Glomerulonephritis Presentation

8/12/2019 Glomerulonephritis Presentation

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Glomerulonephritis

Inflammation and injury of the glomerular capillaries

Generally caused by immunological response resulting in

complement activation, leukocyte recruitment, and

cytokine release.


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Nephritic Syndrome Nephrotic Syndrome

Associated with injury/inflammation tothe glomeruli

Abnormal glomerular permeability

Hematuria

Azotemia & oliguria

Variable proteinuria

Hypoalbuminemia

Hyperlipidemia

Urine protein excretion rate >3.5g/day

RBC casts No casts or fatty casts

HTN

Edema

Edema

Hypercoagulable state

Increased risk of infection


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Case

A 14-year-old Hispanic male presents with a 3-day complaint of

brown urine. He has been your patient since birth and has

experienced no major illnesses or injuries, is active in band and

cross-country, and denies drug use or sexual activity. Two weeks

ago he had 2 days of fever and a sore throat, but he improvedspontaneously and has been well since. His review of systems is

remarkable only for his slightly puffy eyes, which he attributes to

late-night studying for final examinations. On physical

examination he is afebrile, his blood pressure is 135/90 mm Hg,

he is active and nontoxic in appearance, and he has someperiorbital edema. The urine dipstick has a specific gravity of

1.035 and contains 2+ blood and 2+ protein. You spin the urine,

resuspend the sediment, and identify red blood cell casts under

the microscope.


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Post-streptococcal glomerulonephritis

Epidemiology:

Most common between children 5-12 y.o.

Most common cause of acute nephritis worldwide

Clinical course:

Strep. Pharyngitis 1-2 weeks OR Strep. Pyoderma 3-6 weeks

before nephritic syndrome

Proteinuria and HTN should normalize 4-6 weeks after onset

Microscopic hematuria persists 1-2 years

Clinical Manifestations: asymptomatic, microscopic hematuria to full-blown acute nephritic

syndrome

Hematuria, proteinuria, edema, hypertension, and acute kidney injury


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Post-Strep GN cont.

Pathophysiology: Immune complex

Molecular Mimicry

Strep antigen deposition causing complement

Diagnosis Positive Serology(ASO or streptozyme)

AntiDNase B level

Low C3

Prevention Risk not eliminated from early antibiotic therapy

Treatment Control hypertension and renal problems

ACEi, lasix, sodium restriction

Prognosis Excellent

Mortality is due to poor management


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Impetigo and Strep Throat


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Case

A 15 year old boy comes to your clinic complaining of darkurine. He had a URI that recently cleared. Vital signs arestable except for a blood pressure of 145/92.

UA: Protein 1+, WBC 3-6/hpf, RBC 30-50/hpf, RBC casts Serum Chemistry:

Sodium: 138

Potassium: 4.5

Bicarb: 22

BUN: 18

Creatinine: 1.2

Complement levels are normal


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IgA Nephropathy(Berger Nephropathy)

Epidemiology Most common cause of GN in developed nations

Most common cause of chronic GN

15-30 y.o.peak 20-30s

Pathogenesis Etiology Unknown IgA deposition itself does not cause glomerular injury

Clinical course Gross hematuria 2 days of URI or GI sx

40-50% with gross hematuria

30-40% with microscopic hematuria

Nephritic/nephrotic syndrome

Labs and Exams ***Normal C3 levels***

Dx made only by biopsy Mesangial deposition of IgA


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IgA Nephropathy cont.

Prognosis and Treatment

Generally benign

Course depends on severity at onset

Prognosis may be different in adulthood

Medications ACEicontrol BP

Fish Oilcontrol disease progression

Corticosteroidscontrol disease


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Case

A 7 year old boy has cramping abdominal pain and therahs shown mainly on the back of his legs and buttocksas well as on the extensor surfaces of his forearms.Laboratory analysis reveals proteinuria and

microhematuria. In addition to his rash and abdominalpain, what other finding is he likely to have?

A: Chronic renal failure

B: Arthralgias

C: Seizures

D: Unilateral lymphadenopathy

E: Bulbar nonpurulent conjunctivitis


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Henoch Schonlein Purpura

Most common vasculitis in children

90% in children

IgA deposition in mesangium

Follows URI

Clinical Manifestations: Rash on buttocks and legs

Last 3-10 days, can recur up to 4 months after presentation

Edema: Periorbital, dorsa of hands/feet, lips, scalp Arthralgias

GI sxpurpura can be seen in the GI tract

Renal

CNS


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HSP

Diagnosis

Based on rashbut what if rash isnt the first sx?

Clinical

No lab findings are diagnostic

Serology

Elevated IgA

Treatmentsupportive

Prognosis

Self limited

Can recur in 4-6 months


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Minimal Change Disease

Epidemiology:

Most common primary glomerular disease in children

70-90% under 10y.o., peak incidence at 2-4y.o.

Etiology unknown

May be associated with NSAIDS, rifampin, neoplasms such as

Hodgkins disease

Clinical Course:

Nephrotic syndrome features

Diagnosis and Treatment Empiric treatment given prevalence in childhood

Treat symptomatically and give prednisone

Biopsy not made unless there is treatment failure


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Membranoproliferative Glomerulonephritis

(MPGN) Most commonly occurs in children and young adults

Primary, idiopathic and secondary forms

Secondary causes:

Hep B and C, syphilis, lupus, multiple myeloma

Different Forms:

Type I

Immune complex mediated

Type II

Not immune complex mediated. Decreased C3 levels is more common.

C3 levels in MPGN and Post Strep GN

Treatment:

Treat underlying cause


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Rapidly Progressive(Crescenteric)

Glomerulonephritis (CGN) ESRD within weeks to months if untreated


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Rapidly Progressive GN cont. (CGN)

Clinical manifestations:

Gross Hematuria

Oliguria

Edema

Severe form of any GN

Goodpasture diseaseusually goes on to rapidly progressive

Post strep GNrarely goes to rapidly progressive

Treatment

Treat aggressively with high dose steroids and cyclophosphamide

Can lead to ESRD despite treatment


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Most important points

Nephritic vs nephrotic syndrome RBC casts, hematuria, HTN vs hypoalbuminemia, proteinuria >3.5g/day,

edema

Post Strep GN Can come from both strep throat and strep pyoderma

Course of renal involvement cannot be altered

IgA nephropathy and HSP Both have IgA deposition in mesangium

IgA nephropathy and post strep GN Renal involvement in IgA nephropathy comes 2-3 days after URI sx while in

post strep GN, URI sx occur 2-3 weeks beforehand

IgA nephropathy have normal C3 levels while in post strep GN C3 levels are

decreased Lupus nephritis

Diffuse lupus nephritis is the most severe form

MPGN and Post Strep GN C3 levels are consistently low in MPGN while in post strep GN they normalize

in 2 months


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Glomerulonephritis Presentation