Intro to acute renal failure and clearance Flashcards
What is the difference between internal / external balance?
- External balance refers to the relationship between intake from the outside and output to the outside
- Internal balance refers to shifts between intra and extracellular fluid spaces
T/F: the kidney is the primary regulator of balance for sodium, potassium, phosphate, magnesium, calcium, and for acid-base status
True
With the following variables, what equation would you use to calculate GFR?
- Px (plasma concentration)
- Ux (urine concentration)
- V (urine flow rate)
At the whole renal level, we use the concept of clearance. With the same given variables, how could you calculate clearance?
GFR = (Ux * V) /Px
Clearance = same
- Thus clearance of a substance that isn’t secreted or excreted in any tubular segment = GFR
- That’s why we use clearance to estimate GFR
Describe why each of the following is/ isn’t used to measure GFR:
- Inulin
- Urea
- Creatinine
-
Inulin:
- Good: is a polysaccharide that can be used because its not secreted/ excreted.
- Bad: exogenous > has to be infused & expensive
-
Urea:
- Good: Is endogenously produced.
- Bad: is reabsorbed & influenced by muscles
- Underestimates GFR
-
Creatinine:
- Good: Is endogenously produced.
- Bad: slightly secreted
- Overestimates GFR
- METHOD OF CHOICE
What is the equation for creatinine clearance that is used to estimate GFR?
**WILL BE ON EXAM
Creatinine clearance (ml/min)
= [(A) x (140 - age) x weight]/ (72 x SCr)
Where:
- A=l.0 if male, 0.85 if female
- Age is in years
- Weight is in kg
- Serum creatinine is in mg/dL
OR WHEN DOING 24 HOUR TEST:
ClCr = (UCr) V/ PCr
A patient is found to have a plasma creatinine of 2.0 mg/dL and a 24 hr urine volume of 1,500 ml with a urinary creatinine concentration of 100 mg/dL (100 mg/l00 ml).
- Calculate the creatinine clearance
- What would the creatinine clearance be if the patient’s creatinine rose to 4.0 mg/dL (assuming that the patient was again in creatinine balance)?
ClCr = (UCr) V/ PCr
ClCr = 1,500ml/1440 min x 100 mg/dL / 2.0 mg/dL
= 52 ml/min
(remember that there are 1440 minutes in 24 hours)
If the serum creatinine increased to 4.0 mg/dL in a steady state, creatinine clearance would be 26 ml/min
The rate of glomerular filtration at level of a single nephron (SNGFR) is determined by the Starling forces.
What is the equation to calculate SNGFR?
Which variables are not clinically relevant?
SNGFR = [(PGC - PT) - (πGC-πT)] x Kf
- we can generally assume that the oncotic pressure in the tubule (πT) is zero.
- Furthermore, alterations in PT or πGC are generally modest and usually not clinically relevant
- K = takes into account the surface area and permeability of glomerular capillary membrane
- Therefore, in normal individuals under physiologic conditions, PGC controls SNGFR the most and SNGFR is proportional to PGC (glomerular capillary hydrostatic pressure )
What factors maintain PGC (glomerular capillary hydrostatic pressure )?
What chemicals alter these factors?
PGC is influenced by afferent and efferent arteriolar tone (constriction/ dilation)
- Dilation of A.A causes increases in PGC. Constriction of E.A. causes increases in PGC
- SEE IMAGE
- Dilation of A.A. = prostaglandins and nitric oxide
- Constriction of E.A = angiotensin-II
How do the different starling forces affect filtration rate?
- Glomerular capillary hydrostatic pressure (PGC).
- Glomerular capillary oncotic pressure (πGC).
- Tubular hydrostatic pressure (PT).
- Oncotic pressure in the tubule (πT)
How does the change in pressure along the capillary affect filtration?
As you progress along arteriole you get a drop in pressure which decreases filtration
Now explain how each of the following affect arteriolar resistance and subsequently GFR?
- Nitric oxide/ prostaglandins
- Angiotensin-II
- NSAIDs, adenosine, norepinephrine, endothelin, thromboxane
- ACE-I, ARBs
What are the normal lab values of the following:
- Na
- K
- Creatinine
- BUN
- Cholesterol
- Na- 140 ± 3 mEq/L (Tells you about the relative amount of water in the ECF compared with Na. It tells you nothing about total body Na)
- K- 4.5 ± 0.6 mEq/L
- Creatinine- 1.0 ± 0.3 mg/dL
- BUN- 12 ± 4 mg/dL
- Cholesterol- 140-200 mg/dL
Define acute kidney injury and what is azotemia?
AKI: rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine (Pcr) concentration, urea and other nitrogenous waste products
Azotemia: increased nitrogenous waste products in blood, ie BUN, creatinine (azote = nitrogen in french)
Define Uremia, Oliguria, and Anuria
Uremia: refers to the constellation of signs and symptoms of multiple organ dysfunction caused by retention of “uremic toxins” and lack of renal hormones due to acute or chronic kidney injury
Oliguria: Urine volume is < 400 mL/24hrs
Anuria: Urine volume is < 50 mL/24hrs
What are the three broad types of AKI, and what causes them?
- Pre-renal azotemia: a decrease in GFR due to decreases in renal plasma flow and/or renal perfusion pressure (problems before kidney)
- Intrinsic renal disease: a decrease in GFR due to direct injury to the kidneys (may be due to a variety of insults).
- Post-renal azotemia or obstructive nephropathy: a decrease in GFR due to obstruction of urine flow (after kidney)
What are the different causes of pre-renal azotemia?
Decreases in GFR is the hallmark of ATN. What are the vascular factors that can cause this? What are the tubular factors?
- The vascular factors include decreases in renal blood flow and decreases in glomerular permeability (Kf)
- Tubular factors = tubular obstruction (by cellular debris) and backleak of glomerular filtrate (across an incompetent tubular basement membrane)
Mortality in patients with ATN approaches 60%
Common causes of death in these patients include infections and gastrointestinal bleeding.
