Download Urinary Text Lecture This lecture has been written to accompany the

Dr. Carmen E. Rexach
Spring 2008
1
Urinary Text Lecture
This lecture has been written to accompany the slides posted on-line for the Urinary
System lecture. The intention is for you to either print the text lecture or view it on-line
while looking at the slides. You are responsible for all of the material contained in this
lecture. If you have any questions, it is your responsibility to contact me and ask before
you take the exam!
Slide 2:
The urinary system consists of the kidneys, ureters, urinary bladder, and the urethra. Note their
location in the body.
Slide 3:
The kidneys are retroperitoneal in the abdominopelvic cavity and are about the size of your fist.
The left kidney is slightly higher than the right due to the size and shape of the liver. It is
surrounded by and packed in fat to keep it in place. If someone is anorexic or cachexic and loses
the fat around the kidney, the kidney can fall. This is called ptosis and can result in a kinked
ureter, potentially trapping the urine in the bladder.
Slide 4:
The kidney functions primarily to maintain homeostasis in the body by regulating the composition
and volume of extracellular fluid through the formation of urine. Kidneys regulate the amount of
blood plasma by increasing or decreasing the reabsorption of water. They regulate the
concentration of waste products so that they can be efficiently eliminated from the body as urine.
It is in the kidney tubules that hormones act to regulate the concentration of several major
electrolytes, such as Na+ and K+. Kidneys can also help regulate the acid-base balance in the
body by adding H+ or HCO3- to the blood. In addition, the kidneys produce and secrete several
hormones, including erythropoietin, which regulates the formation of red blood cells. Rennin, a
protease which is involved in the maintenance of blood volume, is also produced. It is in the
kidney that Vitamin D is converted to its final active form, 1,25 dihydroxycholecalciferol.
Slide 5:
This slide shows the gross structure of the kidney, which should be familiar to you from your
anatomy class. If it isn’t, please take out your anatomy book and refresh your memory!
Slide 6: Micturition Reflex
Urine is formed in the kidney and then sent to the bladder through the ureters. Peristalisis of the
renal pelvis and the ureters helps to move the urine along. A valve called the ureterovesicular
valve prevents the urine from flowing back up into the ureters from the bladder as it fills. The
bladder contains a special muscle called the detrusor muscle. (Remember that the bladder is
also lined with transitional epithelium, which flattens as it is stretched). The amount of urine in the
bladder can range from close to 0 up to about 500 ml. As the bladder fills up, stretch receptors in
the bladder wall are stimulated. This sends signals to the spinal cord via the hypogastric nerve.
When the bladder pressure reaches a critical level, pelvic nerves from the sacral region respond
by causing reflex contractions of the bladder. This allows the internal urethral sphincter, which is
composed of smooth muscle, to relax, resulting in an urge to urinate. The external urethral
sphincter is skeletal muscle and should be under voluntary control. If you have the urge to
urinate, but suppress it, then contractions will abate temporarily until more urine is added to the
bladder, at which point the stimulus is resumed.
Slide 7: Renal blood vessels
Be sure you know the pathway of blood through the kidney from the abdominal aorta to the
inferior vena cava.
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Spring 2008
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Slide 8 & 9: Nephrons
These two slides show illustrations of the structure of the kidney and of its functional units, the
nephrons. Nephrons are an association of blood vessels and tubules. Each nephron consists of
an afferent arteriole, a glomerulus, an efferent arteriole, and a system of kidney tubules. The next
set of slides describes nephrons in more detail.
Slide 10: Renal tubules
There are two general types of nephrons based on their location. The shorter and more
numerous nephrons are located predominately in the cortex of the kidney and are therefore called
cortical or superficial nephrons. Those with long kidney tubules that extend deep into the medulla
are called juxtamedullary nephrons. The latter hyperconcentrate the urine. The kidney tubules
begin with a cuplike structure that surrounds the glomerular capillaries called Bowman’s capsule.
The combination of the glomerulus and Bowman’s capsule is called the renal corpuscle. From
Bowmann’s capsule, the first region of the tubule is called the proximal convoluted tubule or PCT,
because the tubule twists. It then straightens and forms the descending limb of the loop of Henle.
Next comes the thinner loop of Henle, followed by the ascending limb of the loop of Henle. The
tubule then twists again and becomes the distal convoluted tubule. This then empties into the
collecting duct which carries the urine to the renal pelvis.
Slide 11: Formation of Urine
Blood from the renal artery through as series of blood vessels within the kidney until it enters the
afferent arterioles which lead to the glomerulus, and then to the efferent arterioles. The efferent
arterioles are smaller than the afferent arterioles in diameter, which causes an average pressure
of approximately 60mmHg in the glomerular capillaries. These capillaries are fenestrated, so that
protein free plasma gets forced out into Bowman’s capsule, along with electrolytes and other
solutes that are small and able to pass through the openings. This process is called filtration.
The fluid that is formed in this way is called filtrate. It will be adjusted as it moves through the
kidney tubules. In some areas, reabsorption will occur, returning the majority of water, glucose,
amino acids, some ions, back to the circulation. In addition, some substances which could not be
filtered out, but need to be eliminated, can also be secreted into the tubules from the peritubular
capillaries. H+, K+, creatinine, and some drugs are eliminated in this way.
Slide 12: Glomerular filtration
The filtrate that is formed as the blood moves through the glomerular capillaries is free of protein
and should not contain any cells. Sometimes, both proteins and cells can be present in the urine
if there is a urinary tract infection or a condition such as glomerulonephritis, in which the glomeruli
are inflamed or destroyed. Under normal circumstances, however, there are restrictions as to
what can pass through the fenestrations based on the size of the molecules and their electrical
charge. Specialized folded extensions of the plasma membrane called podocytes wrap around
the filtration slits in the glomerular capillaries and also play a role in restricting the size of the
filtration pores. In general, those molecules which are smaller than 18 Å in size can move freely
through the pores. If the molecules are between 18 and 36 Å, their electrical charge will
determine if they can pass through. If they are greater than 36 Å, they cannot pass through due
to their size. The negatively charged surface of the basement membrane prevents the movement
of proteins.
Slide 13: Ultrafiltrate
You might wonder why all of the plasma doesn’t leave the capillaries and enter the tubules as the
blood moves through the glomerulus. Well, as the protein free plasma moves into Bowman’s
capsule, the concentration of the remaining blood inside the capillaries goes up. This exerts
colloid osmotic pressure (COP) on the blood, preventing all of the water from leaving. The net
filtration pressure in the kidney is about 10 mm Hg because of this. There is a very large surface
area in the kidney with many thousands of glomeruli. The volume of filtrate that is produced by
both kidneys per minute is called the glomerular filtration rate or GFR. It is approximately equal
to 115ml/min in women, and 125 ml/min in men.
Dr. Carmen E. Rexach
Spring 2008
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Slide 14: Regulation of GFR
The sympathetic nervous system provides an extrinsic method of regulating GFR. In a fight or
flight situation, it is important to maintain the blood pressure, since blood will be diverted to
skeletal muscle and to the heart under these circumstances. This means that urine formation
should be decreased. Therefore, the afferent arterioles vasoconstrict in a sympathetic response.
Slide 15: Regulation of GFR
There are also built in or intrinsic methods of regulating GFR. These include renal autoregulation
and tubuloglomerular feedback. In renal autoregulation, the goal is to maintain a relatively
constant GFR inspite of changes in blood pressure. If the systemic arterial pressure drops below
70 mm Hg, this will cause the afferent arteriole to dilate, causing a decrease in blood pressure in
the glomerulus. If the systemic arterial pressure rises above 70 mm Hg, this will cause the
afferent arteriole to vasoconstrict so that the blood pressure will not increase in the glomerulus
and the GFR will not increase. Specialized cells called the macula densa cells detect filtration
flow. If an increase in filtration flow is detected, the macula densa cells cause the afferent
arterioles to constrict.
Slide 16: Reabsorption of water and salt
The average person produces approximately 180 L of filtrate per day. If we only have 4.5-5.5 L of
blood, this could be a huge problem if most of what is filtered out was not reabsorbed. In fact,
about 99% of the filtrate is reabsorbed. We only need to excrete 0.444L of water per day to get
rid of the metabolic wastes we produce. This is called obligatory water loss.
Slide 17: Reabsorption in the PCT
Initially, when the filtrate comes out of the blood into Bowman’s capsule, the osmolarity is the
same as the osmolarity of the plasma. The epithelial cells in the proximal convoluted tubule have
a lower Na+ concentration than the filtrate. They also contain Na+K+ATPase pumps on the
basolateral membranes. This keeps the Na+ low. The osmotic gradient draws the Na+ into the
cell continuously. Cl- follows, moving down the electrical gradient. This results in an increase in
osmolarity in the extracellular fluid, drawing water out from the filtrate. The actual osmolarity of
the filtrate does not change during this process because NaCl and water are reabsorbed in equal
proportions.
Slide 18: Significance
65% of the water and NaCl in the filtrate is absorbed by the end of the proximal convoluted tubule
without changing the osmolarity of the filtrate.
Slide 19: Countercurrent multiplier system
The countercurrent multiplier system takes place in the loop of Henle. Notice first that fluid flows
in the opposite direction in the ascending and descending limbs simultaneously. As the filtrate
moves through, a positive feedback loop multiplies the effects. We always begin talking about
this by describing what occurs in the ascending limb first. The ascending limb actively transports
NaCl out of the filtrate and into the ECF. However, this part of the loop of Henle is not permeable
to water. The descending limb is permeable to water, but lacks the ability to transport NaCl.
Slide 20: Additional factors
Juxtamedullary nephrons loop around the long loops of Henle that extend far into the medulla.
These are also involved in countercurrent exchange to maintain a high concentration of urea in
the medulla. The high concentration of urea increases the hyperosmolarity of the medulla and
draws out additional water as the filtrate passes through these tubules, hyperconcentrating the
urine.
Slide 21: Changes in filtrate osmolarity
This slide illustrates the changes in osmolarity that occur as the filtrate moves through different
regions of the tubule system. Please note that there is no change in the PCT from the blood
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Spring 2008
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plasma (300 mOsm), then there is a drop up to 1200 mOsm at the base of the loop of Henle. The
osmolarity then decreases again to about 100mOsm in the DCT and the collecting duct.
Slide 22: Collecting Duct and ADH
The collecting duct (CD) is permeable to water, but mostly impermeable to salt. Antidiuretic
hormone (ADH) increases the number of water channels in the CD. Although this may appear to
be a “small” change, it provides a huge increase in the amount of filtrate that is reabsorbed. Even
a small change can dramatically alter the amount of urine produced.
Slide 23: Renal plasma clearance
It is sometimes necessary to measure the glomerular filtration rate or the rate of blood flow
through the kidneys. To do this, certain chemicals are used. GFR is measured by using a
substance called inulin. Inulin is freely filtered by the glomerulus, is not reabsorbed or secreted,
is not metabolized or produced by the kidney, and does not alter GFR. Para-aminohippuric acid
(PAH) is used to measure renal blood flow.
Slide 24: Renal clearance of inulin
Inulin is a polymer of fructose (simple sugar) that is filtered freely in the kidneys without any
reabsorption. Renal plasma clearance refers to the amount of time it takes for the kidneys to
remove a particular substance from the blood. The equation for this is renal plasma clearance
(RPC) = V x U/P, where v = the amount of urine produced per minute by the kidneys, and u = the
concentration of the substance (in this case “inulin”) in the urine, and p = the concentration of the
same substance (inulin) in the plasma. Measuring the renal plasma clearance of inulin will give a
good estimate of the glomerular filtration rate.
Slide 25: Clearance of PAH
Measuring the clearance of PAH from the urine gives a good estimate of the blood flow to the
kidneys. This is because PAH (para-aminohippuric acid) is not produced in the body. It is not
filtered by the glomerulus, but is secreted into the proximal convoluted tubule (PCT). It is also
cleared from the blood the first time the blood passes through the kidney (one pass). The
equation used to determine renal blood flow is clearance of PAH/volume of the plasma. The
average value for this is about 1.1L/min.
Slide 26: Renal plasma threshold for glucose
Diabetes mellitus was first discovered by a physician who was doing research with dogs. He had
these dogs penned up in an outside kennel. He noticed that ants were attracted to the urine of
some of his experimental animals. When he evaluated the urine, he discovered that it contained
high concentrations of sugar. As you know, the body works to maintain blood glucose in the
range of 50mlg/100ml and 170mg/100ml by either encouraging cells to take up glucose from the
blood or by liberating glucose from body reserves. When you eat carbohydrates, they get broken
down into monosaccharides and every bit of these is absorbed in the small intestines and taken
into the body. This is because the surface area of the intestines is huge (microvilli + villi + plicae
circularis) and the transit time is slow (time it takes for the food to move through the digestive
system). Also remember that the stomach releases the chyme in very small amounts into the
intestines, ensuring that what is sent into the intestines is completely absorbed. By comparison,
the surface area of the kidneys is very small, and the blood moves through the kidneys very
quickly. So, there is a limit to the amount of glucose you can have in the blood before you start
seeing glucose in the urine. This is called the renal plasma threshold.
Slide 27:
The formula for determining renal clearance of glucose is (UG x V)/PG, where P is equal to the
amount of glucose in the blood, UG is equal to the concentration of glucose in the urine, and V =
volume of urine produced per minute. The average renal plasma flow is about 700 ml/min, and
the average GFR is about 100 ml/min. Recall that glucose is transported by facilitated diffusion.
This means that it relies on the availability of transporter proteins. When all of the transporter
proteins are occupied (saturation), the rate of transport can’t increase because the glucose has to
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Spring 2008
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wait for a “seat” on an empty transporter protein to get into the cell. The transporter maximum ™
in the kidneys is 375 mg/min.
Slide 28:
This illustration from Berne’s Physiology illustrates the effect of plasma glucose concentration on
the appearance of glucose in the urine by comparing two different scenarios. Patient A has a
plasma glucose concentration of 1 mg/ml (amount of glucose in the blood). If you multiply this
number x the renal plasma flow (700 ml/min), you will see that the kidneys are receiving about
700 mg/min of glucose. The filtered load refers to how much glucose is going to be filtered in the
glomerulus of the kidney in one pass. It is equal to the plasma glucose concentration x the
glomerular filtration rate. In the case of patient A, this is 1 mg/ml x 100 ml/min = 100 mg/min.
Recall that the transporter maximum in the kidneys is 375 mg/min. This is way above the 100
mg/min being filtered in patient A. Therefore, all of the glucose is absorbed and there is no
glucose in the urine (Glucose clearance = 0 mg/min).
Now take a look at patient B. In this patient, the plasma glucose concentration is 5 mg/ml.
Therefore, when you multiply the plasma glucose x the renal plasma flow (5 mg/ml x 700 mg/ml),
you see that 3500 mg/min of glucose is entering the kidneys. The filtered load (plasma glucose
concentration x GFR) is 5 mg/ml x 100 ml/min and is equal to 500 mg/min. However, the
maximum amount of glucose the kidneys can absorb is restricted by the transporter maximum,
which is 375 mg/min. This means there are 125 mg/min in the filtrate that cannot be reabsorbed.
Recall that Glucose Clearance (CG = UG x V/PG ). Therefore, the glucose clearance for this patient
is 25 ml/min. He has exceeded the plasma threshold for glucose and glucose will appear in the
urine.
Slide 29: Renal control of electrolyte and acid-base balance
The kidneys are involved in maintaining homeostasis, as we have already seen. One major role
involves regulating the electrolytes in the blood. This role involves hormones which affect the
rate of reabsorption of certain ions. Aldosterone is a hormone produced by the adrenal cortex. It
regulates the absorption of Na+. If aldosterone is increased, more Na+ are reabsorbed. …and,
as always, water follows salt. This will increase the blood volume and decrease the volume of
urine. However, when Na+ are brought back into the body, they are exchanged for other positive
ions, notably K+. Therefore, an increase in aldosterone will cause Na+ to be reabsorbed in
exchange for K+ ions, which will be excreted into the urine. When aldosterone is low, Na+ will be
excreted, and K+ ions will be reabsorbed.
Slide 30: Na+ reabsorption
Under normal conditions without the influence of hormones, 90% of the sodium is reabsorbed
before the filtrate reaches the distal convoluted tubule (DCT). In the DCT, without aldosterone,
8% of the remaining sodium ions are reabsorbed, and 2 % are filtered out in the urine. With
aldosterone, all of the remaining sodium is reabsorbed.
Slide 31: K+ reabsorption
Under normal conditions, without the influence of hormones, 90% of the filtered K+ is reabsorbed
in the proximal convoluted tubule (PCT). Without aldosterone, all of the K+ is reabsorbed in the
DCT. With aldosterone, K+ is secreted into the filtrate in the distal convoluted tubule and the
collecting duct (CD). Remember, K+ is exchanged for Na+!
Slide 32: Control of aldosterone secretion
There are two ways of stimulating the release of aldosterone from the adrenal cortex. The cortex
is directly stimulated by an increase in blood K+, and indirectly stimulated by a decrease in blood
Na+. Recall when we studied respiration and we determined that the primary stimulus for
breathing was not oxygen, but carbon dioxide. This was because CO2 levels effect blood pH. In
this case, you see that the K+ levels are more “important” than the Na+ levels. This is because
the plasma concentration of K+ has a very profound effect on neuromuscular excitability and
cardiac rhythm. It will affect the ability of neurons to send a message, it will affect the ability of
muscle to contract, and it will affect the ability of the heart to beat appropriately. These conditions
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are life threatening. For example, increased K+ can result in hyperexcitability of cardiac muscle,
causing serious cardiac arrhythmias that can be fatal.
As the blood moves through the kidneys, it passes by the juxtaglomerular apparatus (jga,
described in next slide). The jga contains sensors that monitor blood volume. If the blood
volume is too low, the enzyme rennin is released. Renin is a protease that converts angiotensin
II to angiotensin I. This ultimate triggers an increase in the amount of aldosterone that is secreted
by the adrenal cortex. Renin secretion is also affected by the sympathetic nervous system.
Renin secretion causes an increase in blood volume and a decrease in urine production, which is
important when you are trying to maintain your blood volume and blood pressure while shunting
blood to skeletal muscle and to the heart. Another hormone that affects blood volume is naturetic
hormone, which is produced when blood volume is too high. The cells that produce this hormone
are located in the atrium of the heart. An increase in blood volume causes a stretching of the
atrium. This causes an increase in naturetic hormone release, which causes an increase in the
secretion of sodium ions and water in the kidneys.
Slide 33: Juxtaglomerular apparatus
Note: There are some changes here that contradict what you have on your slide. Please correct
your slides accordingly!
The jga is located where the ascending limb of the loop of Henle (ALLH) comes up between
the afferent and efferent arterioles. It is composed of two cell types: granular cells, found in the
afferent arterioles, and macula densa cells, which are located in the ALLH. The granular cells are
sensitive to the amount of blood entering and leaving the glomerular capillaries. When the blood
volume is too low at this point, they secrete renin. The macula densa cells inhibit the release of
renin.
Slide 34: Relationship between Na+, K+, and H+
When sodium ions are reabsorbed, potassium ions are secreted, largely due to the electrical
gradient. However, other ions can also have similar affects. For example, if there is an increase
in extracellular H+ (decrease in pH), this causes H+ to move into the cells in exchange for K+.
Recall that K+ is higher inside the cell than outside. When the H+ and K+ reach the distal
convoluted tubule and the collecting duct of the kidney, they can also be exchanged for Na+.
Therefore, Na+ will be reabsorbed, as the H+ and K+ are secreted into the filtrate and sent out
with the urine.
Slide 35: Metabolic acidosis
When we learned about the respiratory system, we mentioned that there were two types of
acidosis and alkalosis, respiratory and metabolic. Respiratory acidosis is caused by
hypoventilation, so that CO2 is retained and H+ are generated from the splitting of carbonic acid.
Metabolic acidosis is caused by several things including, an increase in the intake of something
that is acidic, metabolic events that cause an increased production of acid, a decrease in the
elimination of acid by the kidneys, and in increase in the loss of alkaline substances that an buffer
the acids. These events can be the result of several pathological conditions, including diabetic
ketoacidosis (remember that diabetics are unable to uptake glucose appropriately, so they must
produce more ketones to use as an energy source instead of glucose), kidney failure, diarrhea
(causes an excess amount of alkaline substances to be lost), starvation (increases the amount of
ketone bodies produced), and hypoaldosteronism (insufficient production of aldosterone by the
adrenal cortex can result in an increased retention or reabsorption of H+ in the kidneys).
Slide 36: Metabolic alkalosis
Respiratory alkalosis is caused by hyperventilation, in which too much carbon dioxide is exhaled,
driving the blood pH up above 7.45. Metabolic alkalosis results when too many H+ are lost from
the body, or too much bicarbonate is either retained or produced. Common causes of metabolic
alkalosis include vomiting (you are throwing up the acid produced by the stomach, driving the pH
up), loop diuretics or thiazide diuretics (loop diuretics block NaCl reabsorption in the loop of
Henle. When Na+ is retained, secretion of K+ and H+ is encouraged, resulting in hypokalemic
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Spring 2008
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metabolic alkalosis), and adrenal steroids (increased aldosterone will cause an increase in Na+
and a decrease in K+ and H+, which will be excreted in the urine).
Slide 37: Acid-Base Balance
The body works to maintain a relatively constant plasma pH in spite of daily variations in the
production of acids from metabolism and from the intake of food. On average, adults will
produced about 100 mmol/day of H+. The kidney has several ways of mediating acid production.
First of all, the kidney can reabsorb all bicarbonate from the filtrate and return it to the blood, and
excrete H+ into the filtrate, which will be eliminated as urine. 90-95% of the bicarbonate is
reabsorbed in the proximal and distal convoluted tubules. However, this is insufficient to balance
all the acid produced. If 1-2 L of unbuffered urine is eliminated, it will only eliminate 1mmol/day of
the hydrogen ions produced (and remember, we produce about 100mmol/day on average).
There has to be something else!
The kidneys are also able to generate new bicarbonate. This can be done by using filterable
phosphate as a primary buffer anion in the urine, and by excreting nitrogen as ammonium rather
than urea, which spares bicarbonate.
Slide 38: Reabsorption of bicarbonate
When we were studying the respiratory system, we talked about the way in which carbon dioxide
is transported in the blood. We said that carbonic anhydrase, the enzyme that mediates the
conversion of CO2 and water to carbonic acid, was located in red blood cells. In the kidney,
carbonic anhydrase is located on the apical membrane and in the cytoplasm of the cells that line
the kidney tubules, especially in the proximal convoluted tubule. If the filtrate is acidic, CO2 and
water form carbonic acid inside the kidney tubule cells. The carbonic acid splits to form H+ and
bicarbonate. The bicarbonate is sent out to the blood to stabilize the pH, while the H+ is sent out
into the filtrate to be excreted in the urine. In alkalosis, the bicarbonate is excreted into the
filtrate, while the H+ are sent into the blood, to lower the pH and bring it back within the range of
7.35-7.45.
Slide 39: Urinary buffers spare bicarbonate for plasma
Two additional methods are typically used to spare bicarbonate when the pH of the blood is too
low. The first of these involves the amino acid glutamine. Glutamine can be split inside the
tubule cells to generate ammonium, which is sent out into the kidney tubules to be eliminated,
and bicarbonate, which is sent into the blood to drive the acidic pH back up. The second involves
using filterable phosphate as a buffer. This is referred to as titratable acidity because the
phosphate will attract H+ from the kidney tubule cells and send it out with the urine, while the
bicarbonate is sent into the ECF to go back into the blood and buffer the low pH. Although the pH
of blood is a very narrow range of 7.35-7.45, the pH of urine has a much wider range (5-7)
because of the kidney’s buffering activities.
Slide 40: Clinical applications
This slide simply describes how the kidneys are affected by diuretics (which inhibit salt and water
reabsorption, causing an increase in the production of urine), the autoimmune disease
glomerulonephritis (causes an inflammation and destruction of the glomerular capillaries, which
results in a decrease in the blood volume and an increase in edema), renal insufficiency
(involving the destruction, damage, or obstruction of the nephrons resulting in renal hypertension,
urea in the blood, and acidosis), and finally pyelonephritis (inflammation of the renal pelvis due to
bacterial infection).
Slide 41: Glomerulonephritis
Autoimmune disorders often result in the formation of antibody/antigen complexes that are not
attached to anything. These large protein “blobs” get caught in the glomerular capillaries,
triggering a complement cascade. The activated complement proteins attack the glomerular
capillaries, destroying them, and allowing the movement of blood cells, and protein and other
large molecules into the filtrate. This causes an increased loss of water and electrolytes due to
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Spring 2008
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an increase in osmotic pressure inside the kidney tubules, drawing fluid in and reducing the
amount of water and electrolytes that are reabsorbed.
Slide 42- Slide 52: Kidney treatment options
These slides are simply for your edification. They show various options in treatment of individuals
with kidney disease, including hemodialysis, peritoneal dialysis, and kidney transplant.