acute renal failure internal medicine lecture series august 10, 2005 julia faller, d.o
TRANSCRIPT
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 25-90%.
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.
Questions or Comments