Kidney Function III Flashcards
How is plasma osmolarity kept constant
Urine- dilute/ concentrated
thirst
Concentrated urine
greater than 300 mosmol/l
1) Have to remove 600 mosmol/day of waste products
2) Max urinary concentration = 1400 mOsmol/l
3) 600/1400= 0.428 L/day
This is the obligatory water loss- anything below this value is called oliguria
Dilute urine
Less than 300 mosmol/l
Min urinary concentration= 50 mOsmol/l
Urine output = 1-2 /day
Anything beyond this is called polyuria
Osmular Clearance
Cosm -ml/min
The volume of plasma cleared of osmotically active particles per unit time that could have resulted in urine isomolar to plasma
The calculation of all osmotically active particles
Cosm= Uosm x V / Posm
Free Water Clearance
(C h20) used to assess renal function
Ch20 = V - (Uosm x V)/Posm
Ch20 > 0 indicates hypo-osmotic urine- dilute urine
Ch20 = 0 indicates isometric urine wrt plasma
ch20 < 0 indicates hyper osmotic urine- concentrated urine
Possible range= -1.3 —> 14.5 ml/min
LOW WATER INTAKE
Plasma osmalality decreases
Osmoreceptors by hypothalamus detects this change
Posterior Pituatory
Increase in ADH
Kidneys
Increase in water reabsorption
Less water excreted in urine
HIGH WATER INTAKE
Plasma osmalality increases
Osmoreceptors by hypothalamus detects this change
Posterior Pituatory
Decrease in ADH
Kidneys
decrease in water reabsorption
More water excreted in urine
Where are osmoreceptors located in the hypothalamus
Organum vasculosum Lamina terminals
Median Preoptic nucleus
Subfomical organ
What do the osmoreceptors do?
Signal to the magnocellular neurosecratory cells in the paraventricular region and supraoptic nuclei in hypothalamus.
These cells contain the precursor for ADH which is released into the blood to the posterior pituitary via the axons. These are changed to ADH which is then released into blood
Why is ADH useful in the short term
Plasma half life is short
ADH release is rapid from the posterior pituatory
What else can osmoreceptors indicate-
Thirst- locates in the lateral preoptic, osmoreceptors aren’t activated until the plasma osmolality has reached 295mosm/kg
What else can affect ADH secretion
BP and BV
As the release is dictated by stretch mediated receptors found in the arteriole which sends neurally mediates signals to ADH containing neurons
1% change in plasma osmalility - plasma vasopressin change
5% change in volume results in plasma vasopresisin change
10% change in pressure results in plasma vasopressin change
Alcohol- decrease in ADH Nicotine- increase in ADH Nausea- increased in ADH Pain- increase ADH Stress- increase in ADH
ADH action in collecting duct
1) ADH binds to the V2 receptor on the basolateral membrane- 2nd messenger cAMP
2) This causes the fusion of AQP2 with the luminal membrane to allow movement of H20 to move by osmosis
3) water molecules then move through AQP3 and AQP4
Diabetes Insipidus
Effects the water reabsorption only
Characteristics- polyuria, thirst, nocturia
Type 1 Diabetes
Neurogenic- congenital
Head Injury
NO ADH
Type 2 Diabetes
Nephrogenic- inherited (mutated v2 receptor)
- acquired (infection/side effect of drug)
Osmotic Diuresis
Characteristic- polyuria and polydipsia
Caused due to the fact that there are small molecules in the renal tube lumen. This means that there’s an increase in [glucose] blood which meant that there’s an increase in glomerular filtration of glucose. This increases the osmolarity in filtrate.
Ultimately this decreases water reabsorption from PT- past saturation
Bad because this will affect osmotic gradient- meaning that less water is being reabsorbed.
Potassium
Major intracellular cation in the body
Renal excretion of Potassium
Filtered, absorbed and secreted
Filtration of K+
Small ion doesn’t bind to proteins so said to be freely filtered in the renal corpuscle
therefore filtration rate = 1.0
Filters 800 m moles/day
Proximal Tubule- K+
65% is reabsorbed passively
due to K+ leak and K+/Cl- cotransporter
Thick ascending limb- K+
30% is reabsorbed passively
Na+/K+/2Cl- con transporter using gradient of Na
Distal Tubule-K+
5% si reabsorbed
K+/H+ exchanger
Collecting Duct- K+
Intercalated cells
Principal cells
Intercalated cells
K+ is being reabsorbed -
exchanged with H+
[K+] increases inside the cells
K+ diffuses out of the cell into the IF
Principal cells-
secretes K+
K+ channels- ROMK and BK depending on the electrochemical gradients
K+/Cl- co transporter
ROMK-renal outer medullary K+ channel
BK- Ca2+ activated by conductance K+ channel
What factors affect the K+ secretion by Principal cells
Acid Base Balance - acidosis inhibits and alkalosis enhances. High H+ in filtrate–> more positive charge —> inhibits movement
Tubular flow rate- high flow rate favours secretion- negative charges are washed away therefore K+ more likely to pass through down the electrochemical gradient
Aldosterone- stimulates the K+ channels
increasing the activity of Na+
