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Case study: acute renal failure

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Case study: acute renal failure Bruce R. Wall, MD, FACP 4/3/06 Renal resident conference Patient P B 80 yo white female with history of HBP for 20 years, and previous ... – PowerPoint PPT presentation

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Title: Case study: acute renal failure


1
Case study acute renal failure
  • Bruce R. Wall, MD, FACP
  • 4/3/06
  • Renal resident conference

2
Patient P B
  • 80 yo white female with history of HBP for 20
    years, and previous Left hemispheric CVA
  • CC Doc, I was playing bridge 2 weeks ago
  • Known lumbosacral spine stenosis/listhesis with
    increasing back pain and loss of strength in
    lower legs
  • 1 week of nausea and vomiting with minimal abd
    pain
  • Two year history of ibuprofen use recent
    conversion of naprosyn for 1 month
  • No abd distension no hematemesis occasional
    pink tinged sputum, while on Plavix
  • Conversion to Ultram, then narcotics, which
    caused constipation

3
H P continued
  • No previous documentation of creat in caregate
    current creat 2.5 to 3.5mg
  • Iron deficiency anemia documented negative
    colonscopy 1 year ago
  • GI consulted for nausea, vomiting, anemia after
    naprosyn exposure EGD WNL
  • Renal consulted for ARF? CRF?
  • Lower leg weakness, poor gait, and GI symptoms
    were her main concerns

4
PAST HISTORY
  • Hypertension 20 yrs
  • Coronary artery stent 2002
  • CVA with mild expressive aphasia
  • Anemia
  • CKD
  • Diverticulae and internal hemorrhoids
  • Lumbar stenosis, moderate, at L3-4
  • Cholecystectomy, appy, TAH

5
History continued
  • FH HBP, CVA ASCVD at young age
  • SH remote smoker, very active, no ETOH
  • ROS ataxia with abnormal gait, requiring walker
    GI symptoms no history of CHF no
    nephrolithiais, no endocrinopathy, no diabetes
    able to drive

6
Medications
  • Amitriptyline
  • Aspirin 81 mg
  • Atorvastatin
  • Clonidine TTS
  • Plavix
  • Iron
  • Lisinopril
  • Metoprolol
  • Protonix
  • Morphine
  • SL nitroglycerin
  • Vitamin K
  • Centrum
  • ALLERGYVoltaren (nausea)

7
Physical exam
  • 140/88 90 14 afebrile
  • Awake, alert, preserved muscle mass
  • HEENT minimal facial asymmetry
  • NECK no nodes, chronic stiffness
  • LUNGS no hemoptysis no rales
  • COR RRR, no murmur, no gallop
  • ABD soft, benign, no hepatomegaly
  • GU positive stool occult blood, no mass
  • EXT impressive 3 edema no purple toes
  • NEURO expressive aphasia abnormal gait no
    hyperreflexia

8
Laboratory exam
  • Hgb 9gms normocytic plts WNL
  • Serum iron 20, ferritin 325, sat 18
  • Nomal LFTs and normal coags
  • Sodium 128 Potassium 5.1 Chloride
    100 BUN 34 creatinine 2.8
    Glucose 100 bicarbonate 23
    calcium 7.6 albumin 2.7
    cholesterol 225

9
Labs continued
  • CXR - borderline cardiomegaly
  • Urinalysis yellow hazy SG 1.01 pH 5
    large blood negative ketones RBC 25/HPF WBC
    35/HPF 2protein
  • Sonography left 10.7cm, right 11.9cm isoechoic
    with the liver
  • 24 hour urine clearance 9ml/min total protein
    1100mg per day

10
Additional information
  • Any additional history required?
  • Any additional physical exam?
  • Labs pending repeat 24hr urine, complements,
    myeloma markers, lupus markers, vasculitis markers

11
Differential diagnosis
  • This slide intentionally left blank

12
Approach to kidney
  • Acute vs chronic disease
  • Nephritic vs nephrotic syndrome
  • Glomerular diseaseacute vs chronic GN
  • Interstitial disease infiltrative, AIN
  • Renal artery disease stenosis or emboli
  • Obstructive disease tubules, stones,
    retroperitoneum, BPH vs prostate CA

13
dont fall in love with your first diagnosis
  • TOXIC EFFECTS of NSAIDS
  • GI toxicity upper and lower
  • Modest worsening of chronic hypertension
  • ARF 2 different types
  • CV effects blocks beneficial effect ASA
  • Hepatic injury
  • Bone marrow toxicity aplasia
  • Anti-platelet effect stop 5 days prior to
    surgery
  • CNS changes tinnitus
  • Skin - TEN

14
NSAID induced renal failure
  • Hemodynamic mediated ARF not a concern in normal
    individuals yet patients with underlying GN,
    CKD, or hypercalcemia all need prostacyclin and
    PGE2
  • Patients with increased vasoconstrictors AII or
    NE states of volume depletion CHF, cirrhosis,
    DM are at greatest risk

15
NSAID induced ARF
  • Inhibition of PG by any NSAID in state of
    vasoconstriction may lead to reversible renal
    insufficiency or ARF
  • Indocin, ibuprofen, and toradol most common
    causes
  • COX II inhibition reported cause ARF
  • Sulindac/clinoril less suppression ARF

16
AIN allergic interstitial nephritis
  • Fenoprofen and Indocin relatively common cause
    hematuria, pyuria, proteinuria yet the full
    blown syndrome of fever,rash, eosinophilia is
    extremely uncommon
  • Nephotic range proteinuria is reported
  • Biopsy is uncommon since pts improve
  • Prednisone not helpful (retrospective)

17
Lab profile
Date BUN Creatinine
2/13/06 34 2.6
2/27/06 40 4.0
3/14/06 50 6.3
3/20/06 55 7.2
3/26/06 86 8.0
3/30/06 85 7.3
4/02/06 90 6.0
18
Renal biopsy
  • Indication
  • Risk
  • Solitary kidney?
  • Complications
  • Follow up monitoring

19
Additional serology
  • Anti GBM negative
  • ANA 140 speckled
  • PANCA 132 with positive MPO (Myeloperoxidase
    IgG) of 55 units

20
biopsy
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26
Overview to classification of RPGN
  • RPGN is the syndrome crescentic GN is the
    pathologic entitiy
  • Crescent formation is a nonspecific response to
    injury of glomerular capillary wall
  • gt80 crescents present -- severe ARF
  • Types of crescentic GN type I anti-GBM
    disease type II immune complex disease type
    III pauci-immune disease
  • Pauci-immune present with necrotizing GN with few
    or no immune deposits by IF or EM. Majority of
    patients with renal-limited vasculitis are P-ANCA
    positive with 75 MPO positive.

27
Overview to classification of RPGN
28
Spectrum of ANCA
  • Described in 1982
  • Technical issues indirect IF assay is more
    sensitive ELIZA more specific
  • C-ANCA pattern staining is diffuse _at_ cytoplasm
    (most are PR3 positive)
  • P-ANCA stains around the nucleus, (most are MPO
    positive)

29
Clinical applications of ANCA
  • Is a positive result a true positive? Yes, if
    ELIZA (), fairly good PPV.
  • Does (-)ANCA exclude ANCA vasculitis? No,
    since 40 test (-) in Wegeners.
  • Does presence of ()ANCA establish the diagnosis
    (no biopsy required)? No, tissue confirmation
    is standard.
  • Does rising ANCA titer correlate with flare? No,
    not a reliable indicator of disease.
  • Does persistant (-)ANCA mean quiescence? No

30
Disease associations
  • ANCA are associated with may cases of WG,
    MPA,Churg-Strauss syndrome, renal-limited
    vasculitis and certain drug-induce syndromes
    (PTU, hydralazine, minocycline)

31
therapy
  • Initial dosing with 1000mg solumedrol for 3 days
  • Intravenous cyclophosphamide every month has less
    toxicity than PO
  • Once in remission, consider PO imuran,
    methotrexate, or ENBREL?

32
Lab profile
Date BUN Creatinine
2/13/06 34 2.6
2/27/06 40 4.0
3/14/06 50 6.3
3/20/06 55 7.2
3/26/06 86 8.0
3/30/06 85 7.3
4/02/06 90 6.0
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