Renal Flashcards
What are the functions of the kidney?
HOMEOSTASIS
Electrolyte homeostasis
Fluid balance
acid base homeostasis
regulation of arterial blood pressure
EXCRETION
excretion of waste - urea, drugs
ENDOCRINE
secretion and metabolism of hormones - Renin, EPO, vitamin D active form
METABOLISM
gluconeogenesis
describe the anatomy of the renal vasculature..
aorta - left and right renal arteries enter at hilum
divide into segmental and then interlobular arteries
eventually afferent arteriole –> glomerulus –> efferent arteriole
efferent arterioles give rise to vasa recta or peritubular capillaries.
the glomerulus is a high pressure capillary network
whereas the vasa recta/ peritubular capillaries are low pressure.
how much blood flows to kidneys?
20-25% of CO
1L/min
90% cortical, 10% medulla
what is the role of the vasa recta?
hairpin capillary system closely related to loop of henle
hairpin arrangment helps maintain ionic concentrations of medulla whilst still delivering O2 to collecting tubules and loop of henle.
what are the peritubular capilaries ?
supply O2 and reabsorb nutrients from PCT, DCT, parts of collecting ducts.
what is meant by autoregulation of renal blood flow?
many organs have an intrinsic mechanism to regulate flow to maintain a constant perfusion pressure to ensure O2 is being delivered and CO2 removed.
In the kidneys autoregulation has the additional role of maintaining GFR.
the main mechanism for this is known as the myogenic response
when MAP increases, causes muscle contaction - to maintain constant flow.
this autoregulation can function between 90-200mmHg
other mechanisms contributing to autoregulation include tubuloglomerular feedback
what factors affect renal blood flow and GFR?
autoregulation/ myogenic response
tubuloglomerular feedback
sympathetic NS
hormonal factors - ATII, catecholamines,
what is tubuloglomerular feedback?
this helps maintain a constant filtrate rate. relies on juxtaglomerular apparatus. the macula densa at DCT senses Na delivery. if this is increased due to high GFR, local metabolites are released which cause afferent arteriole vasoconstriction to reduce GFR.
metabolites invovled depending on if high or low include NO, enodthelin, prostaglandins
how does the sympathetic NS influence renal blood flow and GFR?
activation of sympathetic NS
causes vasoconstriction via a1
reduces blood flow and GFR
water retention
sympathetic NS also causes renin release via B1 receptors. this results in ATII which causes further vasoconstriction.
how does ATII affect renal blood flow and GFR
vasoconstiction of efferent more than afferent
maintains GFR
however also causes contraciton of mesangial cells to reduced filtration
reduces renal blood flow.
(whereas sympathetic afferent more than efferent so both reduced)
describe the strucutre of glomerulus and bowmans capsule?
glomerulus = capillary network of fenestrated capillaries
in close contact with bowmans capsule
so as high pressure blood is filtered, the filtrate enters bowmans capsule.
the barrier between the 2 makes up the filtration barrier and consists of fenetrasted endothelium of capillaries , BM, podocyte foot processes of bowmans
what molecules are filtered at the glomerulus?
depends on size and charge
under 7KDa = freely filtered
then the rate of filtration is proportional to size
above 70kDA = none filtered
slight negative charge of filtration barrier means positive are favoured over negative
give example e.g. small ions, glucose - freely filtered
large proteins - albumin - not filtered
what is meant by glomerular filtration rate?
the rate at which fluid enters the bowmans capsule from the glomerulus. (volume of plasma per min)
normally 125ml/min (180l/day)
what factors determine GFR?
starlings forces of filtration
pressure
* high pressure system within glomerulus, the pressure in both afferent and efferent are high so hydrostatic pressure is maintained across the length, helping to produce filtrate
oncotic pressure
* oncotic pressure of plasma has an opposing force drawing fluid back in, this is higher than in bowmans capsule (near 0)
reflection coefficient / permeability
* this is how leaky the capillaries are. there is high permeability due to fenestrations. however limited to >70Kda
S.A:
contaction of mesangial cells, reduces S.A to regulate fitlration. many humeral factors affect this e.g. ATII constricts them
how does starlings filtration forces differ in kidneys to other tissues?
in normal tissues the arterial end has a high pressure and then there is a big drop at venule end which draws fluid back in
in glomerulus, it is a high pressure system which is maintained across - hence net filtration out of capilaries, not reabsorbed at that point.
in normal tissue = 35mmHg to 10mmHg
in renals = remains at 45mmHg
oncotic pressure in both 25mmHg (slight rise by effrent end as fluid has left)
in bowman oncotic = 0mmHg
bowman pressure is 10mmHg
what is the equation for starlings filtration in kidneys
Kf = filtration coefficient = permeability x S.A
describe the different methods of tubular transport?
simple diffusion - O2, CO2, lipid soluble drugs
fasciliated diffusion - glucose, aa , ions in ion channels e.g. Na
active transport - Na/K ATPase, H+ secretion and H/K ATPase - often sets up gradients for 2nd AT
secondary AT - glucose and aa later in tubules against conc gradient using Na/glucose symporters
osmosis - water follows paracellular or AQUAporins
paracellular movemnet - between cells dragged with water
why is urine a different composition to filtrate?
reabsorption
secretion
what happens in PCT?
majority of substances are reabsorbed
in healthy kidneys, non pregnant
all of glucose
all of aa
60% of sodium , K , Cl
85% HCO3
60% water
occurs via a number of transport mechanisms.
also some secretion - e.g. penicillin, aspirin, histamine, catecholamines, morphine etc
draw a graph to show the filtrate:plasma conc as fluid moves down PCT
initially all equal as equilbrium reached with plasma so ratio is 1
as it moves down, glucose, amino acids and HCO3 are reabsorbed so ratio drops as plasma conc increases and filtrate conc drops.
although Na is reabsorbed, the concentration is unchanged with distance as water is also reabsorbed
inulin is secreted into the tubules so its ratio increases.
urea and creatinine would also increase as these are not reabsorbed but water is so their conc increases
describe how the structure of PCT relates to its function?
brush border - high S.A
many transport proteins
mitochondria - AT
describe the mechanism of glucose reabsorption at PCT…
basolateral membrane Na/K ATPase
luminal - SGLT - sodium glucose symporter
basolateral = glut 2
what is meant by T max?
the PCT has a max rate of reabsorption of molecules. beyond this point, the substance will appear in urine
e.g. for glucose this is 10mM
below this, as glucose conc increases, rate of reabsorption increases up to a max
if glucose conc exceeeds 10mM , the reabsorption pathways are saturated and the remaining glucose is excreted.
therefore Tmax = the max rate of reabsorption of a substance. for glucose this is 300mg/min (which equates to the rate at 10mM)
not all nephrons have the same Tmax value
how is sodium handled by PCT?
Na/K ATPase
Na/Glucose symptor
Na/aa symptors
Na/H antiporter - luminal membrane
how is chloride reabsored
as Na and HCO3 are reabsorbed and water follows, Cl conc increases
passively diffuses down conc gradient
also co-transporter
how is bicarb reabsorbed by the kidneys
carbonic anhydrase, combines H+ and bicarbonate to H2CO3 to make H20 and CO
these can diffuse across back into plasma
how is urea handled by the PCT?
50% is reabsorbed by passive diffusion due to other things being reabsorbed and conc rising
where is water reabsorbed by kidneys?
70% PCT
15% LoH
variable = collecting ducts
describe the structure of the LoH?
hair pin like structure with countercurrent mechanism
fluid flows down descending and up ascending
2 types of nephrons = juxtamedullary (15% to deep medulla) and cortical (85% - only junction of cortex and medulla)
descending = impermeable to solute, permeable to water.
thin ascending limb = impermeable to water, permeable to solule
TAL = permeable to ions and impermeable to water
this aids its mechanism in creating high osmoltic pressure in depths of medulla and hence water conservation.
describe the countercurrent mechanism in LoH…
active transport of solutes out of TAL - Na/K basolateral, Na/2Cl/K luminal, K+ channels basolateral etc
creates high osmotic pressure in interstium
water leaves the DL
as descending travels further down, less water to dilute and thus interstitial fluid increases in osmotic pressure
increases conc of solute within DL
this is fed back round to TAL which is impermeable to water and now has high conc solutes delivered for further AT
the hairpin arrangement creates a countercurrent mechanism which creates very high concs in depths of medulla. 1400mOSm /L at deepest point.
this allows for efficient water reabsorption by collecting duct in times of dehydration.
what is the fluid leaving LoH like?
TAL has pumped out fluid so dilute
100mOSmol/l enters DCT
what is the role of the vasa recta?
capillaries emerging from efferent arterioles
hairpin structure following LoH
this hairpin arrangement and low flow means solutes are not washed away as equilibrium is reached.
however O2 is still supplied
how does ATII affect vasarecta , what about other drugs
vasoconstriction of vasa recta, slows down flow
allowing time to equilbrate and hence maintaining medullary concentrations
hence aids fluid absorption
some drugs will oppose this e.g. ARBs, ACEi
what is the role of DCT?
further reabsorption of solute - Na/ HCO3, K
impermeable to water so delivers hypotonic solution to collection duct for control of water regulation
also contains macula densa - part of juxtamedullary apparatus and communicates with afferent arterioles.
what is the function of the collecting duct?
role in water reabsorption and homeostasis of osmotic pressure
And also in Na reabsorption
OSMOTIC HOMEOSTASIS:
Dilute fluid enters collecting duct
collecting duct passes through medulla
if aquaporins are present, reabsorption of water is allowed by the high osmotic gradient created by LoH
if aquaporins are not present, dilute urine is excreted
this is regulated by ADH
urea recycling also plays a role here.
NA REABSORPTION
collecting duct also plays a role in sodium homeostasis under influence of aldosterone.
how does the body achieve homeostasis of plasma osmolality?
sensors - control centre - effectors
with the hypothalamus and collecting ducts of the kidneys playing a central role in this
Sensors
* paraventricular and supraoptic nucleus of anterior hypothalamus
* detect changes to osmotic pressure
Control centre
* hypothalamus sends impulses to posterior pituitary and ADH is secreted, also sends impulses to initiate thirst
Effector
* ADH travels in blood
* receptors V2 on collecting ducts
* GPCR - Gs - cause vesicles containing aquaporin to fuse with luminal membrane
* (Aquporin channels already on BL membrane)
* now water can flow down osmotic gradient into the renal interstitium and absorbed by capillaries
what is the normal osmotic pressure of the blood?
280-290mOsm/Kg H20
where is ADH produced and stored
produced in hypothalamus (supraoptic)
travels down by axonic transport
stored in vesicles of posterior pituitary
what stimuli can cause ADH release and inhibit it?
stimulus = high osmolarity , ATII (volume depletion), sympathetic NS, opioid receptors, emotions (pain, stress), other drugs nicotine
which drug inhibits ADH
alcohol
what are the roles of ADH?
osmolarity homeostasis - collecting duct
vasoconstriction - helps with volume depletion
role in clotting (desmopressin releases vWF), platelet aggregation
neurotransmitter - release of ACTH
why is homeostasis of osmolarity important?
human cells are subject to osmotic pressure. in hypotonic solutions, water will enter cells and they can burst and in hypertonic they can shrink/ dehydrate
in the brain oedema in a constricted space can result in increase ICP and reduced perfusion and ischeamia
what is the role of urea in osmoregulation
urea is an active osmole
ADH causes urea channels on collecting duct
urea leaves collecting ducts, increases osmolarity of interstitium further, aiding further water reabsorption in times of dehydration
it is recycled by descending limb
what disorders of osmolarity do you know
excess ADH
* SiADH - lung tumours, traumatic brain injury
* low plasma osmolarity, concentrated urine. hyponatraemia
no ADH
* neurogenic diabetes insipidus
* dilute urine 23L/day
* high osmolarity, high sodium plasma conc
* caused by traumatic brain injury, SAH, brain tumour
insensitivity to ADH
* nephrogenic diabetes insipidus e.g. lithium, congential , CKD
* dilute urine 23L/day
* high osmolarity, high sodium plasma conc
how is SiADH diagnosed and treated?
diagnosis = low osmolarity (less than 280) , low sodium ( less than 135), euvolaemic
treatment - lithium, demeclocycline , fluid restriction
how is diabetes inspidus diagnosed and treated
urine production > 3L/day (usually much more)
sodium >145
osmolarity >305
desmopressin and fluids
how is extracellular fluid volume regulated?
since sodium is the main osmotically active solute, mostly via chnages to Na conc
Neuronal
sympathetic NS / baroreceptors
Hormonal:
RAAS
ANP/ BNP
osmolarity and ADH
other:
direct passive influence - more ECF, more GFR, higher excretion rate. more ECF, less reabsorption via peritubular capillaries
psychological and social factors -e.g. diet, fluid intake
how is GFR measured?
tindirect
* clearance of inulin - inulin is a polysaccharide that is freely filtered and not bound by plasma proteins, not reabsorbed or secreted or metabolised
* it is infused into a patient and clearance of it is measured
* this is accurate however time consuming and impractical
indirect / estimation
* using creatinine and cockcroft and gault equation which takes into account age, weight and gender to estimate GFR
* there is also the modification of diet in renal disease (MDRD) equation and the CKD EPI equation
* this is easier as creatinine is a natural byproduct of muscles so no need for an infusion however creatinine is secreted so not completely accurate and will over estimate GFR.
what properties of a substance make it ideal in measuring GFR?
freely filtered
not metabolised
not reabsorbed
not secreted
inert
doesnt influence GFR itself
what are the problems of using creatinine to estimate GFR?
some is secreted so overestimation of GFR
amount produced depends on body muscle amount - so can vary from gender to race to individual.
how can renal blood flow be measured?
plasma clearance of PAH (para-amino-hippuric acid)
as a modification of FICKs principle i.e. flow to an organ is equal to uptake or excretion of a substance divided by the A-V conc difference
PAH is used because it is almost completely removed by kidneys by filtration and secretion and not used by any other organ
When PAH is infused into the bloodstream, nearly all of it is removed from the plasma by the kidneys during a single pass through the renal circulation under normal physiological conditions. Thus, the clearance of PAH is nearly equal to renal plasma flow (RPF), which can be further converted to RBF.
clearance of PAH = estimation of Renal PLASMA flow
can work out the renal blood flow from this by knowing the haematocrit value..
RBF = RPF / 1-Hct
what is meant by clearance?
volume of plasma cleared of a drug / substance per unit time
calculated by
= (urine conc x urine flow) / plasma conc
it combines all methods of clearance by kidneys e.g. filtrations/ secretion.
define osmolarity and osmolality
osmolarity = the number of osmoles per kg of solvent
osmolarity = the number of osmoles per L of solvent - temp dependant as volume changes with temp so less accurate.
define an osmole
1 mole of osmotically active particles
where 1 mole is the same number of particles as there are atoms in 12g of C12 = 6.022x10.23
OR
1 osmole = amount of solute that exerts osmotic pressure of 1atm when placed in 22.4L of solution at 0 degrees.
define osmotic pressure
the pressure required to prevent water travelling via osmosis from area of low to high concentration.
define solvent and solute
solvent = a substance capable of dissolving another solute e.g. water
solute = a substance that dissolves into a solvent e.g. NaCl
what is meant by tonicity?
tonicity is the osmotic pressure of one substance compared to another reference point e.g. hypotonic means it has less osmotic pressure compared to the other solution.
how is osmolarity calculated?
2x (NA + K )+ glucose + urea
(osmolality may be different ie. osmolar gap)
also via vant hoff equation - number of osmoles
PV = nRT. rearrange for P to be pressure
what is meant by the osmolar gap?
osmolality - osmolarity
usually less than 10
increases with increased levels of other osmotically active particles e.g. mannitol, alcohol, methanol (other than glucose, urea, sodium etc)
what is oncotic pressure?
a form of osmotic pressure exerted by presence of proteins
what is the role of renal prostaglandins?
vasodilation of afferent arteriole to maintain GFR
involved in signalling from macula densa when GFR is low to maintain it.
what is the filtration fraction?
proportion of plasma being filtered by glomerulus
GFR / Plasma flow rate
x 100
i.e a %
usually around 20%
what factors can effect GFR
Blood pressure - hypovolvaemia, sepsis
local vasoconstriciton / dilation of afferent/ efferent - hence local mediators (prostaglandins) but also hormones and sympathetic NS
changes to oncotic pressure - hypoalbuminaemia
what device can measure osmotic pressure?
osmometer
uses collagative properties
usually freezing point
sample is supercooled to -7 degrees (using peltier effect - absorption of heat at 2 dissimilar metals), then stired to trigger freezing, freezing point recorded.
the more osmoles, the lower the freezing point
THis will measure OSMOLALITY (rather than osmolarity)
how is body water distributed amoungst compartments?
Extracellular and intracellular
Intracellular = 2/3
extracellular =1/3
extracellular further divided into interstitial (3/4) and plasma (1/4)
in total 42L
ICF = 28L
ECF =14L
what does total body water depend on?
age (higher in neonates, less in elderly)
gender, ethnicity
muscle mass vs fat - fat constains less
pregnancy
compare TBW and fat in neonates and adults
in neonates TBW = 80%
adults TBW =60% of weight
fat is higher in adults
how are different body compartments measured?
ECF = Inulin - crosses endothelium but doesnt go intracellularly.
plasma = radioactive albumin
red cell mass = radioactive Hb
TBW = dueterium oxide - crosses all compartments
worked out via concentration and dose given to work out volume.
how can intracellular compartment be calculated?
no direct measurement
take away others
e.g. Total water - ECF
therfore using dueterium oxide and inulin
how is interstitial fluid compartment measured?
no direct way
ECF - Plasma
what are the roles of sodium in the body?
determines ECF volume as most dominant extracellular cation
determines osmolarity
important for membrane potentials and generation of AP.
normal sodium plasma level
135-145mM
daily sodium requirement
1-2mM /kg /day
how is sodium lost from the body
sweat
faeces
urine
draw a graph to show how the conc of sodium changes throughout the tubules
bowmans capsule - same as plasma = 135 -145
in descending limb water leaves = increase in conc
by end of asending limb = active transport, low sodium entering collecting ducts
depends on ADH
what are the clinical features of hyper and hyponatraemia?
hypo Na
- headache, N&V
- confusion, seizures,
hyper
- thirst
- weakness
- dry mucus membranes
- seizures etc
how is hyponatraemia corrected?
slowly
risk of central potine myelinosis
roles of pottasium
major intracellular cation
determines resting membrane potentials
important in action potentials - repolarisation
important in regulation of cellular processes
normal potasium levels?
3.5 to 5mM
causes of hypokalaemia?
reduced intake - diet, laxatives and poor absorption
increased losses - renal tubular disease, diuretics , cushings, increased aldosterone
intracellular shifts - insulin, salbutamol, adrenaline
what defines severe hypokalaemia?
less than 2.5
less than 3.5 = mild
less than 3 = moderate
clinical signs of hypokalaemia?
CVS - arrythmia (flat T, long PR, Long QT, torsades)
muscle - weakness, ventilatory failure
GI - ileus
what are the causes of hyperkalaemia?
excess intake - bananas, IV potassium
reduced output - K+ sparing diuretics, addisons, CKD
intracellular…
haemolysis / rhabdomyolysis / burns
MH
sux after denervation
what defines severe hyperkalaemia?
above 6.5mM
mild 5.5 to 6
moderate 6 to 6.5
how does DCT handle K+
secreted into tubules
filtrate flow dependant
clinical effects of hyperkalaemia ..
CVS - arrhythmias - tall T , flat P , prolonged PR, sine wave, VF
muscle weakness
malaise
why does VF occur in hyperkalaemia?
high K+ outside
depolarises membrane, less negative resting potential, more excitable cell
as per nernst equation
management of hyperkalaemia?
A B C
calcium gluconate 10% - protect the heart (or CaCl2)
salbutamol nebs
Insulin 10 units actrapid+ dextrose 50ml 50%
sodium bicarb if metabolic acidosis
RRT
other
- calcium resonium - bind and prevent absorption
normal level of Mg?
0.7 to 1mM
causes of hypomagnesium?
loss - diarrhoea, diuretic
reduced intake - diet
features of hypomagnesium?
nausea, anorexia
muscle cramps, lethargy
later - tetany, muscle spasms, seizures , ECG changes (QT prolongation)
anatogonises Ca - hypocalcaemia - hyperexcitable e..g trousseaus sign and chvostek sign
where is Mg found ?
mostly intracellular
2nd most abundant intracellular after potassium
soft tissues, muscle and bone
tell me about the relationship between K+ and Mg?
often low K and low Mg are seen together due renal losses
low K can rarely be corrected with low mg
correct Mg first
Mg promotes K loss by kidneys
and Mg blocks Na/K ATPase - hence poor uptake of K into cells
why is hypokalaemia common in stress and surgery?
cortisol release
causes Na reabsorption, K loss via kidneys
how does macula densa signal renin release?
high Na delivery to macula densa - ATP and adenosine release - inhibits renin
low Na - prostaglandins released - vasodilation of afferent and renin release.
what is the steward theory for acid and base ?
different perspective of how acids and bases are regulated in the body compared to the henderson hasselbach model.
it uses relationship between ions, water dissociation, and the principles of electroneutrality.
3 components
* Strong ion difference - difference of strong cations and anions e..g Na + , Cl-
* weak acids and bases levels
* pCO2
if there are more cations (Na) compared to Anions (Cl) i.e. a large strong ion difference –> promotes acidity as it promotes the dissociation of H20
e.g. after vomitting , loss of Cl, increases the SID. promotes dissociation of H20. to balance loss of Cl, H+ must be lost. hence alkalosis.
normal fluid requirements?
20-30ml/kg
1-2mM/kg Na
1mM / Kg K
50g-100g glucose
risks of IV fluid…
overload
electrolyte disturbance / acidosis
what different fluids do you know?
crystalloid - sollution containing inorganic ions dissolved in water - hartmans, 0.9% saline , dex saline
may be isotonic, hypotonic, hypertonic
colloid - suspension of particles unable to pass through semipermeable membrane and hence remain intravascular. can also be defined as a mixture in 2 phases dispersed amongst one another. can be naturally occuring (albumin) or synthetic (gelatin).
compare pros and cons of colloids and crystalloids..
cystalloids - cheap, long shelf life, low ADR profile. many uses in resusitation, maintainance etc and correction of electolytes. However risk of electrolyte abnormalities, overload and acidosis.
colloids - better at increasing intravascular volume and therefore less risk of peripheral oedema and small amount required to have same effect. however expensive, more ADRs (anaphylaxis)
state the contents of 0.9% saline, hartmans
0.9% saline = 154mM Na and 154mM Cl, pH 5, osmolarity 300
hartmans = 131 Na, 111 Cl, 5K, 2 Ca, pH 6.5, lactate buffer, osmolarity 280
what does plasma lyte contain..
similar to hartmans, however ph 7.4. no lactate instead acetate and glucaonate
what is the risk of normal saline?
hyperchloraemic acidosis
what was the problem with Ringer solution, how was this improved?
similar to hartmans but no lactate
caused metabolic acidosis
lactate added to solution to buffer this = ringers lactate/ hartmans
when and why should hartmans be used cautiously?
liver disease
lactate not metabolised and cause cause acidosis
what colloids do you know?
HAS = human albumin solution 4% or 20%
Starches - no longer used due to safety concerns
Dextrans 40 or 70
Gelatins (type of collagen) e.g. gelofusine - suspended in crysatalooid solution excreted unchanged in kidney
blood products are also classed as colloids - Cyroprecipitate, packed red cells, FFP
tell me about HAS
naturally occuring protein molecule normally synthesised by liver.
HAS is a solution of albumin from donor blood. available in 4.5% and 20% solutions
large protein with 69KDa MW and negatively charged and thus exerts oncotic pressure.
often given in those with ascites, severe sepsis.
it is costly, associated with coagulopathies and can cause allergy
what are the risks of colloids
all anaphylaxis risk especially with gelatins
coagulopathies, itching, flushing , renal dysfunction
what crystalloids do you know?
0.9% saline
hartmans
0.18% saline + 4% dextrose
5% dextrose
how does Hb value change in haemorrhage?
initially doesnt change until fluid moves from interstitium to plasma or fluids are given IV
then will fall.
what are the different types of fluid loss?
haemorrhage
burns
vomitting/ diarrhoea
diuretics
insensible - fever
how is fluid responsiveness assessed?
level of dehydration / fluid loss - clinically via lactate, urine output, mucus membranes, HR/tachy, fluid balance chart
then responsivness by..
1. leg raising - tilt bed by 45 degrees, if haemodynamic improvement e.g. BP, HR, swing on art line reduced then likely fluid deplete. if condition deteriorates potentially overloaded
2. fluid challenge - bolus and look for improvements
3. respiratory swing - i.e. on arterial line, PPV can be analysed. only reliable in ventilated
compare the difference between giving 1L or saline to 1L of dextrose
1L of saline = isotonic solution. Na cannot cross plasma membranes, so stays mostly extracellular. 1/4 plasma 3/4 interstitium
1L dextrose = glucose metabolised = hypotonic, enters cells. less than 10% stays in plasma
what is AKI? including stages
a rapid decline in kidney function
over hours to days
resulting in increase in creatinine and urea
reduction in GFR
defined by serum creatinine >26.5mM in 48hrs
or >1.5x baseline
OR urine output less than 0.5ml/kg/hr for 6 hrs
is classified into 3 stages KDIGO
1. serum creatinine 1.5 to 1.9 x baseline
2. serum creatinine 2 to 2.9 x baseline (or UO less than 0.5 for more than 12 hr)
3. serum creat more than 3 x (or UO less than 0.3 for 24 hrs or anuria for 12 hours
what are the causes of AKI?
pre renal
* sepsis, haemorrhage, renal artery stenosis, NSAIDs or ACEi
* poor CO - HF
renal
* glomerular - nephritic and nephrotic syndromes
* acute tubular necrosis, drug toxicity (gold, penicillamine, gentamicin)
* vasculitis
post renal
* stone, tumour, prostate BPH
what are the complications of AKI?
increase waste - urea , drug half lives
electrolyte disturbances - hyperkalaemia, hyponatraemia
acidosis
hypertension + overload - RAAS activated as kidneys are being underperfused, so think BP is low.
how is AKI avoided?
identify risk - stop nephrotoxic e.g. metformin stopped when in hospital and ACEi and NSAIDs
fluids / avoid dehydration
monitor UEs
maintain good BP intra op
how is AKI managed?
fluids
manage cause - pre, renal, post e.g. may need to relieve obstruction
treat complications - acidosis, hyperkalaemia, overload
may require dialysis
adjust drug doses / stop nephrotoxins
what are the indications for renal replacement therapy?
AEIOU
Acidosis - severe metabolic acidosis
electrolytes - refractory hyperkalaemia
Intoxication - salicylates
Overload - refractory pulmonary oedema
uraemia - with complications such as pericarditis/ encephalopathy
what are the types of RRT?
transplant
peritoneal dialysis
haemodialysis - arteriovenous or venovnous
may be continous or intermittent
- intermittent less haemodynamic stability as achieving larger fluid shifts in shorter space of time.
continous therapies could be
haemodialysis or ultrafiltration or haemodilation
5 types
CAVHD = cont arteriovenous haemodialysis
CVVHD = cont venovenous haemodialysis
CAVH = cont AV haemfiltration
CVVHDF = cont venovenous haemofiltration
SCUF = slow continuous ultrafiltration
what is the difference between ultrafiltration and haemodialysis
ultrafiltration - uses hydrostatic pressure across a filter to push solvent across this filter. good for treating fluid overload.
dialysis - blood and dialysate pass eachother separated by a semipermeable membrane. diffusion occurs across this. the composition of dialysate is chosen depending on need.
what are the indications for continous RRT over intermittent?
haemodynamic instability - wouldnt tolerate intermitted i.e. critically ill
raised ICP
high volume required to be removed
risk of disequilibrium syndrome
disadvantages of continous RRT vs intermittent?
longer time for immbility
more labour intensive and expensive
needs continous anti-coag
how would you prescribe dialysis?
set filtration fracture, clearance rate and blood flow
prescribe the citrate or heparin
pros and cons of citrate vs heparin for anti-coag for dialysis
citrate - limited to machine, not patient, need to monitor Ca levels
heparin - will anticoag patient too (may or may not be useful)
complications of RRT?
access related - infection, thrombosis, bleeding
circuit related = clotting
anticoag related = HIT, bleeding, hypocalcaemia
diaysis related = fluid shifts (hypotension, electrolytes)
