Nephrology Flashcards
Post strep GN
- what age
- after what infection, time frame
age 5-15
after Group A beta hemolytic streptococcus
cellulitis- 5 days after if co-infection with staph aureus otherwise 3 weeks post infection
pharyngitis- 7-10 days after
what is the classical presentation of post strep GN
Hypertension- 50 to 90%
Gross hematuria and edema- 30 to 60%
what happens to C3 and C4 with post strep GN
ANA?
ASO titer?
urine?
low C3 (90% will be low at presentation) C4 normal ANA negative ASO titer may be elevated red cells, red cell casts, positive for leukocytes
when do ASO titers peak?
4 to 6 weeks after strep infection but may remain detectable for several months after the strep infection has resolved
when should your C3 normalize after post-strep GN
8 weeks
if it doesn’t normalize then think membranoproliferazive glomerulonephritis
microscopic hematuria persists for up to a year
List 4 diagnoses that can cause a low C3
post strep GN Lupus membranoproliferative glomerulonephritis subacute bacterial endocarditis shunt nephritis
what is the treatment for post strep GN
supportive fluid and salt restriction Furosemide (1-2mg/kg/day) treat hypertension- resolves by 2 weeks Short-acting or long-acting antihypertensive medications: Nifedipine/Hydralazine or Amlodipine
C3 level should return to normal by 6-8 weeks
proteinuria may last for 4 months
microscopic hematuria may last for 2 years though most cases resolved by 3-6 months
how is IgA nephropathy diagnosed?
renal biopsy
most common in adolescents
when do you see gross hematuria with IgA nephropathy?
Gross hematuria often occurs within 1-2 days of onset of an upper respiratory or gastrointestinal infection, in contrast with the longer latency period observed in acute postinfectious glomerulonephritis
gross hematuria gets better as they get better (typically only lasts 3-4 days)
what happens to C3 and C4 with IgA nephropathy
normal!!
Normal serum levels of C3 in IgA nephropathy help to distinguish this disorder from postinfectious glomerulonephritis.
what are the treatment options for IgA nephropathy
ACE, fish oil, corticosteroids
The primary treatment of IgA nephropathy is appropriate blood pressure control and management of significant proteinuria.
ACE inhibitors and angiotensin II receptor antagonists are effective in reducing proteinuria and retarding the rate of disease progression when used individually or in combination.
Fish oil, which contains antiinflammatory omega-3 polyunsaturated fatty acids, may decrease the rate of disease progression in adults
If a renin-angiotensin system (RAS) blockade proves ineffective and significant proteinuria persists, then addition of immunosuppressive therapy with corticosteroids is recommended.
what is alport syndrome
Alport syndrome (AS), or hereditary nephritis, is caused by mutations in type IV collagen, a major component of basement membranes. 85% are x-linked
what are the clinical features of alport syndrome
all patients have asymptomatic microscopic hematuria
hypertension
proteinuria (commonly progressive by 2nd decade of life)
renal failure
bilateral sensorineural hearing loss
what is seen on electron microscopy for alport syndrome? when do they need renal replacement therapy?
thin basement membrane
renal replacement therapy by 20-30 years of age
why do you refer alport syndrome to an ophthalmologist?
Ocular abnormalities, which occur in 30–40% of patients with X-linked AS, include ANTERIOR LENTICONUS, macular flecks, and corneal erosions.
Anterior lenticonus is pathognomonic for what?
Alport syndrome
what are 4 clinical features of Alport syndrome
AS is highly likely in the patient who has hematuria and at least two of the following characteristic clinical features: macular flecks recurrent corneal erosions GBM thickening and thinning sensorineural deafness.
what are the features of anti-GBM disease (Goodpasture disease)
autoimmune disease characterized by
- pulmonary hemorrhage
- rapidly progressive glomerulonephritis
- elevated anti–glomerular basement membrane antibody titers
- rare in children
what parts of the body are attacked by anti-GBM disease? good pasture syndrome
The disease results from an attack on these organs by antibodies directed against certain epitopes of type IV collagen, located within the alveolar basement membrane in the LUNG and glomerular basement membrane (GBM) in the KIDNEY
how do children present with anti-GBM disease
hemoptysis from pulmonary hemorrhage that can be life-threatening
usually systemic symptoms (malaise, fever, weight loss, arthralgia) are ABSENT
What is the treatment for anti-GBM disease?
plasmapheresis** to remove the antibody
high-dose intravenous methylprednisolone
cyclophosphamide
what is the most important cause of morbidity and mortality in SLE.
lupus nephritis (diagnosed by renal biopsy)
Diagnostic criteria for Lupus
SOAP BRAIN MD need 4/11 criteria Serositis – Pleuritis, pericarditis Oral ulcers Arthritis (2 or more joints) Photosensitivity
Blood disorders- hemolytic anemia, leukopenia <4 or lymphopenia <1.5 or platelets <100 000
Renal involvement- nephritis
Antinuclear antibodies- ANA
Immunologic markers (dsDNA, anti-Sm, anti-ro)
Neurologic disorder- seizures, psychosis
Malar rash
Discoid rash
what is the most common cause of a midline mass of the abdomen in a newborn
mesenteric cyst
you are asked to see a newborn in the nursery for an abdominal mass. what is the most likely origin of this mass? what is the likely diagnosis?
renal mass
hydronephrosis
multi cystic dysplastic kidney
what are the top 3 causes of renal masses
hydronephrosis
multi cystic dysplastic kidney
renal vein thrombosis
what would be your first line modality to evaluate the renal mass?
ultrasound
NS is _____meq/L of Na
154 mEq/L Na
154 mEq/L Cl
how do you calculate body surface area
√height (cm) x weight (kg) ÷ 3600
what is the equation for insensible losses
400mL/m2
what is your minimum glucose requirement
4-6mg/kg/min
what are 2 conditions that present with normal anion gap metabolic acidosis
- RTA
2. Gastroenteritis (diarrhea)
where are most things absorbed in the kidney
65% of anything that goes through your body is predominantly absorbed in the proximal tubule
Proximal RTA
pH <7 acidosis- HCO3 15 often hypoNa can have hypoPhos Glucosuria Mild tubular proteinuria or generalized aminoaciduria Fanconi's syndrome
Distal RTA
urine pH >7 acidosis- HCO3 can go below 10 sodium usually normal nephrocalcinosis may be present** Hypokalemia Hypercalciuria
what is the most common cause of proximal RTA
cystinosis
how do you treat distal RTA
potassium citrate
giving them bicarbonate
how do you treat proximal RTA
sodium citrate (because they are losing sodium through proximal tubule)
what are the 2 main causes of type 4 RTA
aldosterone deficiency
aldosterone resistance
what is the most common cause of distal RTA
idiopathic
what constitutes the single most important risk factor for future loss of kidney function
proteinuria
what is the most common cause of proteinuria in pediatrics?
transient proteinuria
- exercise
- fever
- infection
what is the definition of persistent proteinuria
proteinuria on 2 or 3 separate samples taken 1-2 weeks apart
- if you have a kid with proteinuria you have to repeat the sample 2-3x
<1% have persistent proteinuria
how do we measure urine protein
on urine dipstick
or urine protein/creatinine ratio
- don’t do 24h urine collection
what is a normal protein/creatinine ratio for infants <2 years of age
upc <50mg/mmol
what is a normal protein/creatinine ratio for children >2 years of age
upc <20mg/mmol
what are 3 causes of false positive protein on urine dipstick
semen
menstrual blood
vaginal discharge
what is orthostatic proteinuria
normal, persistant proteinuria
seen in adolescents
assess with two separate night and daytime samples
if am sample upc <20mg/mmol then the diagnosis can be made
Prognosis: No treatment is required; benign disease
what is the average age for idiopathic nephrotic syndrome
2-10 years
what are causes of idiopathic nephrotic syndrome
minimal change disease mesangial proliferation focal segmental glomerulosclerosis membranous nephropathy membranoproliferative glomerulonephritis
Approximately 90% of children with nephrotic syndrome have idiopathic nephrotic syndrome.
what is the initial treatment for nephrotic syndrome
prednisone
2mg/kg/day for 6 weeks
then 1.5mg/kg/ day for alternate days for 6 weeks and then stop
most children respond within 5-10 days of starting steroids
95% with steroid sensitive nephrotic syndrome are in remission by 4 weeks
what is the definition of remission
urine protein/creatinine ratio <20 or urine dipstick negative - trace for 3 days
what is the definition of relapse
after remission, increase in proteinuria of 20g/l for 3 days
what is the definition of frequently relapsing
2 or more relapses within 6 months or >/= 4 in any 12 month period
Cyclophosphamide prolongs the duration of remission and reduces the number of relapses in children with frequently relapsing and steroid-dependent nephrotic syndrome.
how do you manage a patient with nephrotic syndrome
fluid and salt restriction
steroids
lasix/albumin
what is the definition of steroid dependent
relapse during taper or within 2 weeks of discontinuation of steroids
what is the definition of steroid resistant
inability to induce remission within 4 weeks of daily steroid therapy
2nd line agent- cyclosporine or tacrolimus
Children with steroid-resistant nephrotic syndrome require further evaluation, including a diagnostic kidney biopsy, evaluation of kidney function, and quantitation of urine protein excretion (in addition to urine dipstick testing). Steroid-resistant nephrotic syndrome is usually caused by FSGS (80%)
what is the main cause of steroid resistant nephrotic syndrome
FSGS
50% will require dialysis/ transplant within 5 years
in pediatrics it is the most common cause of acquired end stage renal disease
what is the most common cause of chronic kidney disease in pediatrics
congenital
what are the four main features of nephrotic syndrome
- heavy proteinuria
protein: creatinine ratio >20mg/mmol - generalized edema
- hypoalbuminemia (<25g/l)
- hypercholesterolemia
what are the initial investigations for nephrotic syndrome
urine dipstick analysis early morning urine for protein:creatinine ratio urine microscopy and C&S electrolytes, albumin, urea, creatinine CBC VZV status HepB and C serology, HIV C3, C4 \+/- ASOT, ANA, ds-DNA
what are features of an atypical presentation of nephrotic syndrome?
age <12 months or >10 years persistent hypertension impaired renal function hematuria (can be present in 10%) low C3 positive hep B or C serology
what are 3 complications of nephrotic syndrome
1. increased risk for infection especially cellulitis, spontaneous bacterial peritonitis, and bacteremia - s pneumonia - other streptococci - ecoli - enterobacteriaceae - h influenza
- spontaneous bacterial peritonitis must be considered inane child with NS who has severe abdominal pain, fever
- hyper coagulable state (risk of thrombosis)
- decreased antithrombin III
- decreased protein C and S - hyperlipidemia
- kids that are resistant or have FSGS with increased lipids are at increased risk of cardiovascular disease in the future
what vaccinations are required for children with nephrotic syndrome
all routine vaccinations
live vaccinations >3 months off prednisone or cyclosporine
or > 6 mo after cyclophosphamide
annual flu vaccine
how does glomerulonephritis typically present
with gross hematuria
what are some causes of gross hematuria
foods: beets, blueberries, plums, cherries, food colouring hemoglobinuria- intravascular hemolysis myoglobinuria- rhabdo urate crystals drugs- rifampin porphyria munchausen by proxy
what is the most common cause of microscopic hematuria?
gross hematuria?
microscopic= idiopathic hypercalciuria gross= cystitis
what is the most common presenting symptom of nephrotic syndrome
Edema is the most common presenting symptom of children with nephrotic syndrome
how does spontaneous bacterial peritonitis present?
Spontaneous bacterial peritonitis presents with fever, abdominal pain, and peritoneal signs. Although Pneumococcus is the most frequent cause of peritonitis
what is seen on electron microscopy for minimal change disease
85% of total cases of nephrotic syndrome in children
the glomeruli appear normal
electron microscopy simply reveals effacement of the epithelial cell foot processes.
More than 95% of children with minimal change disease respond to corticosteroid therapy.
Barrter Syndrome
Present with hypokalemia, alkalosis, hyperaldosteronism, polyuria, polydipsia, hypercalciuria and salt wasting
Presents early with polyhydramnios
** like giving someone too much Lasix!!! (hypoK, met alkalosis, increased Ca in urine, polyuria)
how does someone with type 4 RTA present
Hyperkalemic non-anion gap MA
Either impaired aldosterone production or impaired renal responsiveness to aldosterone
no aldosterone= high potassium
Teenager found to have struvite stone. What would be next investigation?
urine culture
how do you diagnose hypercalciuria
Hypercalciuria is diagnosed by a 24-hr urinary calcium excretion > 4 mg/kg
what are the treatment options for hypercalciuria
thiazide diuretics
Sodium restriction is important because urinary calcium excretion parallels sodium excretion.
Importantly, dietary calcium restriction is not recommended
what happens if you correct hyponatremia too quickly. What should you aim to increase your sodium by per day?
Na <120
Correcting too quickly can lead to osmotic demyelination
(central pontine myelinolysis)
Overall aim for slow correction < 0.5mmol/l/hr or =10- 12mmol/day
what is multi cystic dysplastic kidney?
what are some associations with multicystic dysplastic kidney
MCDK- congenital condition in which the kidney is replaced by cysts and does not function
unilateral and not inherited (different from polycystic kidney disease)
MCDK is the most common cause of an abdominal mass in the newborn, but the vast majority are nonpalpable at birth
Contralateral hydronephrosis is present in 5–10% of patients.
Contralateral VUR
hypertension
Wilm’s tumor
what is the equation for plasma osmolality
2Na + Glucose + BUN
-Affected by water content
how does SIADH present
low serum osm
increased ADH-inappropriate elevated Urine osm (> 100)
urine sodium >20meq/l
low serum uric acid and high urine excretion of uric acid
Treat with Fluid Restriction and Remove offending agent
How do you calculate anion gap? what’s a normal anion gap?
AG = Na – (Cl +HCo3)
Normal AG < 12mmol/l
Causes of high anion gap metabolic acidosis
MUDPILES
M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Paracetamol, Propylene glycol I — Infection, Iron, Isoniazid (which can cause lactic acidosis in overdose), Inborn errors of metabolism (an especially important consideration in pediatric patients) L — Lactic acidosis E — Ethylene glycol S — Salicylates
Causes of nonanion gap metabolic acidosis
USEDCRAP U- ureteric diversion S- Sigmoid fistula E- Excessive saline D- Diarrhea C- carbonic anhydrase inhibitors R- RTA A- Addisons P- Pancreatic fistula
What is cystinosis
Cystinosis
- autosomal recessive
- lysosomal storage disease
- accumulation of cysteine in various organs
- measurement of cysteine levels in leucocytes can confirm diagnosis
Which of the following is seen in distal RTA Hyperkalemia Hyponatremia Hypophosphatemia Hypercalciuria
hypercalciuria
Febrile UTI > 2ms < 2years. when should they get an ultrasound?
During or within 2 weeks of presentation
what prophylaxis is recommended for grade IV/V VUR
TMP/SMX and Nitrofurantoin recommended unless resistant
If resistant to both consider d/c. Broader spectrum leads to more resistance
what followup is recommended for a solitary kidney
No VCUG if ultrasound is otherwise normal
No antibiotics
Follow by ultrasound to be sure it grows appropriately
Yearly urinalysis, BP
Contact sports – no longer advise against it
Most common renal stone in children
Calcium oxalate
Treatment recommendations to prevents calcium oxalate stone
Increase fluids
Low salt diet to decrease calciuria
Increase citrate in diet as natural inhibitor
Do not restrict calcium in diet unless hypercalcemia
Minimize use of furosemide/steroids/excess vit D
Consider thiazide diuretic to decrease calciuria or potassium citrate to augment stone inhibition
what are some indications for dialysis
AEIOU
A-acidosis
E- electrolyte abnormalities – hyperkalemia, hyponatremia, hyperphosphatemia
I- intoxication/poisoning – ethylene glycol, ASA, lithium
O- overload – fluid
U- uremia - mental status change, pericarditis
14y old boy in your office for pre-camp physical; 3+ protein in urine x2; exam is normal; what is most likely cause?
a) exercise induced
b) IgA nephropathy
c) nephrotic syndrome
d) orthostatic proteinuria
orthostatic proteinuria
What is the most common cause of proteinuria in an otherwise well teen? How would you test for this? Two causes of false +ve proteinuria on dipstick.
Answer: Orthostatic proteinuria
Diagnostic test: 3 consecutive first morning urines with negative protein
False +ve: Concentrated urine (SG>1.010), gross hematuria, fever, exercise
Diabetic patient with microalbuminuria. What drug to start?
a) hydrochlorothiazide
b) nifedipine
c) enalapril
d) salt and water restriction
enalapril
Diabetic nephropathy, how do you diagnose it? what is the treatment?
Diagnosis: First morning urine showing albumin:creatinine ratio (ACR) >2.5mg/mmol on two occasions
Treatment: ACE inhibitors
Inhibit the renin-angiotensin system (RAAS) which results in decreased urinary protein excretion
Patient presents with edema, abdominal distention, and proteinuria. Patient also has fever and is found to have spontaneous bacterial peritonitis. What is the MOST likely pathogen causing the SBP?
a) Streptococcal pneumoniae
b) E Coli
c) Enterococcus
d) Listeria
Streptococcal pneumoniae
what are some complications of steroids
Obesity Labile mood Hirsutism Gastritis Hypertension Infection Hyperlipidemia Osteopenia Diabetes Avascular necrosis Cataracts Adrenal suppression
what is the diagnostic criteria for nephritic syndrome
Gross hematuria
Hypertension (due to salt and water overload)
RBC or granular casts
Renal-limited causes of low C3
Post-infectious GN**
MPGN (type 1 & II)
C3 Glomerulopathy
systemic causes of low C3
SLE **
VP Shunt Nephritis
Subacute bacterial endocarditis
renal causes of normal C3
IgA Nephropathy **
anti-GBM disease
ANCA-associated vasculitis (renal ltd)
Hereditary Nephritis
systemic causes of normal C3
HSP **
Granulomatosis with polyangiitis
Goodpasture’s
Alport’s **
5y old child with recent upper respiratory tract infection, now has respiratory distress and BP 150/110. Most likely diagnosis:
a) anxiety
b) pneumonia
c) myocarditis
d) Henoch-Schonlein purpura
e) post-infectious glomerulonephritis
post-infectious glomerulonephritis
Decreased C3 is a feature of which of the following:
a) IgA nephropathy
b) HUS
c) Post-streptococcal glomerulonephritis
d) Nephrotic syndrome
Post-streptococcal glomerulonephritis
what is the most common cause of acute nephritis in children around the world
post-streptococcal glomerulonephritis
14y old girl with recurrent painless hematuria, best test?
a) C3
b) IgA level
c) Renal ultrasound
d) Hearing test
IgA level (elevated in 35-50% IgA nephropathy) although best test for IgA nephropathy is biopsy
If it was a boy, get the hearing test (Alport’s)
Classic presentation of IgA
age?
First episode usually occurs between 15 -30y of age
Recurrent episodes of gross hematuria concomitant with infection (synpharyngitic)
Gross hematuria lasts <3 days
Microscopic hematuria and/or proteinuria may be the only signs
Not often associated with complete nephritic syndrome
Importantly, high IgA levels are only found in 35-50% of patients
5y old M with intermittent abdominal pain and purpuric rash on thighs. He has joint pains and hematuria. Which of the following lab abnormalities would likely be present?
a) Thrombocytopenia
b) Schistocytes
c) Elevated IgA
Elevated IgA
HSP
Common childhood vasculitis; Peak incidence age 5-7y
Immune complex-mediated vasculitis associated to IgA deposits
Clinical syndrome and multi-system disorder affecting predominantly skin, joints, GI tract, and kidney
Preceded by URTI (30-50%)
*Normal C3
12y old female presents with a 2 week history of fevers, arthralgias, and myalgias. She is pale but otherwise looks well. She has blood and protein in her urine. ESR 50, WBC 3. Platelets normal.
a) Acute rheumatic fever
b) Wegener’s granulomatosis
c) Systemic lupus erythematosus
d) Juvenile rheumatoid arthritis
Systemic lupus erythematosus
what happens to C3/C4 with lupus nephritis
Lupus nephritis: occurs in 80% of childhood-onset SLE; major determinant of prognosis
*Low C3/C4
The most common manifestation of lupus nephritis is? 2nd most common?
The most common manifestation of lupus nephritis is microscopic hematuria (79%)
nephrotic syndrome- 55%
What are the 3 core features of hemolytic uremic syndrome?
Thrombocytopenia
Microangiopathic hemolytic anemia (schistocytes)
Renal failure
Which is important for measuring blood pressure?
a) Weight
b) Height
c) Tanner staging
height
*BP tables are dependent on age, sex, and height.
What is the most common cause of hypertension in the newborn?
a) Renovascular
b) Coarctation
c) Hydronephrosis
Renovascular
*Most commonly renal artery thrombosis or stenosis
11y old girl with hypertension confirmed by ambulatory monitoring, next step?
a) 24h urine catecholamines
b) Renal ultrasound
c) Start enalapril
d) Repeat monitoring
Renal ultrasound
how should you measure blood pressure
Patient at rest for minimum 3 mins, sitting, right arm supported, cubital fossa at heart level
Cuff width at least 2/3 the width of the arm
If cuff too small, BP recordings are falsely high
Most common causes of paediatric hypertension by age group
<1 month
>1 month- 6 years
<1 month Renal artery thrombosis Coarctation of the aorta Congenital renal disease Bronchopulmonary dysplasia
> 1 month - 6 years
Renal parenchymal disease
Coarctation of the aorta
Renovascular disease
Most common causes of paediatric hypertension by age group
>6-10
>10-18
> 6-10 years
Renal parenchymal disease
Renovascular disease
Essential hypertension
> 10-18 years
Essential hypertension
Renal parenchymal disease
Renovascular disease
Initial HTN workup
Blood: CBC, electrolytes (including TCO2, extended), Cr/BUN, (fasting) lipids, optional: LFTs, TSH, renin, aldosterone, catecholamines, Hb A1C, drug screen
Urine: Urinalysis + microscopy, ACR, +/- urine metanephrines
Imaging: Renal US (+ Doppler), CXR
Functional tests: ECG, 24h ambulatory BP monitoring, +/- sleep study
What are the 4 organ systems that should be checked for end-organ damage in a hypertensive paediatric patient?
- Kidney
- Heart
- Eye
- CNS
Initial investigations for end organ damage
Kidney:
Urinalysis/microscopy
Urine protein-creatinine ratio
Renal US (+Doppler)
Heart:
ECG
Chest x-ray
Echocardiography (?LVH)
Eyes:
Fundoscopy (retinal changes, papilledema)
CNS:
History?
Imaging?
School performance?
Treatment options for HTN
Lifestyle:
DASH (Dietary Approaches to Stop Hypertension) diet
Moderate - vigorous physical exercise 3-5d/wk for 30-60mins
Stress Reduction
Pharmacologic Management: Start with ACEi, ARB, long-acting calcium channel blocker (Amlodipine), or thiazide
Normal BP for 1-13y?
Stage I HTN?
Stage 2 HTN?
Children Aged 1-13y
Normal BP: <90th percentile
Elevated BP: ≥90th percentile to <95th percentile OR 120/80mmHg to <95th percentile (whichever is lower)
Stage I HTN: ≥95th percentile to <95th percentile + 12mmHg, or 130/80 to 139/89mmHg (whichever is lower)
Stage II HTN: ≥95th percentile + 12mmHg, or ≥140/90mmHg (whichever is lower)
Normal BP Children >13 ?
Stage I HTN?
Stage II HTN?
Children Aged >13y
Normal BP: <120/80mmHg
Elevated BP: 120/<80 to 129/<80mmHg
Stage I HTN: 130/80 to 139/89mmHg
Stage II HTN: ≥140/90mmHg
what are 3 treatment options for hypertensive crisis
IV Labetalol
IV Nicardipine
IV Hydralazine
what is nephrotic range proteinuria
Nephrotic-range proteinuria is defined as proteinuria > 3.5 g/24 hr or a urine protein:creatinine ratio > 2.
The triad of clinical findings associated with nephrotic syndrome arising from the large urinary losses of protein are hypoalbuminemia (≤2.5 g/dL), edema, and hyperlipidemia (cholesterol > 200 mg/dL).
lab results with SIADH
hyponatremia
an inappropriately concentrated urine (>100 mOsm/kg), normal or slightly elevated plasma volume
normal-to-high urine sodium
low serum uric acid.
how is cerebral salt wasting different from SIADH
Hyponatremia
elevated urinary sodium excretion (often >150 mEq/L), excessive urine output **
hypovolemia **
normal or high uric acid **
suppressed vasopressin
elevated atrial natriuretic peptide concentrations (>20 pmol/L).
what is the treatment for SIADH
Chronic SIADH is best treated by oral fluid restriction.
what are 4 urine tests you would do for evaluation of nephrolithiasis
urinalysis urine culture calcium:creatinine ratio spot test for cystinuria 24h urine collection for: creatinine clearance, calcium, phosphate, oxalate, uric acid
Ddx SIADH (euvolemic)
hypothyroidism
glucocorticoid deficiency
what is prune belly syndrome (whats the triad)
deficient abdominal muscles
undescended testes
urinary tract abnormalities probably results from severe urethral obstruction in fetal life
Oligohydramnios and pulmonary hypoplasia are common
Urinary tract abnormalities include massive dilation of the ureters and upper tracts and a very large bladder
Most patients have vesicoureteral reflux.
what lab abnormalities are associated with ATN
The hallmark of ATN is a progressive increase in the serum creatinine and BUN.
sodium (UNa > 40 mEq/L)
fractional excretion of sodium > 2% (>10% in neonates)
What are two causes of Fanconi syndrome
- cystinosis
- galactosemia
- glycogen storage disease
