Acute Renal Failure (acute kidney injury) Flashcards
Renal function
o Filtration, Reabsorption, Secretion, Excretion
o 21% cardiac output - 0.4% body weight
o Require adequate perfusion
o Functional unit = nephron
o Glomeruli -> ultrafiltrate -> tubules
o Tubules resorb/secrete solute, H2O
“ End product passed to collecting system
o 750ml-2L/day: homeostatically perfect urine
acute renal failure of acute kidney injury
o Defined - precipitous decline in renal filtration function
o Characteristics:
“ Rise in serum creatinine from baseline
“ Decreased GFR
“ Alteration in urine output, concentration
“ Active urine sediment - casts
“ Changes in urine sodium concentration
who gets acute renal failure and whos at risk
o Renal perfusion alterations
“ Hypotension (shock), hypovolemia (volume loss)
o Diabetics, HTN: early end-organ damage
o Kidney injury: drugs, contrast, trauma
o Rheumatologic/Collagen Vascular Dz: progression
o Intrinsic Kidney Disease
o Blood pressure will alter perfusion rates through the kidney
kidney problems - markers
o UA micro and Chem Panel
“ First clues to presence of Dz
o Volume: definitions
“ Polyuria: >2500ml/24hrs
“ Oliguria: <500ml/24hrs
“ Anuria: <100ml/24hrs
o Concentration (specific gravity)
“ On dipstick/UA: 1.005-1.020
“ Sick kidneys don’t concentrate normally
o Urine sediment on micro
“ Active or bland? Casts or no casts?
o Serum Creatinine
“ Chem panel: 0.6-1.2mg/dl
“ Skeletal muscle, diet
“ Filtered and secreted, balanced amount in serum - normally
“ Increase = glomerular/tubular injury/Dz
“ Indicates Dz presence - not etiology of problem
“ Rises late: GFR already reduced by ~50%
“ Normal creatinine does not equal normal GFR
o Cbc contributes NOTHING to kidney function
o These are the first clues that kidney problems are present
o Dialysis patients are usually the people with anuria
o Small increases in creatinine are a big deal
o If you have a rise in creatinine on chem panel, you already have a GFR reduction of 50% because creatinine rises later on in the liver disfunction situation
kidney function - markers
o BUN: Blood Urea Nitrogen " Chem panel: 5-20mg/dl " Nitrogenous waste from cellular protein breakdown " Elevated in: dehydration renal dz, GI bleeding, etc o BUN to Creatinine Ratio " Helpful in determining etiology of AKI o Urine Microalbumin " Albumin to creatinine ratio o Glomerular Filtration Rate " GFR is estimated (120mL/min) " Calculations - not exact " Reduction implies renal Dz " Progression is marker in CKI " Increase = improvement o Cystatin C w/ creatinine " May be useful in early Dz o BUN to creatinine ratio is usually about 10:1 í that's normal o CKI í chronic kidney injury
Azotemia and uremia
o Terms that describe degree of failure
o Azotemia
“ Retention of nitrogenous wastes
“ Inadequate renal filtration, decreased GFR
“ Increased creatinine, renal “insufficiency”
o Uremia
“ Severe azotemia, renal “failure”
“ Creatinine high, GFR very low
“ Clinical symptoms/consequences of renal failure
Disease duration - key to ddx
o Acute - hours to days
o Rapidly progressing - weeks to months
o Chronic - progressive, months/years
“ May have acute insult on chronic failure
o Compare UA, creatinine from previous
“ No previous? Sx duration
o Hospitalized pt’s close monitoring - daily
“ Monitor events - hypotension, drugs, contrast
o You can have an acute hit to your renal function while having chronic kidney
Causes of ARF/AKI
o Think - where in the system?
o Prerenal
o Intrarenal (Intrinsic)
o Postrenal
o How do you think about acute kidney injury í how do you characterize it
“ Is it prerenal, intrarental, or postrenal
Prerenal causes of ARF/AKI
o Think - hypoperfusion o Hypotension - low vascular resistance " Shock - all forms " Medication induced o Volume depletion - intravascular " Dehydration, blood loss (trauma, GI) " "third spacing": burns, hypoalbuminemia o Decreased cardiac output " MI, CHF, arrhythmias, PE, etc.. o Low blood pressure
prerenal AKI
o Most common form - 50-80%
o Acute time course - creatinine elevated
o BUN to Creatinine Ratio =/>20/1
o Glomeruli, tubules are intact
o “Bland” sediment (no casts)
o Most prerenal AKI is reversible if treated promptly
“ GFR will return to near normal if reversed
o Acute prerenal on chronic renal failure
Intrarenal/intrinsic causes
" Structural injury/insult to kidney itself o Prerenal, postrenal causes excluded " Glomerular " Tubular " Vascular
Intrarenal cause - clomerular
o AGN: Acute glomerulonephritis
“ Hx, UA, urine sediment key to DDx
“ Postinfectious, rheum, IgA nephropathy, hereditary Dz, DM, etc
“ BUN to Creatinine ratio also =>20/1
“ Focal or diffuse glomerular damage
“ Focal: mild AKI - dysmorphic RBC’s, red cell casts (nephritic), mild proteinuria
“ Diffuse: signif AKI - nephritic w/ heavy proteinuria (nephrotic), HTN, edema
Intrarenal causes - tubular
o ATN - Acute tubular necrosis
“ Most common cause intrinsic AKI - 80%
“ Common in hospitalized pt’s
“ **Prerenal AKI not resolving with volume
“ BUN to Creatinine ratio <20/1 (10/1 common)
“ Increase in urine Na - >2%
“ Active sediment
“ “Muddy brown” granular & epithelial cell casts
“ Nephrotoxins: Abx, IV contrast, etc…
“ Ischemia: sepsis, rhabdomyolysis, burns, heat stroke, venomous bites
“ Most common kidney infection í prerenal
“ Most common intrarenal = acute tubular necrosis
o AIN - Acute interstitial nephritis
“ Drugs (NSAID’s, Abx), long list
“ Infections, autoimmune disorders
“ Fever, rash, eosinophilia
“ Active sediment - white cell casts
“ White, red cells, variable proteinuria
“ BUN to Creatinine ratio <20/1
“ Dx - renal biopsy but…consider temporal relation to drugs, stop the offender, monitor
“ Rash = vasculitis
Intrarenal causes: vascular
o Large Vessel Dz:
“ Malignant HTN, renal artery occlusion, emboli
o Small Vessel Dz, Vasculitis common
“ Thrombocytopenia (HUS/TTP)
“ Hemolytic uremic syndrome (HUS)
“ Thrombotic thrombocytopenic purpura (TTP)
“ Scleroderma
o Malignant HTN í blood pressure that increases so rapidly that it causes acute end organ damage
Postrenal causes
o Think: obstruction of urine flow out o Anywhere, eminently reversible o Must obstruct both kidneys to cause ARF " Unless the pt has only one… o Prostatic Dz, malignancy - common o Stones, blood clots, crystals
estimating GFR @ bedside
o Cockcroft-Gault: Creatinine Clearance (CrCl)
“ Best for CKD, may overestimate GFR (uses old creatinine assays)
“ ((140-Age) X (weight in kg)) / (serum creat X 72)
“ Normal: 90-140ml/min males; 80-125 females (X 0.85)
o MDRD equation: Modification of Diet in Renal Disease
“ More accurate than CrCl; best for CKD, not acute; commonly used
“ 175 x serum creat x age Add calc: (x .742(F)); (x 1.210(AA))
“ GFR >90 normal, GFR <60 abnormal
estimating GFR
o CKD-EPI: Chronic Kidney Dz Epidemiology Collaboration
“ Better in mild Dz; better for risk prediction
“ Recently: better than CrCl or MDRD
“ GFR = 141 * min(SerumCreat/kappa, 1)alpha * max(SerumCreat/kappa, 1) -1.209 * 0.993Age * Sex * Race
“ Use a calculation app…
o Other methods:
o Serum Cystatin C
“ Alternative to creatinine-based calculations
“ Studies: best in conjunction with creatinine - not superior to others
o Pediatric GFR
“ Schwartz formula
o 24hr urine Creatinine Clearance
Assessing tubular function
o Tubular function assessed by solute concentration in urine over 24hrs. Especially Na " Sodium retention = prerenal " Sodium dumping = sick tubules o Urine osmolarity o Urine Na concentration o Fractional Excretion of Na - FENa
Calculating FENa
” FENa = fractional excretion of sodium
“ Distinguishes ATN from Prerenal AKI
o Best in advanced AKI only
“ Urine Na X Plasma Creatinine/Plasma Na X Urine Creatinine X 100 (as %)
“ Prerenal, AGN <1%
“ ATN: usually high, =/>3%, AIN variable: 1-3%
“ Postrenal =/>1%
Summary of AKI etiologies - prerenal
o Prerenal " BUN/creatinine ratio 20/1 or greater " High urine specific gravity >1.020 " Urine osmolality high >500 " Urine Na <20 " FENa <1% (kidney retaining Na) " Inactive/bland urine sediment " Oliguria
Summary of intrarenal AKI
" AGN o BUN/creatinine ratio >20/1 o Specific gravity variable o Urine osmolality high >500 o Urine Na <20 o FENa <1% o Urine sediment active - RBC casts o Variable urine output o Similar to Prerenal - except the casts o ATN and AIN " BUN/creatinine ratio <20/1 (10/1) " Low urine specific gravity, brown urine " Urine osmolality <300 " Urine Na >20 " FENa usually high " Active sediment - Casts: WBC, fatty, muddy brown granular " Oliguria/anuria
Summary - postrenal
o Variable amount and specific gravity o Hematuria common o BUN/creatinine ratio 10/1 or higher o FENa usually normal o Sediment usually normal - no casts
Workup of AKI patient - hx
” Elicit Sx’s/Hx of pre-, post- or intrarenal
“ Volume loss: dizziness, syncope
“ Urinary abnormalities
“ Systemic - malaise, edema, weakness, n/v
“ Recent illness, new meds, travel, contrast or instrumentation
Workup of AKI patient - PE
” Toxic or not? Vitals: fever, hypotension, tachy?
“ Skin - rash, pettechiae, excoriations
“ HEENT - dehydration
“ Lungs/heart
“ Abdomen - flank pain, bladder, prostate
“ Extremities - edema
“ Neurologic - weakness, reflexes
Workup of AKI patient - labs
" Urine - dip, UA w/ micro, culture " Chem panel, CBC " Spot albumin to creatinine ratio " Urine microalbumin " Calculate CrCl, GFR " 24hr urine collection " Urine Na, urine creatinine, urine osmolarity " FENa
Diagnostics and treatment of prerenal and intrarenal
o Prerenal " Correct volume status, hypotension " Correct source of problem " IV fluids, Abx for sepsis, etc… " Consider admission " Serial BUN/creatinine, urine volume " No need for acute diagnostic imaging " (except to investigate cause) o Measure ins and outs í urine volume vs. intake o Intrarenal " Pre- and postrenal causes eliminated " Consider admission " Remove/Tx the offender if present " Renal ultrasound first " CT scan of abdomen/pelvis " Referral to nephrologist for renal biopsy " Biopsy detects glomerulonephritis, interstitial nephritis, vasculitis
Diagnostics - renal biopsy
o Indications
“ Glomerular hematuria with proteinuria
“ Nephrotic syndrome
“ Acute nephritic syndrome
“ Unexplained acute/subacute renal failure
o Percutaneous procedure - bleeding common
o Contraindications - prior bleeding Dz, hydronephrosis, severe HTN, infection
diagnostics- postrenal
o Postrenal: identify cause of obstruction
“ Post-void residual useful - ultrasound
“ Catheter to relieve retention
“ Renal ultrasound to evaluate size, hydronephrosis, structural abnormalities
“ CT abd/pelvis w/o contrast for stones, with contrast for tumors
“ Urologist vs. nephrologist
o Hydronephrosis is painful, not crying but in pain
o Urologist take care of stuff past the kidneys
o Nephrologists take care of kidneys
when to admit/refer
o Admit new ARF if symptomatic or severe - new creatinine >2.0 above pt’s baseline
o Consult nephrologist early
o Outpatient work-up if stable, subacute
o Admit worsening chronic renal failure when symptomatic
o Admit if prerenal on top of chronic renal fail
Chronic renal failure
o Chronic Kidney Disease - CKD
o End-Stage Renal Disease - ESRD
Overview of CKD
o Rarely reversible decline in kidney function - progressive, months to years
o Initial injury or chronic insults
o Often asymptomatic as kidneys compensate
o Small kidneys - hallmark of CKD
o Nephrons hypertrophy then become sclerotic
o Nephrons are useless, they do not regenerate
o Hallmark is small kidneys
o You have about a million nephrons to begin with
Staging of CKD
o National Kidney Foundation Dialysis Outcomes Quality Initiative (K/DOQI) o Structural or functional kidney abnormalities for >3 months " Includes abnormal UA, imaging, biopsy o OR: GFR <60 for >3 months " With or without evidence kidney damage o K/DOQI: o Stage 1 - GFR >90 - Tx comorbid Dz o Stage 2 - GFR 60-89 - follow progress o Stage 3 - GFR 30-59 - Tx complications o Stage 4 - 15-29 - prepare for dialysis o Stage 5 - <15/dialysis - transplant o Stage 1 is normal o Stage 3 is where you are in the non normal range
Who gets CKD
o Diabetes - 30-40%
o Hypertension - 25-30%
o Glomerular Dz - 15-20%
o Genetic renal Dz, other - the rest
Labs for CKD
o Follow the usual suspects o BUN/creatinine - progressive increases " Compare with prior, track changes o Estimate GFR to stage pt o Monitor serum electrolytes - esp K+ o Imaging " Renal ultrasound - small kidneys " Plain x-rays - renal osteodystrophy " Subperiosteal resorption = hyperparathyroidism " Not used routinely for clinical staging
Complications of CKD/ESRD
o Affects nearly all organ systems
o Cannot predict when Sx’s or complications will occur from Creatinine or GFR
o Azotemia first
o Frank uremia
“ Not a lab value or toxidrome
“ “Constellation” of symptoms
o You cannot predict when (by creatinine or GFR) you will get symptoms
o Constellation of symptoms = all the symptoms together
complications of ESRD
o Hyperkalemia
“ Life threatening - K+ > 6.0 (get EKG)
“ GFR usually <10-20ml/min (<10%)
“ Pt usually oliguric
“ Causes: dialysis non-compliance a big cause
“ Dietary indiscretion
“ NSAID’s, ACE Inhibitors, beta blockers
“ Trauma, acidosis
o Anion gap metabolic acidosis
“ ESRD pt’s chronically acidotic - events causing added acidosis are bad
“ Uremia = “U” in MUDPILES
o Boards question: hyperkalemia is the feared complication of end stage renal disease
o Hyperkalemia à K affects your heart à conduction disturbances
o Renal failure patients (missed dialysis) à need to get a potassium right away
“ If potassium is high, next step is to get EKG immediately
o People with end stage renal disease are chronically acidotic
Cardiovascular sxs of CKD/ESRD
o Hypertension - common SBP>200, DBP>120
“ Most common - 80-85% in CKD
“ Difficult to control, speeds path to ESRD
“ Directly related to Na and water retention
“ Diuretics, multi-drug antihypertensives
“ Diet, Na restriction, nephrologist
o Accelerated atherosclerosis
“ Dyslipidemia common - statin tx OK
“ Risk of death from CAD > risk of eventually requiring dialysis
“ Independent risk for coronary artery Dz
o Accelerated artherosclerosis = MIs at age 40!
o Many people will die of a cardiac even before getting dialysis
o Volume overload í pulmonary edema, CHF
“ Na and intravascular volume balance is maintained until GFR <10-15ml/min - then fluid overload
“ Left ventricular hypertrophy (LVH) and dilated cardiomyopathy (DCM) very common - HTN
“ Acute pulmonary edema = emergent dialysis
“ Tx w/ loop diuretics, ACEI’s, ARB’s
“ Be careful with IV hydration in renal failure pt!
o You have to be very careful in hydrating a renal failure patient because they can’t get rid of it!
o You can cause pulmonary edema if you overload them with fluid
o Pericardial effusion
“ Retention of uremic toxins, fluid overload
“ Fluid collects in pericardial sac, restricts ventricular filling
“ Don’t forget infectious, neoplastic, autoimmune causes
“ Absolute indication for emergent dialysis
“ Cardiac tamponade can develop
o You can get these effusions from infections, parasites, etc.
o If you have an effusion but no tampenade physiology, then you get dialysis if you have time
hematologic sxs of CKD/ESRD
o Anemia
“ Decreased erythrocyte production
“ Normochromic, normocytic - chronic
“ Common when GFR <30ml/min
“ Treat early: recombinant erythropoietin Epogen or Procrit IM
o Coagulopathies
“ Platelet dysfunction
“ Platelet count OK but bleeding time prolonged
“ Treat if symptomatic or prior to surgery
“ Bleeding is indication for dialysis
o Platelets are there, they just don’t work very well
GI sxs of CKD/ESRD
o Anorexia, nausea, vomiting
“ Dietary restrictions make goals difficult
“ Dehydration common, adds to fluid imbalance
o GI bleeding common
“ Anemia and prolonged bleeding time complicate things
neurologic sxs of CKD/ESRD
o Uremic encephalopathy
“ GFR 10-15ml/min
“ Accumulation of uremic toxins
“ Difficulty concentrating to lethargy, confusion, coma
“ Asterixis, hyperreflexia
“ Indication for emergent dialysis - reversible
o Neuopathies
“ Very common, difficult to treat
“ Paresthesias - stocking/glove pattern
“ Restless leg syndrome
“ Motor involvement - lose DTR’s, foot drop
“ Early dialysis may prevent progression
o Asterixis í foot up and down and then keeps going
mineral metabolism CKD
o Mineral/bone disorders of CKD
“ Hypocalcemia, hyperphosphatemia
“ High PTH - secondary hyperparathyroidism
“ àHigh bone turnover, renal osteodystrophy
“ Bone pain, spontaneous fractures
“ Monitor levels Ca, Phosphorus, PTH
“ Diet - low phosphorus (no eggs, coke)
“ Ca to bind phosphorus or binding agents
“ Vit D to suppress PTH, increase Ca
Endocrine sxs in CKD
o Insulin and glucose tolerance issues " Hyper- or hypoglycemia o Thyroid disorders o Low estrogen and testosterone o Impotence and menstrual disorders o Complicated pregnancy - contraception
dermatologic and miscellaneous sxs of CKD
o Dermatologic " Sallow appearance, pallor from anemia " Pruritis - difficult to treat " Uremic frost - severe, late, rareà o Miscellaneous " Immunocompromised state " Malnutrition " Susceptible to infection o Uremic frost í white frost around face and torso o Anyone with renal failure should be considered immunocompromised í very susceptible to infection
Management of CKD
o Treat reversible causes o Involve nephrologist early in course o Renal-protective measures " Tight HTN, DM control " ACE inhibitors, ARB's to slow progression " Nutritionist: low Na, K, protein, phosphorous " Smoking/drug cessation o Identify and prepare pt for dialysis
Dialysis
o Hemodialysis " Blood from body, thru A-V shunt " Semiperm membrane, dialysate " Blood returned to body " 3x/week, 3-4 hour process o Peritoneal dialysis " Dialysate into perioneal cavity, peritoneal membrane acts as dialyzer " At home, ambulatory, continuous o You WANT a thrill in a dialysis shunt
indications for dialysis
o K/DOQI rec's (non-emergent) " Non-DM - GFR <10ml/min, Cr 8 " DM - GFR <15ml/min, Cr 6 o Emergent indications " Hyperkalemia (refractory) " Fluid overload (refractory to diuretics) " Pericardial effusion, coagulopathy (bleeding) " Severe metabolic acidosis " Neurologic Sx's of uremia " Encephalopathy, neuropathy, seizures o KNOW EMERGENT INDICATIONS
Renal transplant
o Treatment of choice for ESRD
o Successful = improved quality of life and reduced mortality risk compared to dialysis
o Not all patients appropriate candidates
o Refer to transplant program when dialysis is initiated (2-3 years wait)
Summary of AKI, CKD
o AKI? Think - prerenal, intrarenal, postrenal " Know the characteristics of each o Know labs to order, calculations o Monitor patients at risk - DM, HTN o Follow hospitalized patients closely o Know, monitor complications of CKD o Know emergent indications for dialysis o Learn renal function and disease well enough to explain it to your patients
