Congenital disease - 60% - obstructive uropathy - renal hypoplasia - Renal dysplasia - Reflux nephropathy - PKD Glomerular disorders - 2nd most common - >12yo - FSGS - membranoproliferative glomerulonephritis - Minimal change disease

Nonglomerular - Polyuria - Elevation in serum creatinine - poor growth Glomerular - Tea colored/colar colored urine - Edema - Inc serum creatinine - Inc BP for age - systemic findings of concurrent systemic disease that affect kidney function - SLE Stage 3 - anorexia, N/V, Fatigue - pericarditis - bone and mineral disease - dec neuro function ``` PE: Growth parameters HTN Hypervolemia Pericardial rub Pallor Deformities or extremities - CKD bone-mineral disorder ```

U/S - widely used - measure size of kidneys against nl values for age - look for deformities

Treat reversible kidney dysfunction Prevent or slow progression - BP control - ACEI/ARB - HTN + Proteinuria - Don’t limit protein intake - No data to support lipid lowering or anemia correction Treat complications Identify and prepare kids/families if RRT needed Mineral/Bone Disease - growth failure, avascular necrosis, skeletal fractures/deformities/pain, vascular calcification - Control - PO4, Ca, PTH, VitD - Tx: diet, binders (sevalemer, Ca, Iron), Vit D2/D3, Vit D analogs Renal Replacement Therapy (RRT) - GFR <30 - start preparing family/child - 1st line - Kidney transplant preferred for best survival - 2nd line - Paranteral Diaylsis - 3rd line - Hemodyalisis - Start before GFR 10-15 if - poor calarie intake, Symptomatic uremia, delay in psychomotor development

Nephrology- Peds Flashcards by Ismerai Reyes

CKD- pathophysiology

GFR <60ml/min for >3min
GFR >60ml/min + evidence for structural damage
- albuminuria, proteinuria, pathologic abnormalities on histology or imaging

Staging - if below 1 standard deviation - more concerned

Reversible Causes
Dec Perfusion to Kidneys
- Hypotension
- Volume depletion - vomiting, diarrhea
- Meds that dec kidney perfusion - NSAIDs, ACE, ARB
Nephrotoxic drugs - NSAIDs, contrast, aminoglycosides

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CKD- cause

Congenital disease - 60%

obstructive uropathy
renal hypoplasia
Renal dysplasia
Reflux nephropathy
PKD

Glomerular disorders - 2nd most common

> 12yo
FSGS
membranoproliferative glomerulonephritis
Minimal change disease

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CKD- S/S & PE

Nonglomerular

Polyuria
Elevation in serum creatinine
poor growth

Glomerular

Tea colored/colar colored urine
Edema
Inc serum creatinine
Inc BP for age
systemic findings of concurrent systemic disease that affect kidney function - SLE

Stage 3

anorexia, N/V, Fatigue
pericarditis
bone and mineral disease
dec neuro function

PE: 
Growth parameters
HTN
Hypervolemia
Pericardial rub
Pallor
Deformities or extremities - CKD bone-mineral disorder

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CKD- diagnosis

U/S - widely used

measure size of kidneys against nl values for age
look for deformities

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CKD- labs & imaging

Serum Cr
UA
Serum Ca
Sphphorous
Vit D
PTH
- if suspect bone and minilaral issues

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CKD- treatment

Treat reversible kidney dysfunction
Prevent or slow progression
- BP control - ACEI/ARB - HTN + Proteinuria
- Don’t limit protein intake
- No data to support lipid lowering or anemia correction
Treat complications
Identify and prepare kids/families if RRT needed

Mineral/Bone Disease

growth failure, avascular necrosis, skeletal fractures/deformities/pain, vascular calcification
Control - PO4, Ca, PTH, VitD
Tx: diet, binders (sevalemer, Ca, Iron), Vit D2/D3, Vit D analogs

Renal Replacement Therapy (RRT)

GFR <30 - start preparing family/child
1st line - Kidney transplant preferred for best survival
2nd line - Paranteral Diaylsis
3rd line - Hemodyalisis
Start before GFR 10-15 if - poor calarie intake, Symptomatic uremia, delay in psychomotor development

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CKD- prognosis

Inc M&M
Inc Hosp
Inc Depression
Worse QOL for pts, and family
\: More likely unemployed
Leading cause of death - CV and infection

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Obstructive uropathy- pathophysiology

Stricture
Stenosis
Stones

In posterior urethral valves

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Obstructive uropathy- treatment

Refer to Urology

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Reflux Nephropathy/ Vesicoureteral Reflux (VUR)- pathophysiology

Retrograde passage of urine from bladder -> upper urinary tract

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Renal Dysplasia- pathophysiology

Malformed kidneys

Microscopic level:

disorganized nephron elements
Dec # of nephrons
maldifferentiation of mesenchymal and epithelial elements
Transformation of tissue to cartilage and bone

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Renal Dysplasia- cause

Kidney’s variable in size - usually small
Unilateral or bilateral
Multicystic - nonfunctioning dysplastic kidney w/ multiple cysts

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Renal Hypoplasia- pathophysiology

Low number of structural nl nephrons -> small kidneys

Reduce renal size by 2 SD of mean size by age
AND
Exclusion of renal scaring

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Renal Hypoplasia- cause

Genetic

No damage or malformations

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Renal agenesis- pathophysiology

Congenital absence of renal parenchymal tissue - only have 1 kidney

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Renal agenesis- epidemiology

M>F

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Renal agenesis- S/S & PE

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Asymptomatic 
Incidental finding on U/S 
- antenatally - during preg 
- part of UTI eval 
- postnatally in dysmorphic kid

Impaired renal function at birth & progressive renal failure

Associated urologic abnormalities - jrenal pelvis, calyces (congenital hydronephrosis), and ureters (Stenosis,VUR, megaureter)
- can lead to complications - UTI, hematuria, fever, abdominal pain

Non renal anomalies - malformations of heart, genitals, bones, GI tract, respiratory tract

Renal agenesis- diagnosis

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Ranal U/S
Frequent association of dysplasia w/ a collecting system anomaly
- get voiding cystourethrography as well

Renal agenesis- treatment

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Monitor

Transplant/RRT

Focal Segmental Glomeruloscerosis (FSGS)- pathophysiology

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Most common Glomerular disorder

Sclerosis in parts/segments of 1 glomerulus in entired kidney biopsy

Focal Segmental Glomeruloscerosis (FSGS)- cause

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Genetic
Injury to podocytes and/or direct toxicity from drugs or viral infections
2nd to - obesity, HTN, HIV, chronic urinary reflux, analgesic or bisphospbonate exposure

Focal Segmental Glomeruloscerosis (FSGS)- S/S & PE

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Acute onset - Most common

Peripheral Edema
Hypoalbuminemia
Proteinuria - >3.5 g/day

Dec GFR
ESRD - develop in 6-8 yr

Focal Segmental Glomeruloscerosis (FSGS)- diagnosis

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Renal biopsy

Genetic testing

Focal Segmental Glomeruloscerosis (FSGS)- treatment

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Diuretics - edema
ACEI/ARB - HTN/proteinuria
Statin/niacin - HLD – controversial

Prednisone
Immunosuppressants - cyclosporine, tacrolimus
Plasma exchange - prior to renal transplant - lower risk of graft loss
- good for those who are about to relapse

Membranoproliferative Glomerulonephritis- pathophysiology

Pattern of glomerular injury on biopsy w/ characteristic changes on light microscopy Rare

Membranoproliferative Glomerulonephritis- cause

Immune - complex mediated | Complement mediated - less common

Membranoproliferative Glomerulonephritis- S/S & PE

Spectrum of nephritidies: - asymptomatic glomerular hematuria - Gross hematuria - Rapidly progressive glomerulonephritis

Membranoproliferative Glomerulonephritis- diagnosis

Renal biopsy

Membranoproliferative Glomerulonephritis- labs & imaging

Cr - nl or inc Complement levels - low Hematuria -dysmorphic red cells and red cell casts Proteinuria - variable

Membranoproliferative Glomerulonephritis- treatment

Mild - ACEI/ARB Severe - cyclophosphamide or MMF + steroids or rituximab ESRD - develop in most even w/ treatment Kidney transplant - still may recur

Minimal Change Disease- pathophysiology

Most common nephrotic syndrome

Minimal Change Disease- cause

``` Idiopathic After Viral URI Neoplams - Hodgkin Meds - lithium Hypersensitivity reaction ```

Minimal Change Disease- S/S & PE

Nephrotic syndrome symptoms Even though inc fluid vol -> will have s/s of dec effective circulating volume - tachy, peripheral vasoconstriction, oliguria, dec GFR, inc plasma renin, aldosterone, and norepinephrine Susceptible to infection - gram + Tendency toward thromboembolic events Severe hyperlipidemia

Minimal Change Disease- diagnosis

Clinical Biopsy - rare - no changes on light microscopy - electron microscopy - effacement of podocyte foot processes

Minimal Change Disease- treatment

Prednisone - 4m to respond - cont several weeks after proteinuria is resolved Cyclophosphamide or Retuximab - resistant to steroids or relapse Prog to ESRD - rare

Horseshoe Kidney- pathophysiology

Most common kidney fusion anomaly One pole of each kidney fuses to the other - 5-9w gestation 1/2 have another congenital anomaly - urological or genital - syndromes - turner, trisomny 13, 18, 21 Inc risk for Wilms tumor

Horseshoe Kidney- S/S & PE

Asymptomatic Pain and/or hematuria - obstruction or infection Hydronephrosis - 80% Renal calculi - 20% Inc inf risk - inc urinary stasis and impaired drainage

Horseshoe Kidney- diagnosis

Incidental

Horseshoe Kidney- labs & imaging

Cr U/S Voiding cystourethrogram

Horseshoe Kidney- treatment

Good prognosis w/out intervention VUR - prophylactic abx for prevention of UTI Obstruction - refer to urology

Nephrology- Peds Flashcards

(40 cards)