Nephrology Flashcards by Bryn Longcroft-Harris

Long term complication of familial mediterranean fever

Amyloidosis

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4 classic features of HSP

Purpuric rash
Abdominal pain
Arthralgias
Glomerulonephritis

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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)

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What are some criteria to refer HSP to nephrology

Proteinuria
Renal insufficiency
Hypertension with hematuria

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MAG3 vs DMSA scan

MAG3 = renal function, drainage, best for obstruction
DMSA = function, scarring, best for pyelonephritis

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SIADH vs CSW

Both hyponatremia
SIADH = euvolemia, low urine output
CSW = hypovolemia, high urine output

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Most common renal stone in children

Calcium oxalate

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Management of hypercalciuric stones

Increase fluids
Decrease Na
Decrease dietary protein
Do NOT decrease dietary Ca

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Orthostatic proteinuria

Benign condition
Protein in the urine when the child is upright, not present when supine
Check first AM urine specimen

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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)

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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

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Serum and urine osmoles in primary polydipsia

Both low!
Drinking so much you dilute your serum and trying to pee it out

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Central vs nephrogenic DI

Central = inadequate ADH production
Nephrogenic = collecting duct is resistant to ADH

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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

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Most common cause of hypertension in infants

Renovascular

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Blood gas abnormality with RTAs

Non-anion gam metabolic acidosis
Hyperchloremic

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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

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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

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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

1. Normal 2. Usually low 3. 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

1. 120/80 2. 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

1. 154 both 2. 77 both 3. 34 both 4. 130 Na, 109 Cl

How to manage 1. Hypovolemic hyponatremia 2. Hypervolemia hyponatremia

1. Saline (fluids) 2. 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