Nephrology Flashcards
Long term complication of familial mediterranean fever
Amyloidosis
4 classic features of HSP
Purpuric rash
Abdominal pain
Arthralgias
Glomerulonephritis
Follow up for HSP
Need monitoring of BP and UA
Weekly during active disease
Monthly x6 months
(some say weekly to biweekly to monthly - main takeaway is monitor for 6 months to 1 year)
What are some criteria to refer HSP to nephrology
Proteinuria
Renal insufficiency
Hypertension with hematuria
MAG3 vs DMSA scan
MAG3 = renal function, drainage, best for obstruction
DMSA = function, scarring, best for pyelonephritis
SIADH vs CSW
Both hyponatremia
SIADH = euvolemia, low urine output
CSW = hypovolemia, high urine output
Most common renal stone in children
Calcium oxalate
Management of hypercalciuric stones
Increase fluids
Decrease Na
Decrease dietary protein
Do NOT decrease dietary Ca
Orthostatic proteinuria
Benign condition
Protein in the urine when the child is upright, not present when supine
Check first AM urine specimen
Alport syndrome
X linked (majority)
Persistent microscopic hematuria with episodes of gross hematuria
Can get proteinuria, HTN
Decline in function to ESRD
Associated with SNHL and ocular defects (anterior lenticonus)
Thin basement membrane nephropathy
AD
Check dip of both parents to look for microscopic hematuria
No long term sequelae, no treatment required
Difference with Alports: no hx of ocular anomalies, SNHL, or ESRD
Serum and urine osmoles in primary polydipsia
Both low!
Drinking so much you dilute your serum and trying to pee it out
Central vs nephrogenic DI
Central = inadequate ADH production
Nephrogenic = collecting duct is resistant to ADH
Diagnostic test for diabetes insipidus
Water restriction test first
Without water, ADH should be able to rise
In DI, cannot rise so urine remains dilute
Then give vasopressin!
In central you are able to replace the ADH so the urine becomes concentrated
But in nephrogenic still resistant so urine remains dilute
Most common cause of hypertension in infants
Renovascular
Blood gas abnormality with RTAs
Non-anion gam metabolic acidosis
Hyperchloremic
Distal RTA
1. Cause
2. Serum K
3. Urine pH
4. Clinical features
5. Management
Type 1
1. Decreased H+ secretion in distal tubule
2. Serum K is low
3. Urine pH is high
4. Hypercalciuria, hearing loss, hypocitraturia
5. Bicarb supplementation
Proximal RTA
1. Cause
2. Serum K
3. Urine pH
4. Clinical features
5. Management
Type 2
1. Decreased resorption of bicarb
2. Low to normal
3. Low
4. Fanconi syndrome (glucosuria, hypophos, proteinuria, hypoK)
5. Bicarb supplementation, may need other supplements
Type 4 RTA
1. Cause
2. Serum K
3. Urine pH
4. Clinical features
5. Management
- Impaired aldosterone production or responsiveness
- High
- Low
- Obstructive uropathy mainly
- Sodium supplementation
Most common cause of Fanconi syndrome
Cystinosis
Management of hypertensive crisis
ICU admission for IV antihypertensives
Except nifedipine can be SL
Decrease by no more than 25% in 8 hours, rest of reduction over 12-24 hours
Rate of hyponatremia correction
0.5 mmol/hr
Not more than 10 mmol in 24 hours
What renal anomaly is associated with Turner’s syndrome
Horseshoe kidney
Disorders with low C3
SHEMPS
SLE
HUS (atypical)
Endocarditis (subacute)
Membranoproliferative GN (C3 membranopathy)
PIGN
Shunt nephritis
PIGN vs MPGN
PIGN C3 is low but returns to normal by 12 weeks
MPGN C3 stays low
C4 levels in
1. PIGN
2. MPGN
3. Lupus
- Normal
- Usually low
- Low
Who needs prophylaxis post UTI
Grades 4-5 VUR or a significant structural abnormality
What to do if UCx post prophylaxis is resistant to both septra and nitrofurantoin
Discontinue both
Best test to look for long term hypertension changes
Echo
Hypertension levels for
1. children 6-11
2. children 12-17
And when to start screening
- 120/80
- 130/85
Annually starting at 3 years
Nephrotic syndrome criteria
PALE
Proteinuria (3 or 4+)
Hypoalbuminemia
Hypercholesterolemia
Edema
Red flags to indicate biopsy before steroids in nephrotic syndrome
< 1 year, > 12 years
Gross hematuria
Hypertensive
Non prerenal AKI
Low C3
Evidence of systemic disease
Steroid resistance (proteinuria after 4 weeks of steroids)
Which vaccine do children with nephrotic syndrome need
Pneumococcal
Most common bug in SBP
Strep pneumo
When to refer undescended testes to surgery
6 months
Prune belly syndrome triad
Abdominal muscle deficiency
Bilateral cryptorchidism
Uro abnormalities (dilation of the urethra, bladder, ureters)
Clinical findings from testicular appendage torsion
Palpable, tender nodule on top portion of testicle
Blue dot sign
Teste is normal and not indurated
Can be red and swollen
Testicular torsion findings
Acute onset of severe scrotal pain
N/V
Scrotal edema, redness
Loss of cremasteric reflex
High lying, horizontal teste
Transient proteinuria
Temporary
In the context of febrile illness, exercise, dehydration, cold stress
Repeat U/A when stressor no longer present
Classic triad of HUS
Microangiopathic hemolytic anemia
Thrombocytopenia
AKI
Often have bloody diarrhea, abdo pain, GI sx, neuro involvement
How much Na and Cl is in
1. Normal saline
2. 0.45% NS
3. 0.2% NS
4. RL
- 154 both
- 77 both
- 34 both
- 130 Na, 109 Cl
How to manage
1. Hypovolemic hyponatremia
2. Hypervolemia hyponatremia
- Saline (fluids)
- Sodium and fluid restrictions +/- diuretics
Multicystic vs polycystic kidney disease
Polycystic = genetic disease that leads to CKD
Multicystic dysplastic kidney = description of a kidney, essentially non functional
4 dietary interventions to decrease further risk of stones
Increase dietary citrate
Drink more water
Reduce salt intake
Normal dietary calcium intake
Steroid responsive vs frequently relapsing vs steroid dependent nephrotic syndrome
Responsive: responds to pred 60 mg/m^2 within 4 weeks
Relapsing: 2+ relapses within 6 mo of initial presentation or 4+ relapses within 1 year
Dependent: 2 consecutive relapses during steroid therapy OR within 2 weeks of stopping therapy, relapse on maintenance therapy
ADPKD vs ARPKD
Dominant: normal or large, liver cysts, cerebral aneurysms, onset in teens or later
Recessive: large and echogenic kidneys, liver fibrosis, onset in childhood/infancy
