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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 Left hemispheric CVA CC: “Doc, I was playing bridge 2 weeks ago…”

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case study acute renal failure

Case study: acute renal failure

Bruce R. Wall, MD, FACP

4/3/06

Renal resident conference

patient p b
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
h p continued
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
past history
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
history continued
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
medications
Amitriptyline

Aspirin 81 mg

Atorvastatin

Clonidine TTS

Plavix

Iron

Lisinopril

Metoprolol

Protonix

Morphine

SL nitroglycerin

Vitamin K

Centrum

ALLERGY:Voltaren (nausea)

Medications:
physical exam
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
laboratory exam
Laboratory exam
  • Hgb 9gms; normocytic; plts WNL
  • Serum iron 20, ferritin 325, sat 18%
  • Nomal LFT’s 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
labs continued
Labs: continued
  • CXR - borderline cardiomegaly
  • Urinalysis: yellow hazy SG 1.01 pH 5 large blood negative ketones RBC 25/HPF WBC 35/HPF 2+protein
  • Sonography: left 10.7cm, right 11.9cm “isoechoic with the liver”
  • 24 hour urine: clearance 9ml/min; total protein = 1100mg per day
additional information
Additional information
  • Any additional history required?
  • Any additional physical exam?
  • Labs pending: repeat 24hr urine, complements, myeloma markers, lupus markers, vasculitis markers
differential diagnosis
Differential diagnosis:
  • This slide intentionally left blank
approach to kidney
Approach to kidney
  • Acute vs chronic disease
  • Nephritic vs nephrotic syndrome
  • Glomerular disease:acute vs chronic GN
  • Interstitial disease: infiltrative, AIN
  • Renal artery disease: stenosis or emboli
  • Obstructive disease: tubules, stones, retroperitoneum, BPH vs prostate CA
don t fall in love with your first diagnosis
“don’t 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

nsaid induced renal failure
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
nsaid induced arf
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
ain allergic interstitial nephritis
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)
renal biopsy
Renal biopsy
  • Indication
  • Risk
  • Solitary kidney?
  • Complications
  • Follow up monitoring
additional serology
Additional serology
  • Anti GBM negative
  • ANA 1:40 speckled
  • P–ANCA 1:32 with positive MPO (Myeloperoxidase IgG) of 55 units
overview to classification of rpgn
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
  • >80% 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.
spectrum of anca
Spectrum of ANCA
  • Described in 1982
  • Technical issues: indirect IF assay is more sensitive & ELIZA more specific
  • C-ANCA pattern staining is diffuse @ cytoplasm (most are PR3 positive)
  • P-ANCA stains around the nucleus, (most are MPO positive)
clinical applications of anca
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 Wegener’s.
  • 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
disease associations
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)
therapy
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?