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Alan Chan MP2

Morning Report. 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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Alan Chan MP2

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  1. Morning Report 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

  2. 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

  3. 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

  4. PMH: POD 22 OHT for nonischemic cardiomyopathy with relatively no post op complications, HTN, DM PSurgH: no others

  5. SH: worked at TMC; no tob, occ EtOH FH: N/C what else do you want to know????

  6. 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

  7. CVS: rrr Abd: lg pannus, BS present, benign Ext: full ROM, but slow due to some stiffness Neuro: wnl

  8. CC: Fever HPI: 54 yo s/p OHT, with some mild nausea, fever, arthralgia PMH: DM, HTN PE Findings Differential Diagnosis

  9. CBC BMP Urinalysis Cardiac Enzymes Liver Function Tests Coagulation Endocrinology Serology Immunologic Studies Other Serology Body Fluid Analysis Cytology Pathology Microbiology CXR EKG Ultrasound CT Scan MRI 2-D Echo Other Studies Other Imaging Clinical Course Differential Diagnosis Discussion Laboratory Data

  10. Please Press to Return

  11. CBC 8.7 167 8.9 28 Neutro 78, Lymph 12, Eos 2 MCV 85 (80-99)

  12. BMP 135 98 56 113 24 2.1 4.7 Ca 8.4 (8.8-10.5) Baseline Cr 1.4

  13. 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 Urine Analysis

  14. CK XX (30-225) CK-MB X (0-6.0) Troponin X (0-1.9) Cardiac Enzymes

  15. 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) Liver Function Tests -wnl

  16. PTT X (21-33) PT X (10.3-13.0) INR X Coagulation

  17. TSH X (0.34-5.6) Free T4 X (0.6-1.6) Endocrinology

  18. Serology

  19. Immunologic Studies

  20. Cytology

  21. Other Serology • Results – U Na 42, U Cr 108 • FeNA – 0.6%, U eos neg x 2

  22. Body Fluid Analysis

  23. Pathology • Enterbacter cloacae

  24. Microbiology • Urine Cx 3/27 GNR • Blood Cx 3/27 no growth to date

  25. CXR • IMPRESSION: • 1. Increasing left lower lobe airspace disease. Stable right basilar • subsegmental atelectasis. • 2. Stable bilateral pleural effusions. • 3. Stable marked cardiomegaly.

  26. EKG

  27. Ultrasound

  28. CT Scan

  29. MRI

  30. 2-D Echocardiogram

  31. Other Imaging

  32. Other Studies

  33. 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

  34. Discussion

  35. Definition, dx, w/u, tx, and mgmt AIN

  36. 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 Acute Interstitial Nephritis

  37. 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 Discussion

  38. 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 Presentation

  39. 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 PP

  40. 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 Dx

  41. Labs • Older individuals may have mild proteinuria (usu < 1 g/day) • Signs of tubulointerstitial damage – like RTA

  42. 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. Tx

  43. Analgesic induced, toxin induced, sarcoidosis, chronic IN, tubulointerstitial nephritis uveitis Other syndromes that mimic

  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. MKSAP – nephro #44

  45. 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 Discussion

  46. 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. A – more calcium

  47. Discussion

  48. Discussion

  49. Discussion

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