Nephrology Case Presentation Douglas Stahura D.O. Grandview Hospital November 20, 2001.
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Transcript of Nephrology Case Presentation Douglas Stahura D.O. Grandview Hospital November 20, 2001.
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Nephrology Case Nephrology Case PresentationPresentation
Douglas Stahura D.O.
Grandview Hospital
November 20, 2001
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Case PresentationCase Presentation
24 y/o AAF referred by PCP c/o fatigue, periorbital edema, lower extremity edema, hematuria, proteinuria
Pt relates a 5 year history of intermittent gross hematuria usually associated with “colds”
Over past four months has noticed increasing fatigue, swelling “around my eyes, especially in the morning” and swelling in the ankles and legs
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Case PresentationCase Presentation
PMH – one pregnancy, uncomplicated PSH – none Allergy – none Meds – Lasix 40 mg QD Social – married, nursing student,
nonsmoker, EtOH socially, caffeine-2 cpd Family – Father deceased age 50 MVA,
Mother DM2 age 56
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Case PresentationCase PresentationROS
– Fatigue, Weight gain 10#, No energy, poor appetite,
– Swelling in feet/ankles, worse at end of the day, legs “feel heavy”
– Denies CP/PALP/DOE, Cough/Sputum/SOB
– Denies N/V/D, +/-Constipation– No recent UTI, hematuria
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Case PresentationCase Presentation
Exam: BP 135/85, T-98.6, P-80, R-14Wt-146, Ht-5’3”NAD, pleasant, cooperativeCV,RESP,GI,MS, LYMPH – WNLSKIN – warm/dry, 3+ pitting up to knees
B/L, no rash/purpura,
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Case PresentationCase Presentation
Lab data:– Na-133, K-4.1, Cl-103, HCO3-25– BUN-8, Cr-0.8– CBC normal– AST-18, ALT-22, ALP-80, ALB-0.6– UA SG-1.020, pH-5, BLO-2+, PRO-4+,
GLU-neg, Ketones-Neg– CXR-normal
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Differential DiagnosisDifferential Diagnosis
Hematuria, grossProteinuriaHypoalbuminuriaNephrotic SyndromeNephritic Syndrome
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Clinical InvestigationClinical Investigation
Imaging: Renal UltrasoundLab:
– ANA, dsDNA– ASO titer, ANCA, anti-GBM Ab– Serum/Urine Electropheresis– HBV, HCV, HIV, C3, C4, CH50– 24 hour Urine: Protein, Creatinine
Renal Biopsy
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Clinical InvestigationClinical Investigation
24 hour urine– 18 grams protein/24 hours– Creatinine Clearance 120 ml/min
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00:00
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IgA NephropathyIgA Nephropathy
Mesangial proliferative glomerulonephritis characterized by diffuse mesangial deposition of IgA
Described by Berger in Paris 1968 Common clinical presentation is gross
hematuria provoked by mucosal infection Diagnosis is made by Immunoflorescence
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IgA NephropathyIgA NephropathyPathogenesisPathogenesis
IgA preferentially deposits in glomerulusAbnormality of host IgA immune system
– No consistent evidence for a specific antigen
Bacterial, viral, food
– Possibly autoimmune against mesangium– Antigen-independent mechanism – IgA
glycosylation
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IgA NephropathyIgA NephropathyPathogenesisPathogenesis
IgA most abundant Ig in the body and provides mucosal defence
Two subclasses: IgA1, IgA2Mucosal Ag challenge provokes pIgA by
plasma cells in MALTBone marrow derived mIgA1
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IgA NephropathyIgA NephropathyPathogenesisPathogenesis
In IgA nephropathy– pIgA1 is deposited in mesangium– pIgA1 is downregulated in mucosa and
upregulated in the marrow– Tonsillar pIgA1 is increased
Mesangial proliferation is a result of cytokines and growth factors (PDGF, TGF-beta)
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IgA NephropathyIgA NephropathyClinical PresentationClinical Presentation
Macroscopic Hematuria in 2nd & 3rd decades of life (40-50%)
“Synpharingitic” hematuria Microscopic hematuria +- proteinuria Nephrotic Syndrome w/ hematuria(5%) Acute Renal Failure (rare)
– Cresentic or tubular occlusion by hematuria
Chronic Renal Failure w/HTN
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IgA NephropathyIgA NephropathyClinical AssociationsClinical Associations
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IgA NephropathyIgA NephropathyPrognosisPrognosis
Clinical– POOR
Increasing Age Duration of symptoms Severity of proteinuria Hypertension Renal impairment
– NO IMPACT Gender Serum IgA level
Histopathologic– POOR
Glomerular sclerosis Tubule atrophy Interstitial fibrosis Vascular wall
thickening Capillary loop wall IgA
deposits
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IgA NephropathyIgA NephropathyTherapyTherapy
Reduce IgA production Tonsillectomy Gluten free diet – neither reduce incidence of
renal failure
Altering Immune and Inflammation In cresentic IgAN – plasmapheresis, steroids,
and cyclophosphamide – poor long term results Steroids – alternate day regimen x 2 years Cyclophosphamide only – no good data
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IgA NephropathyIgA NephropathyTherapyTherapy
Altering Immune and Inflammation Dipyridimole and warfarin – no benefit Cyclosporine – hemodynamic effect only
Slowly Progressive Hypertension – Use of ACE-Inhibitor to target
125/75 will reduce proteinuria Fish Oil – 4-8 grams/day provided renal
protection from progressive disease, but did not lower proteinuria
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My PatientMy Patient
Daily Prednisone, then to alternate day therapy – Failed, no decrement of renal function, but no improvement of proteinuria
Fish Oil – unable to comply and quit therapy after 3-4 months
Cytoxan/Methyprednisolone monthly IV pulses x 6 (Lupus Nephritis regimen)
Albumin =4.1 clinical Nephrotic syndrome resolved
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ReferencesReferences
Comprehensive Clinical Nephrology, RJ Johnson/J Feehally, Harcourt, 2000
The Kidney, Brenner and Rector, 6th Ed, Saunders, 2000
The long term Outcome of Patients with IgA Nephropathy Treated with Fish Oil in a Controlled Trial, Donadio et al., JASN:10;1772-1777, 1999