Nephrology Flashcards
This is secreted by the kidneys and promotes productions of the protein Angiotensin I
Renin converts angiotensin into angiotensin I
and angiotensin converting enzyme AKA ACE converts angiotensin I into angiotensin II
The active form of vitamin D that is produced by the kidneys
1,25-Dihydroxycholecalciferol
Blood seen on dipstick but no red cells on urinalysis: explanation?
Hemolysis or rhabdo (which produces myoglobin) in urine to test positive for blood on dipstic
This is the protein that is tested in a urine dip when looking at protein
Albumin
A notable protein that will not be tested with urine dipstick
Bence-jones protein is not tested by dip stick, if you are working up a patient for MM do not be encouraged by negative protein on dip stick
Interstitial nephritis is commonly tested on boards. you commonly see WBCs and no bacteria on urinalysis. What type of white blood cell is commonly elevated in these cases?
Eosinophils
Knee jerk: Red blood cell casts
Glomerulonephritis
Knee jerk: brown muddy casts
Acute tubular necrosis
Knee jerk: WBC casts
Pyelonephritis
four factors that are used to calculate the modern “eGFR” as determined by the MDRD equation displayed in most hospitals
Serum creatinine
age
sex
X1.2 if african american (more muscle mass on average)
186 * serum creatinine - (1.154age) - (0.203-.742 if female) * (1.1212 if african american)
eGFR as determined by the MDRD equation will ______ (under or over estimate) eGFR if a patient is obese
The Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease and Epidemiology (CKD-EPI) equations do not include total weight but have been reported to also overestimate GFR in obese patients
(the AAFP board review course archive has this backwards! oops…)
Basically, these patient will produce more creatinine which is multiplied by 186 in the MDRD equation.
(Michels WM, Grootendorst DC, Verduijn M, Elliott EG, Dekker FW, Krediet RT: Performance of the Cockcroft-Gault, MDRD, and new CKD-EPI formulas in relation to GFR, age, and body size. Clin J Am Soc Nephrol 5: 1003–1009, 2010)
this measurment is often less effective at measuring true GFR than the MDRD equation but is more useful with dosing medications as it takes weight into account
Creatinine clearance
via the cockcroft-gault equasion
cutoff for nephrotic range proteinuria on 24 hour collection
> 3 grams
minimal criteria for AKI
increase in creatinine greater or equal to 0.3 in 48 hours
increase greater or equal to 1.5 times baseline in 7 days
And the one I never remember the numbers:
urine volume <0.5mL/kg/hr for more than 6 hours
most common cause of AKI in an adult?
- Stones
- Diuretic induced volume loss
- ATN
- Acute interstitial nephritis
- ATN!
45% of AKIs are ATN which includes hypotension and sepsis! as well as surgery, burns, nephrotoxins, ischemia
21% prerenal 13% acute on chronic kidney disease 10% obstruction including stones and BPH 4% glomerulonephritis 2% interstitial nephritis 1% thromboembolic disease
What does MPGN stand for
Membranoproliferative glomerularnephritis, a type of nephritic syndrome
Knee jerk: Fever, Rash, urine eosinophils after starting a new medication
Acute interstitial nephritis. Treatment is get rid of drug. Consult neph for +/- steroids if its bad
Most common drug listed assiciated with AIN:
- pregabalin
- ertapenem
- omeprazole
- fluoxetine
omeprazole
class effect and NOT dose related
nephritic or nephrotic: RBCs in urine, hypertension, and mild proteinuria
nephritic syndrome
Nephritic or nephrotic: hypercoagulable state
nephrotic: liver attempts to maintain serum osmolality by increasing production of clotting factors
nephritic or nephrotic: IgA nephropathy
nephritic
nephritic or nephrotic: diabetic nephropathy
nephrotic
nephritic or nephrotic: HSP
nephritic
Which of the following most likely decreases the possibility of the highly debated phenomenon of contrast induced nephropathy in iodonated contrast ajents
- hydration prior
- acetylcystine prior
3 acidification of urine prior - use of hyperosmolar contrast medium
- hydration prior
(with modern IV contrast it is questionable whether or not this happens but nephrologists in general have not accepted this yet)
name some nephrotoxic medications for fun
Nsaids Lithium aminoglycosides vanc amphotericin B IV acyclovir (PO is pretty ok) ace/arb diuretic ppis methotrexate
dont start metformin if gfr is less than what
<45
consider reduction in dose by 50 % once your patient who is already on metformin hits less than this GFR
<45
dont use metformin if GFR less than
<30
be careful with this once daily injectable anticoagulant once creatinine clearance becomes less than 30
enoxaparin - typicaly can use but needs to reduce dose by 50% and I would talk with pharmacy
Fena <1% with AKI means what
pre-renal
think kidneys are trying to hold on to sodium because water will follow and keep your volume up
Fena >2-3% with AKI means what
intrarenal, if very high likely ATN
kidney is injured and can’t keep the sodium that you want
four measurements needed to calculate fena
urine sodium and creatinine, plasma sodium and creatinine
consider this test when working up an AKI patient who is on a diuretic
FeUrea (urine sodium is affected by diuretics but urea is not as much)
AKI causes which of the following
- metabolic alkalosis
- metabolic acidosis
- hypophosphatemia
- hypokalemia
- metabolic acidosis
simplified: working kidneys overall excrete potassium, phosphorus and acidic substances, broken kidneys cannot
goal MAP to maintain renal perfusion
> 65
MAP equation (this has been seen on boards)
(systolic + diastolic *2)/3
next best step in treatment for AKI with creatinine of 5 with fluid overload and pulmonary edema with SOB but normal o2 sat
Give lasix and dont be afraid, start with 20-100 mg IV every six hours. Pulmonary edema will kill your patient way faster than an oliguric AKI, and in patient’s with high Creatinine, they need larger doses for the medicaiton to reach the part of the tubules where it will actually work.
If it doesn’t work you talk to nephrology who will probably say either lasix drip, bumex, or dialysis depending on what is going on and for how long
what is patiromir
new fancy potassium binder, still works slow though
pH threshold at which you give a patient bicarb
<7.2
Situations where you DONT need urgent dialysis
- hyperkalemia refractory to medical therapy
- volume overload unresponsive to diuretics
- metabolic acidosis with pH = 7.25
- uremic pericarditis
- metabolic acidosis with pH 7.25
True or false, one AKI increases your chances at developing CKD
true
True or false: ace inhibitors dilate efferent arterioles
True
Afferent brings the blood to the arteriole because it comes first in alphabet
Efferent takes blood away from glomerulus
Here is key concept that is easy to confuse:
Dilating the outflow tract will decrease the pressure on your glomerulus but ALSO increase flow through the glomerulus.
Excretion of creatinin is a function of PRESSURE inside the glomerulus and not flow through it, which is why you can get increased serum creatinine concetrations in people on ACE’s even though you are increasing their true GFR.
An small amount of increasing Creatinine on a patient on an ACE inhibitors does not necessarily mean you are hurting them and continuing the ACE still provides long term benefits
Kidney Int 997;51: 793-7
buildup of what substance causes a dry cough in patients on an ACE inhibitor
bradykinin
an increase of what percent of Creatinine after initiation of an ACE should you actually discontinue the med
more than 30% - and you start a workup for OTHER CAUSES and not just think it was the ACEi (look for dehydration, other meds like nsaids, or renal artery stenosis)
