Acute Kidney Injury Flashcards
Group of dx that all result in ￬ GFR and subsequent ￪ BUN and/or serum Cr, often with ￬ urine volume
AKI
by the time serum Cr rises, GFR usually has already fallen significantly
AKI Criterias
- KDIGO - Most recent, most preferred
- RIFLE Criteria - Risk, Injury, Failure, Loss, ESRD
- AKIN (Acute Kidney Injury Network) Criteria
- All correlate with prognosis in AKI patients
Increase by 1.5-1.9x baseline w/n 7 d OR increase by >0.3 mg/dL w/n 48 hrs
<0.5 mL/kg/h x 6-12 hrs
what is this KDIGO stage?
1
increase by 2-2.9x baseline
<0.5 mL/kg/h for >12 hrs
what is this KDIGO stage?
2
increase by >3x baseline, >4mg/cK, OR pts <18 y/o with decrease in estimated GFR to <35 mL/min/1.72m2
<0.3 mL/kg/h for >24 hrs OR anuria for >12 hrs
what is this KDIGO stage?
3
normal urine output amount
800-2000 mL/day
< 50 mL/24 hrs of urine output is considered what?
anuria
Ominous finding!
Acute obstruction, cortical necrosis, aortic dissection, etc.
< 400 mL/24 hrs of urine output is considered what?
Oliguria
Poor prognostic sign in AKI
Higher mortality and poorer recovery than non-oliguric AKI
excessive urine (2500 - 3000 mL/day +) is considered what?
Polyuria
￪ nitrogenous wastes in the blood
is called what?
Azotemia
nonspecific sx caused by elevated nitrogenous waste (esp urea) in the blood is called what?
what are the sx?
Uremia
General - weakness, fatigue
Neuro - tremors, seizures, encephalopathy, confusion, coma
Skin - itching, dryness
CV - pericardial effusion, pericarditis, HTN
GI - anorexia, N/V
Other - shallow breaths/tachypnea, metabolic acidosis
risk factors for AKI
- renal problems
- History of CKD or AKI
- Single functioning kidney - meds
- ACEIs or ARBs
- Antimicrobials - Aminoglycosides, Amphotericin B, PCNs, Vancomycin
- Immunosuppressants - Cyclosporine, Methotrexate
- Diuretics
- Iodinated contrast agents
- NSAIDs
- PPIs - hypoperfusion
- Hypovolemia - Trauma, hemorrhage, GI loss
- Sepsis - Comorbidities
- HF, Liver disease, DM, BPH
- Infection (renal or systemic)
- Cancer
- >65 y/o
what can determine the risk of developing mod-severe AKI in next 12 hrs in critically ill patients
NephroCheck - emerging technology
MCC of AKI (40-80%)
Caused by renal hypoperfusion
Prerenal azotemia
major categories of AKI
- Prerenal azotemia
- Intrinsic kidney injury
- Postrenal obstruction
Up to 50% of all cases of AKI
Direct injury to 1+ renal structures
Intrinsic kidney injury
LCC of AKI (5-10%)
Caused by obstruction of urinary flow
Postrenal obstruction
causes of Prerenal Azotemia
Inadequate renal perfusion
1. Hypovolemia - dehydration, hemorrhage, GI loss, diuresis, pancreatitis, burns, peritonitis, etc.
2. Decreased CO - decompensated HF, cardiogenic shock, PE, pericardial tamponade, arrhythmias, liver failure (hepatorenal syndrome)
3. Changed vascular resistance
- ￬ - sepsis, anaphylaxis, anesthesia
- ￪ - EPI, high-dose dopamine, RAS
- Meds interfering renal vascular autoregulation - NSAIDs, iodinated contrast, ACEIs/ARBs
￬ GFR and ￪ BUN/Cr with BUN:Cr ratio > 20:1 is usually seen in what category of AKI
Prerenal Azotemia
for prerenal azotemia, If oliguric, there should be a ____ fractional excretion of sodium (FENa+) in the urine
low - <1%
Kidney can still reabsorb sodium
Often have normal urine osmolality
what would the urinary sediment look like with prerenal azotemia
usually normal
may see hyaline casts - Formed from Tamm-Horsfall mucoprotein secreted by tubule
s/s of prerenal azotemia
- Uremia is possible (depending on stage)
- Signs of cause - vary, may include:
- Dehydration and/or hypovolemia
- Arrhythmias, cardiomegaly
- Sepsis - Nonspecific diffuse abdominal pain and ileus
- May see decreased urine output
tx for prerenal azotemia
- resolve underlying cause
- Maintain euvolemia
- Correct abnormal electrolytes
- Avoid nephrotoxic drugs
Obstruction of urinary outflow can affect the kidneys how?
Postrenal Obstruction
- Affecting both kidneys or a single functioning kidney
- Affecting one kidney and the second kidney cannot compensate
Elevated intraluminal pressure → damaged renal parenchyma
causes of postrenal obstruction
Obstruction of urethra, bladder, ureters, or renal pelvises
1. In men - BPH MCC
2. Devices - Obstructed Foley catheter
3. Meds - anticholinergic
4. Other causes - cancer, retroperitoneal fibrosis, neurogenic bladder
- Rare - blood clots, stones or strictures of the urethra or bilateral ureters, bilateral papillary necrosis
s/s of Postrenal Obstruction
- Anuria or polyuria possible
- May have lower abdominal pain
- May see large prostate, distended bladder, pelvic/abdominal mass
what can be helpful to look for hydroureter and obstruction
Bladder catheterization and/or abdominopelvic US
lab findings of postrenal obustrction
- ￬ GFR and ￪ BUN/Cr with BUN:Cr > 20:1 usually
- Urine sodium - varies
- Urine osmolality - 400 mosm/kg or less
- Urine sediment - often normal; may see RBCs, WBCs, crystals
intrinsic kidney injury is usually caused by ?
direct damage
infections, sepsis, nephrotoxins, ischemia
possible sites of intrinsic kidney injury?
tubules, glomeruli, interstitium, vasculature
in many causes, what is a precursor cause of tubular injury?
prerenal azotemia
3 types of intrinsic kidney injury
- acute tubular necrosis (MC)
- acute glomerulonephritis
- acute interstitial nephritis
AKI due to tubular damage
acute tubular necrosis (ATN)
85% of intrinsic AKI
3 causes of ATN
- ischemia - inadequate GFR and blood flow
- prolonged hypotension or hypoxemia - nephrotoxins - endo- or exogenous
- EXO MC - sepsis - both hypoperfusion and direct injury
what are the exogenous nephrotoxins that cause ATN (6)
- aminoglycosides: up to 30% of pt
- 5-7 days of tx
- Can remain in renal tissues up to 1 month
- Trough levels are most useful to predict toxicity - amphotericin B - >2-3g
- other antimicrobials
- abx - vanc, sulfonamides, cephalos, tetracycline
- Antivirals - acyclovir, foscarnet - radiographic contrast media
- Pre-existing DM and kidney dysfunction poses greatest risk (15-50%) - chemo/immunosuppressant - MTX, cyclosporine, cisplatin
- environmental toxins
- Heavy metals
- Ethylene glycol
- Insecticides/herbicides
what aminoglycoside is least nephrotoxic
Streptomycin
what may reduce the risk of exogenous nephrotoxin from radiographic contrast media?
3 mL/kg/hr IV 0.9% NS over 4-6 hrs before and after contrast
due to rhabdomyolysis, muscle necrosis causing ATN
Myoglobinuria
what can cause myoglobinuria that eventually leads to endogenous nephrotoxins
- Directly damaging to tubules; can also cause tubule obstruction
- Crush injury, muscle necrosis from prolonged unconsciousness
ATN from directly damaging to tubules can lead to a CK of ?
> 20,000-50,000 IU/L
what can happen to the urine with Myoglobinuria - ATN
- false (+) dipstick for hemoglobin
- appears dark brown, but has no RBCs on microscopy
tx for ATN - Myoglobinuria
-
rehydration
- Hypocalcemia may occur but usually self-corrects with rehydration
— No calcium replacement needed unless severe or symptomatic
- Hyperkalemia, hyperphosphatemia, hyperuricemia may also occur
what endogenous nephrotoxin is seen in transfusion reactions and hemolytic anemia
Hemoglobinuria
tx for Hemoglobinuria ATN
Reversal of underlying disorder, hydration
which endogenous nephrotoxin is seen in rapid cell turnover and lysis
hyperurcemia
usual cause of hyperuricemia
chemo for germ cell neoplasms, leukemia, lymphoma
Intratubular deposition of ___ causes hyperuricemia ATN?
uric acid crystals
Serum uric acid often > 15-20 mg/dL
Medications to lower uric acid level can help
what endogenous nephrotoxin is directly toxic, obstructs tubules that causes ATN
Seen in association with multiple myeloma
Bence Jones Protein
s/s ATN
Signs of underlying cause
May see arrhythmias, abdominal pain, uremia
Oliguric or nonoliguric
labs for ATN
- Hyperkalemia and hyperphosphatemia MC
- ￬ GFR and ￪ BUN/Cr with BUN:Cr < 20:1 usually
- Urine Na elevated
- Urinary sediment - pigmented granular casts or “muddy brown” casts, renal tubular cells, epithelial cell casts
tx for ATN
remove cause, avoid complications
1. Avoid volume overload and hyperkalemia
- Volume overload - loop diuretics or dialysis (if persistent/severe)
— Diuretics not shown to improve recovery or reduce risk of death
- No improvement in outcomes with diuretics in oliguric AKI
2. Dietary changes
- Protein restriction - to prevent metabolic acidosis
- ￪ or ￬ dietary phosphate, calcium, magnesium
MCC of acute glomerulonephritis
nephritic
almost all acute glomerulonephritis involves the development of ?
inflammatory glomerular lesions
crescent lesions = severe breaks in glomerular walls
pt comes in with HTN, edema, and urine containing protein, RBCs, WBCs, and RBC casts
what is most likely the diagnosis?
acute glomerulonephritis
what are the types of acute glomerulonephritis
- Immune Complex Deposition
- Anti-GBM-associated acute glomerulonephritis
- C3 Glomerulopathy
- Monoclonal Ig-Mediated Glomerulonephritis
- Pauci-Immune Glomerulonephritis
when antigen excess over antibody production occurs
what type of acute glomerulonephritis?
Immune Complex Deposition
what lodge in glomerular basement membrane (GBM) that causes immune complex deposition?
antigen-antibody complexes
Complement activation to resolve complexes → destruction of GBM
MCC of Immune Complex Deposition
1. post-infectious - endocarditis and strep
2. autoimmune disease - lupus
3. IgA nephropathy (Berger disease)
4. membranoproliferative (MPGN)
5. cryoglobulinemic glomerulonephritis (HCV)
Autoantibodies against glomerular basement membrane (GBM)
May be confined to kidney or involve lungs as well
what type of acute glomerulonephritis
anti-GBM-associated acute glomerulonephritis
Can cause pulmonary hemorrhage
what type of acute glomerulonephritis is renal + pulmonary involvement
Goodpasture’s Syndrome - Anti-GBM-associated acute glomerulonephritis
deposition in the glomerulus, +/- Ig deposition
Minimal role played by immunoglobulins, unlike other GN
Caused by abnormalities in the alternative complement pathway
what type of acute glomerulonephritis?
C3 Glomerulopathy
(C3 deposition)
what lab can help identify C3 glomerulopathy
Low serum C3 levels
normal C3 DOES NOT r/o
deposited in GBM and/or tubular basement membrane
No excess amounts of antigen as seen in immune complex GN
Associated with monoclonal gammopathies
what type of acute glomerulonephritis?
Monoclonal Ig-Mediated Glomerulonephritis
what can help identify Monoclonal Ig-Mediated Glomerulonephritis, and what other tests?
- Serum Protein Electrophoresis (SPEP)
- immunofixation and free light chain analysis
small-vessel vasculitis associated with ANCAs
Can see manifestations in other areas of the body
Tissue injury secondary to cell-mediated immune processes
what type of acute glomerulonephritis?
Pauci-Immune Glomerulonephritis
Other Causes of pauci-immune glomerulonephritis besides cell-mediated immune processes
HTN emergencies, thrombotic microangiopathies (HUS, TTP)
pt comes in with severe HTN and swelling of his scrotum, what is the most likely diagnosis?
Acute Glomerulonephritis
Often have HTN and edema
Edema seen first in body parts with low tissue tension - Scrotal edema, periorbital edema
potential labs to get and their results of glomerulonephritis
- Serum Cr rises over days - months
- BUN:Cr ratio not reliable kidney fxn marker, but can help assess volume status - Urinalysis - hematuria, moderate proteinuria
- Urine sediment - RBCs, WBCs, RBC casts
- Complement levels - low levels may help
- C3 and C4 low in immune complex GN
- C3 alone low in C3 glomerulonephropathy - ASO titers - help evaluate for recent strep infection
- anti-GBM antibodies
- SPEP
- P-ANCA and C-ANCA levels
- Other general autoimmune labs - CRP, ESR, ANA
tx for acute glomerulonephritis
- underlying disease process!
- High-dose corticosteroids
- Cytotoxic agents may be used
- Plasma exchange - Goodpasture disease, pauci-immune glomerulonephritis
Interstitial inflammatory response
Edema and possible tubular damage
Cell-mediated immune reactions predominate
what type of intrinsic AKI?
Acute Interstitial Nephritis
causes of acute interstitial nephritis
- meds (MC)
- Antimicrobials - PCNs (β-lactams), cephalosporins, rifampin, sulfonamides, HIV drugs
- Others - diuretics, NSAIDs, rifampin, anticonvulsants, allopurinol, PPIs, H2 blockers - Infections -
- Bacterial - strep, staph, diphtheria, legionella, rickettsia (RMSF)
- Viral - CMV, EBV
- Fungal - histoplasmosis - Immunologic - SLE, Sjogren’s, sarcoidosis, etc.
- MCC glomerulonephritis - Others - allergic reaction, collagen vascular disease
fever, rash, arthralgia is the classic triad for what intrinsic AKI?
Acute Interstitial Nephritis
labs of Acute Interstitial Nephritis
- CBC - eosinophilia
- Urine sediment - WBCs (95%), RBCs, eosinophiluria, WBC casts
- < proteinuria unless NSAID-related - Renal biopsy - inflammatory cells within renal interstitium
tx for Acute Interstitial Nephritis
-
removal of cause, supportive care
- IV or oral corticosteroids if renal injury
persists
- Urgent dialysis may be necessary in up to ⅓ of all pts
Serum BUN:Cr - > 20:1
Concentration of Na - < 20
Fractional Excretion of Na - < 1%
Osmolality (mosm/kg) - > 500
Urine Sediment - Benign or hyaline casts
what type of AKI?
Prerenal Azotemia
serum BUN: Cr > 20:1
Na concentration Varies
fractional excretion of Na Varies
osmolality - < 400
urine sediment - Benign or RBC, WBC, crystals
what type of AKI?
Postrenal Azotemia
BUN:Cr < 20:1
Na concentration > 20
fractional excretion of Na > 1% (if oliguric)
osmolality 250-300
urine sediment - Granular (muddy brown) casts, renal tubular casts
what type of AKI
ATN - intrinsic kidney injury
BUN:Cr > 20:1
[Na] < 20
fractional excretion of Na < 1%
osmolality Varies
urine sediment - RBC, WBC, RBC casts
what type of AKI
Acute Glomerulonephritis
Intrinsic Kidney Injury
BUN:Cr < 20:1
[Na] Varies
fractional excretion of Na < 1%
osmolality Varies
urine sediment - RBC, WBC, WBC casts, eosinophiluria
what type of AKI
Acute Interstitial Nephritis
Intrinsic Kidney Injury
other diagnostic tools for AKI
- Abdominal/Pelvic US
- Most AKI - normal-sized kidneys
- Acute interstitial nephritis - Enlarged kidneys
- Hx of CKD - normal, or may see small or polycystic kidneys
- Postrenal AKI - May see dilated urine collecting system proximal to point of obstruction - Urethral Cath - r/o urethral obstruction
- Bladder Scan - r/o urethral obstruction
- Kidney Biopsy
- Primarily when prerenal, postrenal, and ischemic/nephrotoxic AKI etiologies have been ruled out
- Can help dx glomerulonephritis, vasculitis, interstitial nephritis, etc.
