Transcript MR-AC2aa

'But I don't want to go among mad
people,' said Alice. 'Oh, you can't
help that,' said the cat. 'We're all
mad here.'
Lewis Carroll
Alan Chan
MP2
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Chief Complaint: Nausea
HPI: you are on cardiology call on a quiet night. You
are called about a 54 yo WF s/p orthotopic heart
txp doing fairly well post op. He is on
immunosuppressant therapy. He has had nausea
dry heaving x2 d, currently mild fever to 100.8, and
malaise x2 d.
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Medications
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NovoLog and Lantus insulin
CaCO3 1250 mg b.i.d.
Epogen 10,000 units MWF
Vitamin D 50,000 units MTh
CellCept 1000 mg b.i.d.
Protonix 40 mg b.i.d.
Paxil 10 mg daily.
Pravastatin 20 mg daily.
Tacrolimus 2 mg b.i.d.
Prednisone 10 mg qday
Valcyte 450 mg daily.
Cipro 250 mg q12
Allergies NKDA
PMH: POD 22 OHT for nonischemic
cardiomyopathy with relatively no post op
complications, HTN, DM
PSurgH: no others
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SH: worked at TMC; no tob, occ EtOH
FH: N/C
what else do you want to know????
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VS: Temp 100.8, Resp 16, BP 134/68, Pulse 68
Significant findings….
General: NAD obese male
Skin: 2+ pitting edema – not new; stage II wound
on his coccyx, no drainage, mild TTP
HEENT: wnl
Neck: large neck
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Chest: CTA bilat
CVS: rrr
Abd: lg pannus, BS present, benign
Ext: full ROM, but slow due to some stiffness
Neuro: wnl
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Differential Diagnosis
CC: Fever
HPI: 54 yo s/p OHT, with
some mild nausea, fever,
arthralgia
PMH: DM, HTN
PE Findings
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Laboratory Data
CBC
BMP
Urinalysis
Cardiac Enzymes
Liver Function Tests
Coagulation
Endocrinology
Serology
Immunologic Studies
Other Serology
Body Fluid Analysis
Cytology
Pathology
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Microbiology
CXR
EKG
Ultrasound
CT Scan
MRI
2-D Echo
Other Studies
Other Imaging
Clinical Course
Differential Diagnosis
Discussion
Please Press to Return
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CBC
8.7
167
8.9
28
Neutro 78, Lymph 12, Eos 2
MCV 85 (80-99)
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BMP
135
4.7
98
24
56
113
2.1
Ca 8.4 (8.8-10.5)
Baseline Cr 1.4
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Urine Analysis
color
sp gr
pH
Hgb
ketone
glu
prot
LE
nitrite
urobil
bili
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clear yellow
1.020
5
sm
neg
neg
30
pos
neg
neg
neg
Microscopic
21-40 wbc
1-5 rbc
Cardiac Enzymes
CK
CK-MB
Troponin
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XX (30-225)
X (0-6.0)
X (0-1.9)
Liver Function Tests -wnl
AST
ALT
Alk Phos
Albumin
T Bilirubin
D Bilirubin
I Bilirubin
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XX (15-41)
XX (7-35)
XXX (32-91)
X.X (3.5-4.8)
X.X (0.3-1.2)
X.X (0.1-0.5)
X.X (0-0.7)
Coagulation
PTT
PT
INR
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X (21-33)
X (10.3-13.0)
X
Endocrinology
TSH
Free T4
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X (0.34-5.6)
X (0.6-1.6)
Serology
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Immunologic Studies
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Cytology
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Other Serology
• Results – U Na 42, U Cr 108
• FeNA – 0.6%, U eos neg x 2
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Body Fluid Analysis
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Pathology
• Enterbacter cloacae
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Microbiology
• Urine Cx 3/27 GNR
• Blood Cx 3/27 no growth to date
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CXR
• IMPRESSION:
• 1. Increasing left lower lobe airspace disease.
Stable right basilar
• subsegmental atelectasis.
• 2. Stable bilateral pleural effusions.
• 3. Stable marked cardiomegaly.
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EKG
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Ultrasound
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CT Scan
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MRI
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2-D Echocardiogram
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Other Imaging
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Other Studies
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Clinical Course
• You find out that he had mild fever the other day and was
pan cultured. He was started on avelox and then changed
to cipro after sensitivities of organisms.
• You suspect AIN and started him on higher dose steroids
with continued taper
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Discussion
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AIN
• Definition, dx, w/u, tx, and mgmt
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Acute Interstitial Nephritis
• Immune mediated tubulo-interstitial injury
• Usu abrupt
• Infection – bacteria (Corynebacterium diphtheria,
legionella, staph/strep, yersinia), viral (CMV, EBV,
HSV, hep C, HIV), other (leptospira)
• Immune – acute rejection of kidney, GNs, vasculitis,
SLE
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Discussion
• Drug induced, but not necessarily dose related
• Abx – cephalosporins, cipro and other quinolones,
PCNs, rifampin, sulfonamidees
• Most NSAIDs
• Diuretics – lasix, thiazides, triamterene
• Misc – allopurinol, cocaine
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Presentation
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Nonspecific s/s
Fever (27%)
Skin rash – nonspecific diffuse (15%)
Arthralgia
Above triad present 5-10% in practice, but 80% on
the boards
Malaise
Nausea +/- vomiting
Eosinophilia (23%)
Flank pain
PP
• Inflammatory cells in interstitium – edema, but
vessels and glomeruli ok
• Fibrosis later – either diffuse or patchy, from cortex
out to medullocorticol jxn
• Mononuclear and T lymphocytes, with plasma cells
and eosinophils
• NSAIDs – a/w minimal change disease
• Antigen driven – T cell mediated hypersensitivity and
cytotoxic T cell injury
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Dx
• Gold std bx – but not typically done
• Urine eos – in mid 80s, thought Hansel stain more
sensitive than Wright’s stain. Recent studies show
not very good test
• PPV 38%, sens 40%
• Imaging – U/S – no specific findings; Gallium 67 –
may only be useful to tell ATN from AIN
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Labs
• Older individuals may have mild proteinuria (usu < 1
g/day)
• Signs of tubulointerstitial damage – like RTA
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Tx
• Stop offending agent or treat the infection
• Typically quick recovery, NSAIDs may take up to
18months
• Steroids – no trials support use. Small studies have
shown faster diuresis and improvement in Cr; others
have had conflicting data (IC evidence)
• Can try Cytoxan if steroids don’t work in 2-3 wk
• Use slow steroid taper of your choice if seems to
work.
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Other syndromes that mimic
• Analgesic induced, toxin induced, sarcoidosis,
chronic IN, tubulointerstitial nephritis uveitis
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MKSAP – nephro #44
• A 44 yo man with a history of nephrolithiasis
requests nonpharmaceutical interventions for stone
prevention. His last symptomatic kidney stone was 2
years ago. He does not recall the exact type of stone
that he formed but believes that it contained calcium.
Previous laboratory studies have showed normal
renal function and normal levels of calcium,
phosphorus, and uric acid. A plain abdominal
radiograph performed 1 year ago revealed no
genitourinary calcifications. He does not have a
family history of nephrolithiasis wishes to reduce his
chances of developing further kidney stones.
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Discussion
• In addition to increasing fluid intake to >2 L/d,
which of the following is the best initial therapy for
this patient?
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A Increase dietary calcium intake
B Decrease dietary sources of citrate
C Increase dietary animal protein intake
D Increase dietary sodium intake
A – more calcium
• Increasing calcium intake decreases the risk for
calcium oxalate stones because calcium binds to
gastrointestinal sources of oxalate and therefore
prevents absorption.
• Dietary modifications such as decreasing animal
protein intake, decreasing sodium intake, and
increasing citrate can reduce the risk for recurrent
kidney stones without additional medical therapy.
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Discussion
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Discussion
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Discussion
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