AKI/CKD Flashcards
eGFR can be calculated using etither of these 2 equations:
- Cockcroft-Gault equation
- MDRD equation
PCT almost complete reabsorption of: (5)
1- glucose 2- AA 3- lactate 4- water soluble vitamins 5- electrolytes
What electrolytes are included in the PCT reabsorption: (4)
1- sodium
2- potassium
3- bicarb
4- chloride
PCT excretion includes:
1- organic cations and anions as end-products of metabolism (oxalate, urate)
2- minimal exogenous organic compounds: ASA, morphine, and penicillin (2/2 bound to proteins and difficulty entering ultrafiltrate)
Taken as a whole the Loop of henle always reabsorbs more of this molecule than water
NaCl
Loop of Henle’s major role
determining the concentration of urine by establishing a high concentration of osmotically active particles in the renal parenchyma surrounding the medullary collecting tubules where ADH exerts it’s effects
Declining renal function leads to increased levels in these substances in the serum: (4)
- creatinine
- phosphate
- urea
- potassium
Renal clearance is dependent on: (2)
1- the ability of the glomeruli to filter the substance
2- the capacity of the renal tubules to reabsorb or secrete it
Kidneys excrete H+ ions in urine for regulating pH via these 3 buffers:
1- Ammonia
2- Phosphate
3- Bicarbonate
Increases in urea can be seen in these 3 conditions:
1- GI bleed
2- Tissue breakdown
3- increase PRO diet
AKI Dx Criteria: Only need 1
1- Increase in serum Cr by 0.3 mg/dL or more in 48 hours
2- Increase in serum Cr by 150% or more in 48 hours
3- Oliguria of less than 0.5 mL/kg/hr for more than 6 hours (in a 150 lb pt. that equal UOP<35 cc/hr)
Two situations in when you cannot rely on Cr levels:
1- HD
2- pt is not in a steady state
Nephrotoxins that cause Intrinsic or Renal Azotemia:
- NSAIDs
- Aminoglycosides
- contrast
When is imaging with AKI required? (2)
1- likely obstructive pathology
2- determine if it is chronic renal failure when no baseline labs are available
early renal bx in AKI dx looks for: (4)
- HUS
- TTP
- vasculitis
- GN
Renal bx in AKI indicated in pts. w/ these sxs: (3)
1- clinical situation suggesting vascular pathology
2- oliguria >4 weeks
3- If based on hx, pre-renal and ATN unlikely, and no improvement w/ conservative care
Deadly complications of uremia: (4)
1- sz
2- arrhythmias
3- fluid overload (pulmonary edema)
4- metabolic acidosis
Indications for Urgent HD: (4)
1- hyperkalemia
2- sxs of uremia (coma, confusion, pericarditis, sz, coagulopathy, n/v, GIB)
3- fluid overload- unresponsive to tx
4- metabolic acidosis
Name the phases in the patho remodeling of ATN: (3)
1- initiation
2- management
3- recovery
Etiologies of the Initiation phase in the patho remodeling of ATN: (5)
1- loss of ET border of lumen, leading to back-leak of filtrate
2- damage to Na/K ATPase pumps, leading to increased Na and Ca retention and swollen cells
3- sloughing, leading to granular casts
4- decreased vasodilator production (NO, prostacyclin)
5- Increased free radicals and resultant damage
Describe the Maintenance phase in the patho remodeling of ATN:
- stable, but very low GFR (lasts 1-2 wks)
Describe the Recovery phase in the patho remodeling of ATN:
- some tubular cell regeneration
- abnormal diuresis sometimes occurs resulting in salt and water loss with occasional hypovolemia
List the aminoglycosides: (3)
1- gentamycin
2- tobramycin
3- neomycin
aminoglycosides induced ATN presentation:
5-10 days after exposure and is generally mild and non-oliguric
Specific NSAID’s that can lead to AIN: (3)
1- fenoprofen
2- ibuprofen
3- naproxen
Other drugs that can lead to ATN: (8)
1- Antivirals 2- Amph. B 3- Acyclovir 4- ACE/ARB 5- Cephalosporins 6- Cannabinoids (synthetic forms) 7- Foscarnet 8- Vancomycin
Rhabdomyolysis can be seen in which pts: (4)
1- elderly who fall and cannot get up
2- Statin SE
3- extreme exercise
4- crush injury
Sxs/Labs seen with Rhabdomyolysis: (7)
1- dark, brown urine 2- elevated Cr 3- elevated Myoglobin 4- Urine w/ false positive for Hemoglobin 5- hyperphosphatemia 6- hyperuricemia 7- hyperkalemia
Two main causes of CKD:
HTN and DM
SXS of CKD:
- Pts. typically remain asxs until stage 4 or 5
- General: appears chronically ill w/ fever, malaise, and weakness
- GI: hiccups, anorexia, n/v, metallic taste in mouth
- CV: “overload sxs”-> rales, peripheral edema, pericardial friction rub, and cardiomegaly
- Neuro: asterixis, clonus, cognitive deficits, irritability, difficulty concentrating, RLS, rarely coma
- Skin: carotinemic color changes, severe itching (secondary to elevated BUN), easy bruising
As CKD becomes more severe, pts typically get these sxs: (3)
1- fluid overload
2- hyperkalemia
3- metabolic acidosis
What medications are nephroprotective? (3)
1- ACE
2- ARB
3- CCB (Both DHP and Non-DHP)
Criteria for initiating HD: (2)
1- GFR 10-15mL/min
2- higher GFR w/ sxs of ESRD
MC cause of mortality overall in ESRD
CV dz
MC cause of sudden death in CKD is due to:
hyperkalemia (usually due to non-compliance with diet or missed HD)
5 year survival rate of HD pts
36%
- but dependent etiology of uremia and on comorbidities and compliance
C/I for a kidney transplant: (4)
1- active substance abuse
2- active infx
3- chronic illness w/ short life expectancy
4- active malignancy
Kidney transplant anti-rejection medications (2)
1- cellcept
2- Cyclosporine
Nephrogenic systemic fibrosis involves what structures? (5)
1- skin 2- heart 3- muscle 4- fascia 5- lungs
Dx for Nephrogenic systemic fibrosis
skin biopsy
Tx for Nephrogenic systemic fibrosis
No known tx
Etiology for Nephrogenic systemic fibrosis
- occurs secondary to MRI w/ Gadolinium contrast in renal insufficiency pts.
- avoid in anyone after stage 3B CKD
Skin appearance in Nephrogenic systemic fibrosis:
symmetrical, B/L fibrotic indurated papules, plaques, or subQ nodules +/- erythema
- often preced by edema and frequently misdx for cellulitis
Types of anemia associated w/ CKD: (3)
1- IDA
2- anemia of CKD
3- anemia secondary to erythropoietin deficiency
List the phosphate binders used to tx secondary hyperparathyroidism in CKD: (4)
- all given w/ meals
1- Calcium acetate (PhosLo)- only Ca containing one
2- Selevamer (Renvela, Renagel)
3- Fosrenol (Lanthanum)- chewable and crushable
4- Sucroferric oxyhydroxide (Velphoro)
List the Vitamin D substitutes used to tx secondary hyperparathyroidism in CKD: (3)
1- Calcitriol (rocaltrol)- active metabolite; QD IJ or after HD; want serum Ca to be 9-10 mg/dL
2- Doxercalciferol (hectoral)- rq. kidney metabolize to active form; takes 10-12 wks. for effects
3- Paricalcitol (zemplar)- synthetic form which binds to and activates Vitamin D receptors in kidney; dosed Q2-4 wks.
List the calcimimetic used to tx secondary hyperparathyroidism in CKD: (1)
- Cinacalcet (Sensipar)
Tx mild hyperkalemia and asxs:
- phosphate binder
- sodium polysterene sulfonate- kayexelate
Tx more severe hyperkalemia and sxs:
- IV calcium gluconate to stabilize cardiac membranes, glucose, and insulin
