanisms are actually much more
22:12term and permanent in nature it is also
22:14a bit slower so if we talk if we look at
22:18respiratory regulation this is actually
22:20initiated within one to three minutes
22:22but the effect is also short lasting
22:25whereas with rental regulation it is
22:28initiated within a few days to a few
22:30weeks but it is it lasts longer so it's
22:33more time intensive and permanent in
22:35nature
22:36so how does a kidney regulate acid-base
22:40balance that's the question
22:42well there are three mechanisms and
22:44first which and the first one is through
22:47proton excretion and carbonate
22:49reabsorption second is protein buffer
22:52and third is phosphate buffer so let's
22:55look at the first mechanism what does it
22:56mean when we say regulation of proton
22:58excretion and carbonate reabsorption
23:00basically it means how does the kidney
23:03throw hydrogen hydrogen protons out and
23:07take carbonates in so the renal tubules
23:12can regulate that it can either increase
23:14the secretion of protons or it can
23:18increase the conservation of protons
23:21depends if we have acidosis then it will
23:23probably increase it if we have our
23:25closes and it will conserve it and let's
23:28take an example of acidosis let's say a
23:31patient has a really low pH bad acidosis
23:35so how does the kidney respond this is
23:38the mechanism there's a really nice
23:39little figure from the Atlas we can see
23:41here so all the carbon dioxide's that
23:44the kidney can take from the plasma you
23:45will take and it will break this down
23:48sorry with together with water it will
23:52form carbonate and also protons now what
23:56does the carbonate do it goes back into
23:58the plasma why because it's a base
24:00reserve having more carbonate will make
24:03the blood more basic increase the pH and
24:07then that what happens to the protons
24:09well we have to get rid of it somehow we
24:13can either throw it out or we can turn
24:14into something basic in this mechanism
24:17we're looking at how it's turning into
24:19something basic so what happens the
24:22person first needs to get out
24:24and can only get out if we swap it or
24:28extinct exchange it with sodium so once
24:32we can swap it with sodium the proton is
24:35now in the urine what happens in the
24:37urine once again we can either throw it
24:39out there are some other mechanism or we
24:43can find some we can find something and
24:46we can turn it into so we can find some
24:49carbonate and together with carbonate we
24:53join this together and make new carbon
24:56dioxide and the new carbon dioxide will
24:58go then into the tubular cells and form
25:01more carbonate or get reabsorbed into
25:04the plasma or carbon dioxide so
25:06basically here we're looking at how the
25:08kidney takes the protons and either
25:11kicks it out or uses it to make more
25:14base now talking about the protein
25:19buffer system we're looking at how the
25:22body can get rid of protons using
25:25proteins and what protein is usually
25:27used well we use an amino acid called
25:29glutamine so the Kimmy takes a lot of
25:32glutamine in turns it into glutamate and
25:36turns it into ammonia and what happens
25:41is that the ammonia here inside the
25:44urine can combine with any random
25:46protons hanging around and will happen
25:49is that they combine together and turn
25:51into ammonium and ammonium is their is
25:54unable to be reabsorbed back into the
25:56tubules so what happens that we have to
25:58actually excrete it so that's another
26:00way to get rid of protons now let's look
26:04at phosphate buffer system another way
26:06to get rid of protons so here recall
26:09when you recall that Rennell tubules
26:12into renal tubules we can only get rid
26:14of protons and we can swap it with
26:16sodium so in this system though what we
26:20have is a specific compound called Dyne
26:23atrium hydrogen phosphate it's got to
26:25nee treants how does it provide for
26:28natrium and get rid of H+ so this
26:32compound in the phosphate buffer system
26:34will donate one natrium so that
26:37our proton can get in to exchange these
26:41compounds and what happens is this
26:43random proton going in will combine with
26:45the leftover natrium hydrogen phosphate
26:48now with one sodium so one sodium
26:51hydrogen phosphate will combine with the
26:53proton and create sodium dihydrogen
26:57phosphate now as you can notice it now
26:59has two hydrogens so it's a dihydrogen
27:02phosphate and it will then be excreted
27:04through the urine there we go
27:06three different ways the kidney can
27:08throw protons out in the case of
27:11acidosis now how does the kidneys
27:14regulate electrolytes we've looked about
27:17how it regulates acid-base now how does
27:19irregular electrons so the first
27:21electrolyte that we're going to look at
27:22is sodium so reabsorption of sodium
27:26occurs through active transport and this
27:29mostly occurs here in the proximal
27:33convoluted tubules about 65% of
27:36reabsorption occurs here and although it
27:39can also occur around the loop of Henle
27:42the distal convoluted tubule and the
27:43collecting duct and this active
27:46transport mediator is absorption is
27:48actually affected by a couple of
27:51hormones when we have a lot of
27:53aldosterone hormones more sodium is
27:57reabsorbed so it increases reabsorption
27:59but when we have a lot of atrial
28:01natriuretic peptide then that decreases
28:04reabsorption so more sodium is excreted
28:08and thrown out of the body now how does
28:11it regular potassium is a little
28:13different to the way the body regulates
28:16sodium potassium is actually mediated
28:18through both active and passive
28:21transport mechanisms so it can be first
28:24transported passively by following
28:27following the transport of sodium or it
28:31can also be reabsorbed actively through
28:36active pumps in that loop of Henle
28:40in hyperkalemic conditions intercalated
28:43sells reabsorbs potassium while it is
28:47excreted by the principal cell and this
28:49is affected by the activity of
28:51aldosterone now moving into the last
28:54function of the kidneys which is the
28:55Andorran or function so the first
28:58hormone that the kidney produces is
28:59calcitriol calcitriol is basically an
29:02inactive vitamin d now where do we get
29:04the vitamin d from it can either read
29:06from a diet or it can be from 70 Hydra
29:09cholesterol that is found in the skin
29:11and is converted into vitamin D using
29:13sunlight now in the kidneys the inactive
29:17vitamin D will be converted into an
29:18active vitamin D through an enzyme that
29:21we call one alpha
29:22hydroxylase now the second hormone that
29:27we'll talk about is Ipoh so EPO is
29:30basically a glycoprotein responsible for
29:32erythropoiesis
29:33or the formation of red blood cells EPO
29:36how does it work well if it goes to the
29:39bone marrow and stimulates the
29:40differentiation of progenitor cells and
29:43it turns it into erythrocytes EPO is
29:46formed in the kidney as a response of
29:48heart towards hypoxia so when there's a
29:50low oxygen level then EPO is formed and
29:53this synthesis is occurs in mesangial
29:55cells and Rennell tubular cells so
29:57patients with kidney failure often
29:59experience disturbed ePro synthesis and
30:01hence results in am Lamia now in the
30:05renin-angiotensin system the kidney
30:07synthesizes renin which is a hormone
30:09that is responsible for increase in the
30:12renin-angiotensin system and what
30:14happens is when there's a condition of
30:16low blood pressure the kidney will
30:18respond by synthesizing renin and this
30:21will convert angiotensinogen into
30:23angiotensin one and this will then be
30:25converted into Angie intention to by ACE
30:28and then this will create
30:30vasoconstriction or increase blood
30:31pressure now the last one is metabolic
30:34function of the kidneys and the kidney
30:37beside the liver is another organ
30:39capable of performing gluconeogenesis as
30:41you can see it occurs mostly in the
30:43fourth phase of starvation and
30:46substrates included in the kidneys what
30:48precursor exclude men that take glycerol
30:51and fructose and beside that Rennell mr.
30:53is also responsible for amino acid
30:55metabolism not only in degradation as we
30:58can see from urine cycle but also
31:00instances synthesis such as in carnitine
31:03synthesis and also from for argument
31:07synthesis so there we go in conclusion
31:09the kidney has a lot of functions
31:11it could be excretory nature for
31:13homeostatic function in doctrinal and
31:16also metabolic so we've covered all
31:18those topics and I hope this video helps
31:19and these are the references that can be
31:23read further

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