Exam 2: Renal Flashcards
Kidneys maintain homeostasis: Regulatory function
Control composition and volume of blood - maintain stable conc of cations (Na, K, Ca)
Maintain acid-base balance
Kidneys maintain homeostasis: Excretory function
Produce urine
Remove metabolic waste (urea and other waste products)
Kidneys maintain homeostasis: Hormone function
Produce renin for BP control
Produce erythropoietin which stimulates marrow production of RBC
Activate 25(OH)-D (inactive vit d) to 1,25(OH)D (active vit D)
Kidneys maintain homeostasis: Metabolic function
Gluconeogenesis
Metabolize drugs and endogenous substances (insulin)
Kidneys maintain homeostasis: BP function
Decrease kidney perfusion stimulates the release of renin from juxtaglomerular cells of the kidneys
Renin converts angiotensinogen to AT1
AT2 a potent vasoconstrictive agent
- stimulates Na retention in the nephron (particularly in PCT)
- stimulates release of aldosterone from the adrenal gland to increase Na
Kidney primary functions
Filtration (glomerulus)
Reabsorption and secretion (tubule)
If tubular cells are damaged, ____ will be wasted and increase _____
sodium/electrolytes and increase urine sodium (normally reabsorbed but tubule cells damaged and unable to)
Explain relationship with BUN and low perfusion pressure
If perfusion pressure is low (CHF, dehydration, hypotension, then tubular cells will reabsorb sodium and water to maintain homeostasis and urea will follow sodium
reabsorption of urea increases BUN
Creatinine is ___% filtered and ____ secreted
80-90 and 10-20
Synonym of prerenal AKI
Prerenal azotemia
Doubling of ___ is evidence of AKI
SCr
Def: Azotemia
Increase in waste products (Cr and urea)
What does AIN stand for
Acute interstitial nephritis
What does ATN stand for
Acute tubular necrosis
What are 3 types of intrinsic/intrarenal AKI?
acute interstitial nephritis (AIN), acute tubular necrosis (ATN), and glomerulonephritis
Def: Nonoliguria
> 500 ml/day
Def: oliguria
100-500ml/day
Def: anuria
<100ml/day
Key determinants of AKI
x2 SCr Decrease UO (<0.5ml/kg/hr over 12 hrs) Abrupt change over short period of time (hours to days) and sustained for over 24 hrs
AKI cases in hospital is a/w increased ____, ____, and _____
risk of death (7x), length of stay (4x) and risk of transfer to ICU (x4)
What are non-modifiable risk factors of AKI
CKD DM Older age Chronic liver disease (cirrhosis) CHF Renal artery stenosis Peripheral vascular disease
What are modifiable risk factors of AKI?
Volume depletion HTN/Hypotension Hypoalbuminemia sepsis/shock Nephrotoxic meds Major surgery/anesthesia
Prerenal AKI: Results of hypoperfusion of the kidneys
Volume depletion (burns, hemorrhage, GI loss like diarrhea)
HYPOtension (sepsis, shock)
Renal artery stenosis
Prerenal AKI: What are the effects of ACEI/ARBS?
Vasodilation of efferent arteriole
Prerenal AKI: What are the effects of epinephrine?
Vasoconstriction of afferent arteriole
Prerenal AKI: What are the effects of high-dose dopamine?
Vasoconstriction afferent arteriole
Prerenal AKI: Diagnostic parameters
BUN/SCr 20:1 ratio (Scr x2, BUN rapidly increase, usually faster than Cr)
UO usually decrease to conserve (dark urine, more concentrated)
Urine sediment/RBC/WBC/protein - none
Urina Na <20 mEq/L
FeNa <1% (conserving Na)
What is the relation between cirrhosis and low flow
decrease in albumin production and water cannot be stored in bloodstream so intravascular volume depletion
Prerenal AKI: 3 causes
Low volume, flow, and drug-induced
DIKD: Prerenal: Agents
NSAIDs, ACEI/ARBs, Radioconstrast media, loop diuretics and metolazone
