20. Acute Kidney Injury Flashcards
what does a small amount of highly concentrated urine with low Na mean?
warning that irreversible cell damage is imminent.
reason: water has been reabsorbed due to ADH, and salt has been reabsorbed due to aldosterone. Both were upreg’d due to sympathetic stimulation
definition of acute kidney injury?
reduction in GFR by 25% or more
how is GFR measured?
serum creatinine concentration. accumulates in serum if not cleared by kidneys
which artery supplies the tubular structures?
efferent. but decr blood flow in either will cause possible ischemia to the nephron blood supply
generally, a decrease in circulating blood (ECV) supply activates what?
What causes decr. in ECV?
sympathetics!
tachy, vasoconstriction, RAAS system, thirst, ADH
also aldo, AtII –> incr reabsorption of Na
causes: CHF, cirrhosis, sepsis, vasodilators, nephrotic syndrome, RAS, ACEi - anything that decreases GFR
define pre-renal azotemia
moderate decrease in renal perfusion (GFR decreases)
renal sympathetics activate, sodium is reabsorbed –> low urine Na concentration
water is reab –> concentrated urine
define acute tubular necrosis (ATN)
What do you see on labs?
severe/sustained fall in renal perfusion (sustained decr. ECV) –> cell death; tubular fluid is not processed, results in accumulation of toxins/electrolytes, may result in isothenuria (urine = plasma osmolarity)
incr. serum creatinine/BUN in the setting of decr ECV (incr. HR, decr. BP, cool skin, diaphoresis)
what marks the transition point between pre-renal azotemia and ATN?
urine osmolality approach PLASMA values (i.e., tubular fluid not altered much by action of tubular cells) = ISOTHENURIA
at the point of ATN, what is the significance clinically?
past the point of being able to restore renal function by restoring circulating volume
Pre-renal AKI treatment:
ATN treatment
pre-renal: restore ECV to maintain perfusion
ATN: decr. fluid intake, K, correct A/B balance, dialysis (basically maintain homeostasis until the tubules regenerate)
ATN: what will be seen on urine microscopy?
muddy brown casts
ATN clinical labs demonstrate:
FENa: if 2% (since tubules aren’t working properly and are unable to respond to aldosterone/AII and are excreting too much Na)
how should I monitor patients with Pre-renal AKI?
monitor serum creatinine, minimize blood loss, restore ECV
calculation for FENa?
What does FENa 1?
(USPC)/(UCPS) x 100
1 = tubules aren’t reabsorbing Na properly
What is intrinsic AKI? Where can it happen? 3
toxic or immunologic injury within the kidney compartment.
can be glomerular, tubulo-interstitial, or vascular
with a tubular injury, will I see proteinuria?
no, will see proteinuria with a glomerular injury
What would you see with glomerular AKI?
oliguria with HTN
cola-colored urine
hematuria (dysmorphic RBC + casts)
What is tubular-interstitial AKI caused by? 3 broad categories
Allergic Interstitial nephritis (AIN) Endogenous toxins (myoglobin, light chains, uric acid) Exogenous toxins (nsaids, contrast, Calcineurin inhibitors, Aminoglycosides, crystals, acetaminophen, ETOH, Lithium)
What is allergic interstitial nephritis?
labs? creatinine? oliguric or non-oliguric? urine findings? bx findings? systemic findings?
trmt:
hypersensitivity rxn to exogenous chemicals/meds that can act as haptens (penicillin, cephalosporin, PPIs, sulfur-based Rx, NSAIDs, etc)
Labs: incr serum creatinine non-oliguric (>0.5ml/kg/hr) urine: sterile pyuria (+WBC) bx: lymphocytes + eosinophils systemic: rash
discontinue offending agent
How does myoglobin cause AKI?
causes? labs? creatinine? oliguric or non-oliguric? urine findings? bx findings? systemic findings?
Trmt?
contraindications?
myoglobin released from muscle damage (crush injury, rhabdomyolysis, NMS) cause VASOCONSTRICTION of afferent arteriole and direct toxicity to RTE
labs: incr. CPK can be oliguric or non-oliguric pink urine + pink plasma systemic: edematous
trmt: hydration, alkalinazation, dialysis
contraindications: diuretics
How does light chains cause AKI?
causes? labs? creatinine? oliguric or non-oliguric? urine findings? bx findings? systemic findings?
Trmt?
contraindications?
Multiple myeloma, plasma cell dyscrasias produce light chains that accumulate in the PCT –> toxic
Insidious loss of GFR over days-months
Non-oliguric
May have RTA Type II
decr. AG (due to incr serum globulins, which are + charge)
incr. risk of AKI in response to minor changes in ECV
urine dipstick = NEGATIVE
Urine microscopy: no cells, casts, or crystals
Trmt: Alkylating agents (melphalan) & Prednisone Velcade/Bortezomib Thalidomide and lenalidomide (Revlamid) Autologous transplantation
How does uric acid cause AKI?
causes?
labs?
oliguric or non-oliguric?
urine findings?
Trmt?
contraindications?
Tumor lysis syndrome or defects in purine metabolism (Lesch-Nyhan Syndrome); Uric acid accumulates in peri-tubular fluid and precipitate into uric acid crystals -> inflammatory response
Labs: Hyperuricemia Urine sediment: bland, urate crystals Oliguric or non-oliguric High FENa phosphate & LDH (due to cell lysis)
Trmt: Hydration Alkalination Allopurinol + Febuxostat Recombinant IV uricase
Exogenous toxins that can cause AKI?
NSAIDs Iodinated Contrast Calcineurin Inhibitors Aminoglycosides Crystals Acetaminophen ETOH Lithium
How does NSAIDs cause AKI?
Lab findings?
Inhibit vasodilator prostaglandins -> afferent arteriole vasoconstriction -> medullary ischemia
low FENa (due to afferent arteriolar vasoconstriction) high K + metabolic acidosis due to distal inhibition of K/H secretion
