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'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 Z A CD 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. Z A CD Medications Z A CD • • • • • • • • • • • • 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 Z A CD SH: worked at TMC; no tob, occ EtOH FH: N/C what else do you want to know???? Z A CD 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 Z A CD Chest: CTA bilat CVS: rrr Abd: lg pannus, BS present, benign Ext: full ROM, but slow due to some stiffness Neuro: wnl Z A CD Differential Diagnosis CC: Fever HPI: 54 yo s/p OHT, with some mild nausea, fever, arthralgia PMH: DM, HTN PE Findings Z A CD Laboratory Data CBC BMP Urinalysis Cardiac Enzymes Liver Function Tests Coagulation Endocrinology Serology Immunologic Studies Other Serology Body Fluid Analysis Cytology Pathology Z A CD Microbiology CXR EKG Ultrasound CT Scan MRI 2-D Echo Other Studies Other Imaging Clinical Course Differential Diagnosis Discussion Please Press to Return Z A CD CBC 8.7 167 8.9 28 Neutro 78, Lymph 12, Eos 2 MCV 85 (80-99) Z A CD BMP 135 4.7 98 24 56 113 2.1 Ca 8.4 (8.8-10.5) Baseline Cr 1.4 Z A CD Urine Analysis color sp gr pH Hgb ketone glu prot LE nitrite urobil bili Z A CD 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 Z A CD 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 Z A CD 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 Z A CD X (21-33) X (10.3-13.0) X Endocrinology TSH Free T4 Z A CD X (0.34-5.6) X (0.6-1.6) Serology Z A CD Immunologic Studies Z A CD Cytology Z A CD Other Serology • Results – U Na 42, U Cr 108 • FeNA – 0.6%, U eos neg x 2 Z A CD Body Fluid Analysis Z A CD Pathology • Enterbacter cloacae Z A CD Microbiology • Urine Cx 3/27 GNR • Blood Cx 3/27 no growth to date Z A CD CXR • IMPRESSION: • 1. Increasing left lower lobe airspace disease. Stable right basilar • subsegmental atelectasis. • 2. Stable bilateral pleural effusions. • 3. Stable marked cardiomegaly. Z A CD EKG Z A CD Ultrasound Z A CD CT Scan Z A CD Z A CD MRI Z A CD 2-D Echocardiogram Z A CD Other Imaging Z A CD Other Studies Z A CD 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 Z A CD Discussion Z A CD AIN • Definition, dx, w/u, tx, and mgmt Z A CD 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 Z A CD 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 Z A CD Presentation • • • • • • • • • Z A CD 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 Z A CD 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 Z A CD Labs • Older individuals may have mild proteinuria (usu < 1 g/day) • Signs of tubulointerstitial damage – like RTA Z A CD 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. Z A CD Other syndromes that mimic • Analgesic induced, toxin induced, sarcoidosis, chronic IN, tubulointerstitial nephritis uveitis Z A CD 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. Z A CD Discussion • In addition to increasing fluid intake to >2 L/d, which of the following is the best initial therapy for this patient? • • • • Z A CD 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. Z A CD Discussion Z A CD Discussion Z A CD Discussion Z A CD