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#DAY4_PEDIATRICS > NEPHROLOGY > Flashcards

NEPHROLOGY Flashcards

1
Q

Management of Minimal Change Disease

A
  • Corticosteroid
  • Tuberculosis must be first ruled out
  • Uncomplicated nephrotic syndrome between 1-8yo are likely to have steroid responsive MCNS
    • Initiate steroids even without biopsy
  • Do biopsy if with features less likely of MCNS
    • Gross hematuria, hypertension, renal insufficiency, hypocomplementemia, < 1yo or > 12yo
  • Prednisone or Prednisolone (60mg/BSA/day or 2mg/kg/day, max 60mg daily) for 4-6 weeks
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2
Q

Linear IgG and C3 on Immunofluorescence is seen in

A

Goodpasture syndrome

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3
Q

Children who fail to respond to prednisone therapy within 8 week

A

Steroid resistant

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4
Q

Cloudy urine

A

can be normal; due to crystal formation at room temp.

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5
Q

In APSGN, what major noxious products of complement activation are produced after C3 activation?

A

anaphylatoxin (increases vascular permeability) & C5a (release substances that damage cells & basement membranes)

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6
Q

The most common cause of gross hematuria in pediatric population is?

A

Urinary Tract Infection

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7
Q

Relapse within 28 days of stopping prednisone therapy

A

Steroid dependent

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8
Q

Nephrotic Syndrome most responsive to steroids

A

Minimal Change DIsease

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9
Q
A
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10
Q

GRANULAR IgG, C3 on Immunofluorescence is a characteristic of

A

APSGN

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11
Q

Triad of Hemolytic Uremic Syndrome

A
  1. Microangiopathic Hemolytic Anemia (mechanical damage to RBCs as they pass through damaged endothelium)
  2. Thrombocytopenia (d/t intrarenal platelet adhesion or damage)
  3. Uremia
  • Onset is preceded by gastroenteritis (fever, vomiting, abdominal pain, bloody diarrhea)
  • Sudden onset of pallor, irritability, weakness, lethargy & oliguria usually occurs 5-10 days after the initial gastroenteritis or respiratory illness
  • PE: dehydration, petechiae, hepatosplenomegaly, marked irritability
  • Peripheral smear: helmet cells, burr cells, fragmented RBCs
  • Increased reticulocyte count, negative Coombs test, leukocytosis, thrombocytopenia, anemia, hematuria & proteinuria, normal PT & PTT, stool culture is often negative
  • Supportive care: fluids & electrolytes, early institution of peritoneal dialysis, BP control, red cell transfusion
  • Platelets NOT generally administered regardless of platelet count (almost immediately consumed by active coagulation and can worsen the clinical course)
  • NO antibiotic therapy (can lead to increased toxin release)
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12
Q

Laboratory criteria for diagnosis of TTP

A

The following are both present at some time during the illness:

  1. Anemia (acute onset) with microangiopathic changes (schistocytes, burr cells, helmet cells) on peripheral blood smear
  2. Renal injury (acute onset) evidenced by hematuria, proteinuria, or elevated creatinine level: equal or > 1 mg/dL in < 13 years old or >1.5 mg/dL in > 13 years old or equal or >50% increase over baseline
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13
Q
  • The urinalysis reveals 3+ or 4+ proteinuria
  • Spot urine protein/creatinine ratio exceeds 2.0 and urinary protein excretion exceeds 3.5 g/24 hr in adults and 40 mg/m 2 /hr in children.
  • The serum albumin level is generally <2.5 g/dL, and the serum cholesterol and triglyceride levels are elevated.
  • C3 and C4 levels are normal.
  • Renal biopsy is not required for diagnosis in most children.

• >95% respond to corticosteroid therapy

A

NEPHROTIC SYNDROME (MINIMAL CHANGE DISEASE)

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14
Q

In APSGN, When wil microscopic hematuria resolve and normalize?

A

1-2 years

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15
Q

Best single Ab titer to document skin infection s DNAse B antigen

A

DNAse B antigen

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16
Q

Nephrotic Range 24 hr urine protein

A

Nephrotic range > 40mg/m2 /hr

o Normal is = 4mg/m2/hr

o Abnormal 4-40mg/m2/hr

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17
Q

NEPHRITIC SYNDROMES

A
  • PSGN
  • RPGN
  • IgA Nephropathy (berger disease)
  • Alport Syndrome
  • GoodpastureSyndrome
  • MPGN - Nephrotic/Nephritic
  • SLE - Nephrotic/Nephritic
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18
Q

In PSGN, C3 sould normalize within ___

A

8 weeks

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19
Q

Children who continue to have proteinuria (+2 or greater) after 8 week of steroid therapy

A

Steroid resistant

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20
Q

BOTTOM-UP approach - identify upper and lower tract abnormalities

A

UTZ then VCUG then DMSA

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21
Q

In APSGN, patient develops nephritic syndrome how many weeks after skin infection?

A

3 - 6 weeks

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22
Q

Subepithelial humps are seen in

A

PSGN

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23
Q

Diffuse mesangial deposits are seen in

A

IgA nephropathy

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24
Q

Detect posterior urethral valves

A

VCUG

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25
Q

In APSGN, patient develops nephritic syndrome how many weeks after throat infection?

A

1-2

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26
Q

Renal parenchyma is involved in what type of UTI?

A

Pyelonephritis

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27
Q

Documentation of prior strep infection on the skin

A

antideoxyribonuclease B

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28
Q
  • LM: Diffuse thickening of glomerular capillary walls
  • IF: Granular IgG and C3
  • EM: Sub-epithelial deposits of electron dense material
  • “Spike and Dome” appearance
A

Membranous Glomerulonephritis

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29
Q

Relapse on alternate-day steroid therapy

A

Steroid dependent

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30
Q

TOP-DOWN approach

A

UTZ then DMSA then VCUG

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31
Q

UTI prevalence with age

A

o 1 st year of life = male predominance

o Beyond 1-2yo = female predominance

32
Q
A
33
Q

Clinical Pictures of Glomerular Diseases

A
34
Q

Grossly red urine with or without blood clots

A

from the lower urinary tract

35
Q

In APSGN, When will the abnormalities resolve and normalize during acute phase?

A

6-8 weeks

36
Q

What is involved in pyelitis?

A

Renal PELVIS

37
Q

Nephrotic Range Urine protein: creatinine ratio

A

>2 is nephrotic range proteinuria

o <0.5 in <2yo is normal

o <0.2 in >2yo is normal

38
Q

LM: normal

EM: diffuse effacement of epithelial foot process, no deposits

A

Minimal Change Disease

* often preceded by URTI and prophylactic immunization

39
Q
  • LM: Large, hypercellular glomeruli
  • Increased mesangial matrix
  • Double Contour or Tram-track appearance
A

Membranoproliferative Glomerulonephritis

40
Q

How is HUS different from thrombotic thrombocytopenic purpura (TTP)?

A
  • TTP has the same triad but can include CNS involvement and fever and has a more gradual onset
  • Fewer cases of TTP can occur after diarrhea compared to HUS
41
Q

Clinical picture of nephritic syndrome:

A
  • Hematuria
  • Oliguria
  • Hypertension
  • Azotemia
42
Q

What is the pathogenesis of PSGN?

A

Ab is produced & combines with a circulating Ag unrelated to the kidney → IC accumulate in glomeruli & activate the complement system → immune injury (Type III hypersensitivity)

43
Q

In APSGN, what hypothesis is given to explain the predilection to damage the glomeruli?

A

Localized in the glomeruli due to negatively charged capillary wall, mesangial trapping, hydrodynamic forces

44
Q

Presumptive UTI

A

Bag sample, positive urinalysis, symptomatic AND single organism with culture colony count > 100,000

45
Q

Fever may be the only manifestation.

A

PYELONEPHRITIS

46
Q

Nephrotic Syndromes

A
  • Idiopathic Nephrotic Syndrome
    • Minimal change disease
    • Focal segmental glomerulosclerosis
    • Mesangial proliferation
  • Glomerular diseases
    • Membranous nephropathy
    • Membranoproliferative glomerulonephritis
47
Q

In APSGN, when will urinary protein excretion and hypertension resolve and normalize?

A

6 mos

48
Q

CAUSES OF TRANSIENT PROTEINURIA

A
  • Fever
  • Exercise
  • Dehydration
  • Cold exposure
  • Congestive heart failure
  • Seizure
  • Stress
49
Q
A
50
Q

Normal specific gravity of urine

A

1.015-1.025

51
Q

If C3 levels did not go back to normal and the proteinuria persited after 8 weeks in PSGN, what would be your differential?

A

Membranoproliferative Glomerulonephritis (MPGN)

52
Q

Microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency

A

HEMOLYTIC-UREMIC SYNDROME

53
Q

In APSGN, why does serum C3 decrease?

A

Inflammatory reaction follows immunologic injury due to activation of classic and alternative pathways which converge at C3 → lysis of cell membranes → hypocomplementemia

54
Q

Indications for Renal Biopsy in APSGN

A
  • Acute renal failure
  • Nephrotic syndrome
  • Absence of evidence of strep infection
  • Normal complement level
  • Hematuria and proteinuria
  • Low C3 that persists more than 2 months
55
Q

best to assess renal scarring

A

DMSA scan

56
Q

UTI if with ff lab findings

A

o > 50,000 colonies of single pathogen from suprapubic tap or catheterized sample OR

o 10,000 colonies + symptoms

57
Q

Small vessel vasculitis characterized by:

  • purpuric rash
  • arthritis
  • abdominal pain
  • glomerulonephritis with IgA deposits
A

HSP

58
Q

False negative hematuria

A

o Formalin

o High urinary ascorbic acid

59
Q
  • Presence of persistent microscopic hematuria and isolated thinning of the GBM on E/M
  • Often initially observed in childhood and is intermittent
  • Isolated hematuria in multiple family members without renal dysfunction is termed as benign familial hematuria
  • Important to monitor for hypertension, progressive proteinuria, or renal insufficiency
A

THIN BASEMENT MEMBRANE DISEASE

60
Q

GAS Serotype following throat infection

A

1, 2, 4 , 12, 18 25

61
Q

GAS Serotype following skin infection

A

49, 55, 57, 60

62
Q

GLOMERULONEPHRITIS VS NEPHROTIC IN CHILDREN

A
63
Q

Clinical picture of nephrOtic syndrome:

A
  • Proteinuria (nephrotic range)
  • Albumin low
  • Lipid High
  • Edema
64
Q

Patients who respond well to prednisone therapy but relapse 4 or more times in a 12 month period

A

Frequent relapser

65
Q

What are the only causes of Renal Insufficiency that cause decreased C3?

A

1. PSGN

2. MPGN

3. Lupus Nephritis

66
Q

Documentation of prior strep infection in the throat

A

ASO

67
Q

Crescentic GN is a characteristic of

A

RPGN

68
Q

In APSGN, when will the C3 level resolve and normalize?

A

6-8 weeks

69
Q

True or False. Administering antibiotics will NOT alter the natural history of PSGN.

A

TRUE

Antibiotics do not alter the course of PSGN. We give it to prevent the spread of nephritogenic steptococcus.

70
Q
  • LM: Focal segmental sclerosis and hyalinosis
  • EM: Loss of foot process, epithelial denudation
A

Focal Segmental Glomerulosclerosis

* least responsive to steroids

71
Q

Brown-colored / tea-colored urine

A

glomerular in origin

72
Q

The major complication of nephrotic syndrome is

A

infection

* The most frequent type of infection is spontaneous bacterial peritonitis.

* The most common organism causing peritonitis is pneumococcus.

73
Q

brown, cola, tea, burgundy colored urine. Proteinuria >100mg/dl on dipstick, RBC casts, dysmorphic RBCs (acanthocytes)

A

Glomerular source of hematuria

74
Q

False positive

A

o Alkaline urine (pH>8)

o Hydrogen peroxide

75
Q

Where is the site of the pathology as seen in the electron microscope in MPGN?

A

Subendothelial

76
Q
  • Bilateral sensorineural hearing loss (never congenital)
  • Ocular abnormalities (30-40%) such as anterior lenticonus (its presence is pathognomonic), macular flecks, & corneal erosions
  • Critical in the diagnosis: family history, screening urinalysis of 1 st -degree relatives, audiogram, ophthalmologic exam
  • Highly likely: (+) hematuria and at least 2 of the ff: macular flecks, recurrent corneal erosions, GBM thickening or thinning, sensorineural deafness
A

ALPORT SYNDROME (HEREDITARY NEPHRITIS)

#DAY4_PEDIATRICS (15 decks)

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