Case Management:Acute Glomerulonephritis

Presentor: Ma. Nieves Elizabeth N. Cruz, MD

Rizal Provincial HospitalRizal Provincial HospitalMay 25, 2010May 25, 2010

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• J.C., 8/f• Cardona, Rizal

• Admitted: April 22, 2010• Discharged: April 26, 2010

GENERAL DATA

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CHIEF COMPLAINT

tea-colored-urine

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HISTORY OF PRESENT ILLNESS

4 days PTA fever, intermittent; resolved with intake of Paracetamol

3 days PTA tea-colored urine dec.urine output

1 day PTA consult with a PMD

RPH

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PERTINENT P.E. FINDINGS

• Wt = 28kg• Temp = 36°C• BP = 100/70 mmHg• CR = 100 bpm• RR = 23 cpm

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PERTINENT P.E. FINDINGS

•No pallor•No facial edema•+ clear breath sounds•No respiratory distress•No abdominal distension•No visible lesions/wounds on extremeties

•No scrotal/bipedal edema

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ADMITTING DIAGNOSIS

T/C Acute Glomerulonephritis

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COURSE IN THE WARD

1st HD low salt dietIVF: D5W x kvoDx’cs: CBC, PC, UA, 24hr-urine-chon, BUN, Crea, ASO, C3, KUB-UTZ

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120/90mmHg

Tx’cs: Pen G, Paracetamol,Furosemide

Nifedipine, 5mg/cap, half cap/SL

COURSE IN THE WARD

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COURSE IN THE WARD

2nd HD

Yellowish urine

IVF: D5 0.3%NaClOral fluids limited

(accdg.to BSA)

BSA (wt)4(9)/100 x 100

Furosemide IV shifted to p.o.

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COURSE IN THE WARD

3rd HDu.o. = 0.8cc/24°/kg

4th HDu.o. = 0.9 cc/24°/kg

Furosemide ↑ q6°

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COURSE IN THE WARD

6th HD DischargedHome meds: TMP-SMZ Furosemide x 3daysAscorbic acid

Advised repeat KUB-UTZ after 2 weeks

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Urinalysis:

(4/19/10) (4/21/10) (4/25/10)

Color: dark yellow, turbid yellow, turbid yellow,sl.turbidpH: acidic acidic acidicsp.gr.: 1.010 1.010 1.010Albumin: +4 +4 traceRBC: loaded plenty 5-7WBC: 5-7 plenty 1-2

LABORATORY RESULTS

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CBC (4/19/10) WBC 8.0 seg 0.89 lympho 0.30 eos 0.01

Hgb 110 hct 0.33 Platelet 232

LABORATORY RESULTS

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(4/22/10) ASO 400IU/ml

C3 28.774 mg/L BUN 6.30

Crea 0.70 24°-urine-chon 793.8mg/ 24°

LABORATORY RESULTS

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KUB-UTZ:

pelvicocaliectasia, rt kidney; left kidney & UB, normal

LABORATORY RESULTS

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Acute glomerulonephritis (AGN)

is a disease characterized by the sudden appearance of edema, hematuria, proteinuria, and hypertension.

It is a representative disease of acute nephritic syndrome in which inflammation of the glomerulus is manifested by proliferation of cellular elements secondary to an immunological mechanism.

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PATHOPHYSIOLOGY

Immune-complex disease

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A schematic representation of the proposed mechanism for acute poststreptococcal glomerulonephritis (APSGN). C = Activated complement;

Pl = Plasmin; NAPlr = Nephritis-associated plasmin receptor; SK = Streptokinase; CIC = Circulating immune complex.

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Normalization of urine sediment

Parameter

• Gross hematuria• Complement level• Proteinuria• Micro-hematuria

Resolved by

• 2-3 weeks• 6-8 weeks• 2-6 months• 6-12 months

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TYPICAL COURSE

• Latent - few days to 3 weeks• oliguric – 7 to 10 days• diuretic – 7 to 10 days• convalescent – 7 to 10 days

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CLINICAL & LABORATORY PROFILE

• hematuria (gross) 100%• proteinuria 86%• edema 85%• hypertension 82%• hypocomplementenemia 80%• cryoglobulinemia 63%• gen. malaise, weakness 55%• oliguria 52%• nausea & vomiting 15%• dull, lumbar pain 5%

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ETIOLOGY

1. InfectionsBacterial: GABS, Strep. Viridans, strep.

Pneumoniae, S. aureus, S. epidermidis, T. pallidum, Leptospira, S. typhi

Viral: hep B, measles, mumps, CMV, enterovirus, GBS, onconavirus

Parasitic: toxoplasma, P. malariae, P, falciparum, schistosoma

Rickettsial: scrub typhusFungal: coccidioides immitis

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2. Drugs: toxins, antisera, vaccines, DPT

3. Misc: tumor antigen, thyroglobulin, autologous Ig

ETIOLOGY

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Group A Beta-hemolytic streptococcus (GABS) Nephritogenic strains

Sites: 1. Upper resp. tract: pharyngitis, M1, 2, 4, 12, 18, 252. Skin: pyoderma, M49, 55, 57, 603. Middle ear : rare

ETIOLOGY

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LABORATORY DIAGNOSIS:

Urinalysis

• dec. volume & sp. gravity• casts (fine & granular)• hematuria (dysmorphic rbc)• proteinuria

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Bacteriology/serology• culture of GABS• strp antibody titers – ASO

(pharyngitis) antiDNAse B (pyoderma), streptozyme

• serum complement – C3, generally dec. in acute phase, rises during convalescence, normal in 10% of cases

LABORATORY DIAGNOSIS:

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Renal function

• BUN, Crea – usually normal• In marked azotemia – metab.acidosis,

hyperK, hypoNa, inc. crea

LABORATORY DIAGNOSIS:

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• Hematology: +dilutional anemia, transient hypoalbuminemia

• Radiography: CXR – sunburst in congestion, renal utz

LABORATORY DIAGNOSIS:

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DIFFERENTIAL DIAGNOSES

• Low serum complement level• Systemic diseases• SLE (focal, 75%; diffuse, 90%)• Subacute bacterial endocarditis (90%)• Visceral abscess• "Shunt" nephritis (90%)• Cryoglobulinemia (58%)

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• Renal diseases

• Acute postinfectious glomerulonephritis (>90%)

• MPGN - Type I (50-80%), type 2 (80-90%)

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DIFFERENTIAL DIAGNOSES

• Normal serum complement level• Systemic diseases• Polyarteritis nodosa group• Hypersensitivity vasculitis• Wegener granulomatosis• HSP• Goodpasture syndrome

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DIFFERENTIAL DIAGNOSES

• Renal diseases• IgA (or IgG-IgA) nephropathy• Idiopathic rapidly progressive

glomerulonephritis (RPGN)• Anti-glomerular basement membrane

(GBM) disease• Negative immunofluorescence findings• Immune complex disease

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DIFFERENTIAL DIAGNOSES

MANAGEMENT

Supportive & Symptomatic• bed rest, prn• fluid & salt restriction• Fluids: 400-600 ml/m2/day + UO 24h• NaCl ≤ 2g/day• K ≤ 40mEq/day

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Antibiotics: • Penicillin 50000-100000 u/kg/d tid-qid x

10days

Specific interventions:• hypertension• CHF• Furosemide 2mg/kg/dose/IV• Dialysis: if refractory indications: uremia,

intractable hyperK, CHF

MANAGEMENT

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NORMAL BP VALUES

Age

NB8-30days1 mo – 2 yrs2-5y6-11y>12y

Upper limit

95 mmHg, systolic

105115/75130/80135/85140/90

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PROGNOSIS

• complete resolution • 5-10% progress to chronic state

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Mortality Rate:

• 0-7% due to sepsis, CHF, hypertensive enceph

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Consultation with a pediatric nephrologist isnecessary when one or more of the following arepresent:

• Severe hypertension• Severe oliguria• Severe edema• Nephrotic-range proteinuria• Azotemia (moderate to marked)• Recurrent episodes of gross hematuria• Persistently depressed C3 (past 8-10 wk)

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Consultation with a pediatric nephrologist is necessary when one or more of the following are present:

Atypical onset

• Absence of latent period• No evidence of streptococcal illness

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Failure of expected resolution of clinical signs• Gross hematuria within the preceding 10-14

days• Microscopic hematuria within 1 year• Edema within 2 weeks• Proteinuria (>50 mg/dL) within 6 months• Azotemia within 1 week• Hypertension within 6 weeks

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Consultation with a pediatric nephrologist is necessary when one or more of the following are present:

FOLLOW-UP

Further Inpatient Care

Only a small percentage of patients with acute glomerulonephritis (AGN) require initial hospitalization, and most of those are ready for discharge in 2-4 days.

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Further Inpatient Care

As soon as the blood pressure (BP) is under relatively good control and diuresis has begun, most children can be discharged and monitored as outpatients.

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Further Outpatient CareFollow up at 0-6 weeks as frequently as

necessary to determine the following:Hypertension has been controlled.Edema has started to resolve.Gross hematuria has resolved.Azotemia has resolved.

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Follow up 8-10 weeks after onset to determine the following:Azotemia has subsided.Anemia has been corrected.Hypertension has resolved.C3 and C4 concentrations have returned

to normal.

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Follow up at 3, 6, and 9 months after onset to check the following:Hematuria and proteinuria are subsiding

gradually.BP is normal.

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Follow up at 2, 5, and 10 years after onset to check the following:Urine is normal.BP is normal.Serum creatinine level is normal

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Follow up at 12 months after onset to determine the following:Proteinuria has disappeared.Microscopic hematuria has disappeared.

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