Renal Physiology Flashcards
What are the main functions of the kidneys
Regulate body fluid composition, volume, osmolarity,and pH
Excrete water,electrolytes and waste products
What is glomerular filtration
The process of filtering blood in the glomerulus to form urine, driven by starling forces
What is glomerular filtration rate (GFR)
Measure of how quickly urine is formed by filtration, typically +125 ml/min
What forces drive glomerular filtration
Hydrostatic and osmotic pressure differences between blood and bowman’s space
What forces affect GFR
resistance in afferent and efferent arterioles, autoregulation mechanisms, and renal clearance
what is renal clearance
measure of how effectively a substance is removed from the blood by the kidneys
what is used to measure GFR
inulin clearance and creatinine clearance
what does low creatinine clearance indicate
possible kidney disease or failure
Why doesn’t GFR increase significantly with high blood pressure
due to autoregulation mechanisms: myogenic and tubulogenic feedback
what is the myogenic mechanism
reflex where smooth muscle cells in the afferent arteriole constrict in response to increased pressure, stabilizing GFR
what is the tubulogenic feedback mechanism
the macula densa senses increased NaCl levels and signals the juxtaglomerular apparatus to constrict the afferent arteriole, reducing GFR
what are the four renal transport processed
filtration, reabsorption, secretion, excretion
what is the nephron
the functional unit of the kidney where urine is formed
what happens in the proximal tubule
major reabsorption of water, ions, and nutrients
what is the function of the loop of henle
creates an osmotic gradient to concentrate urine
what happens in the distal tubule and collecting duct
fine tuning of water and electrolyte balance through hormonal regulation
what happens when the afferent arteriole constricts
decreased GFR and RBF
what happens when the efferent arteriole constricts
increased GFR but decreased RBF
what substances influence vasoconstriction and vasodilation in the kidneys
Vasoconstrictors: norepinephrine, epinephrine, angiotensin II
vasodilators: nitric oxide, bradykinin, prostaglandins
what is the formula for excretion in the kidneys
excreted=filtered - reabsorbed + secreted
where does the most sodium reabsorption occur
proximal tubule (67%), ascending limb of loop of henle (25%), early distal tubule (5%), late distal tubule & collecting duct (3%)
how is Na+ transported across renal epithelial cells
transcellular(active through cells) and paracellular( passive between cells)
how is sodium absorbed in the proximal tubule
active Na+ transport (Na+/K+ ATPase) and passive movement coupled to glucose, Cl- and other solutes
what transporter is responsible for Na+ reabsorption in the ascending loop of henle
NKCC (Na+, K+, 2 Cl- co transporter), inhibited by loop diuretics
what transporter is responsible for Na+ reabsorption in the early distal tubule
NCC (Na+, Cl- co transporter), inhibited by thiazide diuretics
what transporter is responsible for Na+ resorption in the late dista; tubule and collecting duct
ENaC, targeted by K+ sparing diuretics
how does sodium balance affect blood pressure
increased sodium retention=increased ECF volume=increased blood pressure
decreased sodium retention=decreased ECF volume=decreased blood pressure
what factors regulate Na+ balance and ECF volume
sympathetic nervous system, oncotic pressure, renin-angiotensin-aldosterone system (RAAS) , and atrial natriuretic peptide (ANP)
what stimulates renin release
low blood pressure, low sodium levels, and sympathetic nervous activity
what are the effects of angiotensin II
stimulates Na+ reabsorption
increases Na+/H+ exchanger activity
stimulates aldosterone release
how does aldosterone regulate sodium
increases ENaC Na+ channels in the collecting duct
increases Na+/K+ ATPase expression
promotes Na+ reabsorption and K+ excretion
how does ANP affect sodium excretion
increase GFR
decrease renin, angiotensin II, aldosterone, and ADH secretion
inhibits Na+resorption, increasing Na+ excretion
what are the three major classes of diuretics
loop diuretics- inhibit NKCC in loop of henle
thiazide diuretics-inhibit NCC in distal tubule
K+ sparing diuretics-inhibit ENaC in collecting duct
how do diuretics lower blood pressure
by reducing Na+ reabsorption, leading to natriuresis(sodium loss), diuresis(water loss), and decreased ECF volume
what is pseudohypoaldosteronism
loss of function mutation in ENaC, leading to increased Na+ excretion, low ECF volume and hypotension
what is liddles syndrome
gain of function mutation in ENaC, leading to decreased Na+ excretion, increased ECF volume and hypertension
where is most of the water filtered by the kidneys reabsorbed
in the proximal tubule
how is water reabsorbed in the nephron
passively, following osmotic gradients created by Na+ transport
how does water move between body fluid compartments
from areas of lower osmotic pressure to areas of higher osmotic pressure
which part of the nephron is impermeable to water
the ascending limb of loop of henle
what regulates water permeability in the distal tubule and collecting duct
anti-diuretic hormone (ADH)
what is the role of the descending limb of the loop of henle in water reabsorption
water is passively reabsorbed to match the osmolarity of the surrounding interstitial fluid
where is ADH secreted from
the posterior pituitary gland
what stimulates ADH secretion
increased plasma osmolarity and decreased blood volume/pressure
what does ADH do to the distal tubule and collecting duct
increases water permeability by inserting aquaporin-2 channels into the apical membrane
what happens in the absence of ADH
water is retained in the tubule, resulting in water diuresis (high volume,dilute urine)
what happens in the presence of high ADH
water is reabsorbed resulting in antidiuresis(low volume, concentrated urine)
what is the corticopapillary osmotic gradient
gradient of increasing osmolarity from the renal cortex to the renal medulla, created by countercurrent multiplication
how does countercurrent multiplication work
NaCl is reabsorbed in the ascending limb (without water)
water is passively reabsorbed in the descending limb
this creates an osmotic gradient that helps concentrate urine
what is the role of the vasa recta in maintaining osmotic gradients
countercurrent exchange in the vasa recta helps preserve the corticopapillary osmotic gradient by preventing washout of solutes
what happens to urine osmolarity as it travels through the nephron
proximal tubule: isosmotic with plasma
loop of henle: becomes hyperosmotic at the tip
distal tubule: becomes hypoosmotic
Collecting duct: final osmolarity depends on ADH levels
how does urea contribute to urine concentration
under high ADH conditions, urea is reabsorbed from the collecting duct, increasing interstitial osmolarity and enhancing water reabsorption
what is the effect of low ADH
low water permeability in the collecting duct
high urine volume, low osmolarity (dilute urine)
what is the effect of high ADH
high water permeability in the collecting duct
low urine volume, high osmolarity
what are symptoms of diabetes insipidus
excessive urination (polyuria), dehydration and extreme thirst
what is central diabetes insipidus
Failure to secrete ADH from the pituitary
what is nephrogenic diabetes insipidus
Failure of the kidneys to respond to ADH
why is potassium homeostasis important
small changes in extracellular K+ can be fatal
affects nerve and muscle function
what are normal and abnormal plasma K+ levels
normal: 4mM
hypokalemia: <3.5mM
hyperkalemia: >5mM
how is K+ excretion regulated
by plasma K+ levels and aldosterone
where does most K+ reabsorption and secretion occur
in the distal tubule and collecting duct
which cells are involved in K+ regulation
principal cells: secret K+ via apical K+ channels
alpha intercalated cells: reabsorb K+ via H+/K+ ATPase
how does aldosterone regulate K+ secretion
increase Na+/K+ ATPase activity
increase apical K+ permeability
enhances Na+ reabsorption via ENaC, creating a driving force for K+ secretion
what is the normal plasma pH
7.35-7.45
how is extracellular fluid pH maintained
by the bicarbonate/CO2 buffer system
what is the henderson hasselbalch equation for pH
pH=pK + log ([HCO3-]/[CO2])
how do the lungs and kidneys regulate pH
lungs regulate CO2 via ventilation
kidneys regulate HCO3- and H+ excretion
where is most HCO3- reabsorbed
in the proximal tubule (80%)
how is HCO3- reabsorbed in the proximal tubule
HCO3- is converted to CO2 and H2O by carbonic anhydrase
CO2 diffuse into cells and reforms HCO3- which is transported into the blood
how does HCO3- secretion occur in alkalosis
by beta intercalated cells in the distal tubule using Cl-/HCO3- exchangers
how do the kidneys excrete H+
as a titrate acid
as ammonium generated from glutamine metabolism
what happens in acidosis
more H+ is excreted as NH4+and titratable acid generating new HCO3-
what are the four main acid base disorders
metabolic acidosis (low HCO3-)
metabolic alkalosis (high HCO3-)
respiratory acidosis (high CO2)
respiratory alkalosis (low CO2)
how do the lungs compensate for metabolic acidosis
hyperventilation to reduce CO2 and raise pH
how do the kidneys compensate for respiratory acidosis
increased H+ excretion and HCO3- reabsorption
what happens in renal compensation for alkalosis
the kidneys reduce H+ secretion and increase HCO3- excretion
