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Acute Renal Failure Internal Medicine Lecture Series August 10, 2005 Julia Faller, D.O.

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Presentation on theme: "Acute Renal Failure Internal Medicine Lecture Series August 10, 2005 Julia Faller, D.O."— Presentation transcript:

1 Acute Renal Failure Internal Medicine Lecture Series August 10, 2005 Julia Faller, D.O.

2 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

3 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.

4 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.

5 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.

6 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.

7 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

8 History and Physical  Hypotension  Volume contraction  Congestive heart failure  Nephrotoxic drug ingestion  History of trauma or unaccustomed exertion  Blood loss or transfusions

9 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

10 Causes of ARF 1.Prerenal 40-80% 2.Intrarenal 50% 3.Postrenal 5-10%

11 Prerenal  Hypotension  CHF  Hypovolemia from renal losses  Hypovolemia from extrarenal losses  Vasoconstriction

12 Intrarenal  Vascular causes  Interstitial nephritis  Glomerular factors

13 Postrenal  Bladder outlet obstruction due to prostatic hypertrophy  Uretheral stictures

14 Lab studies  BUN and creatinine  CBC with peripheral smear  Urinalysis  Urine Electrolytes

15 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.

16 CBC and peripheral smear  Results can increase differential diagnosis to include TTP, multiple myeloma, DIC

17 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

18 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.

19 Imaging studies  Ultrasound  Doppler scans  Nuclear scans  Renal biopsy

20 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.

21 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

22 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.

23 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

24 Past Medical History  HTN  Type II Diabetes  Psychiatric history  Hypercholesterolemia

25 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)

26 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

27 Lab studies  Second set on day of admission Creat 8.8 Bun 74  Day one BUN 63 Creat 6.4

28 Day four  BUN 13  Creat 1.1  Patient discharged to home.

29 Questions or Comments


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