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Clin Med Exam 4 > Pediatric Nephrology: Paulson > Flashcards

Pediatric Nephrology: Paulson Flashcards

1
Q

What counts as pediatric CKD?((According to KDIGO)

A

Must meet one of the following:

  • GFR <60 ml/min for >3 months
  • GFR >60 ml/min + evidence for structural damage (like albuminuria, proteinuria, pathologic abnormalities on histology or imaging)
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2
Q

Stages of Chronic Kidney disease

A

add image

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3
Q

Pediatric CKD: causes

-list 2

A
  • Congenital disease: 60% of cases

- Glomerular disorders: 2nd most common cause

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4
Q

Pediatric CKD: describe Congenital disease

A 
Obstructive uropathy
Renal hypoplasia
Renal dysplasia
Reflux nephropathy
PKD
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5
Q

Pediatric CKD: describe Glomerular Disorders

A

-More common in kids >12 years
FSGS
Membranoproliferative glomerulonephritis
Minimal change disease

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6
Q

Presenting S/S of Pediatric (nonglomerular) CKD

A

Polyuria
Elevation in serum creatinine
Poor growth

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7
Q

Presenting S/S of Pediatric glomerular CKD

A

Tea-colored or cola-colored urine–>Look for hematuria, RBC casts
Edema
Elevation in serum creatinine
Elevated BP for age
Systemic findings indicative of a concurrent systemic disease that can affect kidney function (ie: SLE)

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8
Q

Things to look for on exam

A 
Growth parameters
Hypertension
Hypervolemia
Pericardial rub
Pallor (anemia)
Deformities of extremities from CKD-caused bone-mineral disorders
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9
Q

Diagnostics: best studies to use

A

-**Ultrasound-Most widely used—>Measure size of kidneys against normal values for age. *Look for deformities

Serum creatinine

UA may be helpful

Serum calcium, phosphorous, 25-hydroxyvitamin D, and PTH helpful if you suspect abnormalities in bone and mineral metabolism

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10
Q

General Management of Pediatric CKD

A

Treat reversible kidney dysfunction
Prevent or slow progression
Treat complications of CKD
Identify and prepare kids/families if RRT will be needed

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11
Q

Reversible Causes of CKD

A

-Decreased perfusion to kidneys:
Hypotension
Volume depletion
Medications that ↓ kidney perfusion

-Nephrotoxic drugs:
NSAIDs, contrast materials, aminoglycosides, as a few examples

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12
Q

How to Slow CKD Progression

A

-BP control:
ACEI/ARB preferred for kids with HTN + proteinuria

  • Differences from adults:
  • -Don’t limit protein intake
  • No data to support lipid lowering therapy or anemia correction in kids
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13
Q

Symptoms for CKD in peds, usually start around CKD stage ___

-list other Sx

A 
Start around CKD stage 3
Anorexia
Fatigue
N/V
Pericarditis
Bone and mineral disease
↓ neurocognitive function
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14
Q

Management of MBD(mineral bone disease):

  • Sx/clinical manifestations: list Ex’s
  • Tx: diet and ____
A

Mineral/Bone Disease:

  • Growth failure
  • Avascular necrosis
  • Skeletal fractures/deformities/pain
  • Vascular calcification
  • Control PO4, Ca, PTH, 25D

Tx: diet, binders (Sevalemer, Calcium, Iron), Vitamin D2/D3, Vitamin D analogs

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15
Q

Renal Replacement Therapy (RRT):

-initiated once GFR is less than ___

A

-Once GFR <30, start preparing the child/family

  • **Kidney transplantation is the preferred treatment for best survival and growth outcomes
    2nd: PD (peritoneal dialysis)
    3rd: HD (hemodialysis)
  • RRT often started earlier than GFR 10-15 because:
  • Poor calorie intake –> FTT (failure to thrive)
  • Symptomatic uremia
  • Delay in psychomotor development
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16
Q

CKD prognosis:

A
  • Higher morbidity & mortality
  • Increased hospitalizations
  • Increased depression
  • Worse QOL for patients, their parents, and their siblings
  • More likely to be unemployed
  • Leading causes of death are CV disease and infection
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17
Q

Obstructive Uropathy:

  • causes?
  • tx?
A
  • Stricture
  • Stenosis
  • Stones
  • Posterior urethral valves
  • ->Refer to urology
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18
Q

Reflux Nephropathy (Vesicoureteral reflux)(VUR)=

A

=Retrograde passage of urine from bladder–> upper urinary tract

-these kids are at higher risk for UTIs–> leads to renal scarring and..
Please refer to Brian Miller’s powerpoint for a review of this topic

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19
Q

Renal dysplasia=

  • kidneys may be variable in ____
  • Unilateral or bilateral?
A

=Malformed kidneys

  • Kidneys may be variable in size, but most are smaller than normal
  • May be unilateral or bilateral
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20
Q

Renal dysplasia:

-on a microscopic level:

A
  • Disorganized nephron elements
  • Decreased number of nephrons
  • Maldifferentiation of mesenchymal & epithelial elements
  • Transformation of tissue to cartilage and bone
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21
Q

Multicystic dysplasia=

A

a nonfunctioning dysplastic kidney with multiple cysts

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22
Q

Renal hypoplasia=

A

=Low number of structurally normal nephrons –>= a small kidney

  • ->Reduction of renal size by 2 SD for the mean size by age –and-
  • ->Exclusion of renal scarring (done by DMSA radionucline scan)
23
Q

Renal hypoplasia: etiology

A
  • Thought to be genetic

- No damage or malformations

24
Q

Renal agenesis=

A

Congential absence of renal parenchymal tissue

25
Q

Renal agenesis:

  • demographic?
  • Sx?
A
  • Males&raquo_space; females
  • Most asymptomatic: Solitary kidney is usually an incidental finding on an ultrasound–> Antenatally or as part of UTI eval
26
Q

Renal agenesis:

-Associated nonrenal anomalies (list)

A

Malformations of heart, genitals, bones, GI tract, respiratory tract

27
Q

Renal agenesis:

-Presentation?

A
  • May be discovered on routine antenatal screening –or-
  • Postnatally in a dysmorphic kid
  • May have:
  • -Impaired renal function at birth & progressive renal failure
  • -Associated urologic abnormalities of renal pelvis, calyces (congential hydronephrosis), and ureters (stenosis, VUR, megaureter)
  • –Can lead to symptomatic presentation from complications of the above: UTI, hematuria, fever, abdominal pain
28
Q

Renal Agenesis:

-Dx?

A
  • Renal ultrasound

- Frequent association of dysplasia with a collecting system anomaly–> consider voiding cystourethrography as well

29
Q

Renal Agenesis: tx?

A
  • Monitoring for progression

- Transplant/RRT

30
Q

Glomerular disorders: (list 3)

A
  • FSGS
  • Membranoproliferative glomerulonephritis
  • Minimal change disease
31
Q

Focal Segmental Glomerulosclerosis=

A

Sclerosis in parts (segmental) of at least 1 glomerulus (focal) in the entire kidney biopsy specimen when examined histologically

32
Q

Focal Segmental Glomerulosclerosis:

-etiology?

A

Can be from:
Genetics
Injury to podocytes and/or direct toxicity from drugs or viral infections
Secondary causes: obesity, HTN, HIV, chronic urinary reflux, analgesic or bisphosphonate exposure

33
Q

Focal Segmental Glomerulosclerosis:

-MC presentation?

A

Most commonly: acute onset of nephrotic syndrome

  • Peripheral edema
  • Hypoalbuminemia
  • Proteinuria (usually >3.5 g/day)
34
Q

FSGS:

____ GFR in about half of patients

A

decreased

35
Q

FSGS:

What do these Pts usually develop by 6-8 yrs?

A

ESRD

36
Q

FSGS:

-diagnosis made by**?

A

**Diagnosed by renal biopsy

May do genetic testing

37
Q

FSGS Treatment

A

Diuretics for edema
ACEI/ARB for HTN/proteinuria
Statin/niacin for HLD

Prednisone or immunosuppressants (ie: cyclosporine, tacrolimus)
Plasma exchange helpful prior to renal transplant to lower risk of graft loss
Also helpful in those who appear like they are about to relapse

38
Q

Membranoproliferative Glomerulonephritis= pattern of ____

A

glomerular injury on renal biopsy with characteristic changes on light microscopy
–>Relatively rare

39
Q

Membranoproliferative Glomerulonephritis: Variety of causes, 2 major causes are:

A
  • Immune-complex mediated

- Complement-mediated

40
Q

Membranoproliferative Glomerulonephritis:

Clinical Presentation

A

Anywhere on the spectrum of nephritidies:
Asymptomatic glomerular hematuria to
Gross hematuria to
Rapidly progressive glomerulonephritis (RPGN)

41
Q

Membranoproliferative Glomerulonephritis: dx?

A

Hematuria, often with dysmorphic red cells and red cell casts
Variable amount of proteinuria
Creatinine may be normal or elevated
Low complement levels

*Diagnosis by renal biopsy

42
Q

Membranoproliferative Glomerulonephritis: tx of mild diseases?

A

ACEI/ARB

43
Q

Membranoproliferative Glomerulonephritis: tx of severe diseases?

A

Cyclophosphamide or MMF + steroids –or- rituximab

  • Despite therapy, ESRD will develop in most
  • May do kidney transplant…but may recur afterwards
44
Q

Minimal Change Disease (MCD)= MC cause of _____

A

nephrotic syndrome in kids

Can be:
Idiopathic
After a viral URI
Associated with neoplasms (ie: Hodgkin disease)
From meds (lithium)
Hypersensitivity reactions
45
Q

Minimal Change Disease: Clinical Findings

A

-Nephrotic syndrome symptoms
Even though there’s an increase in extracellular fluid volume, some kids will present with s/s decreased effective circulating volume:
Tachycardia, peripheral vasoconstriction, oliguria, decreased GFR, elevation of plasma renin, aldosterone, and norepinephrine
More susceptible to infection
Have a tendency toward thromboembolic events
Develop severe hyperlipidemia

  • or question on horse shoe kidney
    Ex: pance question: child with nephrotic syndrome (or proteinuria and edema etc) what is the cause of this? MCD
46
Q

Minimal change disease: Dx?

A
  • Clinical diagnosis:Biopsy rarely done–No changes seen on light microscopy
  • -On electron microscopy, effacement of podocyte foot processes is seen
47
Q

Minimal change disease: tx?

A

Treated with:

  • Prednisone–>Can take up to 4 months to respond
  • Continue for several weeks after proteinuria is completely resolved
  • Cyclophosphamide or rituximab –>If resistant to steroids or for relapse
  • Progression to ESRD is rare
48
Q

Horseshoe kidney= MC kidney _____

A
    • fusion anomaly

- One pole of each kidney fuses to the other–> Usually between weeks 5-9 of gestation

49
Q

Horseshoe Kidney:

-up to half of these PTs have ?

A

Up to half have another congenital anomaly:

  • -Urological and genital anomalies
  • -Syndromes: Feature of Turner syndrome, and Trisomy 13, 18, and 21
50
Q

Horseshoe kidney:

-these Pts are at increased risk for ____ tumor

A

*Wilms (Please reference oncology slides)

51
Q

Horseshoe Kidney: Sx?

A

-Most patients are asymptomatic & diagnosed incidentally

-Some have pain and/or hematuria from obstruction or infection
80% get hydronephrosis
20% with renal calculi
Increased infection risk (from ↑urinary stasis) and impaired drainage

52
Q

Horseshoe Kidney: Labs?

A

Evaluate with:
Creatinine
Ultrasound
Voiding cystourethrogram

53
Q

Horseshoe Kidney: tx/prognosis?

A
  • Most have excellent prognosis without any intervention
  • If they have VUR (vesicoureto reflux) –> consider prophylactic antibiotics for prevention of UTI
  • If obstruction present –> refer to urology

Clin Med Exam 4 (14 decks)

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