Case study: acute renal failure

Download Report

Transcript Case study: acute renal failure

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…”
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





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








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



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)
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




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




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



Any additional history required?
Any additional physical exam?
Labs pending: repeat 24hr urine,
complements, myeloma markers,
lupus markers, vasculitis markers
Differential diagnosis:

This slide intentionally left blank
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…”
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


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




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




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)
Lab profile
Date
2/13/06
2/27/06
3/14/06
3/20/06
3/26/06
3/30/06
4/02/06
BUN
34
40
50
55
86
85
90
Creatinine
2.6
4.0
6.3
7.2
8.0
7.3
6.0
Renal biopsy





Indication
Risk
Solitary kidney?
Complications
Follow up monitoring
Additional serology



Anti GBM negative
ANA 1:40 speckled
P–ANCA 1:32 with positive MPO
(Myeloperoxidase IgG) of 55 units
biopsy
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.
Overview to classification of
RPGN
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





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

ANCA are associated with may cases
of WG, MPA,Churg-Strauss syndrome,
“renal-limited vasculitis” and certain
drug-induce syndromes (PTU,
hydralazine, minocycline)
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?
Lab profile
Date
2/13/06
2/27/06
3/14/06
3/20/06
3/26/06
3/30/06
4/02/06
BUN
34
40
50
55
86
85
90
Creatinine
2.6
4.0
6.3
7.2
8.0
7.3
6.0