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Clin Med Exam 4 > Pediatric Nephrology: Paulson > Flashcards

Pediatric Nephrology: Paulson Flashcards

(53 cards)

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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=

Study These Flashcards
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

Study These Flashcards
A
  • Thought to be genetic

- No damage or malformations

24
Q

Renal agenesis=

Study These Flashcards
A

Congential absence of renal parenchymal tissue

25
Renal agenesis: - demographic? - Sx?
- Males >> females - Most asymptomatic: Solitary kidney is usually an incidental finding on an ultrasound--> Antenatally or as part of UTI eval
26
Renal agenesis: | -Associated nonrenal anomalies (list)
Malformations of heart, genitals, bones, GI tract, respiratory tract
27
Renal agenesis: | -Presentation?
- 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
Renal Agenesis: | -Dx?
- Renal ultrasound | - Frequent association of dysplasia with a collecting system anomaly--> consider voiding cystourethrography as well
29
Renal Agenesis: tx?
- Monitoring for progression | - Transplant/RRT
30
Glomerular disorders: (list 3)
- FSGS - Membranoproliferative glomerulonephritis - Minimal change disease
31
Focal Segmental Glomerulosclerosis=
Sclerosis in parts (segmental) of at least 1 glomerulus (focal) in the entire kidney biopsy specimen when examined histologically
32
Focal Segmental Glomerulosclerosis: | -etiology?
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
Focal Segmental Glomerulosclerosis: | -MC presentation?
Most commonly: acute onset of nephrotic syndrome - Peripheral edema - Hypoalbuminemia - Proteinuria (usually >3.5 g/day)
34
FSGS: | ____ GFR in about half of patients
decreased
35
FSGS: | What do these Pts usually develop by 6-8 yrs?
ESRD
36
FSGS: | -diagnosis made by**?
**Diagnosed by renal biopsy | May do genetic testing
37
FSGS Treatment
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
Membranoproliferative Glomerulonephritis= pattern of ____
glomerular injury on renal biopsy with characteristic changes on light microscopy -->Relatively rare
39
Membranoproliferative Glomerulonephritis: Variety of causes, 2 major causes are:
- Immune-complex mediated | - Complement-mediated
40
Membranoproliferative Glomerulonephritis: | Clinical Presentation
Anywhere on the spectrum of nephritidies: Asymptomatic glomerular hematuria to Gross hematuria to Rapidly progressive glomerulonephritis (RPGN)
41
Membranoproliferative Glomerulonephritis: dx?
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
Membranoproliferative Glomerulonephritis: tx of mild diseases?
ACEI/ARB
43
Membranoproliferative Glomerulonephritis: tx of severe diseases?
Cyclophosphamide or MMF + steroids –or- rituximab - Despite therapy, ESRD will develop in most - May do kidney transplant…but may recur afterwards
44
Minimal Change Disease (MCD)= MC cause of _____
nephrotic syndrome in kids ``` Can be: Idiopathic After a viral URI Associated with neoplasms (ie: Hodgkin disease) From meds (lithium) Hypersensitivity reactions ```
45
Minimal Change Disease: Clinical Findings
-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
Minimal change disease: Dx?
- Clinical diagnosis:Biopsy rarely done--No changes seen on light microscopy - -On electron microscopy, effacement of podocyte foot processes is seen
47
Minimal change disease: tx?
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
Horseshoe kidney= MC kidney _____
* * fusion anomaly | - One pole of each kidney fuses to the other--> Usually between weeks 5-9 of gestation
49
Horseshoe Kidney: | -up to half of these PTs have ?
Up to half have another congenital anomaly: - -Urological and genital anomalies - -Syndromes: Feature of Turner syndrome, and Trisomy 13, 18, and 21
50
Horseshoe kidney: | -these Pts are at increased risk for ____ tumor
*Wilms (Please reference oncology slides)
51
Horseshoe Kidney: Sx?
-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
Horseshoe Kidney: Labs?
Evaluate with: Creatinine Ultrasound Voiding cystourethrogram
53
Horseshoe Kidney: tx/prognosis?
- 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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