Chapter
1 – Acute Kidney Injury (AKI)
v History
o AKI can (+) sympt’ of chronic kidney disease (CKD) but for shorter
time: fatig’, ↓ed weight, anorex’, noctur’, sleep disturban’, & pruritus.
o (Important) (+) history of etio’ factors: Volume restrict’ (eg: low fluid intake,
gastroenterit’); Nephrotoxic drugs; Trauma or unaccustomed exertion; Blood loss or transfusions; Toxic agent exposure, eg: ethanol,
& ethylene glycol; Exposure to
mercury vapors, lead, cadmium, or other heavy metals which are encounterable in
welders & miners.
o Higher risk of AKI
if (+): Hypertensi’; Congesti’ ♥ Fail’(CHF); Diabetes; Multiple Myeloma;
Chronic Infection; Myeloprolifer’ ill’; Connective tissue ill’; &
Autoimmune ill’.
o Oliguria general’ favors AKI. Abrupt anuria suggests acute urin’ obstruction, acute & +++
GNephrit', or embolic renal artery obstruction. Gradual’ ↓ed urin’ output ~ indica’ urethr’ strict’ or bladd’
outlet obstruct’ due to prostate enlargem’.
o ↓ed normal nephron
à easy (+) AKI due
to nephrotoxin @ Px w/ chronic renal
insuffici’.
o Can help classify AKI’s pathophysiol’
(prerenal, intrinsic ren, or postrenal fail’) à ~ suggest specific etio’.
o Prerenal fail’
§ Common’ present (+) hypovolem’-related sympt’: thirst, ↓ed urine
output, dizzi’, & orthostatic hypotens’. Look for volume loss ~ due to: emesis, diarrh’, sweati’, polyur’,
hemorrha’. Advanced ♥ fail’ à ↓ ren’ perfus’ à ~ present w/ orthopnea &
paroxysm’ nocturnal dyspnea.
§ Elder w/ vague mental status change is common’ (+)
prerenal or normotens’ ischem’ AKI. Insensib’
fluid loss can lead to +++ hypovolem’ @ restricted fluid access (should suspect @ elder, sedated, or
comatose Px).
o Intrinsic Ren fail’
§ AKI’s etio’ classes: glomerular (indica’
by: Nephritic syndr’ of hematur’, edema, hypertens’); or
tubular (Acute Tubular Necrosis (ATN)
suspect’ @ Pxs presenti’ after period of hypotens’ due to: ♥ arrest, hemorrha’,
sepsis, overdose, or surgery).
§ Nephrotoxin history: all of current
medications, & radiol’ exam’ (radiocontrastant expos’). Pigment-induced AKI suspect @ rhabdomyolysis (myalg’, recent coma,
seizu’, intoxic’, overexercise, limb ischem’), or hemolysis (recent blood transfus’). Allergic interstiti’ nephrit’ suspect’ w/ fever, rash, arthralg’,
& certain drugs (s.as: NSAID, & antibiot’) expos’.
o Postrenal
fail’
§ Usu’ @ Elder ♂ w/ prostat’ obstruction & sympt’ of urgency, frequency,
& hesitan’. ~ present w/ asympt’,
high-grade ((oft’ provides clue: history of gynecol’ surgery or abdominopelvic
malignancy) urin’ obstruction due to chronic sympt’.
§ Flank pain & hematur’ ↑ concern on renal
calculi or papil’ necrosis as etio’ of urin’ obstruction. Acyclovir,
methotrexate, triamterene, indinavir, or sulfonamide ~ crystallize to obstruct tubuli.
v Physic’ Exam’
o Skin
§ ~ (+): Livido reticularis, digit’
ischem’, butterfly rash, palpab’ purpura (sign of System’ vasculit’); maculopapul’ rash (sign of Allergic interstiti’ nephrit’); track marks (IV drug abuse) (sign
of Endocardit’).
§ Petech’, purpura, ecchymos’, & livedo reticularis clues for
inflammato’ & vascul’ etio’ of AKI. Infectious ill’, thrombotic
thrombocytopenic purpura (TTP), DICoagulation, & embolic phenomena can (+) typic’ cutan’ find’.
o Eyes & Ears
§ Eye ~ (+): keratit’, iritis, uveit’, dry conjunctiva (sign
of Autoimmu’ vasculit’); jaundice (sign
of Liver ill’); band keratopathy
(hypercalcem’) (sign of Multiple myeloma);
DMellitus’s signs; hypertension’s signs; atheroemboli (sign of Retinopathy). Find’ suggesti’ of +++
hypertens’, atheroembol’ ill’; endocardit’ ~ (+).
§ Uveitis’s evidence ~ indicate interstiti’ nephrit’
& necrotiz’ vasculit’. Ocul’ palsy
~ indicate ethylene glycol poisoni’ or necrotiz’ vasculit’.
§ Ear ~ (+): hearing loss (sign of Alport disease & aminoglycoside toxicity); mucosal or
cartilagin’ ulceration (sign of Wegener
granulomatosis).
o ♥vascul’ syst’
§ Most important: ♥vascul’ syst’ &
volume status assessm'. Must include: pulse rate & BPressu' measured while standing
& supine; close exam’ of JVein
pulse; careful exam’ of ♥ & lung, skin turgor, & mucous membran’;
assessi’ peripher’ edema.
§ ~ (+): Irregular rhythm’ (atrial fibrilla’) (sign
of Thromboemboli); murmurs (sign of Endocardit’); pericard’ frict’ rub (sign
of Urem’ pericardit’); ↑ed
JVDistenti’, rales, S3 (sign of ♥ fail’).
§ Important @ inPx: accurate daily record of fluid
intake, urine output, & Px weight. If hypovolem’ or +++ ♥ fail’ à hypotens’ (Ø necessari’ sign of
hypovolem’).
§ ♥ fail’ ~ (+)
hypotens’, volume expans’ is (+) & effective ren perfus’ is poor (~ à AKI).
§ +++ hypertens’ w/
ren fail’ suggest 1 of these: renovascul’ ill; GNephrit’; vascul’; &
atheroembol’ ill’.
o Abdomen
§ ~ (+): pulsatile mass or bruit (sign of Atheroemboli); abdomin’ or costoverteb’
angle tendern’ (sign of Nephrolith’,
papillary necrosis, renal artery
thrombosis, renal vein thrombosis); pelvic masses, rectal masses, prostat’ hypertrophy,
bladd’ distenti’ (sign of Urin’
obstruction); limb ischem’, edema (sign of Rhabdomyolys’).
§ Can detect bladd’ obstruction as etio’ of ren fail’.
Epigastric bruit suggests renovascul’ hypertens’ (~ predispose AKI).
o Pulmon’ syst’
§ ~ (+): rales (sign of Goodpasture Syndr’, Wegener
Granulomatosis); Hemoptysis (sign of Wegener
Granulomatosis).
v DDx
o AKI can be (+) @ chronic ren fail’. Find reversibility
of AKI by tracking rate of ren function’s deterioration: if the rate is ↑ed à find & treat the etio’ of the
↑ed rate.
o Changes in urine output general’ correlate poor’ w/
GFR’s changes. ± 50-60% etio’ of AKI are
Øoliguric. Urine output w/ in DDx:
§ Anuria (< 100mL/day) – Urin’ tract
obstruction, ren artery obstruction, Rapid’ Progress’ GlomeruloNephrit’ (RPGN),
diffuse Bilateral Renal Cortical Necrosis (BRCN).
§ Oliguria (100-400mL/day) – Prerenal fail’, hepatorenal
syndr’.
§ Øoliguria (> 100mL/day) – Acute Interstiti’
Nephrit’ (AIN), Acute GNephrit’, partial obstructi’ nephropathy; nephrotoxic
& ischem’ ATN, radiocontrast-induced AKI, & rhabdomyolysis.
o Abdominal aneurysm
o Alcohol toxicity
o Alcoholic ketoacidosis
o Chronic renal failure
o Dehydration
o Diabetic ketoacidosis
o Gastrointestinal (GI) bleeding
o Heart failure (♥ fail’)
o Metabolic acidosis
o Obstructive uropathy
o Protein overloading
o Renal calculi
o Sickle cell anemia
o Steroid use
o Urinary obstruction
o Urinary tract infection
o Acute Tubular Necrosis
o Azotemia
o Chronic Kidney Disease
o Emergent Management of Acute Glomerulonephritis
o Hemolytic Uremic Syndrome in Emergency Medicine
o Henoch-Schonlein Purpura (HSP) in Emergency Medicine
o Hyperkalemia
o Hypermagnesemia
o Hypernatremia
o Hypertensive Emergencies
v Workup
o Can help assess AKI’s etio’ & aid in proper Tx:
CBC; serum biochemistry; Urine analysis
w/ microscopy; urine electrolytes.
o Ren imaging can be useful in some cases, espec’ @ ren
fai’ due to obstructi’. American College
of Radiology recommends Doppler method of USG as most appropriate imaging
method in AKI.
o Ren Funct’ Studies
§ (Rate of ↑ depends on level of renal insult; BUN’s also
affected positively by protein intake) ↑ed
BUN & creatinine, hallmarks of ren fail’. BUN ~ ↑ed @ GI or mucosal
bleed’, steroid Tx, or protein loading
§ BUN:creatinine can > 20:1 in (+) ↑ reabsorp’ of
urea (eg: @ volume restrict’); this suggests prerenal AKI.
§ Assumi’ Px has no renal funct’:
· BUN’s rise in 24
hours is rough-predictab’ by this formula: [[24-hour
protein intake in milligrams][0.16]/[Total body water in mg/dL]] added to
BUN value.
· Creatinine’s rise
is predictab’ by this formula:
o For ♂: [[weight in kilograms][28 -
0.2(age)]/[Total body water in mg/dL]] added to creatinine value.
o For ♀: [[weight in kilograms][23.8 -
0.17(age)]/[Total body water in mg/dL]] added to creatinine value.
§ (General rule) if creatinine gets to > 1.5mg/dL/day à rule out rhabdomyolysis!
o CBC, peripher’ smear, & sero’
§ Peripher’ smear ~ (+) schistocyt’ in conditions s.as
Hemolytic Uremic Syndr’ (HUS) or
TTP. ↑ed roleaux formation suggests multiple
myeloma (should direct workup toward serum & urine’s
immunoelectrophoresis).
§ (These + related find’ aid defini’ AKI’s etio’):
· Myoglobin or free
Hemoglobin (Hb) ((+) @ eg: pigment
nephropathy).
· ↑ed serum uric acid ((+) @ eg: tumor lysis syndr’).
· ↑ed Serum LDH ((+) @ eg: ren infarc’).
§ Serolo’ tests (only if indicated): Complement Levels;
Antinuclear antibody (ANA);
Antineutrophil cytoplasmic antibody (ANCA);
Anti-glomerular basement membrane (anti-GBM) antibody; Hepatitis B and C virus
studies; Antistreptolysin (ASO).
o Urinalysis
§ (+) tubular cells or their casts à supports ATN’s Dx (oft’ + oxalate crystals).
(Figure right below) Sloughing of cells à (+) granular, muddy brown casts à high’
sensitive of tubular necrosis.
§ Reddish or dark brown urine suggests (+)
myoglobin or Hb, espec’ @ (+) dipstick for heme & no RBC @ microscopy. On
Dispstick, ~ (+) signifi’ proteinur’ due to tubular injury.
§ In urine: eumorphic RBCs suggests
collecting system’s bleed’; dysmorphic
RBCs or RBC casts indicate glomerulit’; WBCs or WBC casts suggest pyelonephritis or AIN; (+) eosinophil, Ø necessari’ (+) allergic interstiti’
nephrit’, but helps its Dx.
§ On wright stain or Hansel stain, (+) eosinophil (also (+) @ urinary tract infections
(UTIs), GN, & atheroembolic ill’) suggests interstiti’ nephrit’.
§ (+) uric acid crystal ~ represent ATN
relat’ to uric acid nephropathy. Usu’ (+)
calcium oxalate @ ethylene glycol poisoni’.
o Fractional Exretion of Sodium & Urea (FENa &
FEUrea)
§ Sodium
· Interpret’ @ Px w/
Øoligur’ states, GN, or use diuretics can
lead to misDx.
· FENa only useful
in AKI if (+) oligur’. FENa (%) = [[UNa/PNa]/[UCr/PCr]].
@ Prerenal azotem’, FENa usu’ < 1%. In
ATN, FENa > 1% (except: @ ATN due to radiocontrast nephropathy, +++ burns,
acute GN, & rhabdomyolysis).
· If (+) liver ill’, FENa can be < 1% @ (+) ATN. Diuretic ~ cause FENa > 1% à FENa can’t be sole predictor of AKI.
§ Urea
· Diuretic Ø affect urea transport, thus also Ø affect
FEUrea. FEUrea < 35% is suggests prerenal state. FEUrea (%) = [[UUrea/PUrea]/[UCr/PCr]].
o Bladd’ Pressu’
§ (Considered normal) Intraabdomin’ pressu’ < 10 mmHg
suggest
AKI Ø due to abdomen compartment syndr’. (Abnormal)
Intraabdomin’ pressu’ > 10 mmHg (if it’s 15-25 mmHg à particular risk for abdomen compartment syndr’). Intraabdomin’ pressu’ > 25 mmHg à suspect AKI due to abdomen
compartment syndr’.
o Emerging Biomarker
· ↑ed creatinine (reflects +++’ ↓ed glomerular filtration
rate (GFR)), late marker of renal dysfunct’.
· Urine neutrophil gelatinase-associated lipocalin (NGAL), detects AKI @ Px w/ ♥pulmon’
bypass surgery.
· Plasma B-type natriuretic peptide (BNP) & NGAL, predictors of
early AKI in lower respirat’ tract infection (LRTI). BNP > 267 pg/mL or NGAL > 231 ng/mL suggests AKI (94%
sensitivity, 61% specificity).
o Ultrasonography (USG)
· Hydronephrosis’s degree on USG Ø necessari’
correlate w/ obstruction’s degree. Small ren suggests chronic ren fail’.
· Doppler USG
o For detecting (+) & nature of ren blood flow (↓ed
@ prerenal, & intrarenal AKI). Quite useful for Dx of thromboembolic & renovascul’ ill’. ↑ed resistive indices’re observable @ hepatorenal syndr’.
o Nuclear Scanning
· Radionuclide imaging w/ technetium-99m-mercaptoacetyltriglycine
(99m Tc-MAG3), 99m
Tc-diethylenetriamine penta-acetic acid (99m
Tc-DTPA), or iodine-131 (131
I)-hippurate can be used to assess renal blood flow, tubular funct’. (+)
marked delay in tubular excretion of radionuclide in prerenal & intrarenal AKI, limiting nuclear scans’s value.
o Aortorenal Angiography
· Can help in Dx of renovascul’ ill: renal artery
stenosis; renal atheroembol’ ill; atheroscleros’ w/ aortorenal occlusi’;
certain cases of necrotizi’ vasculit’ (eg: polyarterit’ nodosa).
o Renal Biopsy
· Can be used to identify AKI’s intrarenal causes, justifiab’ if
results ~ change Tx (eg: initiati’ of immunosupression). Also ~ indicated if (+) prolong’ ren dysfunct’, & prognosis’s needed to develop long-term
Tx. Ren biopsy (+) unexpected Dx @ 40%
cases.
· Acute cellu’ or humoral rejecti’ in transplanted ren is definitiv’ diagnosab’ by ren biopsy.
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