Renal - 06 - Acute And Chronic Renal Failure

Front 1

pre-renal causes of renal failure

Back 1

hypovolumia, low cardiac output, low oncotic pressure, renal artery stenosis, atheroemboli

Front 2

post-renal causes of renal failure

Back 2

obstructions - prostate hypertrophy, stones, ureteral strictures, tumors

Front 3

intrinsic causes of renal failure

Back 3

glomerular problem (glomerularnephritis)

interstitial - acute allergic interstitial nephritis - drugs

vascular (vasculitis, renal infarction, renal vein occulsion, hemolytic uremia syndrome, scleroderma)

tubular (acute tubular necrosis) - e.g. aminoglycoside tox

Front 4

acute tubular necrosis ischemic vs toxic

Back 4

ischemic type see patchy distribution of damage - mostly localized proximally

toxic type see continuous proximal tubule damage

Front 5

mechanism of decreased GFR in acute renal failure

Back 5

vasoconstriction of afferent

backleak of urine into intersitium puts pressure on other nephrons - capsule of kidney means limited space

tubular obstruction

Front 6

how does ischemia cause damage to nephrons

Back 6

severe ischemia -> decreased ATP, activation of degradation process, impaired synthesis of required molecules

-> reversible damage -> cell swelling -> increased membrane perm to Ca++ -> calcium overload -> irreversible damage

necrosis -> cytosolic content release -> inflammation -> damage to other nephrons

____

lesser severity triggers apoptosis

Front 7

vascular and hematologic factors in acute renal failure

Back 7

ezymes, reactive mediators, inflammatory mediators -> vasoconstriction attraction of additional inflam mediators

Front 8

why is the kidney susceptible to ischemia

Back 8

unique anatomy - no collaterals

uses a lot of ATP (high metabolism)

intense vasoconstriction in response to endothelin and depressed NO

Front 9

T/F during ischemia you can find Na/K ATPase on lumnal and basolateral sides of the tubular cells

Back 9

True

Front 10

urinary findings in pre-renal disease

Back 10

BUN/serum creatinine > 15:1
----because urea is reabsorbed, creatinine isn't

Urine Na < 20meq/liter

U/P creatinine ration > 20:1

urine osmolarity > 100 above serum - kidneys can still concentrate the urine

no casts, or cell debris

fraction of Ne excretion < 1%

Front 11

urinary findings in ATN

Back 11

BUN/serum creatinine 10:1 (since both BUN and creatinine increase at same rate)

urinary Na > 20 meq/liter

U/P creatinine ratio < 20:1

Urine osmolarity = serum osmolarity (loss of ability to concentrate urine)

see casts, cell debris

fraction of sodium excretion is > 3% (unable to reabsorb properly)

Front 12

acute renal failure vs chronic

Back 12

acute - all nephrons hit at same time

chronic - some damaged, the healthy ones have to hypertrophy to meet the needs of the body - eventually these nephrons burn out -> failure

Front 13

progression to renal failure

Back 13

4 stages:

loss of renal reserve - GFR<50% - no biochemical abnormalities detected, minimal elevation of creatinine and BUN

renal insufficiency - GFR <25% - mild anemia, raised BUN and creatinine

renal failure - GFR 10-15ml/minunte - bad azotemia, anemia, concentration and dilution defects, electrolyte imbalances, alkalosis/acidosis

Uremic Stage - GFR < 10-15 - multisystem involvement - GI, CV, CNS

Front 14

signs of chronic renal failure

Back 14

non-oliguria, small kidney size, increased PO4, low Ca+, anemia, acidosis

Front 15

most common cause of chronic renal failure

Back 15

chronic glomerulonephritis

followed by: diabetic nephropathy, htn, polycystic kidney disease, etc

Front 16

adaptive changes to increased neprhon load (due to damage to other nephrons)

Back 16

on the nephron: increased filtration, increased secretion, reduced reabsorption

increased K+ excretion by GI

increased utilization of urea by liver

increased phosphate excretion via PTH

Front 17

what happens to nephrons during hyperfiltration

Back 17

eventual sclerosis

Front 18

factors beside glomerular hypertension that are important in progression renal failure

Back 18

hyperlipidemia

release of growth factors by platelets/mesangial cells (TGF beta stimulates collagen formation -> sclerosis)

angiotension II (vascular effects and increased production of TGF- beta)

Front 19

serum osmolality equation

Back 19

2(Na+) + glucose/18 + BUN/2.8