Renal Part 2 Flashcards
what are normal levels of BUN and creatinine (SCr)?
BUN: 7-20
Cr: 07-1.2
BUN:Cr for pre-renal, intra-renal, post-renal
pre-renal: >20:1
intra-renal: 10-20:1
post-renal: 10-20:1
ATN is < __:__ (BUN:SCr)
20:1
BUN:Cr mechanism: pre-renal
BUN reabsorption is increased. BUN is disproportionately elevated relative to creatinine in serum. Dehydration or hypoperfusion is suspected.
BUN:Cr mechanism: intra-renal
Renal damage causes reduced reabsorption of BUN, therefore lowering the BUN:Cr ratio.
BUN:Cr mechanism: post-renal
Normal range. Can also be postrenal disease. BUN reabsorption is within normal limits.
ARF:
Sudden loss of renal function over ______,
decreasing ____,
Rise in serum creatinine by at least ____
hours/days/weeks
decreasing GFR
0.5 mg/dL over patient’s baseline
anuric vs oliguric vs nonoliguric
Anuric: urine output < 50 mL/day
Oliguric: urine output < 400 mL/day
Nonoliguric: urine output > 400 mL/day
ARF pts usually have symptoms of _____ and _____ ( in acute reduction urine output)
peripheral edema, shortness of breath
causes of ARF: pre-renal
pre-renal: decrease in blood flow without ischemic injury (prerenal azotemia)
causes of ARF: intra-renal
ischemic, toxic, or obstructive tubular injury (you can have a post-renal source that goes on to cause intrinsic renal failure)
causes of ARF: post-renal
obstruction of urinary tract outflow (examples- kidney stones, tumors, strictures in ureters, etc.)
most common cause of ARF. is this reversible
pre-renal failure (aka azotemia)
YES reversible!
what type of drugs can cause decreased renal perfusion?
endotoxins, cyclosporine, epinephrine, high doses of dopamine.
ACEs and ARBs are _______ _____ in pts with HTN and DM. however, if used with ______, can cause ____ ______
renal protective in pts with HTN and DM. However, if ACEI or ARBs are used with diuretics, they can cause prerenal failure.
ACEs and ARBs are renal protective. how?
reduces the effect of angiotensin (a renal vasoconstrictor) on the blood flow
NSAIDs cause reduced renal blood flow, how?
NSAIDs can reduce renal blood flow b/c they block with vasodilation properties of prostaglandins
what do the labs show for pre-renal failure?
- decreased GFR
- Increased creatinine (but BUN increases MORE, so…)
- elevation in the ratio of BUN to creatinine from a normal value of 10:1 to a ratio of greater than 20:1
- FeNA <1%
Intrinsic Renal Failure: caused by _____ which results from conditions that cause ….
ATN: Results from conditions that cause injury to structures (tubules) within the kidney (ischemia, injury)
part of ATN: Tubulointerstitial disorder: destruction of ____ _____ _____ with acute suppression of renal function.
Tubulointerstitial disorder
destruction of tubular epithelial cells with acute suppression of renal function.
ATN can be caused by…
acute tubular damage d/t ischemia, sepsis, nephrotoxic effects of drugs, tubular obstruction, toxins from massive infections.
ATN: the GFR does or does not improve with the restoration of renal blood flow in ARF caused by ischemic ATN? what about creatinine?
does NOT
creatinine will be restored to normal
ATN caused by intratubular obstruction is most often caused by what 4 things?
ATN caused by intratubular obstruction is most often caused by multiple myeloma light chains, excess uric acid, myoglobin, or hemoglobin in the urine
3 stages of ATN?
- onset or initiation phase
- maintenance phase
- recovery phase
what is normal GFR?
about 90
majority of intrinsic renal failure is caused by what? at what percent ?
ATN 85%
*intrinsic- theyll have normal range BUN/Creatine 10-20 but…
creatinine will be ABNORMAL
ATN stage 1: onset or initiation phase: how long does it last? from when to when?
lasts hours or days, time of the onset of precipitating event until tubular injury occurs
ATN stage 2: maintenance phase: what is the key factor of this stage?
marked decrease in GFR!
ATN stage 3: recovery phase: what happens here?
when renal tissue repair takes place. Onset is heralded by gradual increase in urine output and a fall in serum creatinine
***pre-renal vs ATN: urine osmolality
pre-renal: >500
ATN: <350
***pre-renal vs ATN: urine sodium
pre-renal: <20
ATN: <40
***pre-renal vs ATN: FENa
pre-renal: <1
ATN: >2
***pre-renal vs ATN: BUN:Cr
pre-renal: >20
ATN: <20
***pre-renal vs ATN: urine sediment
pre-renal: bland, nonspecific
ATN: muddy brown granular casts
Risk of Contrast-induced-neuropathy (kinda weeds…)
Score Risk of CIN Risk of Dialysis 0-5 7.5% 0.04% 6-10 14.0% 0.12% 11-16 26.1% 1.09% > 16 57.3% 12.6%
3 ways to reduce risk of ARF with imaging
- Hydration with IV normal saline 12 hours before and after procedure
- Administering acetylcysteine (Mucomyst®) before/after procedure
- Discontinuing Metformin prior to procedure (if possible) and held for 48 hours
most common underlying problem for post-renal failure
BPH
post-renal failure, can be caused by ____ _____ ____ or _____ _____ ______
can be caused by bilateral ureteral obstruction (unilateral if bad enough) or bladder outlet obstruction
Txt for post-renal failure: 2 parts
Identify/reverse the causes (get rid of obstruction), maintain fluid volume, and maintain electrolyte concentrations.
what labs will you check for post-renal GFR? (4)
Check UA, GFR and serum BUN and creatinine.
overview: txt of the 3 different kinds of ARF
Pre-renal: identify the cause and treat/reverse it, d/c nephrotoxic drugs, hydrate the patient
Intrinsic: identify the cause and treat/reverse it, d/c nephrotoxic drugs, possibly use dopamine, hydrate the patient, reperfusion of the kidney
Post-renal: identify/remove the obstruction
Dialysis or CRRT if needed for any type of ARF if it’s indicated
CKD is defined by presence of kindey damage or loss of kindey function for …
three or more months
CKD results in … and leads to ….
permanent loss of nephrons and frequently leads to renal failure.
how is CKD classified? what is the staging based on?
Kidney Disease Outcome Quality Initiative (KDOQI)
GFR
what are two of the most common causes for CKD?
DM and HTN
what are the stages for CKD?
G5: GFR<15 (kindey failure)
count up in intervals of 15 … (G4, G3b, G3a, G2, G1)
G1: GFR >90 (kindey damage with normal or increased GFR)
Stage 2 CKD is mildly reduced kidney function but also required
evidence of kidney disease (protienuria or hematuria)
increased protien in urine indicates what? excretion of albumin leads to ____
increasing levels of protein in urine indicate kidney damage.
Excretion of albumin leads to CKD
5 most common lab abnormalities in CKD
GFR is decreased! Proteinuria Broad waxy casts anemia BUN (can go >800 )
hyperkalemia in CKD: what stage does it occur and what is the txt?
is advanced- stage 5.
“C BIG K” (calcium, bicarbonate/beta-agonist, insulin + glucose, Kayexalate)
metabolic acidosis in CKD?
Metabolic acidosis may occur when the pt is faced with a high acid load or loses alkali (like in diarrhea).
anemia in CKD? what is the first line txt?
First line treatment: recombinant human erythropoietin (rhEPO),
when should patients be monitored(have GFR checked) for the different stages of CKD?
Consensus recommendations are: Stage 1 and 2 annually Stage 3A and B every 6 months Stage 4 every 3 months Stage 5 every 6 weeks
Decrease in ________ that occurs in CKD results in less protein-bound drugs and greater amounts of free drugs.
plasma proteins (particularly albumin)- it is important in oncotic pressure for fluid shifts
insulin with renal failure? what to do?
dose adjust!
key to management of CKD: what stage does referral need to be made?
Timely Referral to a Nephrologist!!!!
At least by stage 3b CKD you need to be putting referrals into place!!!
4 parts to general management of CKD
- treat UTIs appropriately
- Avoid smoking. (causes vasoconstriction that makes perfusion issues worse)
- Encourage weight loss.
- Evaluate for and treat reversible causes
what are nephotoxic meds to avoid in CKD?
NSAIDs, COX 2 inhibitors, various abx (Macrobid, Bactrim).
5 parts to treating complications of CKD?
- Volume overload
- Hyperkalemia
- HTN
- Acidosis
- Hyperphosphatemia/Hypocalcemia
volume overload with CKD?
Early CKD: balance usually maintained
As CKD progresses, pt cannot respond to rapid changes in Na/H2O
Tx:
a. Na/H2O restriction
b. Loop diuretics (avoid thiazide diuretics)
MAP for management of HTN and CKD (3 parts)
what is the MAP goal?
- Lower the MAP = slows progression (goal is <92 mmHg)
- Same in nondiabetics/diabetics
- Achieving BP goals is difficult
MAP Goal: 60-92 mmHg
HTN with CKD: what is the overall HTN goal? BP goal?
HTN Goal: lower BP –> reduce proteinuria –> renoprotective and cardioprotective effects
BP GOAL: Systolic 110-129
Diastolic < 85
what are the BP goals for proteinuric CKD pts?
In proteinuric patients: even lower BP goals
< 1 g/d: < 130/85
> 1 g/d: < 125/75
4 parts of RAAS from glomerular HTN
- Glomerular HTN (occurs in efferent arteriole)
- Increases pro-inflammatory protein
- Stimulates aldosterone
- Proliferative effects of AT II –> tubular harm
ACEs and ARBs: what do they do?
ACEIs – decrease production of angiotensin
ARBs – block receptor to accepting protein-direct Renin inhibitors, which reduces the effect of angiotensin on the blood flow and is renal protective
management of CKD with HTN: 3 drug therapies
- ACEIs – drugs of choice HTN/proteinuria
- Diuretic – HCTZ-mild/moderate HTN (but to be avoided in late-stage CKD)
- Combination with ACEI or ARB – effective in nondiabetics/diabetics
txt for acidosis in CKD?
Tx: Maintain HCO3 = > 22;
Give NaHCO3, 0.5 to 1 meq/kg/day; Na Citrate
DO NOT GIVE Al3+ containing antacids
hyperphosphatemia and hypocalcemia: when does it start? what happens?
Starts early in renal disease
Drop in Calcium stimulates PTH –> decreased phosphorus resorption and increased calcium resorption from bone
= stimulates bone turn over and resorption
3 goals of treatment for hyperphos and GFR <30: what levels do you want serum Calcium/phosphorus product, phosphorus, and serum total calcium?
(Ca x P) Product; <55
phosphorus: <5.0
calcium: 8.4-8.5
hyperphosphatemia and GFR <30 requires txt, what will you do?
Treat with Phosphorus Binders:
- Calcium Acetate
- Calcium Carbonate
- Non-Calcium Sevelamer (polymer)
what is “AEIOU” for?
indications for dialysis
what does AEIOU stand for?
Acidosis Electrolyte disturbance (severe hyperphosphatemia) Ingestions (overdoses) Overload (pulmonary edema) Uremia (uremic pericarditis)
what are the risks of hemodialysis: what often results post-dialysis?
post-dialysis: hypotensive, low K+, nausea, etc.
what is often the txt of choice for CKD patients?
transplant
success of kidney transplant depends on what 3 things? what meds must patients take prior to transplant?
Success depends on histocompatibility, organ preservation, and immunologic management.
Pts will need immunosuppressive meds to control the T and B cell activation.
what is continuous renal replacement therapy?
blood purification therapy intended to substitute for impaired renal function, normally the patient is hooked up for 24 hrs - good for unstable pts
dietary management for CKD: what do you restrict and what do you want to make sure they are taking?
Restrict dietary proteins
ensure adequate caloric intake in the form of carbs and fats, sodium and fluid restrictions
-When GFR is very low or during hemodialysis, K+ restriction is recommended.
- Limit phosphorous
renal dz of glomerular origin vs tubular dysfunction: how will each effect sodium in the body?
Renal dz of glomerular origin: Na retention
Tubular dysfunction: Na wasting
water restriction of _____ -_____ for dialysis
500-800 mL
CKD in children: can they get the same treatment as adults? what must you monitor?
if over 2 yo can get the same renal treatments as adults
-need to watch their BP
what are age-adjusted measurements for GFR?
if youre older than 75, your GFR will NOT be 90, new normal for this age population.
60-89 GFR —> do age-adjusted meansurements
uremic frost: what does it look like and what does it mean?
Bad sign- means they are uremic, especially if they have chest pain. looks like dandruff
NOTICE THIS
