The kidney as a producer, regulator and excoriator Flashcards
what cells in the kidney secrete EPO
peritubular cells
Vitamin D is made in the kidney too and this raises serum calcium by promoting GI absorption and decreasing renal excretion ( increased tubular reabsorption) and stimulating bone reabsorption what form of Vitamin D is made here
1,25 dihydroxycholecalciferol- calcitriol
what is interstitial fluid
found in spaces around cells
aquaporins found each side of tubular cell
role of golmerulus
filter plasma to produce glomerular filtrate - normal is about 120ml/min/hour
- primary maker of renal function
CKD stages with GFR above 90 then each stage reduce by 30 then last to 15
what are podocytes
epithelial cells with extensive branching cytoplasmic processes ( pedicles and foot processes) prevent proteins in
cut off around 55,000-60,000
what is net filtration pressure - 14mmHg
total pressure that promotes filtration - hydrostatic pressure gradient moves out and then oncotic gradient moves it back in
creatinine is a product of muscle metabolism and maker of renal function
what other protein can be used as a marker of renal function that is produced by most cells that contain a nucleus and there is no tubular secretion
Cystatin C
what two autoregualtion physiological changes occur when a drop is arterial pressure leads to fall in both RBF and GFR
afferent arteriole can dilate improving RBF at a lower arterial pressure or efferent arteriole constructs improving the GFR at a lower RBF therefore increasing the filtration fraction ( proprotion of fluid reaching the kidneys that passes into the renal tubules ( GFR/plasma flow))
autoregulation of the arterioles can be controlled by myogenic mechanisms or bu tubulo-golmerular feedback what are they
Adenosine - produced in hydrated states constricted afferent arteriole reducing GFR and then is switched off with decreased filtrate flow
angiotensin II - constrict the efferent arteries to maintain pressure and therefore GFR - beware of ATII inhibition in hypovolaemia
PGE2 - produced in DCT in response to reduced filtrate flow. Dilates afferent arteriole to maintain RBF - antagonises vasopressin - NSAIDS in hypovolaemia
( also inhibits platelet aggregation and increase uterine stimulation)
In the PCT reabsorption of sodium occurs by 2 main methods what are they
Sodium hydrogen antiporter ( sodium into tubular cell and hydrogen out into tubule lumen) - this has come from dissociation of carbonic acid - the sodium is then cotransported out into blood with the bicarbonate
sodium glucose symporter
( ATPASE pump moving more sodium into the blood)
transport maximum - divide by 1000
in the PCT sodium leaves and water flows to save energy - how does water leave
through leaky junctions allowing easy passage between the tubular cells
in diabetic situations in the pct like ketoacidosis - glycourias reusults leading to osmotic diuresis if the transport maximum is exceeded which is the GFR multiplied by the 4.5mmol of glucose divided by 1000 - this pull on the glucose and on sodium leads to what
dehydration of patients
main role of loop on henle
hypotonic fluid is descending tubule
as ions are lost and water retained tubular fluid becomes progressively more dilute whilst the interstitial fluid becomes more concentrated as ascending limb is impermeable to water is this due to the very tight junctions
yes
Loop diuretics block the NKCC2 cotransporter what is an example of one
furosemide
in the descending limb water is lost via aquaporins by osmosis and sodium retained tubular fluid becomes progressively more concentrated. The osmolarity ( conc of solution based on particles present) changes from 300-1200. Interstitial fluid in medulla is strongly….
hypertonic
on DLOH what venue system takes away electrolytes in the blood
vasa recta - countercurrent system runs other way to nephron
finish the sentence water pass from the descending LoH to ascending limb of what
vasa recta
opposite for ions - ascending LoH to descending vasa recta
what cells in the DCT and CD reabsorb sodium and secret potassium controlled by aldosterone?
principal cells
what cells reabsorb potassium and secrete hydrogen driven by ATPase
intercalated cells
what channel is only found in the principal cells of the DCT
ENaC coupled channel - sodium and potassium contrnsporter - stimulated by aldosterone which also acs on the ATPase pump on the blood side
also a ROMK
what channel are only found in the intercalated cells of the DCT
active proton potassium ATPase transport which acts to secrete hydrogen and reabsorb potassium stimulated by acidosis and hypokalaemia
what is the main role of the medullary collecting duct
Main role in final regulation of water excretion and thereby urine conc
insertion of aquaporins into luminal membrane
what are aquaporins
Transmembrane with narrow shaped and charged walls allowing only water to pass
Without them water moves slowly by osmosis
what is the only aquaporin found in collecting duct on the luminal membrane( tubular cell and lumen) and inserted in response to ADH with variable water reabsorption
Aqu-2
1 - PCT and DLoH basal membrane ( closer to blood) and has constant presence with continuous rebasoptin
3,4 - collecting duct basal membrane side - constant presence and continuous water reabsorption
Aquaporin 4 - miller fisher syndrome
ADH bind to what receptor causing inserting of Aqu-2 into luminal surface
V2 receptor
hypertonic interstitum - near complete water reabsorption when needed - ultra tight junctions imperabele to all
morphine and hypoxia and nausea can stimulate increase ADH - what are the effects of this
increased plasma osmolarity( dehydration)
decreased blood volume and decreased blood pressure
resulting in increased water reabsorption, more concentrated urine and less concentrated blood plasma
decrease ADH - opposite caused by Alcohol and antihypertensives
what are the 3 types of receptors( where are they found and their roles) for ADH that all G protein coupled receptors
V1a - peripheral circulation - vasoconstriction
V2- renal collecting duct and endothelium and Aqu-2 insertion and clotting factor release
V3(V1b) - CNS - ACTH release
final urine acidity is determined in the DCT by what cells
intercalated cells - protons
acidosis increase proton excretion at the expense of potassium retention
normal urine ph is 4.5-8 , where is the bulk of proton secretion and bicarbonate reabsorption taking place
PCT
Acid constantly being produced - impaired renal elimination leads to acidosis
what are the 3 cellular components of the juxtaglomerular apparatus
macula densa ( part of DCT) cells extraglomerular mesangial cells and juxtaglomerular cells( granular cells- secrete renin)
macula densa senses decreased pressure so granular cells then secrete renin to increase pressure
Triggering of the JGA leads to
Dilations of the afferent arteriole - local action ( decrease adenosine and PGE2 )
Release renin ( granular cells)
Note rennin action and release also triggered by sympathetic beta 1 stimulation
Hypovolaemia - renin released, AG AG2 in lungs via ACE and then AG2 affects vasoconstriction on efferent arteriole ( maintain filtration rate as glomerular cap pressure maintained)
aldosterone
increases sodium reabsorption ( variable) determines final urine sodium content
LoH - creates are of interstitial hyperosmolarity
