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Alan Chan

MP2

'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

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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.

Chief Complaint: Nausea

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Medications• 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

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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

Chest: CTA bilat

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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: FeverHPI: 54 yo s/p OHT, with

some mild nausea, fever, arthralgia

PMH: DM, HTN

PE Findings

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Laboratory Data

CBCBMPUrinalysisCardiac EnzymesLiver Function Tests CoagulationEndocrinologySerology Immunologic StudiesOther SerologyBody Fluid AnalysisCytologyPathology

MicrobiologyCXREKGUltrasoundCT ScanMRI2-D EchoOther Studies Other Imaging

Clinical CourseDifferential DiagnosisDiscussion

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Please Press to Return

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CBC

8.98.7

28167

Neutro 78, Lymph 12, Eos 2

MCV 85 (80-99)

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BMP

135

4.7

98

24

56

2.1113

Ca 8.4 (8.8-10.5)

Baseline Cr 1.4

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Urine Analysis

color clear yellow

sp gr 1.020

pH 5

Hgb sm

ketone neg

glu neg

prot 30

LE pos

nitrite neg

urobil neg

bili neg

Microscopic

21-40 wbc

1-5 rbc

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Cardiac Enzymes

CK XX (30-225)

CK-MB X (0-6.0)

Troponin X (0-1.9)

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Liver Function Tests -wnl

AST XX (15-41)

ALT XX (7-35)

Alk Phos XXX (32-91)

Albumin X.X (3.5-4.8)

T Bilirubin X.X (0.3-1.2)

D Bilirubin X.X (0.1-0.5)

I Bilirubin X.X (0-0.7)

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Coagulation

PTT X (21-33)

PT X (10.3-13.0)

INR X

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Endocrinology

TSH X (0.34-5.6)

Free T4 X (0.6-1.6)

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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

• 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

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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?

• A Increase dietary calcium intake• B Decrease dietary sources of citrate• C Increase dietary animal protein intake• D Increase dietary sodium intake

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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