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FRCPC > Nephrology/Urology > Flashcards

Nephrology/Urology Flashcards

1
Q

How do you differentiate true from pseudohyponatremia?

A

Measure serum osmomalility

True hyponatremia should be hypoosmolar

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2
Q

Name 3 conditions that can cause pseudohyponatremia

A

IVIg
Multiple myeloma
Hypertriglyceridemia
Hypercholesterolemia

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3
Q

Name 6 conditions in the differential of hyponatremia

A

1) Hypovolemic Hyponatremia:
-Extra-Renal Losses:
• Vomiting/Diarrhea
• Sweat (e.g. CF)
• Burns
-Renal Losses:
• Diuretics (thiazides, loop, osmotic)
• ATN
• ARPKD
• Cerebral salt wasting
• RTA (Proximal aka typeII)
• Lack of aldosterone (e.g. CAH, pseudohypoaldosteronism)

2) Euvolemic Hyponatremia:
•	SIADH
•	Hypothyroidism
•	Glucocorticoid deficiency
•	Water intoxication → excess IVF, feeding infants water, swimming lessons, tap water enema, diluted formula, psychogenic polydipsia, marathon running w/ excessive drinking, beer potomania
3) Hypervolemic Hyponatremia:
•	Nephrotic syndrome
•	CHF
•	Liver cirrhosis
•	Sepsis
•	Protein-losing enteropathy
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4
Q

Below what Na level are seizures likely?

A

Na <120

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5
Q

What test is most helpful in determining cause of hyponatremia?

A
  1. Urine Osmolality
    - If Osm>100, ADH present, check urine Na
    - If Osm<100-water intoxication, let them pee it out
  2. Urine Na
    - <20=dehydrated, appropriate ADH response (treat with saline)
    - >40=inappropriate ADH response (treat with lasix or hypertonic saline)
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6
Q

How quickly should you correct Na to avoid central pontine myelinolysis?

A

Avoid correcting the [Na] by >12 mEq/L in 24h or >18 mEq/L in 48h

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7
Q

How do you treat seizures secondary to hyponatremia?

A

3% NaCl bolus (3-5 ml/kg)

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8
Q

List 3 causes of SIADH

A

CNS lesion
Post-op
Malignancy
Medications (vincristine, cyclophosphamide, carbamezipine

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9
Q

List 6 causes of hypernatremia

A

Excessive Sodium:
• Improperly mixed formula
• Seawater ingestion
• Hyperaldosteronism

Water Deficit:
• Diabetes Insipidus (nephrogenic or central)
• Increased insensible losses – e.g. prems, phototherapy, radiant warmers
• Inadequate intake – e.g. breastfeeding, neglect

Water + Sodium deficits:
•	GI losses (vomiting/diarrhea) – uncommon
•	Burns/sweating
•	Polyuric phase of ATN
•	DM
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10
Q

What is the most important investigation in hypernatremia?

A

Urine osmolality (if kidneys working, should be high >800 mmol/L)

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11
Q

What brain lesion are patients with rapid hypernatremia at risk of?

A

CSVT

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12
Q

Rapid correction of hypernatremia can lead to….

A

Cerebral edema

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13
Q

Rapid correction of hyponatremia can lead to…

A

Central pontine myelinosis

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14
Q

How do you calculate free water deficit?

A

Free water deficit (mL) = 4x weight (kg)xdesired change in [Na] (mmol/L)

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15
Q

List 10 causes of hyperkalemia

A 
1. Spurious:
•	Hemolysis
•	Thrombocytosis/Leukocytosis
2. Increased Intake:
3. Transcellular Shift
•	Acidosis
•	Rhabdomyolysis/Exercise
•	TLS
•	Tissue necrosis
•	Succinylcholine
•	Hemolysis/bleeding
•	B-blockers
•	Hyperosmolality
•	Insulin deficiency
•	Malignant hyperthermia
4. Decreased Excretion
•	Renal Failure
•	Adrenal Disease (e.g. Addison, CAH)
•	Hypoaldosteronism
•	Renal tubular disease (e.g. pseudohypoaldosteronism, Bartter syndrome)
5. Medications:
•	ACE inhibitors, Angiotensin II blockers
•	Diuretics (potassium sparing)
•	NSAIDs
•	Trimethoprim
•	Heparin
•	Calcineurin inhibitors
•	Yasmin28
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16
Q

List 6 features on ECG in hyperkalemia

A
  1. Peaked T waves
  2. ST-segment depression
  3. Increased PR interval
  4. P wave flattening
  5. QRS widening
  6. Ventricular fibrillation/Asystole
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17
Q

List 3 options for management of hyperkalemia

A

A. Stabilize the heart to prevent life-threatening arrhythmias
o Calcium to stabilize the cardiac cell membrane

B. Shift K+ intracellularly
o Ventolin
o Insulin + Glucose
o Bicarbonate

C.	Remove potassium from the body
o	Stop all sources of K+
o	Loop diuretic (e.g. Lasix)
o	Kayexelate
o	Dialysis
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18
Q

List 5 causes of hypokalemia

A 
1, Spurious:
•	Leukocytosis
2, Decreased Intake:
•	Anorexia nervosa
3. Transcellular Shift
•	Alkalosis
•	Insulin
•	alpha-Agonists
•	Refeeding syndrome
•	Drugs/Toxins
•	Hypokalemic periodic paralysis/Thyroxic periodic paralysis
5. Extra-Renal Losses
•	Diarrhea
•	Sweating
•	Laxative abuse
6. Renal Losses:
•	DKA
•	Medications, e.g. diuretics, penicillin
•	Tubular disorders
•	CF
•	Chloride-losing diarrhea
•	Lots of different syndromes/adrenal/renal disorders+malignancies (e.g. Bartter Syndrome, Gitelman Syndrome, Liddle Syndrome)
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19
Q

Describe the clinical features of Barrter’s syndrome

A

AR
Impaired NaCl reabsorption, volume depletion
Low BP
Hypokalemia
Metabolic alkalosis
Can be developmentally N or have FTT, delays

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20
Q

Describe the clinical features of Liddle’s syndrome

A 
AD
Severe HTN
Metabolic alkalosis
Hypokalemia
Normal/low aldosterone
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21
Q

List 3 ECG changes in hypokalemia

A
  1. Flattened T waves
  2. ST-segment depression
  3. U wave
  4. Ventricular fibrillation/Torsades
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22
Q

List 3 medications that can cause renal stones

A 
Topamax
Lasix (esp in neonates)
Ifosfamide
Indinavir
Allopurinol
Acetazolamide
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23
Q

When should you think about urinary tract infection in a child <3 years?

A

Fever (>39) with no source

Especially highly likely if fever >39 for >48H!

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24
Q

When should you think about UTI in a child >3 years?

A

Only if urinary symptoms

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25
Q

After what age is it unusual for males to have a UTI?

A

> 3 years

Unless urinary tract abnormalities or instrumentation

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26
Q

For cystitis, what is a reasonable duration of antibiotics?

A

2-4 days

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27
Q

Within what time frame should renal ultrasound be obtained in first febrile UTI?

A

<2 weeks

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28
Q

What are the disadvantages of performing VCUG?

A

Exposure to radiation
Discomfort to child
Risk of causing UTI

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29
Q

List 5 risk factors for recurrent UTI

A 
Uncircumcised (esp if boy >1 year)
VUR
Voiding dysfunction
Obstructive uropathy
Constipation
Neurogenic bladder
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30
Q

What is the triad of prune belly syndrome?

A 
Deficient abdominal muscles
Undescended testes (usually intrabdominal)
Urinary tract abnormalities
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31
Q

What are the renal complications of Prune Belly syndrome?

A 
Hydronephrosis
Massive dilation of ureters
High grade VUR
Dysplastic kidneys
PUV
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32
Q

What are the renal complications of Prune Belly syndrome?

A 
Most common-progression to CKD (50%)
Hydronephrosis
Massive dilation of ureters
High grade VUR
Dysplastic kidneys
PUV
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33
Q

List causes of obstructive uropathy

A
  1. PUV-most common cause of severe obstruction
  2. Urtheral strictures
  3. Ureterocele
  4. Ectopic ureter
  5. UPJ obstruction-most common
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34
Q

List causes of hydronephrosis

A
  1. PUV-most common cause of severe obstruction
  2. UPJ obstruction-most common obstructive uropathy
  3. VUR
  4. Other obstructive uropathies:
    - Urtheral strictures
    - Ureterocele
    - Ectopic ureter
    - Congenital megaureter
  5. MCDK
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35
Q

What is the classification of severity of hydronephrosis in 3rd trimester?

A

Mild: <9 mm
Moderate: 9-15 mm
Severe: >15mm

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36
Q

When should you perform an postnatal ultrasound for hydronephrosis?

A

If severe and bilaterally (>15 mm)-within 2 days
If severe and unilateral-after 2 days
If not severe-after 7 days (between 1-4 weeks of age)(fluid shifts underestimate the degree of hydronephrosis)

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37
Q

If post natal ultrasound shows mild hydronephrosis (RPD <9mm), what should you do?

A

U/S at 3 months

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38
Q

If post natal ultrasound shows moderate/severe hydronephrosis (RPD>9mm), what should you do?

A

VCUG

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39
Q

When do you start prophylactic antibiotics for antenatal hydronephrosis?

A

If severe (RPD >15 mm) in 3 rd trimester while awaiting ultrasound

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40
Q

What is the best test to detect renal scarring?

A

Renal nuclear scan (DMSA)

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41
Q

How does urethral prolapse typically present?

A

Black girls 1-9yo

Presents as bloody spotting on the underwear, dysuria or perineal discomfort

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42
Q

How do you treat urethral prolapse?

A

Estrogen cream

Surgery

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43
Q

What is a paraurethral cyst?

A

Results from retained secretions in the Skene glands secondary to ductal obstruction

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44
Q

What is the natural history of paraurethral cyst?

A

Present at birth, and regress in size during the first 4–8 wk

If not, surgical drainage

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45
Q

How does prolapsed ectopic ureterocele present?

A

Cystic mass protruding from the urethra

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46
Q

What investigation should you order for ectopic ureterocele?

A

Ultrasonography should be performed to visualize the upper urinary tracts to confirm the diagnosi

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47
Q

List risk factors for renal vein thrombosis in infants

A 
Asphyxia
Dehydration
Sepsis
Thrombophilia
Maternal diabetes
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48
Q

List risk factors for renal vein thrombosis in kids

A 
Nephrotic syndrome
CHD
Thrombophilia
Sepsis
Post-kidney transplant
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49
Q

How does renal vein thrombosis present?

A 
Sudden onset gross hematuria
Flank mass
Flank pain
Hypertension
Oliguria
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50
Q

Treatment of renal vein thrombosis

A

Supportive
Correction of fluid and electrolyte imbalance
Treatment of HTN

If refractory HTN-nephrectomy

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51
Q

How do you distinguish between AR and AD PCKD?

A

AD

  • Normal at birth
  • Cysts in kidneys, liver, pancreas, spleen

AR

  • Large echogenic kidneys on fetal U/S
  • Oligohydramnios
  • Large cysts
  • Severe HTN and pulmonary hypoplasia
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52
Q

How does ARPCKD typically present?

A

Neonates/infants!

Large kidneys and cysts
Hepatic fibrosis
Bilateral flank mass in neonates
Oligohydramnios-pulmonary hypoplasia
HTN within first few weeks of life
ESRD
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53
Q

What are the liver complications of ARPCKD?

A 
Bile duct proliferation
Hepatic fibrosis 
Ascending cholangitis
Varices
Hypersplenism
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54
Q

Genetics of ADPCKD

A

PKD1, PKD2 encoding polycystin

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55
Q

How does ADPCKD typically present?

A

Symptomatic in 4th/5th decade! (rarely in neonates)
Enlarged kidneys (but not usually at birth)
Hematuria
Flank pain
Abdominal masses
HTN

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56
Q

Where can you have cysts in ADPCKD?

A

Liver
Spleen
Pancreas
Ovaries

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57
Q

List complications associated with ADPCKD

A

Intracranial aneurysms
Mitral valve prolapse
Renal cell carcinoma

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58
Q

How do you diagnose ADPCKD?

A

U/S

Parent U/S

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59
Q

What is multicystic dysplastic kidney?

A

Usually unilateral
Not typically inherited
Kidney replaced by non-functioning cysts

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60
Q

List associations with multicystic dysplastic kidney

A

Contralateral hydronephrosis (30%)
VUR (15%)
Risk of Wilms tumour***
HTN (1%)

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61
Q

What is the most common cause of neonatal abdominal mass?

A

MCDKD

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62
Q

What investigations do you order for MCDKD?

A

U/S-multiple cysts that do not communicate, no renal parenchyma

DMSA scan-will show no function; helps differentiate from severely obstructed kidney

VCUG if significant hydronephrosis in contraleteral kidney

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63
Q

Follow up of patients with MCDKD

A

Serial US
Monitor BP
Monitor function of other kidney

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64
Q

Indications for nephrectomy in MCDKD

A

Enlargement of cysts
Increase in stromal core
Hypertension

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65
Q

In renal agenesis, what happens to contralateral kidney?

A

Compensatory hypertrophy

Low grade VUR

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66
Q

What test to confirm diagnosis of renal agenesis?

A

DMSA

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67
Q

List conditions associated with renal cysts

A 
Autosomal recessive polycystic kidney disease
Autosomal dominant polycystic kidney disease
Hereditary cystic disease with interstitial nephritis
Cerebello-ocular-renal syndromes
Cystic dysplastic kidneys
Joubert syndrome
Juvenile nephronophthisis
Meckel-Gruber syndrome
VATER syndrome
Trisomy 21, 18, 13
Tuberous sclerosis
VonHippel-Lindau syndrome
Orofacial digital syndrome
Bardet-Biedel syndrome
Simple benign cysts
Autosomal dominant hereditary angiopathy with nephropathy
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68
Q

Features of hyperaldosteronism

A 
Hypertension
Hypokalemia
Metabolic alkalosis
Plasma aldosterone/renin is high
HTN
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69
Q

Inheritance of Bartters syndrome and Gitelman syndrome

A

AR

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70
Q

What is the defect in Bartters syndrome?

A

LIKE LASIX!

Defect in sodium and chloride resorption in the loop of Henle

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71
Q

What is the defect in Gitelmans syndrome?

A

LIKE THIAZIDE!

Defect sodium and chloride transporter in the distal tubule

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72
Q

What are the features of Bartters and Gitelman syndrome and how are they different?

A 
Both have:
Urinary loss of Na and chloride
Secondary hyperaldosteronism
Hyperreninemia
Hypokalemia
Metabolic alkalosis
Normal BP
Polyuria polydipsia (decreased urine concentrating ability)

Bartters:

  • Dysmorphic features
  • Growth and mental retardation
  • Hypercalciuria

Gitelman:

  • Less growth failure
  • Hypocalciuria and hypomagnesemia
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73
Q

Fluid requirement formula

A

Insensible (400 x m2) + urinary losses

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74
Q

Differential diagnosis of daytime urinary incontinence

A

Overactive bladder-most common cause of daytime incontinence

Neurogenic

  • Spina bifida
  • Spinal cord injury

Anatomic

  • Ectopic ureter
  • Bladder outlet obstruction

Functional

  • Overactive bladder
  • Voiding postponement and underactive bladder
  • Vaginal voiding
  • Non-neurogenic neurogenic bladder/Dysfunctional voiding
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75
Q

Investigations for daytime incontinence

A 
Urinalysis
C&amp;S
Bladder diar
Validated symptom assessment scores
Imaging (Renal u/s, bladder scan (post void residual)
VCUG
Urodynamic studies
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76
Q

What is the pathophysiology of overactive bladder

A

Abnormal bladder contraction during the filling phase

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77
Q

What is the hallmork symptom of overactive bladder?

A

Urgency
Urge incontinence
Vincent’s curtsy

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78
Q

Treatment for overactive bladder

A 
Treat constipation 
Treat UTIs
Timed voiding (q1.5-2hrs)
Biofeedback (Kegel exercises/pelvic floor exercises)
Anticholinergics
Alpha adrenergic blockers
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79
Q

What is non-neurogenic neurogenic bladder/dysfunctional voiding?

A

Failure of the external sphincter to relax during voiding

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80
Q

Hallmark of non-neurogenic neurogenic bladder/dysfunctional voiding?

A

Stacatto stream

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81
Q

What investigations should you do for suspected dysfunctional voiding?

A

MRI spine

Urodynamic studies

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82
Q

List complications of non-neurogenic neurogenic bladder/dysfunctional voiding

A

VU reflux
Hydronephrosis
Renal insufficiency

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83
Q

What is vaginal voiding?

A

Incontinence usually occurs after urination after the girl stands up

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84
Q

What is the most common cause of vaginal voiding?

A

Labial adhesion

Others:
Don’t separate legs widely during urination

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85
Q

What symptoms would indicate ectopic ureter as cause of incontinence?

A

Constant dripping all da

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86
Q

Causes of neuropathic bladder

A

Spina bifida
Spinal trauma
Spinal tumour
Sacrococcygealteratoma

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87
Q

How do you treat neuropathic bladder?

A

Usually treated around 4yr

Clean intermittent catheterization

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88
Q

Features of daytime frequency syndrome of childhood

A

Severe urinary frequency (q10-15min)

No dysuria, incontinence

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89
Q

In what group is daytime frequency syndrome of childhood most common

A

Boys 4-6 (after toilent training)

Emotional stress!

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90
Q

What is the natural history o f daytime frequency syndrome?

A

Resolve in 2-3 months

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91
Q

What is the definition of secondary enuresis?

A

When incontinence reoccursa fter at least 6 months of continence

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92
Q

Diagnostic criteria of nocturnal enuresis

A

Regular (more than twice per week) wetting persists ≥ 5 years of age.

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93
Q

Non pharmacologic measure to manage nocturnal enuresis (CPS)

A

Avoid caffeine-containing foods and excessive fluids before bedtime.

Have the child empty the bladder at bedtime.

DO NOT PUNISH CHILD

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94
Q

When should you treat nocturnal enuresis? (CPS)

A

When it is distressing to the child

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95
Q

What is the purpose of alarm therapy in nocturnal enuresis? (CPS)

A

To teach the child to respond to a full bladder while asleep

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96
Q

What is the success of alarm therapy dependent on? (CPS)

A

Child being motivated
Willingness of child and parent to be awoken
Requires a commitment from other siblings

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97
Q

Above what age is alarm therapy most effective? (CPS)

A

> 7 years

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98
Q

How long should a therapeutic trial of alarm system be continued? (CPS)

A

3-4 months

May take 1-2 months to start seeing an imporvement

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99
Q

How long after achieving bladder control should alarm therapy be continued? (CPS)

A

Continue until there have been 14 consecutive dry nights.

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100
Q

What is cure rate for alarm therapy? (CPS)

A

Just under 50%

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101
Q

When should DDAVP be used for enuresis management? (CPS)

A

Useful for short-term treatment i.e. camp, sleepovers

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102
Q

Side effects of DDAVP

A

Abdominal pain
Headache
Epistaxis
Dilutional hyponatremia

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103
Q

When should fluid intake be limited when taking DDAVP? (CPS)

A

Fluid intake be limited to eight ounces (240 mL) from 1 hour before to 8 hours after administration of desmopressin

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104
Q

When should imipramine (TCA) be used in treatment of nocturnal enuresis? (CPS)

A

Age >6
Distressed,older children if other treatments unsuccessful or are contraindicated
Parents are judged to be reliable
Parents counselled about safe storage of the medication
Needs 2 week therapeutic trial

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105
Q

Causes of nocturnal enuresis

A

Maturational delay
Genetics (chromosome 13q)-esp PRIMARY enuresis
Detrusor overactivity
Small bladder capacity (constipation)

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106
Q

What counseling should you give a parent re: nocturnal enuresis in a child <5 years regarding natural history?

A

Should be regarded as a variation in the development of normal bladder control.

Improves with age

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107
Q

When does foreskin typically become retractable?

A

50% by 6 years

95% by 17 years

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108
Q

What is phimosis?

A

Scarring and thickening of the foreskin that prevents retraction back over the glans

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109
Q

List causes of phimosis

A

Recurrent posthitis/balanoposthitis
Recurrent paraphimosis
Lichen sclerosis

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110
Q

Treatment of phimosis

A

1) Topical steroid and gentle retraction

2) Circumcision if fails

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111
Q

Advantages of circumcision

A

Prevention of phimosis
Decrease in early UTI (in first few months of life)
Decrease in UTI in males with risk factors
Decreased acquisition of HIV, HSV, HPV
Decreased penile cancer
Decreased trichomonas, bacterial vagniosis, cervical cancer risk in female partners

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112
Q

Short term complications of circumcision

A

Post procedural pain
Minor bleeding to life threatening hemorrhage
Local infection to sepsis

113
Q

Long term complications of circumcision

A

Meatal stenosis (MOST COMMON)

114
Q

How do you prevent meatal stenosis?

A

Apply petroleum jelly to the glans for up to six months following circumcision

115
Q

Contraindications to circumcision

A

Hypospadius
Webbed penis
Bleeding diathesis

116
Q

What is the natural history of cryptorchidism?

A

Most descend spontaneously by 4 mo

117
Q

List consequences of cryptorchidism

A

Infertility (even after treatment)

Testicular cancer (risk reduced if orchidopexy before age 2)

Inguinal hernia

118
Q

What is a retractile testes?

A

Descended at birth

Doesn’t remain in scrotum at age 4-10yrs

119
Q

Management of retractile testes

A

Monitor Q6-12 months

If become acquired undescended testes (1/3)-refer to urology

120
Q

BY what should you refer an infant for orchidopexy and when should it be performed?

A

Refer at 4 months
Ideally repaired 6-12 months
No later than 9-15 months

121
Q

List 2 reasons to perform orchidopexy for UTD

A

Improved fertility

Improved examination for cancer

122
Q

DDx for painful scrotal mass in boys

A 
Testicular torsion
Torsion of appendix testis
Epididymitis
Trauma: ruptured testis, hematocele
Inguinal hernia (incarcerated)
Mumps orchitis
123
Q

Ddx for painless scrotal swelling in boys

A 
Hydrocele
Inguinal hernia*
Varicocele*
Spermatocele*
Testicular tumor*
Henoch-Schönleinpurpura*

*May be associated with discomfort

124
Q

Ddx of scrotal swelling in newborn

A 
Hydrocele
Inguinal hernia (reducible)
Inguinal hernia (incarcerated)*
Testicular torsion*
Scrotal hematoma
Testicular tumor
Meconium peritonitis
Epididymitis*
125
Q

Above what age is testicular torsion more common?

A

> 12 years

126
Q

After how many hours of testicular torsion can you have irreversible loss of spermatogenesis?

A

4-6 hours

127
Q

What is the most common cause of testicular pain 2-10 years of age?

A

Torsion of appendix testis

In >12 years-testicular torsion!

128
Q

Physical findings consistent with torsion of appendix testis

A

Blue dot sign
Tender mass on upper pole
Testicular pain
Scrotal erythema

129
Q

Treatment of torsion of appendix testis

A

Bed rest and analgesia with NSAIDS x5days

Resoves in 3-10 days

130
Q

What bacteria cause epididymitis?

A

E.Coli in young boys

Post pubertal – usually STI (gon/chlam)

131
Q

Above what age does varicocele typically present?

A

Usually after puberty

>10 years

132
Q

What sided does varicocele typically present?

A

Left

133
Q

With right sided varicocele, what must you consider?

A

Abdominal/retroperitoneal mass

134
Q

Why repair varicocele?

A

Maximize fertility

135
Q

What is the difference between communicating and non-communicating hydroceles?

A

Non-communicating:

  • Disappears by 1yr – no surgery needed
  • If older children – can result from inflammatory process (torsion (test/appendix), epididymitis, tumour)

Communicating:

  • Persistently patent processus vaginalis
  • Hydrocele becomes larger during day and smaller in am
  • Long term risk of developing inguinal hernia
  • Needs surgery
136
Q

When should hydroceles be repaired?

A

After 12 months (most should resolve by then)

137
Q

Work up for suspected testicular tumour

A
  1. Scrotal U/S

2. Tumour markers (AFP, BHCG)

138
Q

Treatment of testicular tumour

A

If markers negative-Partial orchidectomy

If markers positive-radical orchiectomy (incl spermatic cord)

139
Q

Difference between acute hydrocele and incarcerated hernia

A

Incarcerated hernia
kids are probably sicker – signs of abdominal obstruction (vomiting, abdo distention, not stooling, ill)

NOTE: Both can look ill

140
Q

List 2 important physical exam findings in acute scrotal pain

A

Absence of cremaster reflex

No relief with prehn maneuver (pain doesn’t subside when elevate scrotum)

141
Q

What is the inheritance pattern of nephrogenic DI?

A

Most are X-linked (90%), but can be AD, AR

142
Q

List causes of diabetes inspidus

A
  1. Genetic
  2. Acquired
    - Hypercalcemia
    - Hypokalemia
    - Drugs (lithium, demeclocycline, foscarnet, clozapine, amphotericin, methicillin, and rifampin)
    - Kidney disease (ureteral obstruction, chronic renal failure, polycystic kidney disease, Sjögren syndrome, and sickle cell disease)
143
Q

List associations with hypospadius

A 
DSDs
Cryptorchidism (think DSD!)
Inguinal hernias
Anorectal malformations
Congenital heart disease
144
Q

When should hypospadius be repaired?

A

6-12 months of age

145
Q

What is paraphimosis?

A

Incomplete retraction

Retracts past coronal sulcus but not over glans

146
Q

What is the definition of micropenis?

A

In neonates <2 cm

147
Q

List causes of micropenis in the neonate

A

Hypogonadotropic hypogonadism

  • Kallman
  • Praderwilli
  • Lawrence Moon Biedl

Hypergonadotropic hypogonadism
-Gonadal dysgenesis

GH deficiency

148
Q

What is the definition of priapism?

A

Persistent penile erection > 4 hrs

149
Q

How does meatal stenosis present?

A

Usually 3-8 years old

Forceful fine stream that goes far

150
Q

What is a normal urine protein/creatinine ratio and what is nephrotic range?

A

Normal:
In 1:1 units
<0.5 in children <2 yo
<0.2 in children ≥2 yo

In mg/mmol:
<25

Nephrotic:
In 1:1 units:
>2

In mg/mmol:
>250

151
Q

What is normal, abnormal and nephrotic range 24 hour protein excretion?

A

≤4 mg/m2/hr considered normal(or ≤150 mg/24h)

Abnormal is 4-40 mg/m2/hr

Nephrotic range is >40 mg/m2/hr

152
Q

What is the most common cause of persistent proteinuria in children/adolescents?

A

Orthostatic proteinuria

153
Q

Investigations for orthostatic proteinuria?

A

3 consecutive first AM urine sample

Diagnostic if dipstick negative/trace for protein
UPr:UC ratio <0.2 for 3 consecutive days

154
Q

Differential diagnosis of fixed proteinuria

A

Glomerular

  • Minimal change nephrotic syndrome
  • FSGS
  • Mesangial proliferative glomerulonephritis
  • Membranous nephropathy
  • Diabetic nephropathy
  • Obesity-related glomerulopathy

Tubular proteinuria

  • ATN
  • Reflux nephropathy
  • PKD
  • Renal dysplasia
  • Galactosemia
  • Wilson disease
  • Cystinosis
155
Q

Workup of fixed proteinuria

A
  • Serum creatinine
  • Electrolytes
  • Albumin
  • Complement (c3, c4, CH50)
  • First morning UA, UPr:UCr ratio
156
Q

Causes of false negative proteinuria on dipstick

A
  1. Dilute urine

2. Disease where predominant urinary protein is not albumin

157
Q

Causes of false positive proteinuria on dipstick

A
  1. Concentrated urine (SG >1.010)
  2. Gross hematuria
  3. Exercise, fever
  4. Alkaline urine
158
Q

What is the definition of nephrotic range proteinuria?

A

> 40 mg/m2/h
50 mg/kg/day
UPr:UCr ratio of >2 or >250 mg/mmol
First morning void urine dipstick 3+/4+

159
Q

List features that distinguish nephritic from nephrotic syndrome

A 
Hematuria
Azotemia (↑ BUN)
RBC casts
Oliguria
HTN
160
Q

List the causes of nephrotic syndrome from most to least common

A

MCD > focal segmental glomerular sclerosis (FSGS) >membranoproliferative glomerulonephritis (MPGN)

161
Q

What percentage of nephrotic syndrome is MCD?

A

85-90% of patients <6 yo

162
Q

List systemic diseases that cause secondary nephrotic syndrome

A 
SLE
HSP
Malignancy (lymphoma, leukemia)
Infections (HBV, HCV, HIV, malaria, schistosomiasis, syphilis)
Drugs (NSAIDs, phenytoin)
163
Q

What is the typical age of presentation of nephrotic syndrome?

A

2-6 years

164
Q

What features are in keeping with MCD?

A

Age 1-10 years of age

Hypertension

Gross hematuria

Marked elevation in serum creatinine

Normal complement levels

No extra-renal symptoms such as malar rash or purpura

165
Q

Ddx of anasarca

A 
Protein-losing enteropathy
Hepatic failure
Heart failure
Acute or chronic glomerulonephritis
Protein malnutrition
166
Q

Differential for nephritis with low C3

A

Low C3-MPGN, postinfectious GN, , endocarditis, shunt nephritis

Low C3/C4-Lupus

167
Q

Management of nephrotic syndrome

A

Salt restriction
Fluid restriction
Daily first AM dipstick and weights
Prednisone 60 mg/m2/day (80 mg max) x 4-6 weeks, then taper

168
Q

In what time frame to most children achieve clinical remission on steroid therapy?

A

Most within 4 weeks

Short response time (<7 days) is associated with a better prognosis

169
Q

Indications for biopsy in nephrotic syndrome

A

<1 year, >12 years

HTN

Gross hematuria

Marked elevation in Cr
Abnormal C3/C4

Steroid resistant nephrotic syndrome

Extra-renal symptoms such as malar rash or purpura

170
Q

What percentage of patients with MCD have relapses?

A

30 % relapse frequently (2+) within 6 months

20% have single relapse

171
Q

What is the definition of clinical remission in nephrotic syndrome?

A

3 consecutive days of negative urine

172
Q

What is the definition of steroid resistance in nephrotic syndrome?

A

Fail to respond to steroids within 4-8 weeks

173
Q

What is the definition of steroid dependent nephrotic syndrome?

A

Relapse when weaning (within 2 weeks of stopping steroids)

174
Q

What is the definition of frequently relapsing nephrotic syndrome?

A

Respond well but relapse ≥4x in 12-mo period

175
Q

Management of relapsed nephrotic syndrome***

A

Repeat course high dose prednisone
Fluid and salt restriction
Consider cyclophosphamide

176
Q

List side effects of cyclophosphamide

A

Neutropenia
Hemorrhagic cystitis
Alopecia
Increased risk of future malignancy

177
Q

What is the most frequent bacteria cause spontaneous bacterial peritonitis?

A

S pneumo!

H. flu and E. coli also seen

178
Q

What additional vaccne should children with nephrotic syndrome get and when should they get it?

A

PPSV-23

When in remission and off prednisone

179
Q

Should live vaccines be given to children with nephrotic syndrome?

A

Live virusvaccines should not be given during steroid treatment of >2 mg/kg/day prednisone

180
Q

In a nephrotic syndrome patient with headache, what complications should you think about?

A

CSVT

They are prothrombotic!

181
Q

What is the prognosis of steroid resistant nephrotic syndrome?

A

Poor!
Progressive renal insufficiency
ESRD
Transplant

182
Q

When and how often should patients with T1DM be screening for nephropathy?

A

Annually starting at age 10 and >5 years after diagnosis

183
Q

What treatment would you consider in T1DM patient with persistent microalbuminuria?

A

ACEi

184
Q

What are the 4 types of renal tubular acidosis?

A

Distal (type I) RTA
Proximal (type II) RTA
Combined proximal and distal (type III) RTA
Hyperkalemic (type IV) RTA

185
Q

Describe the pathophysiology of distal RTA

A

Impaired secretion of H+ from distal tubule–>metabolic acidosis

Compensatory increased K+ secretion–>Hypokalemia

186
Q

Clinical presentation of distal RTA

A 
Growth failure
Non-AG metabolic acidosis
Hypokalemia
Urine pH >5.5
Hypercalciuria
Nephrocalcinosis (due to hypercalciuria and hypocitraturia)
187
Q

Pathophysiology of proximal RTA

A

Problem with reabsorption of HCO3 in proximal tubule

188
Q

Laboratory features of Fanconi’s proximal RTA

A 
Non-AG metabolic acidosis
Hyponatremia
Hypokalemia
Hyperchloremia
LMWH proteinuria (beta 2 microglobulin)
Glucosuria (with normal serum glucose)
Phosphaturia
Aminoaciduria
189
Q

List causes of proximal RTA

A
  1. Inherited idiopathic
2. Syndromes:
Cystinosis***most common
Lowe syndrome (oculocerebralrenal syndrome)
Galactosemia
Tyrosinemia
Wilsons
Hereditary fructose intolerance
  1. Drugs
    Ifosfamide, cisplatin, gentamicine, valproate
  2. Renal disease
    Transplant rejection, sjogrens
190
Q

Difference between proximal and distal RTA

A

Proximal RTA
-Urine pH <5.5 (because distal H+ secretion intact)
-Associated phosphaturia, aminoaciduria, glycosuria,
uricosuria in Fanconis
-Growth failure occurs earlier than dRTA

Distal RTA
-Urine pH >5.5

191
Q

What is cystinosis?

A

Systemic disease caused by a defect in lysosomal metabolism of cystine

Accumulation of cystine in kidney, liver, eye, and brain

192
Q

Clinical presentation of cystinosis

A
  1. Fanconi proximal RTA
    - Polyuria and polydipsia
    - FTT
    - Rickets
    - Dehydration
  2. HSM
  3. Hypothyroidism
  4. Delayed puberty
  5. ESRD
193
Q

How do you diagnose cystinosis?

A

Leukocyte cystine level

Genetic testing

194
Q

Explain the pathophysiology of Type IV RTA?

A

Impaired aldosterone production (hypoaldosteronism)
OR
Impaired tubular responsiveness to aldosterone (pseudohypoaldosteronism)

Aldosterone stimulates H+H+/ATPase responsible for H+ secretion (thus ↓aldo = acidosis)

Aldosterone also potent stimulant for K+ secretion (thus ↓aldo = hyperkalemia)

195
Q

Clinical presentation and laboratory features of type IV RTA

A

Hyperkalemia
Acidosis
Urine pH can be high or low

196
Q

Which of the RTAs is associated with hyperkalemia?

A

Type IV RTA

197
Q

Which of the RTAs has urine pH <5.5?

A

Distal RTA

198
Q

Which of the RTAs has a increased urine anion gap ([UNa+ + UK+] −UCl−) ?

A

Distal RTA

A positive gap suggests a deficiency of ammonia genesis

199
Q

Which RTA is associated with hypercalciuria?

A

Distal RTA

200
Q

List long term complications of Fanconi syndrome ***

A

Rickets

FTT

201
Q

List 3 symptoms of hypernatremia

A

Lethargy
Irritability
Thirst

202
Q

List 3 symptoms of hyponatremia

A

Confusion
Muscle cramps
Lethargy
Seizures

203
Q

Do the number of nephrons change with age?

A

No

But functional maturation with tubular growth/elongation continues until 1st decade

204
Q

What is the definition of renal failure as per the pediatric modified rifle (PRIFLE) criteria?

A

<0.3 ml/kg/h x 24 hours or anuric x 12 hours

205
Q

List pre-renal causes of AKI

A

Dehydration
Sepsis
Hemorrhage
Hypoalbuminemia Cardiac failure

206
Q

List renal causes of AKI

A 
Glomerulonephritis
ATN
AIN
TLS
HUS
207
Q

List post-renal causes of AKI

A 
PUVs
Bilateral UPJ obstruction
Neurogenic bladder
Tumour compression
Urolithiasis
208
Q

List laboratory abnormalities found in AKI

A 
Hyponatremia
Metabolic acidosis
Elevated Cr/BUN
Elevated uric acid
Elevated PO4, low Ca
Hyperkalemia
209
Q

How do you distinguish between pre-renal and renal AKI with the following tests:

i) SG
ii) Urine osmolality
iii) Urine Na
iv) FeNa

A

i) SG
- Pre-renal: ↑SG(>1.020)
- Renal: ↓ SG (<1.010)

ii) Urine osmolality
- Pre-renal: ↑ urine osmolality (UOsm> 500 mOsm/kg)
- Renal: ↓ urine osmolality (UOsm< 350 mOsm/kg)

iii) Urine Na
- Pre-renal: ↓ urine Na (UNa< 20 mEq/L)
- Renal: ↑ urine Na (UNa> 40 mEq/L)

iv) FeNa
- Pre-renal: <1% (<2.5% in neonates)
- Renal: > 2% (>10% in neonates)

210
Q

How do you calculate FeNa?

A

(NaUrine/NaPlasma)/(CrUrine/CrPlasma)

211
Q

What are the principles of management of AKI?

A

1) Volume optimization
- Fluids if prerenal
- Fluid restriction if renal
2) Treat electrolyte abnormalities
- HyperK
- Hypocalcemia-treat with low phos diet and phosphate binders
- Hyponatremia-fluid restriction
- Metabolic acidosis-only correct if severe
3) HTN
- Salt and water restriction
- Diuretics
- CCBs
4) Nutrition
- restrict Na, K, PO4

212
Q

What are the different types of dialysis and when would you use each?

A

Hemodialysis
-Stable hemodynamic status

Peritoneal dialysis
-Neonates/infants

CVVH
-Unstable hemodynamic status

213
Q

With which type of dialysis do you need anticoagulation?

A

HD

214
Q

List indications for dialysis

A
  • Volume overload refractory to diuretics
  • Persistent hyperkalemia
  • Severe metabolic acidosis unresponsive to medical management
  • Neurologic symptoms (altered mental status, seizures)
  • Blood urea nitrogen ↑↑ or rapidly rising
  • Calcium:phosphorus imbalance, with hypocalcemic tetany
215
Q

What is the definition of CKD?

A

Renal injury (proteinuria)and/or a GFR<60 mL/min/1.73 m2 for>3 mo

216
Q

List causes of CKD in children

A

A third a third a third!

1/3: Glomerulonephritis
1/3: Renal dysplasia and other renal malformations
1/3: Obstructive uropathy

Others:

  • Prune belly
  • FSGS
  • ARPKD
  • RVT
  • Alport syndrome
  • Cystinosis
  • Hyperoxaluria
217
Q

What parameters are required to calculate eGFR by Schwartz formula?

A

Height

Serum creatinine

218
Q

Lab findings in CKD

A

↑ BUN
↑ K (↓ GFR, acidosis)
Acidosis (impaired HCO3- reabsorption, H+ secretion)
Anemia (↓ EPO, Fe deficiency, ↓ RBC survival)
Hyperlipidemia (↓ plasma lipoprotein lipase)
Hyperglycemia (insulin resistance)

219
Q

Long term complications of CKD

A

Renal osteodystrophy
FTT (↓ caloric intake, acidosis, anemia, GH resistance)
HTN
Anemia
Pericarditis
Infections
Cardiomyopathy (uremia, HTN, fluid overload)
Bleeding diathesis (platelet dysfunction)

220
Q

Management of CKD

A
  1. Fluid and electrolyte management
  2. High calorie diet
  3. Short stature: GH
  4. Renal osteodystrophy: low phosphate diet, phosphate binders, vitamin D
  5. Anemia: EPO
  6. Adjust drug doses
221
Q

List 4 reasons for normocytic anemia in CKD

A

Reduced EPO
Decreased life span of RBC
Anemia of chronic disease
Dilutional with fluid retention

222
Q

What is the definition of microscopic hematuria?

A

≥5 RBCs per HPF

223
Q

What is can cause red urine without RBCs present?

A

Heme-positive

  • Hemolglobinuria
  • Myoglobinuria

Heme-negative

  • Drugs
  • Dyes – e.g. beets, blackberries, rhubarb, food colouring
  • Metabolites – e.g. melanin, methemoglobin, porphyrin, tyrosinosis, urates, homogentisic acid
224
Q

List 10 causes of hematuria

A

Upper Urinary Tract:

  • Glomerular disease
  • Pyelonephritis
  • ATN
  • Vascular Disease → thrombosis, AVMs, aneurysms, hemoglobinopathy
  • Hydronephrosis
  • PCKD
  • Tumour
  • Trauma
  • Hypercalciuria

Lower Urinary Tract:

  • Cystitis
  • Urethritis
  • Urolithiasis
  • Trauma
  • Coagulopathy
  • Heavy exercise
  • Bladder tumour
225
Q

How do you distinguish between glomerular and extraglomerular hematuria?

A

Glomerular:

  • Coca cola
  • No clots
  • Proteinuria
  • Dysmorphic RBCs
  • RBC casts
226
Q

List 3 causes of hemorrhagic cystitis

A

Toxins (cyclophosphamide, penicillins, busulfan)
Virus (adenovirus, influenza A)
Radiation
Amyloidosis

227
Q

If patient has recurrent episodes of gross hematuria, what are 3 possible etiologies?

A

IgA nephropathy
Alport-think in BOYS
Thin basement membrane disease

228
Q

Workup for isolated microscopic hematuria

A
  • If persists on at ≥3 urinalyses over ≥2-week period:
  • Urine culture
  • Urine Ca:Cr ratio
  • +/- Sickle cell screen
  • Renal/bladder US

If these studies are normal:

  • Urinalysis of first-degree relatives
  • Serum Cr and lytes
229
Q

Workup for suspected glomerulonephritis

A 
CBC, diff
Lytes, Cr, BUN
Albumin
Cholesterol
C3/C4
ASOT
ANA
ANCA
Throat/skin culture
230
Q

Causes of glomerulonephritis in children

A

Primary renal disease

  • PIGN
  • MPGN
  • IgA nephropathy
  • Alport
  • ANCA + glomerulonephritis

Systemic disease

  • SLE
  • Endocarditis
  • Shunt nephritis
  • HSP
  • ANCA associated disease (Wegener’s, microscopic polyangitis)
  • Anti-GBM disease
231
Q

How many weeks after initial infection does post-streptococcal GN typically present ?

A

1-2 weeks after strep pharyngitis

3-6 weeks after streppyoderma

232
Q

Over what time period does PSGN resolve?

A

Proteinuria and HTN usually normalize by 4-6 weeks after onset

Persistent microscopic hematuria can persist for 1-2 years

233
Q

When should C3 normalize in PSGN?

A

6-8 weeks

234
Q

When should renal biopsy considered in PIGN?

A 
ARF
Nephrotic range proteinuria
No evidence of strep infection
Normal complement levels
Lab abnormalities lasting >2 months
235
Q

Treatment of PSGN

A

Pencillin x 10 days
Salt and fluid restriction
Diuretics
CCB for HTN

236
Q

In a patient with PSGN who has persistently low C3 after 8 weeks, what diagnosis should you think of?

A

MPGN

237
Q

How does IgA nephropathy most commonly present?

A

Recurrent episodes of hematuria with URTIs

238
Q

What abnormalities on bloodwork would be consistent with IgA nephropathy?

A

Normal C3

High IgA

239
Q

How do you treat IgA nephropathy?

A

Treat HTN

Fish oil decreases rate of disease progression in adults

240
Q

Describe the genetics of Alport syndrome

A

Mutation in type IV collagen (COL4A5)

Majority X-linked (also AR, AD)

241
Q

Clinical presentation of Alport syndrome

A 
1) Asymptomatic microscopic hematuria
Gross hematuria with URTIs
Progressive proteinuria
2) Bilateral acquired SNHL
3) Eye problems
-Anterior lenticonus=pathognomonic!
242
Q

What 3 tests should you order in a patient with suspected Alports?

A

U/A of 1st degree relatives
Eye exam
Hearing test

243
Q

List 3 risk factors for progression to ESRD in Alports

A

Gross hematruia in childhood
Nephrotic syndrome
Prominent GBM thickening

244
Q

Describe the genetics of thin basement membrane disease

A

Sporadic or AD

Defect in type IV collagen

245
Q

Clinical presentation of thin basement membrane disease

A

Microscopic hematuria
Gross hematuria with URTIs
Rarely progresses to proteinuria, HTN, renal insufficiency

246
Q

What is the goal of treatment of lupus nephritis?

A

To induce clinical and serologic remission

Normalization of anti-dsDNA, C3, and C4

247
Q

How often and for how long should you monitor for nephritis in HSP?

A

Weekly U/A + BP Measurement during active disease

Then monthly x 6 months

248
Q

What are the two defining clinical features of Goodpastures?

A

Pulmonary hemorrhage

Glomerulonephritis

249
Q

How do you diagnose Goodpastures?

A

Anti-GBM antibodies

250
Q

Triad of HUS

A

1) Microangiopathic hemolytic anemia
2) Thrombocytopenia
3) Renal insufficiency

251
Q

List 3 infectious causes of HUS

A
  1. Verotoxin-producing E. Coli
  2. Shigella
  3. Neuraminidase producing S. pneumonia
252
Q

List 3 conditions other than HUS that have microangiopathic hemolytic anemia and thrombocytopenia

A

SLE
Malignant HTN
Bilateral renal vein thrombosis

253
Q

List 3 non-infectious causes of HUS

A
  1. Genetic-inherited deficiencies of vWF, complement factors
    - THINK ABOUT THIS IF HUS WITHOUT diarrheal prodrome
  2. Drugs (e.g. cyclosporine)
  3. Systemic diseases (SLE, malignant HTN)
254
Q

List the causes of nephrolithiasis in children

A
  1. Hypercalciuria
  2. Hyperoxaluria
  3. Hypocitraturia
Others (less common):
Hyperuricosuria
Cystinuria
Struvite stones
Indinavir
255
Q

What % of renal stones are visible on AXR?

A

90% are radioopaque

256
Q

List 3 types of stones that are radiolucent

A

Cystine
Xanthine
Uric acid stones

257
Q

List the components of a stone workup

A

Serum:

  • Calcium
  • Phosphate
  • Uric Acid
  • Lytes and VBG
  • Creatinine
  • AlkPhos

Spot Urine:

  • Urinalysis
  • Culture
  • Ca:Cr ratio
  • Nitroprusside screen

24h Urine

  • Cr clearance
  • Calcium
  • Phosphate
  • Oxalate
  • Citrate
  • Uric Acid
  • Dibasic amino acids (if cysteine spot test positive)
258
Q

What are the two most common stone types in North America?

A

Calcium oxalate

Calcium phosphate

259
Q

Treatment of calcium renal stones

A 
Hydration (3L/1.73m2)
Stop extra vit D
Avoid excess Ca
Thiazide diuretics (if persistent nephrocalcinosis or recurrent stones)
Potassium citrate
260
Q

Describe the pathophysiology of struvite stones

A

Associated with UTIs caused by urea-splitting organisms

Leads to urinary to urinary alkalinization and excessive ammonia production

Leads to precipitation of magnesium ammonium phosphate (struvite) and calcium phosphate

261
Q

List 3 bacteria associated with struvite stones

A

Urea-splitting organisms

  • Proteus
  • Klebsiella
  • E. Coli
  • Pseudomonas
262
Q

List 3 conditions associated with uric acid stones

A

Inborn error of purine metabolism
Lesch-Nyhan
G6PD
Short gut

263
Q

List 2 conditions associated with struvite stones

A

Neurogenic bladder

Reconstructed bladder

264
Q

Treatment of uric acid stones

A

Allopurinol

Urinary alkalinization

265
Q

Describe the pathophysiology of cystinuria

A

Rare AR disorder of renal tubular epithelial cells

Prevents absorption of the 4 dibasic amino acids (cystine, ornithine, arginine, lysine)

266
Q

Treatment of cystine stones

A

Urinary alkalinization

D-Penicilliamine

267
Q

List 5 causes of nephrocalcinosis

A 
Lasix
Distal RTA
Hyperparathyroidism
Hypophosphatemic rickets
Medullary sponge kidney
Hyperoxaluria
Hyperuricosuria
268
Q

Most common cause of microscopic hematuria

A

Idiopathic — 36%

Benign familial hematuria

Hypercalciuria — 22%

IgA nephropathy —16%

Post-streptococcal glomerulonephritis — 7%

Other glomerulopathies including thin basement membrane disease — 2%

Congenital anomalies (eg, UPJ obstruction or renal dysplasia) — 2%

Sickle cell trait — 1%

269
Q

List 5 findings on ultrasound that might indicate reflux and need for VCUG

A 
Pelviectasis 5mm or greater
Size discrepancy kidneys
Significant hydroureter
Thick walled trabeculated bladder
Renal cysts
270
Q

What percentage of children with nephrotic syndrome respond to steroids?

A

80%

271
Q

Differential for nephritis with normal C3

A

Kidney only:
IgA nephropathy
Anti-GBM disease
Alports

Systemic:
Good pastures
ANCA positive GN

272
Q

List 3 stone promoters

A 
Calciuria
Oxaluria
Urate
Cystine
Urinary stasis 
Infection
273
Q

List 3 stone inhibitors

A

Citrate
Phosphate
Magnesium
High urine flow

274
Q

What is significant antenatal pelviectasis?

A

Abnormal if >10mm at >=32 weeks GA

275
Q

If baby has >10mm antenatal pelviectasis at >32 weeks, what should be done postnatally?

A

Trimethoprim prophylaxis

Ultrasound 3-10 days

276
Q

What would you do with the following postnatal ultrasound results:
RPD<1 cm
RPD 1-1.2cm
RPD >1.2 cm

**NOTE: will not be tested-this is a sickkids guideline

A

RPD<1 cm

  • Stop TMP
  • No more U/S

RPD 1-1.2cm

  • Continue TMP
  • Repeat US at 3 mo

RPD >1.2cm
Continue TMP
VCUG

277
Q

What is nuclear scan with lasix washout used for?

A

Assess for:

1) Obstruction
2) Differential kidney function

278
Q

List 3 steps in management of solitary kidney

A
  1. Serial US to ensure proper growth
  2. Avoid ccontact sports, sky diving
  3. Yearly U/A and BP
279
Q

What does the creatinine of a newborn baby represent?

A

Mom’s creatinine

FRCPC (27 decks)

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