Random Kidney Review Flashcards
blood flow through kidney?
renal aa -> arcuate artery - affarent arteriole - glomerular capillaries - efferent arterioles - peritubular capillaries - vasa recta - arcuate v –> renal v.
kidney autoregulation of blood flow?
- myogenic response: when smooth mm. is stretched it contracts
- tubuloglomerular feedback (TGF): increased MAP leads to increase in RBF and GFR. high delivery of sodium ions to macula densa (TAL/DT) –> results in adenosinie and ATP secretion –> vasoconstriction of afferent arteriole –> decreased RBF and GFR
essential HTN? how does that affect the GFR? renal artery stenosis?
increased renal artery pressure –> vasoconstriction of affarent arterioles and vasodilation of efferent aa.
—-> high pressure in the JG apparatus –> decreased renin secretion –> low AngII –> vasodilation of efferent arterioles
patient w/ renal artery stenosis has low renal artery pressures –> low pressure at affarent arterioles: vasodilation of affarent arterioles vosconstriction of efferent arterioles (leads to increased renin secretion and increased ANGII)
nephrogenic DI?
ADH receptors are functioning and it not possible to increase reabsorption at CD
patient loses free water and develops hypernatremia
tx is reduction of EC volume w/ thiazide diuretic = increases peritubular oncotic pressure, increases water reabosprtion in PT
effects of symp. NS on the kidney?
causes vasoconstriction of arterioles, has greater effect on affarent arteriole
thus RPF PGC, PPC and GFR decrease, FF increases
the oncotic pressure of the PC increases
greater forces promote reabsorption in the peritubular capillaries b/c of low peritubular capillary hydrostatic pressure and increase in plasma oncotic pressure (FF increases)
effects of ANG II?
ANG II is vasoconstrictor, constricts both affarenent and efferent arterioles, but has bigger effect on efferent arteriole
RPF decreases PGC increases GFR increases FF increases PPC decreases oncotic pressure in PC increases
thus increased forces promototing reabsorption in the peritubular capillaries b/c of lower peritubular capillary hydrostatic pressure and increase in plasma oncotic pressure (FF increases)
kidneys rxn to stress?
symp input and ANGII secretion increased –> vasoconstriction of affarent and efferent arterioles –> drop in RPF and only small drop in GFR
results in net increase in FF –> increase in oncotic pressure –> increase in reabsorption in PTs
overall less fluid is filtered and greater percentagle of fluid is reabsorbed in the PT, leading to preservation of volume in volume depleted state
increase in ADH due to low volume state, and increased renin release
net effect of ANGII is to preserve GFR in volume-depleted state (and for it to not be too large of decrease in GFR)
what causes an increase in FF?
decrease in glomerular capillary flow –> results in increased oncotic Peritubular capillary pressure and also decreased PPC - resulting in net increase in reabsorption in the peritubular capillaries of fluid
transport mechanisms?
simple diffusion = ions movming down EC gradient, no energy reqd
facilitated diffusion = molecule or ion moving across membrane down its concentration attached to specific membrane bound protein - doesn’t req energy
active transport: protein mediated transport using ATP
Uniport: transporter moves molecule down gradient = facilitated diffusion
symport: coupled transport of solutes in same direction
antiport = mvmt of two solutes in opp. dxn
secondary active transport
Na/K ATPase establishes low intracelluar sodium concentration, creating large gradient across cell membrane for sodium on the luminal side to transport glucose via secondary active transport
inulin
amount filtered = amout excreted
clearance of inulin is independent of plasma concentration - lies on the X axis (rise in plasma concentration results in rise in plasma filtered load)
creatine
freely filtered and very small amount is secreted
- thus creatine clearance always parallels inulin and is slightly higher
calculate reabsorption rate
= filtered load - excretion rate
= (GFRxPx) - (Ux x V)
= (GFR x Plasma glucose) - (Urine glucose x urine flow)
clearance
= theoretical volume of plasma from which a substance is removed over a period of time
= if substance has concentration of 4 molecules/L and excretion is 4 molecules/min = then the volume of plasma cleared of x is IL/min
Clearance = Excretion rate of x / plasma concentration of X Clearance = (Ux * V) / Px Clearance = (urine concentration of X * Urine flow rate) / plasma concentratino of X
measures of GFR
would use inulin as gold standard b/c it is freely filtered and not reabsorbed or secreted
clinically use Creatinine b/c its released from skeletal mm. at constant rate protpprtional to mm. mass
creating production = creatine excretion = filtered load of creatinine = Plasm Creatinine x GFR
glucose
at low plasma levels, clearance is zero
at high plasma levels glucose appears in urine
PAH
at low plasma concentrations the clearance equals renal plasma flow
as plasma concentration rises the carriers hit TM and results in some PAH appearing in renal venous plasma
Plasma concentrations above TM reduce the clearance of PAH
as plasma levels rise further the clearance approaches but never equals GFR b/c some PAH is always secreted
highest to lowest clearance?
PAH > creatinine> inulin > urea > sodium > glucose = albumin
urea
freely filtered but partially reabsorbed
ADH increases reabsorption of urea in medullary CD –> increasing BUN –> decreasing clearance
proximal tubule:
Na+: 2/3 reabsorbed here: sympathetic and Ang II stimulate basolateral ATPase and enhance fraction of Na+ absorbed here
Water reabsorbed here, glucose reabsorbed, 80% bicarbonate reabosrbed here
potassium and AAs also absorbed ehre
bicarb reabsorption?
bicarb combines w/ luminal H+ and is converted to water and CO2 by luminal carbonic anhydrase
H+ is pumped into the lumen via sodium antiporter along with an H+ ATPase on the luminal membrane
CO2 is very soluble and crosses the luminal membrane where it combines with water to reform H+ and bicarb due to the CA in the cell
H+ is pumped back into the lumen while bicarbonate exits the basolateral membrane
Ang II stimulates the Na+/H+ antiporter, thus in volume depleted states, the amount of bicar reabsorbed in PT increases –> contraction alkalosis
contraction alkalosis?
thiazides, sweating in desert, vomiting…
low volume state –> increase in renin/AngII –> activation of sodium/hydrogen exhcnager via AngII –> increased reabsorption of bicarb and metabolic alkalosis ensues f
loop of Henle?
descending loop = water reabsorption
Thick ascending limb: sodium reabsorption via Na+/K+/2Cl- cotransporter
Increase in K+ concentration in the cells causes back diffusion of K+ into the tubular lumen, allowing a lumen-positive electrical potential to drive reabsorption of cations (Mg2+, Ca2+) via the paracellular pathway
Calcium sensing receptor
basolateral membrane of cells in ATL contain CaSR, which is influenced by plasma concentration of calcium
when there is high level of blood calcium it inhibits Na/K/Cl- transporter = results in reduction of K+ back diffusion and no positive luminal potential
thus Ca2 not reabsorbed as much in TAL
Distal convoluted tubule
NaCl crosses membrane due to cotransporter
Principal cells in CD
This is where aldosterone acts
- have Epithelial sodium channel (ENaC) thus sodium flow in following its gradient: creates a negative luminal potential
- K+ has high level in cell and thus moves through a channel into the lumen
- ALDOSTERONE results in net influx of Na+ and excretion of K+
THUS hypokalemia is seen with metabolic alkalosis due to increased ALDO secretion
Principal cells also express aquaporins which are regulated by ADH and result in water and urea reapsorption
Intercalated cells in CD
- involved in acid base regulation
- luminal membrane has H+ ATPase which pumps H+ into the lumen, combines with ammonia and is excreted as urea
- for every H+ excreted, bicarb is adde to the body
ALDO stimulates the H+/ATPase of intercalated cells restulting in metabolic alkalosis
Proximal Renal tubular acidosis?
due to diminished capacity of proximal tubule to rebsorb bicarb
- see low plasma bicarb and acid urine
- serum potassium is low, when bicarb is lost in urine, it is lost as sodium bicarb and that pulls water with it creating osmotic diuresis
- diuresis leads to loss of potassium in urine
Distal renal tubular acidosis
due to inability of distal nephron to excrete fixed acid
results in metabolic acidosis w/ high urine pH
and hypokalemia
what changes rate of potassium excretion?
increased flow (diuresis) or ALDO = increased potassium secretion
decreased flow (antidiuresis) or low ALDO = decreased potassium secretion
what promotes hyperkalemia?
metabolic acidosis
CKD
hypoaldosteronism
consequences: mm. weakness, general fatigue, ventricular fibrillation, metabolic acidosis
promoters of hypokalemia?
metabolic alkalosis
increase in insulin or sympathetic stimulation
diarrhea, vomiting, low potassium diet
diuretics, hyperaldosteronism (adrenal adenoma or renal arterial stenosis)
consequences:
mm. weakness and fatigue, metabolic alkalosis
acute renal failure
loss of renal function , results in accumulation of waste products (BUN and CR)
pre renal
decreased renal perfusion due to decreased renal perfusion pressure (hypovolumia, hemorrhage, diarrhea, vomiting, CHF)
see reduced GFR
Na+ reabsorption is increased due to Ang II and catecholamines elevated
elevated BUN:Cr ; both are elevated, the high reabsorption of urea (water reabsorption is elevated and urea through aquaporin channels) - causes BUN elevation more the Cr
intrarenal
tubular damage occurs resulting in tubular dysfunction
ex: toxins, interstitial nephritis, ischemia, rhabdomyolysis, sepsis
See decreased reabsorption of Na+
See casts/cells in urine
Low plasma BUN:Cr - tubular damage prevents reabsorption of urea
Postrenal
caused by obstruction of fluid outflow from kidneys
ex: renal calculi, enlarged prostate
Early: characteristics are similar to prerenal - elevated BUN:Cr
Late: build up of pressure results in tubular damage and causes intrarenal failure, so see low plasma BUN:Cr
Chronic renal failure
see inability to excrete waste products: rise in plasma BUN and Cr
Inability to regulate water and sodium = hyponatermia, volume overload and edema
hyperkalemia and metabolic acidosis
hyperphosphatemia , reduces plasma calcium, cause ing rise in PTH and bone resoprtion (renal osteodystrophy)
inability to excrete EPO –> anemia
normal values
pH = 7.4 PCO2 = 40 mm Hg HCO3- = 24 mEq/L
4 primary disturbances?
resp acidosis = too much CO2
Met acidosis = addition of H+ or loss of bicarb
resp alkalosis = not enough CO2
met alkalosis = loss of H+ or addition of base
if CO2 and HCO3- go in opposite directions it is probably a mixed disorder
measuring anion gap
Na+ - (Cl + HCO3-)
normal PAG = 12 +/- 2
Isosmotic volume contraction
Osmolarity remains the same in ECF & ICF
Only changes ECF volume (ICF remains unchanged)
Examples: vomiting& diarrhea, hemorrhage/
Isosmotic volume expansion
Osmolarity remains the same in ECF & ICF
Only changes ECF volume (ICF remains unchanged)
ex: infusion of 0.9% NaCl
Hyperosmotic volume contraction
loss of water
Osmolarity of ECF increases as ECF volume decreases
ICF volume decreases as water shifts from ICF to equilibrate osmolarity
Examples: dehydration; diabetes insipidus
Hyperosmotic volume expansion
(gain of NaCl):
Osmolarity of ECF increases as ECF volume increases
ICF volume decreases as as water shifts from ICF to equilibrate osmolarity
Examples: excess NaCl intake; mannitol infusion
Hyposmotic volume contraction
(loss of NaCl):
Osmolarity of ECF decreases as ECF volume decreases
ICF volume increases
Examples: hypoaldosteronism; adrenal insufficiency
Hyposmotic volume expansion
(gain of water):
Addition of pure water decreases ECF osmolarity
Water proportionately increases ECF and ICF volumes
Examples: SIADH; psychogenic polydipsia
body fluid compartments
total = 42 L ECF = 14 L Plasma = 4 L
contraction of mesangial cells
shortens capillary loops and thus lowers GFR
symp stimulation
Constriction of afferent and, to a lesser extent, efferent arterioles: ↓RBF, ↓GFR
Diverts the renal fraction to vital organs
Increased renin secretion by granular cells
Angiotensin II thus produced restores blood pressure (systemic vasoconstriction)
Angiotensin II promotes arteriolar constriction (efferent > afferent): raises blood pressure, may stabilize GFR (moderate ang II)
Stimulates Na+ reabsorption in proximal tubule, thick ascending limb of Henle’s loop, distal convoluted tubule, collecting duct
clearance
creatinine clearance ~ GFR
CL = Ux * V / Px
ALDO, ANP, ADH
Aldosterone stimulates Na+ reabsorption, K+ secretion, H+ secretion in this segment
Atrial natriuretic peptide inhibits Na+ reabsorption (medullary collecting duct)
Antidiuretic hormone [aka arginine vasopressin (AVP)] stimulates water reabsorption
what does ANP do?
ANP increases GFR: Afferent arteriolar dilation, efferent arteriolar constriction
ANP inhibits Na+ reabsorption in medullary collecting duct
ANP suppresses renin secretion
ANP suppresses aldosterone secretion
ANP is a systemic vasodilator
ANP suppresses AVP secretion, actions
osmolar gap
Plasma solute concentration, mOsm/kg H2O =
(2 · Na+, mEq/l) + (glucose, mg/dl / 18) + (BUN, mg/dl / 2.8)
Osmolar gap: Difference between plasma osmolality estimated as above and true plasma osmolality measured with an osmometer. Normally < 10 mOsm/kg H2O
