Acute Renal Failure
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Transcript Acute Renal Failure
Acute Renal Failure
Internal Medicine Lecture Series
August 10, 2005
Julia Faller, D.O.
Objectives
Define acute renal failure (ARF)
Describe the pathophysiology of ARF
Outline appropriate testing to diagnose the
cause of ARF
Recommendations for treating ARF
Case presentation
Acute Renal Failure
An abrupt or rapid decline in renal function.
Recognized by a rise in BUN or serum
creatinine concentrations.
With or without a decline in urine output.
Often transient and completely reversible.
Pathophysiology
ARF may occur in 3 clinical settings
1. An adaptive response to severe volume
hypotension.
2. In response to cytotoxic insults to the
kidney.
3. With obstruction to the passage of urine.
Classifying ARF
ARF is classified as oliguric or nonoliguric.
Oliguria is defined as a daily urine volume of
less than 400 mL/d.
Anuria is defined as a urine output of less
than 50 mL/d
If anuria is abrupt in onset, it is suggestive of
obstruction.
Frequency of ARF
Approximately 1% of patients admitted to
hospitals have ARF at the time of admission.
The estimated incidence rate of ARF is 2-5%
during hospitalization.
Approximately 95% of consultations with
nephrologists are related to ARF.
Morbidity and Mortality
The mortality rate estimates vary from 2590%.
The mortality rate is 40-50% in general and
70-80% in intensive care settings
History and Physical
Hypotension
Volume contraction
Congestive heart failure
Nephrotoxic drug ingestion
History of trauma or unaccustomed exertion
Blood loss or transfusions
History and Physical
Evidence of connective tissue disorders
Exposure to toxic substances such as ethyl
alcohol or ethylene glycol
Exposure to mercury vapors, lead, or other
heavy metals, which can be encountered in
welders and miners
Causes of ARF
1. Prerenal 40-80%
2. Intrarenal 50%
3. Postrenal 5-10%
Prerenal
Hypotension
CHF
Hypovolemia from renal losses
Hypovolemia from extrarenal losses
Vasoconstriction
Intrarenal
Vascular causes
Interstitial nephritis
Glomerular factors
Postrenal
Bladder outlet obstruction due to prostatic
hypertrophy
Uretheral stictures
Lab studies
BUN and creatinine
CBC with peripheral smear
Urinalysis
Urine Electrolytes
BUN and Creatinine
BUN values that increase disproportionately
larger than those of creatinine suggest
prerenal azotemia
The ratio of BUN to creatinine greater than
20:1 suggest volume contraction.
CBC and peripheral smear
Results can increase differential diagnosis to
include TTP, multiple myeloma, DIC
Urinalysis
Granular muddy-brown casts—ATN
Reddish brown colour—acute glomerular nephritis,
presence of myoglobin or HgB
Eosinophils—UTI’s, glomerulonephritis, acute
embolic disease, drug-induced interstitial nephritis
RBC casts—glomerular disease
WBC—pyelonephritis, or acute interstitial nephritis
Urine Electrolytes
Fractional excretion of sodium (FENa).
With decreased GFR, the kidney will reabsorb salt and water
avidly if there is no intrinsic tubular dysfunction. Thus,
patients with prerenal failure should have a low fractional
excretion percent of sodium (< 1%).
FENa = (UNa/PNa) / (UCr/PCr) X 100
Oliguric states are more accurately assessed with this
formula than nonoliguric states because the kidneys do not
avidly reabsorb water and sodium in nonoliguric states.
Imaging studies
Ultrasound
Doppler scans
Nuclear scans
Renal biopsy
Treatment
Balancing volume status and correcting
biochemical abnormalities.
All nephrotoxic agents must be discontinued
or used with extreme caution.
All medications cleared by renal excretion
should be discontinued or their doses should
be adjusted appropriately.
Treatment
Correct acidosis with bicarbonate
administration
Correct hyperkalemia by decreasing the
intake of potassium, delaying the absorption
of potassium, using potassium-binding
resins, controlling intracellular shifts, and
instituting dialysis if necessary
Correct hematologic abnormalities
Case presentation
Pt is a 47 y/o WM who presented to MCH ER via
ambulance after he was found by counselors at
stairways falling and complaining of dizziness. Pt
states unsteadiness has been going on for the past
week with associated nausea, vomiting, and change
in urine stream. Pt states he cannot hold any food
down. He denies fevers/chills or diarrhea, CP,
SOB. Pt has psych history. Pt had previously
normal renal function.
Medications
Lithium ER 450 mg bid
Promethazine 25 mg q 6hour prn
Topamax 150 po bid
Wellbutrin SR 150mg 2 in am 1 in pm
Clonidine 0.1 mg bid
Lamictal 25 mg 2 hs
Lisinopril/HCTZ 20/25 qd
Glipizide XL 5 qd
Lipitor 40 mg qd
Diltiazem 240 mg qd
Paroxetine 20mg qd
Past Medical History
HTN
Type II Diabetes
Psychiatric history
Hypercholesterolemia
LABS in ER
BUN 81
Creat 10.5
Potassium 3.1
Albumin 1.7
Myoglobin 442
UA yellow, hyaline casts
Lithium 3.00 (0.60-1.20)
Admission
Pt was admitted to ICU and was hydrated
aggressively
Nephrology consult was obtained
U/S was significant for R hydronephrosis
Pt was started on dopamine drip in the ER
CT chest with contrast was done in ER
Urine output was good and responded nicely to
fluids
Lab studies
Second set on day of admission
Creat 8.8
Bun 74
Day one
BUN 63
Creat 6.4
Day four
BUN 13
Creat 1.1
Patient discharged to home.
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