nephrology division king khalid university tutorial med course 441 tutorial case
TRANSCRIPT
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Nephrology DivisionKing Khalid University
Tutorial Med Course 441
Tutorial Case
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14 year old Saudi Malec/o fever-headache for 10 daysGeneral malaiseDark urine x 3 days
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HPIFever
intermittentMuscular joint
painUrine character Edema No skin rash
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PH & Med◦Antibiotic and NSAID
Social HxS. reviewFH
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Examination
BP : 160/90 mmHg and pulse rate 120/min◦Temp : 39 ºC Resp 25/min.
paleLook SickPuffiness in faceHead and neckJVP
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Chest ExaminationNormal percussionNormal TVFNormal breath soundVesicular breathingS1 increaseS2 NS3 positivePansystolic murmur
◦Radiation to axilla◦Grade IIII
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Abd◦Tend epigastic◦Tend loins◦BS +ve
CNS◦Normal
M.S. /Normal
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Initial Diagnosis
Fever? Infection vs autoimmune DiseaseMurmur ; M R vs VSDHEAMATURIA
Urine Sample with hematuria
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Initial Diagnosis
Hematuria Systemic
◦ Hemolytic Anemia◦ Embolization ◦ Anti-coagulant
Surgical◦ Stone ◦ Tumor◦ Papillary◦ APKD
Medical◦ Acute kidney injury◦ Glomerulonephritis◦ Rapid pogressive glomerulonephrtis◦ IgA Nephropathy
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Differential Diagnosis of Hematuria
ARF-AKI-ATN◦ Acute glomerulonephritis (post-
infection)◦ RPGN◦ IgA◦ Hemolytic uremic syndrome◦ NSAID
Hemolytic Anemia
IgA Nephropathy hemolytic uremic
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InvestigationWBC 15,000 cells/microliter
◦ Hb – 100 g/L◦ Plat – 150 g/L◦ ESR 90
PT normal◦ PPT normal Sec◦ BI normal Sec
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U&E Scr - 210µmol/LUrea – 20mmol/LK – 6mmol/LNa – 125 mmol/LCa – 1.9 mmol/LAlbumin – 28 g/L
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Urine Analysis
Many RBCRed cell cast
abscentProtein – 1.2 g/24
hr
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U/S : kid size ENLARGE 12.2 cm
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Treatment
Patient receive ceftriaxone IV and IV fluid
TREAT HYPERKALEMIA
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Follow – up:
S Cr – 300 µmmol/LJVPOliguriaEdema
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Investigations for Glomerulonephritis
Regular follow-up and U&EAntistreptolysin O (ASO)ANA, Anti-DNAC3-C4
ANCA (p,c)HCV Antibody (HBsAg)HIVRFCryoglobulinAnti-basement membrane anti-body
(with lung hemorrhage
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Management IV LasixRepeat urine analysis
◦RBC castKidney biopsy : RPGNSerology tesy : all negativeRF: -negativeFinal diagnosisAnti-glomerular basement
membrane anti-bodies
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Glomerular Disease – Acute Glomerulonephritis
Post infectious glomerulonephritis
Group A Strep Infection Infective endcarditis
Membranoproliferative glomerulonephritis:
Systemic lupus erythematosus
Hepatitis C virus
IgA Nephropathy (Buerger’s Disease)
Rapidly progressive glomerulonephritis
Type I RPGN (direct antibody) Good Posture syndrome
Type II RPGN (immune complex)
Post infectious Systematic lupus erythematosus Henoch – Schonlein pupura (IgA)
Type III RPGN (pauci-immune) Vasculitis (, Wegener
granulomatosis; poiyarteritis nodosa-microscopic polyangitis)
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Complications of acute glomerulonephritis
HypertensionPulmonary edemaHyperkalemiaEncephalopathy convulsionElectrolyte disturbancePericaditisGastroentritisPeptic ulcer
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Management of Glomerulonephritis
Treat the causeConservative managementDialysis
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Acute post-infection glomerulonephritis
Often associated with group AB-hemolytic streptococcal type 12
infectionAlso staphylococcus or viruses
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Acute Glomerulonephritis
Symptoms occur 10-21 days after infection◦Hematuria◦Proteinuria (<1gm/24 hr)◦Decreased GFR, oliguria◦Hypertension◦Edema around eyes, feet and ankles◦Ascites or pleural effusion
Antistreptolysin O (ASO), Low C3, normal C4
◦Kidney biopsy immune complexes and proliferation
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Proliferative GN-poststretococcal
This glomerulus is hypercellular and capillary loops are poorly defined This is a type of proloferative glomerulonephritis known as post-
streptococcal glomerulonephritis
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Post-streptococcal GN
Post-streptococcal glomerulonephritis is immunologically mediated, and the immune deposits are distributed in the capillary loops in a granular, bumpy pattern because of the focal nature of the deposition process
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Post-streptococcal glomerunephritis
Conservative Treatment (acute kidney injury
Improves 1 – 4 weeks, C3 normalizes in 1 – 3 months, hypertension improves 1 – 3 months, intermittent hematuria x 3 years
99% complete recovery in children and 85% in adult
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IgA nephropathy (Buerger’s Disease)
Most common acute glomerulonephritis in US, South East Asia
Associated with H.S. Purpura Upper respiratory (50%) in 1
– 2 days (synpharyngitic hematuria)
Primary versus secondary (IBD, Liver disease, SLE, vasculitis)
50% risk of CRF Proteinuria, hypertension,
renal insufficiency predict worse prognosis
50% increase IgA, normal compliments
TREATMENT OF CONSERVATIVE ACEi
HIGH RISK: patient prednisone and alkylating agent
Cyclophosphamide-azothroprim & ASA & ACEi & tosilectomy
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Rapid Progressive GN
Type I RPGN (direct antibody)◦Good pasture syndrome
Type II RPGN(immune complex)◦Post infectious◦Systematic lupus erythematosus◦Henoch-schonlein purpura (IgA)◦ cryoglobulinemia
Type II (pauci-immune)◦Vasculitis (, Wegener
granulomatosis, microscopic polyangitis,poplyarteries nodosa)
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Rapidly progressive GN
Develops over a period of days and weeks
Primarily adults in 50’s and 60’sProgresses to renal failure in a few
weeks or monthsHematuria is common, may see
proteinuria, edema or hypertension
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Rapidly progressive (Crescentic) Glomerulonephritis
Morphology◦Crescent formation◦Crescents are formed by
proliferation of parietal cells◦Infiltrates of WBC’s & fibrin
deposition in Bowman’s space◦EM reveals focal ruptures in the
GBM
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Goodpasture Syndrome
Antibody formation against pulmonary and glomerular capillary basement membranes
Damage glomerular basement membrane
Men – 20 to 30 years of agePulmonary hemorrhage and renal
failureTREATMENT
Early treatment is essential Pulse steroid (10 mg/kg/day for 3 – 5
days)CyclophosphamidePlasmapheresis
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Goodpasture’s syndrome
This immunoflourescence micrograph shows positivity with antibody to IgG has a smooth, diffuse, linear pattern that is characteristic for glomerular basement antibody with Goodpasture’s syndrome
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Microscopic PolyangitisNecrotizing vasculitis of small – and
medium – sized vessels in both the arterial and venous circulations
Frequently involves the lung and the kidney with typical complications of hemorrhage and glomerulonephritis
Usually positive p-ANCA (anti-myeloperoxidase)
Usually positive c-ANCA (ant-proteinase 3)
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Treatment Initial TherapyCombination cyclophosphamide-
corticosteroid therapyPulse methyl prednisone (10
mg/kg/day for 3-5 days)A slow steroid taper, with the goal of
reaching 20 mg of prednisone per day by the end of two months and an overall glucocorticoid course of between 6 and 9 months
Either daily oral or monthly intravenous cyclophosphamide
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Treatment
PlasmapheresisSevere manifestations of
pumonary hemorrhage on presentation
Dialysis – dependent renal failure unpon presentation
Concurrent anti-GBM antibodies
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