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A. PEDIA BOARD REVIEW > NEPHRO Chap 508-536 > Flashcards

NEPHRO Chap 508-536 Flashcards

1
Q

At least 5 RBC in urine

A

Hematuria

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2
Q

MC chronic glomerular disease in children

A

IgA Nephropathy

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3
Q

Focal and segmental mesangial proliferation and ibcreased mesangial matrix

A

IgA Nephropathy

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4
Q

Renal histo: epithelial crescent formation and sclerosis

A

IgA Nephropathy

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5
Q

Gross hematuria that occurs 1-2 days after an upper respiratory or GI infection
(+) loin pain
Normal C3

A

IgA Nephropathy

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6
Q

Nephritis associated with gene mutations for Type IV collagen

A

Alport Syndrome (Hereditary Nephritis)

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7
Q

Renal histo:
- mesangial proliferation and capillary wall thickening leading to PROGRESSIVE GLOMERULAR SCLEROSIS
- diffuse thickening, splittinh and layering of glomerular and tubular basement membranes
(+) FOAM CELLS (lipid containing tubular or interstitial cells)

A

Alport Syndrome (Hereditary Nephritis)

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8
Q

Asymptomatic microscopic hematuria, intermittent
1-2 days after URTI
Bilateral SENSORINEURAL HEARING LOSS (NEVER CONGENITAL)
ANTERIOR LENTICONUS
(+) family history of renal disease

A

Alport Syndrome (Hereditary Nephritis)

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9
Q

Sudden onset of GROSS hematuria, edema, hupertension and renal insufficiency
(+) history of yhroat or skin infection

Renal histo: lumpy bumpy appearance of glomerulus

Low C3

A

Post streptococcal Glomerulonephritis

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10
Q

Weeks to develop GN post strep pharyngitis

A

1-2 weeks after

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11
Q

Weeks to develop GN post strep pyoderma

A

3-6 weeks

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12
Q

Urinary protein excretion and hypertension normalizes by… in GN

A

4-6wks

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13
Q

Serum C3 level normalizes by… in GN

A

6-8 weeks

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14
Q

Microscopic hematuria persists for… in GN

A

1-2 years after

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15
Q

Renal histo: diffuse thickening of basement membrane WITHOUT cell proliferative changes

Electron Microscopy (EM): granular deposits of IgG and C3

NEPHROTIC SYNDROME with RENAL VEIN THROMBOSIS

A

Membranous Nephropathy

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16
Q

GN associated with Hepatotis B and Syphilis

A

Membranoproliferative Glomerulonephritis (MPGN)

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17
Q

MC Membranoproliferative Glomerulonephritis

Renal histo: accentuated lobular pattern of glomeruli

A

Type I MPGN

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18
Q

Type of MPGN with prominent C3 immunofluorescence

EM: lamina densa is very dense WITHOUT evident immune-complex deposit

Markedly depressed C3

A

Type II MPGN

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19
Q

MPGN associated with partial lipodystrophy (diffuse loss of adipose tissue and decreased complement

A

Type II MPGN

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20
Q

Gold standard for establishing SLE nephritis

A

Kidney biopsy

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21
Q

Classification of nephritis?

No histologic abnormalitis but with present mesangial immune deposits

A

WHO Class I nephritis

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22
Q

Classification of nephritis?

Mesangial hypercellularity with deposits

A

WHO Class II nephritis

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23
Q

Classification of nephritis?

Mesangial and endocapillary lesions with <50% of glomeruli involvement

A

WHO Class III nephritis

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24
Q

Classification of nephritis?

Mesangial and endocapillary lesions with >50% of glomeruli involvement

A

WHO Class IV nephritis

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25
Q

Monitoring for HSP Nephritis

A

Urinalysis weekly during active disease then

Monthly up to 6 months

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26
Q

Hallmark of Rapidly Progressive GN

A

Crescents in glomeruli

*proliferation of epithelial cells in Bowman’s space

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27
Q

Pulmonary hemorrhage and Glomerulonephritis

A

Goodpasture disease

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28
Q

Pulmonary hemorrhage and Glomerulonephritis

A

Goodpasture disease

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29
Q

Kidney biopsy: cresenteric GN
Immunofluorescence: continuous linear deposition of IgG along BM

Serum ANTI-GBM antibody is present
Normal C3
ANCA elevated

A

Goodpasture Disease

30
Q

Triad of Microangiopathic hemolytic anemia, thrombocytopenia and renal insufficiency

A

Hemolytic Uremic Syndrome

31
Q

Most common form of HUS

A

Diarrhea associated HUS (E. coli)

32
Q

Approved treatment for atypical HUS

A

Eculizumab

33
Q

Unilateral bleeding of the left ureter due to compression of the left renal vein (mesoaortic compression)
Persistent hematuria, left lower abdominal pain, orthostatic hypotension

A

Nutcracker syndrome

34
Q

Thrombus formstion due to endothelial injury secondary to hypoxia, endotoxin or contrast media
SUDDEN ONSET of GROSS HEMATURIA & UNILATERAL or BILATERAL FLANK MASSES

UTZ: Marked renal enlargement
Radionuclide study: no renal function of affected kidney

A

Renal vein thrombosis

35
Q

Thrombus formation due to endothelial injury secondary to hypoxia, endotoxin or contrast media
SUDDEN ONSET of GROSS HEMATURIA & UNILATERAL or BILATERAL FLANK MASSES

UTZ: Marked renal enlargement
Radionuclide study: no renal function of affected kidney

A

Renal vein thrombosis

36
Q

Treatment of Renal Vein thrombosis

A

Heparin

37
Q

Severe hypertension secondary to RVT refractory to medications

Tx?

A

Nephrectomy

38
Q

Autosomal dominant

Recurrent gross hematuria, persistent microscopic hematuria, dysuria in the ABSENCE of STONE FORMATION

A

Idiopathic hypercalciuria

*Dx: 24h urine calcium >4mg/kg
Spot urine Ca:crea >2
*Tx: Hydrochlorothiazide 1-2mg/kg/24h single morning dose

39
Q

Main site of electrolyte reabsorption

A

Proximal tubule

40
Q

Promotes calcium reabsorption

A 
Parathyroid hormone
Calcitonin
Vitamin D
Thiazide diuretics
Volume depletion
41
Q

Promotes calcium excretion

A

Volume expansion
Increased sodium intake
Diuretics

42
Q

Sites of bicarbonate reabsorption

A

Proximal tubule

Collecting tubule

43
Q 
Proximal Renal Tubular acidosis (pRTA)
Ocular abnormalities 
Short stature 
Enamel defects
Intellectual impairment
Basal ganglia calcification
A

Isolated autosomal recessive pRTA

44
Q 
Proximal RTA
Low molecular weight proteinuria
Glycosuria
Phosphaturia
Aminoaciduria
A

Fanconi syndrome

45
Q

Defect in metabolism of cysteine leading to accumulation of cystine crystals in major organs

A

Cystinosis

46
Q

Most sever form of cystinosis

A

Infantile or Nephropathic cystinosis

  • 1st 2 years of life
  • growth failure and severe tubular dysfunction
47
Q

Treatment of cystinosis

A

Cysteamine

- binds to cystine and converts it to cysteine

48
Q

NAGMA
Growth failure
Phosphate and bicarbonate wasting
Urine is acidic (pH<5.5)

A

Proximal RTA (Type II)

49
Q 
NAGMA 
Growth failure 
Severe metabolic acidosis
NEPHROCALINOSIS
HYPERCALCIURIA
Hypokalemia
Urine pH>6

May be associated with sensorineural deafness

A

Distal RTA (Type I)

50
Q

Cystic dilation of terminal portions of collecting ducts

Medullary calcinosis on UTZ

A

Medullary sponge kidney

51
Q

Hyperkalemia
Hypoaldosteronism (impaired aldosterone production) or
Pseudohypoaldosteronism (impaired renal responsiveness to aldosterone)
Hyperkalemic NAGMA

A

Hyperkalemic RTA (Type IV)

52
Q

Formula for anion gap

A

Na - (Cl + HCO3)

53
Q

Normal anion gap

A

12-20

54
Q

Formula for urine anion gap

A

(Urine Na + Urine K) - urine Cl

55
Q

Mainstay of therapy for RTA

A

Bicarbonate replacement

56
Q

Inability to concentrate urine

A

Nephrogenic DI

57
Q

Polyuria, hypernatremia, diluted urine

Serum Osm >/=290
Urine Osm <290

A

Nephrogenic DI

58
Q

Hypokalemic Metabolic Alkalosis
HYPERCALCIURIA
Salt wasting
Recurrent episidoes of dehydration

*maternal history of polyhydramnios8

Urinary calcium, sodium and potassium are ELEVATED
Serum renin, aldosterone and prostaglandin E are ELEVATED

A

Bartter Syndrome

59
Q

Hypokalemic Metabolic Alkalosis
HYPOcalciuria
HYPOMAGNESEMIA

Late childhood
Recurrent muscle cramps and spasms
*DO NOT have history of recurrent dehydration

Urinary Calcium is LOW
Urinary Magnesium is ELEVATED

A

Gitelman Syndrome

60
Q

Associated with Rickets

A

Proximal RTA

61
Q

Tubulointerstitial inflammation & damage with relative sparing of glomeruli

A

Tubulointerstitial nephritis (TIN)

62
Q 
Fever, rash and arthralgia (1-2 weeks after antibiotics)
Rising serum creatinine
Flank pain
Nonoliguric
Normotensive

UA: white blood cell casts

Lymphocytic infiltration of tubulointerstitium, tubular efema and tubular damage

A

Acute TIN

*rbc casts (sign of glomerular disease) are absent

63
Q

Type of TIN that presents with nephrotic syndrome

A

Acute TIN secondary to NSAIDs

64
Q

T/F: Corticosteroid administration within 2 weeks of the discontinuation of the offending agent can hasten recovery and improve long-term prognosis in drug-induced TIN

A

True

65
Q

Most important factor predicting progression to ESRD in Chronic TIN

A

Severity of interstial disease

66
Q

Nephrotoxic?

ACE Inhibitors

A

Yes. Causes
Nephrotic syndrome
Acute renal failure

67
Q

Nephrotoxic?

ACE Inhibitors

A

Yes. Causes
Nephrotic syndrome
Acute renal failure

68
Q

Nephrotoxic?

Amphotericin

A

Yes. Causes
Nephrogenic DI
Acute renal failure
Renal tubular acidosis

69
Q

Newborn
Massive polyuria, volume depletion, hypernatremia, hyperthermia
Irritabile
Constipation
Poor weight gain despite adequate caloric supplementation
Behavioral problems

A

Congenital Nephrogenic DI

70
Q

Rare cause of acute renal failure secondary to extensive ischemic damage to renal cortex

Commom in neonates (hypoxic or ischemic insult) and adolescents

(+) Hypertension
Hematuria, proteinuria on UA
Anemia and thrombocytopenia

A

Cortical necrosis

A. PEDIA BOARD REVIEW (13 decks)

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