Renal System and Electrolyte/Fluid Balance Terms Only

renal system includes what

kidneys, ureters, urinary bladder, urethra

functions of the renal system

1. regulates plasma electrolyte balance

2. regulates plasma volume and osmolality

3. regulates plasma pH

4. excretion of metabolic waste products and foreign substances

5. endocrine functions (RAAS, erythropoietin)

3 main regions of the kidney

• renal cortex (outer)

• renal medulla (middle)

• renal pelvis (inner)

__ of total cardiac output is delivered to the kidneys (blood supply)

1/4

renal cortex and medulla _________ urine while the renal pelvis ________ urine

filter and produce; secretes

nephron

functional unit of the kidney made of the glomerulus, PCT, loop of henle DCT, and collecting duct

nephron functions

1. filtering blood

2. reabsorption

3. secretion

4. excretion

where does filtration occur

glomerulus

______ brings blood to glomerular capillaries

afferent arteriole

____________ pushes blood across the capillary wall and glomerular filtration membrane

hydrostatic pressure

after the glomerular capsule where does filtrate go

it enters the bowman’s capsule and tubule system

what 3 layers of the glomerulus do substances have to pass through to be filtered

capillary endothelium, basement membrane, podocytes with the space between each layer getting smaller and smaller

it filters like a brita filter where large molecules cannot pass through

__% of fluid filtered through the bowman’s capsule is reabsorbed

99

reabsorption

substances moving from kidney tubules back into the blood

secretion

substances moving from blood into the kidney tubules

glomerular filtration rate (GFR)

a way to evaluate kidney function through calculating the rate at which plasma is filtered through the glomeruli into the bowman’s capsule

uses net pressure

inulin clearance can help calculate this (inulin clearance is about 125 mL/min

creatinine

natural byproduct of creatine secreted by the kidney that is used as an index for GFR

creatinine and GFR are _________ related

inversely (low blood creatinine means high GFR aka high net pressure meaning the kidneys are cleaning and excreting creatinine)

GFR is driven by what

starling forces

hydrostatic pressure

pushing force exerted by fluid (in blood vessels this would be the pressure of the blood against the vessel wall)

osmotic pressure

pulling force driven by plasma proteins with the movement of fluid through a permeable membrane (in blood vessels this would be like if there is more solute outside the vessel and there is a permeable membrane for the fluid to leave, then there would be osmotic pressure pulling the fluid out towards the solute)

tissue hydrostatic pressure

pushes fluid into the intravascular space

blood hydrostatic pressure

pushes fluid out into the interstitial space

tissue osmotic pressure

pulls fluid out of blood

plasma osmotic pressure

pulls fluid into blood

HPgc

pressure exerted by blood pushing out of glomerular capillaries and into bowman’s capsule

HPbc

pressure exerted by filtrate in bowman’s capsule pushing fluid from bowman’s capsule into blood

OPbc

always 0 because no proteins enter bowman’s capsule meaning there is no pulling pressure towards the bowman’s capsule towards any proteins there

OPgc

pressure pulling fluid into blood because there are more proteins in the blood of the glomerular capillary than the bowman’s capsule so fluid moves towards blood

GFR equation

(HPgc+OPbc) - (HPbc+OPgc)

(pressure towards bowman’s capsule) - (pressure away from bowman’s capsule)

if we have vasoconstriction how are starling forces affected

vasoconstriction is going to decreases HPgc (pressure pushing fluid into the bowman’s capsule) because there is less blood flowing through to push outwardly

HPbc (pressure pushing fluid into the blood) would likely stay the same because the bowman’s capsule is not smaller so there is not any less or more fluid in that space to influence pressure out of that

OPgc (pressure pulling fluid into blood because of proteins in the blood) would likely stay the same cause protein content in the vessel is not changing

OPbc (pressure pulling fluid into bowman’s capsule because of proteins in bowman’s capsule) would still be zero cause there are not any proteins in bowman’s capsule

so GFR = (HPgc decreases + OPbc same) - (HPbc same + OPgc same) = GFR decrease

if we have a kidney stone how are starling forces affected

HPgc (pressure of fluid pushing into bowman’s capsule from blood in glomerular capillaries) is not impacted because fluid amount in blood is not chaning

HPbc (pressure of fluid pushing into blood from bowman’s capsule) should increase because the kidney stone creates less space for fluid in the bowman’s capsule so there is more pressure to get the fluid out

OPgc (pressure pulling fluid to blood) should be unchanged because there is no change in protein concentration

OPbc (pressure pulling fluid to bowman’s capsule: always 0

GFR = (HPgc unchanged+OPbc unchanged) - (HPbc incerased+OPbc unchanged) = GFR decreases

PCT is where we have selective reabsorption and secretion of what

reabsorbed: glucose, amino acids, Na, water

secreted: urea, drugs

by the end of the PCT about ___ of Na, K, and water remain

1/3

loop of henle’s descending loop is only permeable to _____

water

the loop of henle’s ascending loop of only permeable to ______

solutes using Na, K, or 2Cl transporters

loop of henle’s countercurrent mechanism

countercurrent means flow in opposite directions, basically the fluid undergoes a lot of water reabsorption in the descending loop so it’s super concentrated at the bottom and then the ascending loop is where we reabsorb more Na so it becomes less concentrated on the up

vasa recta

this is the countercurrent exchanger at the bottom of the loop of henle wherewater moves into the ascending vasa recta while solutes move out

this is the blood just outside the loop of henle where things are secreted from and reabsorbed into,,, hence countercurrent,,, cause going both ways

basically blood version of loop of henle so opposite directional movement

almost all ___ is secreted in the DCT

K

______ is reabsorbed in the DCT is PTH is present

calcium

aldosterone increases ____ reabsorption, therefore it pulls __ into and K out of blood hence also increasing K secretion

Na; Na

generally the DCT is impermeable to water, but with ___ we will still reabsorb water

ADH

in the collecting duct we reabsorb water through __________ channels

aquaporin

collecting duct secretes what

ammonia, drugs, toxins, H ions

collecting duct maintains what

pH levels

• intercalated A cell secretes H to increase pH in acidic conditions

• intercalated B cell reabsorbs H to decrease pH in alkaline conditions

long looped nephrons are good for what

conserving more water (think camels)

BP regulation happens locally and systemically, list the 2 local regulations and the 1 systemic regulation we discussed

local: myogenic response and tubuloglomerular feedback

systemic: renin aldosterone angiotensin system (RAAS)

myogenic response to high BP

• short term increase in BP increases GFR

• stretch from blood vessels activates Ca channels in smooth muscle

• afferent arteriole vasoconstricts restoring normal GFR and BP

myogenic response to low BP

• short term decrease in BP decreases GFR

• smooth muscle relaxes

• afferent arteriole dilates, increasing blood flow which increases GFR and BP

tubuloglomerular feedback response to high BP

• short term high BP increases GFR

• more solutes filtered = increased Na and Cl ions

• macula dense cells release adenosine or ATP to cause afferent arteriole constriction

• afferent arteriole constriction decreases GFR and BP

tubuloglomerular feedback response to low BP

• short term low BP decreases GFR

• low Na and Cl levels

• macula densa cells release prostaglandins and nictric oxide to cause vasodilation

• vasodilation causes an increased GFR and BP

goal of RAAS

retain water and increase blood pressure

first step of renin aldosterone angiotensin system

juxtaglomerular (JG) cells detect a decrease in BP

what happens in RAAS after JG cells detect a decrease in BP

JG cells release renin

what happens after renin is released in RAAS

renin converts angiotensin to angiotensin I

what happens in angiotensin converts to angiotensin I in RAAS

ACE converts angiotensin I to angiotensin II

what happens once we have angiotensin II in RAAS

angiotensin II is the main player for restoring BP levels and starts 4 pathways

1. posterior pituitary pathway

2. adrenal cortex pathway

3. PCT pathway

4. arteriole pathway

what does angiotensin II cause in the posterior pituitary

the production of ADH which increases water reabsorption which increased blood volume which increases BP

what does angiotensin II cause in the adrenal cortex

the production of aldosterone which increases sodium and water reabsorption in the DCT which increases blood volume which increases BP

what does angiotensin II cause in the PCT

increased sodium and water reabsorption which increases blood volume and therefore BP

what does angiotensin II cause in the arterioles

vasoconstriction which increases BP

micturition

process of emptying urine from the urinary bladder

step 1 of micturition

stretch receptors detect filled bladder

what happens after stretch receptors detect filled bladder in micturition

the pelvic nerve contracts the detrusor muscle

what happens after the pelvic nerve contracts the detrusor muscle in micturition

the pudental nerve relaxes the external urethral sphincter

what happens after the pudental nerve relaxes the external urethral sphincter in micturition

the hypogastric nerve further contracts the detrusor muscle and also relaxes the internal urethral sphincter

what happens after the hypogastric nerve contracts detrusor and relaxes internal sphincter

the pontine micturition center in the pons is stimulated which tells the 3 nerves to keep going (also the pontine storage center is inhibited)

sacral spinal tract pathway

sacral spinal cord → pelvic nerve → detrusor muscle

sacral spinal cord → pudental nerve → external urethral sphincter

thoracolumbar spinal tract pathway

thoracolumbar spinal cord → hypogastric nerve → detrusor muscle and internal urethral sphincter

incontinence (what are the 3 types)

stress, urge, overflow

stress incontinence

increased intraabdominal pressure (from coughing, sneezing, etc, or even from pregnancy or obesity)

this increases bladder pressure and causes urine to leak out

urge incontinence

detrusor hyperactivity due to neurological activity or UTI

causes us to to lose inhibition of pontine micturition center

overflow incontinence

decreased detrusor muscle activity: basically we are compressing sphincter muscles which doesn’t allow for complete emptying so we have urine “leftover” that sort of leaks out later

usually due to neurological disorder like MS

this increases bladder filling and distention

nephritic diseases

inflammation of the glomerulus or inflammatory rupture of glomerular capillaries

urine ends up containing some RBCs and some protein, decreased GFR, increase in urea and creatinine in urine, low urine output

nephrotic diseases

damage to the glomerulus resulting in urinary loss of plasma proteins (primarily albumin)

caused by infectious disease, DM, drugs, autoimmune disorders, metabolic disorders

causes increased basement membrane permeability and increased permeability of proteins

chronic glomerulonephritis

inflammation and scarring to the glomerulus characterized by proteinuria (protein in urine), hematuria, and hypertension

causes progressive loss of functioning nephrons leading to kidney failure and dialysis

renal calculi

kidney stones

4 types of renal calculi

calcium, struvite, uric acid, cystine

formation of kidney stone

1. supersaturation: presence of salt in a higher concentration than the volume able to dissolve the salt (low fluid intake or excessive fluid loss)

2. precipitation: salt moving from liquid to solid state; low pH (acidity) helps form solid crystals

3. growth via crystallization or aggregation: small particle or bacteria in urine acts as nucleus for crystals to grow around (nucleation)

kidney stone treatment based on size of stone

less then 5mm: pass on own within 4 weeks

less than 1 cm: receive shockwave treatment to break up stone

over 1 cm: ureteroscopy with laser

chronic kidney disease

decreased kidney function determined through GFR

damages glomerulus, reducing surface area and GFR

kidneys unable to regulate fluid, move wastes, balance pH

risk factors for chronic kidney disease

DM, hypertension, prolonged NSAID use, glomerulonephritis

stage 1 of chronic kidney disease

no overt symptoms, gradual kidney damage, reversible

stages 2 and 3 of chronic kidney disease

capillaries damaged, albumin in urine, creatinine may increase in stage 3

stages 4 and 5 of chronic kidney disease

kidneys can’t excrete toxins, hypertension, proteinuria, uremia (waste products build up in blood), anemia

chronic kidney disease treatment

treat underlying disease, prevent further loss of kidney function, dialysis (artificial filtering of blood), kidney transplant

UTI

inflammation of the urinary epithelium following invasion and colonization by a pathogen

lower UTI

cystitis (bladder infection), urethritis

upper UTI

pyelonephritis (kidney infection, primarily affects the interstitial area and the renal pelvis (less common but still occurs: renal tubules)

UTI pathogenesis

usually ascending: from urethra to bladder

UTI defense mechanisms

normal voiding eliminates some organisms because certain chemical properties of the urine are antibacterial

lower UTI symptoms

urinate frequently and urgently, painful urination (dysuria), subpubic or flank pain, hematuria

upper UTI symptoms

rapid onset of high fever, chills, and flank pain, also back pain, cloudy urine, and nausea/vomiting