Why Kidneys Fail Flashcards
KEY FUNCTIONS OF THE KIDNEY
for each aspect explain what happens to each in disease and what the outcome is
i) electrolyte balance
ii) fluid balance
iii) acid base balance
iv) normal BP
v) maint of Hb
vi) maint of vit D
vii) toxin clearance
i) electrolytes > hyper/hypo K+/Na > tented T waves, wide QRS, asystole, confusion, coma, death
ii) oedema, ascites, pulm oedema > breathless, HF, mitral regurg
iii) acid base > acidaemia < reduced CO, bone destruction
iv) normal BP > HTN > IHD, stroke, HF, AAA
v) Hb main (via EPO prod) > renal anaemia > fatigue, HF
vi) maint vit D > hyperparathyroidism (second or tertiary) > BV wall calcification
vii) toxin clear > uraemia > weight loss, subfert, anorexia, bleeding, pericarditis
WHAT IS KIDNEY FAILURE?
i) when are irreversible, slow, progressive loss of nephrons seen? is urine output preserved?
ii) when are potentially reversible rapid onset loss of nephrons seen? what will urine output likely be?
iii) which type of kidney failure has 5 stages? which type has 3?
iv) which type of kidney failure uses albumin to creat ratio? which one uses serum creat and urine output in staging?
i) loss of func nephrons
- slow/irreversible > CKD
- urine output is preserved til late stages (CKD5)
ii) rapid onset nephron loss > AKI
- usually oliguria (low urine output) or anuria (no urine output)
iii) 5 stages in CKD
3 stages in AKI
iv) CKD - alb:cr
AKI - serum creat and urine output
WHAT GOES WRONG
i) what are the three main things that go wrong in the tubules? explain each
ii) name three things that can go wrong in the glomeruli?
iii) name three things that can go wrong with the blood vessels?
iv) what is the interstitium aka? what is the main problem here? what can cause it?
i) tubule - acute tubular injury (mostly AKI from sepsis or hypovol which cause decreased perfusion pressure and ischaemic enviro)
myeloma - abnormal clone of IgA light chains > block the tubule
rhabdomyolysis - muscle breakdown causes bup of myosin deposits that clog the tubules
ii) glomeruli > any blood in urine is always a glomerular problem
- diabetes, vasculitis, SLE, glomnephritis
iii) blood vessels > diabetes
- renal vasc disease (prob w blood supp to kidney / high BP for long time causes damage to BV, lumen gets smaller > ischaemia)
- HTN
iv) intersititium = final common pathway (all kidney issues lead to scaring/fibrosis in the interstitium)
- tubulo-interstitial nephritis > inflam drugs can cause it eg abx, furosemide, PPIs > treat with steroids and removing offending agent
GLOMERULI - DIABETIC KIDNEY DISEASE
i) what happens to the podocytes? what does this lead to?
ii) what are mesangial cells? what happens to them in diabetes?
iii) what happens to the glom BM and the capiliary loops?
iv) what does a high glucose environment lead to an increase in? what is the consequence of this?
v) what ultimately happens
vi) is there a strong relationship between glucose control and kidney disease development in T1DM/T2DM? which ethnicity is diabetic kidney disease most common in?
i) podocyte damage/loss > albuminuria (loss of sieve)
ii) mesangial cells lie between capillaries > in diabetes they expand which can cause the capillary loops to be squeezed > damage
iii) glom BM thickens and cap loops are squeezed
iv) high glucose enviro leads to dev of reactive oxygen species > vasc endothelial cell damage
v) ultimately you get tubulo-interstitial and glomerular fibrosis (scarring)
vi) there is not much relation between glucose control and dev of kidney disease
- may help in T1DM but no assoc in T2DM
- diabetic kidney diasease is most common in south asian, black african/carribean
ACUTE TUBULAR NECROSIS/INJURY
i) what is it? what is it the most common cause of
ii) what can be used to correct it in the first few hours?
iii) what are the tubules unresponsive to after they have become ischaemic? how long may it take to recover
iv) name four things that can cause ischaemic injury
v) name four toxins that can cause toxic ATN
vi) what happens in sepsis that can cause ATN? (3)
i) damage to the kidney tubules that can lead to acute kidney failure
- most common cause of renal cause of acute kidney injury
ii) fluids and abx can correct in the ‘pre renal’ phase when at risk but before injury
iii) once ischaemic then tubule doesnt respond to fluid
- cam take days to recover
iv) D+V, bleeding, dehydration, burns, renal loss via diuretics, nephroic synd, oedematous states > reduced kidney perfusion
v) aminoglycosides (gentamicin), light chain accum in myeloma, myoglobin accum in rhabdomyolysis, cisplatin, acylovir
vi) sepsis = systemic hypoperfusion, endotoxins can cause vasoconstric, inflammatory cytokines > ROS > injury
TREATING AKI
i) what are the goals of therapy? name two ways it can be prevented
ii) name three things that are effective tx once an AKI is present?
iii) name three things that are ineffective/harmful in tx
iv) name three things that have unknown effetiveness in tx
i) goals are to prevent AKI or the need for renal replacement therapy
- prevent by rehydration pre contrast and hold an ACEi if there is low BP pre operatively
ii) hydration is the best treatment (0.9% saline)
- prevent hypotension by stopped HTN medication
- avoid nephrotoxins
- treat the cause
iii) ineffective - diuretics, dopamine, renal vasoactive drugs eg DA-1 agonist, PDE blocker, Ca blockers
iv) unknown- N acetyl cysteine, sodium bicarb and prophylactic haemofiltration
INTERSTITIUM/TUBULE
i) name three drugs that may be nephrotoxic and affect the intersititum?
ii) which two UTI causative agents are directly toxic to the tubule?
iii) how may interstitium injury be treated?
i) gentamicin, vancomycin, NSAIDs, ethylene glycol
ii) leptospirosis and CMV
iii) treat with steroids
RENAL BLOOD VESSELS
i) what does the renal artery divide into? (3) which size vessels is disease the most common in?
ii) is it common or rare to have damage in the renal artery itself? how is it treated?
ii) where is disease most common? what is seen in the urine? what is it usually associated with?
i) renal artery > interlobar arteries > arcuate arteries > interlobular arteries
- most commonly get small vessel disease > kidney starved of oxygen
ii) rare - tx with angioplasty (only if narrowing was causing rapid kidney func decline or lack of control of BP)
iii) common in small vessels
- slowly progressive > see low grade proteinuria
- assoc with vascular disease elsewhere
FINAL COMMON PATHWAY
i) what happens as a result of disease progression?
ii) name four things renal injury causes and their consequence
iii) what ultimately happens to the kidney? how does this affect BP? what does this loop back round to contribute to?
iv) how may the tubules appear in the fibrotic kidney? how is cap density affected? how is ECM affected (3)
i) CKD
ii) decreased nephron mass
glom capillary hypertension
inc glom permeability to macromolecs and filtration of plasma proteins causing proteinuria
excessive tubular protein reabs
tubulointerstitial inflam
iii) this all leads to renal scarring which causes systemic hypotension as reduced ability to produce renin > hypotension then contrib to renal injury again
iv) dilated atrophic tubules
- cap density is reduced
- increased intertitial ECM, increased corss linking, stiff ECM
TREATMENT IN CKD
i) each condition will have a spec tx - what is a good tx for diabetes? rhabdomyolysis?
ii) what is the first line generalised tx for all patients with CKD? why?
iii) what can also be used to treat CKD? why?
iv) how does treating HTN affect renal function?
v) what can be used to determine the progress of CKD?
i) diabetes > good glycaemic control
rhabdomyolysis > IV fluids inc IV bicarb to dilute the myoglobin out
ii) ACEi/ARB (ramipril)
- want to decrease BP inside glom to protect it from damage
iii) can also use SGLT2 inhibitors eg flozins
- decreases pressure in glom therefore reduces dev of albuminuria
iv) patients with better BP control have a slower decline in GFR
v) albuminuria
RENAL REPLACEMENT THERAPY - DIALYSIS
i) what is haemodialysis? where does it principally take place? how often is it done?
ii) what is peritoneal dialysis? where does it principally take place?
i) blood is cleaned by a machine then reperfused in
- mostly done in hospital 3 times per week
ii) peritoneal - plastic tube into abdomen and use peritoneal membrane to filter > put fluid in peritoneal space for a few hours and urea/alb will be drained out
- mostly done at home and takes a few hours
