Transcript Finance Subcommittee Update March 17, 2005

Metro NY/ NJ Pediatric Board
Review Course
Pediatric Fluid/ Electrolytes and
Nephrology
June 2014
Leonard G. Feld MD PhD
Levine Children’s Hospital
Charlotte, NC
Outline
• Fluid and Electrolyte abnormalities
– Dehydration
• Renal
– Hematuria
– Proteinuria
– Hypertension
– Urinary tract infections
– Glomerulonephritis
Case 1
4 mo old infant with 4-5 day history of fever (38.5oC),
numerous watery diarrhea and decreased activity.
Child refused to take breast milk or solid foods.
Mother substituted non-carbonated soda (Coca-cola,
etc ~550-700 mOsm/kg H2O & < 5 mEq/L Na.
Over last 12 hrs few episodes of emesis and less wet
diapers.
EXAM:
lethargic, dry mucous membranes, no tears, sunken
eyeballs & reduced skin turgor.
BP 74/43 mmHg; Temp 38.5oC, RR 36 , HR175 beats
WT 6 kg. Weight 7 days ago was 6.6 kg.
There were no other significant findings.
Electrolyte Composition of Body
Fluid Compartments
March 17, 2005
BODY WATER DISTRIBUTION
TOTAL BODY WATER (TBW)
0.6 x Body Weight (BW)
EXTRACELLULAR FLUID
(ECF)
0.2 x BW
Interstitial Fluid
¾ of ECF
Plasma
¼ of ECF
INTRACELLULAR FLUID (ICF)
0.4 x BW
Clinical Assessment
Fluid
Deficit
Mild
( 3-5%)
~50 cc/kg
Clinical
Status
Compensated
Clinical
Assessment
Thirsty, HR, Normal BP
tears, slightly dry mucosa,
alert/restless, [urine]
Moderate ~100 cc/kg Decompensated
(6-9%)
Very dry mucosa, < skin
turgor, sunken eyes, deep
resp, weak pulses, cool
extremities, oliguria
Severe
(>10%)
Intense thirst,  BP, cap refill
> 3 sec, weak pulses,
apnea/rapid breathing, coma,
anuria
>100 cc/kg Shock
Maintenance Requirements
Body wt
0-10 kg
10-20 kg
20 kg
TBW
100 ml/kg
1000 ml +
50 ml/kg for
each kg >
10kg
1500 +
20 ml/kg for
each kg >
20kg
Na+
3 mEq/kg
3 mEq/kg
3 mEq/kg
K+
2 mEq/kg
2 mEq/kg
2 mEq/kg
Cl-
5 mEq/kg
5 mEq/kg
5 mEq/kg
Laboratory
Sodium 124 mEq/L
Chloride 94 mEq/L
Potassium 4 mEq/L
Bicarbonate (or total CO2) 12 mEq/L
Serum creatinine 0.8 mg/dL
Blood urea nitrogen 40 mg/dL
Blood glucose 70 mg/dL
Complete blood count was normal except for a
hemocrit of 38% (normal ~ 36%)
Hyponatremia
•
•
•
•
•
Serum [Na+] < 130 mEq/L
Water shifts into cells – lower ECF volume
<125 mEq/L – nausea and malaise
< 120 mEq/L – headache, lethargy,
<115 mEq/L – seizure and coma
Loss of hypertonic Fluid and Sodium from the ECF secondary to Dehydration
NORMAL
0.25 Liters
0.40 Liters
280
280
mOsm/L
35 Na
64 K
0
0
Loss
0.10 LIters
AFTER LOSS
400
0.15 Liters
10 K
10 Na
280
200
55 K
10 Na
15 Na
0
0.40 Liters
0
0
AFTER OSMOTIC ADJUSTMENT
0.116 Liters
0.434 Liters
258
258
15 Na
54 K
10 Na
0
NORMAL ECF
0
NORMAL ICF
Question 1: What is the appropriate
parenteral solution
A. 5% dextrose + 0.45% isotonic saline +
40 mEq KCl /L
B. 0.45% isotonic saline + 40 mEq KCl /L
C. 0.33% isotonic saline + 40 mEq KCl /L
D. 5% dextrose + 40 mEq KCl /L
E. 5% dextrose + 0.2% isotonic saline
Causes of SIADH
•
•
•
•
Neurological conditions
Pulmonary conditions
Tumors
Medications
Criteria
• Hypotonic hyponatremia.
• Inappropriate urine osmolality compared to
plasma osm. Patients with medical condition
associated with occurrence of SIADH, a urine
osmolality > maximal dilution (75-125
mosm/L) and low plasma osm is
“inappropriate” to state of water balance.
• Absence of thyroid, adrenal, cardiac, or renal
disease
• Absence of volume contraction
• High urinary sodium concentration
Additional hints for SIADH
•
•
•
•
•
•
Fluid balance even or positive
CVP > 6
Urine volume decreased
Uric acid decreased
BUN and Cr decreased
Urine Na > 20 mEq/L
Points on Hypernatremic Dehydration
NORMAL
0.25 Liters
0.40 Liters
280
280
mOsm/L
35 Na
64 K
0
0
413
0.15 Liters
AFTER LOSS
0.40 Liters
280
Loss
0.10 LIters
31 Na
62 K
2 Na
80
2K
2 Na
0
0
0
AFTER OSMOTIC ADJUSTMENT
0.195 Liters
0.355 Liters
318
318
37 Na
62 K
2 Na
0
NORMAL ECF
0
NORMAL ICF
Hypernatremia – SLOW and CLOSE
Key points: look quiet then irritable on stimulation; may look
better than % of dehydration based on weight
Fluid selection: 5% dextrose + ¼ isotonic saline (~30-40 mEq/L of
Na) + 20 mEq KCl /L (D5W with 1/2/ NS + KCl is also OK).
• 1st 24 hrs: 24 hrs of Maintenance + ½ deficit
• 2nd 24 hrs: 24 hrs of Maintenance + ½ deficit
• Close monitoring of serum sodium every 2-3 hours.
Some have suggested using a higher [sodium] – 0.45% isotonic
saline or even isotonic saline to restore ECF volume then
moving to a lower
• sodium containing solution to restore the water deficit. This
approach may also reduce the possibility of dropping the
serum sodium too quickly and preventing neurological
problems.
Case 2
Susan an 8 yr old noted on routine exam to
have moderate hematuria on dipstick.
Unremarkable past medical hx.
Family hx is negative in the parents and
siblings for any renal disease. Hx of
hematuria is unknown.
Repeat urine in 1 wk still positive, urine
culture showed no growth.
Question 2: Which of the following test is the next
step in the evaluation?
A. VCUG and urine culture
B. Renal sonogram and urine calcium to
creatinine ratio
C. Urology referral
D. CBC and Direct Coombs
E. Recheck in two years
More on Hematuria
• BIG 3
1 Repeat a first AM void following restricted activity ,
perform a microscopic on a fresh urine
2 Check the family members
3 If there is still blood without protein, casts, crystals,
normal BP with or without a strong family history, no
further work-up is generally required. However a
renal sonogram and urine calcium to creatinine
ratio
Glomerular v. Non-glomerular bleeding
• Glomerular
– oliguria, edema, hypertension, proteinuria, anemia
• Non-glomerular – THINK LOWER TRACT
–
dysuria, frequency, polyuria, pain or colic, hx
exercise
–
crystals on microscopic
–
mass on exam
–
medication history - sulfas, aspirin, diuretics
Initial evaluation of the patient with hematuria
•
All patients: BUN, creatinine, kidney and bladder ultrasound, urine
calcium to creatinine ratio
•
Who should be worked up
– Presence of proteinuria and/or hypertension ,
– History consistent with infectious history, HSP, systemic symptoms, medication
use or abuse, strong family history of stones or renal disease/failure.
– Persistent gross hematuria
– Family anxiety - limit evaluation
•
Probable glomerular hematuria
– C3, ASO titer
– possible: hepatitis, HIV, SLE serology , SSD
– renal biopsy – not for persistent microscopic without proteinuria, decreased renal
function, and/or hypertension
•
Probable non-glomeurlar hematuria
–
–
–
–
urine culture, urine Ca/creatinine ratio
possible: hemoglobin electrophoresis,
coagulation studies, isotope scans,
Flat plate, CT, ??IVP, cystoscopy
Pearls for Hematuria
• Hematuria may be an important sign of renal or
bladder disease
• Proteinuria (as we will discuss) is the more
important diagnostic and prognostic finding.
• Hematuria almost never is a cause of anemia
• The vast majority of children with isolated
microscopic hematuria do not have a treatable
or serious cause for the hematuria, and do not
require an extensive evaluation. So a VCUG,
cysto and biopsy are not indicated.
More Pearls
• Urethrorrhagia – boys with bloody spots in the
underwear
– Presentation – prepuberal ~ 10 yrs
– It is painless
– Almost 50% will resolve in 6 months and > 90% at 1
year; it may persist for 2 yrs
– Treatment – watchful waiting in most cases
• Painful gross hematuria – usually infection,
calculi, or urological problems; glomerular
causes of hematuria are painless.
More Pearls – gross hematuria
• Gross hematuria is often a presentation of
Wilms’ tumor
• All patients with gross hematuria require
an imaging study.
• If a cause of gross hematuria is not
evident by history, PE or preliminary
studies, the differential includes
hypercalciuria or SS trait
• Cysto is rarely helpful
Case 3
7 yr old boy developed gross tea colored hematuria after
a sore throat and URI. No urinary symptoms but urine
output was decreased. Complained of mild diffuse lower
abdominal pain. No fever, rash or joint complaints. Past
med hx was unremarkable but had intermittent
headaches 2 years ago.
EXAM
Afebrile, BP 95/65 mmHg, no edema, some suprapubic tenderness,
red tympanic membranes. Mother thinks that a similar episode occur
on vacation a few months ago.
Urinalysis - 20 RBCs/hpf, 5-10 WBCs, 100 mg/dL protein, rare
cellular and hyaline casts. Serum creatinine is 0.8 mg/dL, C3 100
(normal).
.
Question 3: The most likely cause
of the gross hematuria is:
A.
B.
C.
D.
E.
Myoglobinuria
Urinary tract infection
Obstructive uropathy
IgA nephropathy
Benign familial hematuria
IgA
• IGA nephropathy
– Boys > girls
– Mostly normotensive, with persistent
microscopic hematuria
– Chronic glomerulonephrits – up to 40% of
primary glomerulonephritis
– Complement studies are nl, some inc IgA
– Prognosis – not so good if > 10 yrs of age,
proteinuria, reduced GFR, hypertension and
no macrohematuria
Work of AGN
1. Obtain UA, renal US, 24 hr urine protein/creatinine, spot
urine protein and creatinine ratio
2. Glomerulonephritis –active sediment (protein, RBCs,
dysmorphic RBCs/or RBC casts), 300 mg - >1 gm/day
proteinuria, HTN, edema
3. Low complement GN:
Systemic: SLE, SBE, cryoglobulinemia, shunt nephritis
Isolated renal: post-infectious GN, MPGN
Normal complement GN:
Systemic: HSP, ANCA-associted (Wegener’s, PAN),
Goodpasture’s syndrome, hypersensitivity vasculitis
Isolated renal: IgA nephropathy, anti-GBM disease,
RPGN
Red or Tea colored/ Brown Urine
Fresh Centrifuged Urine Sample
Sediment Red with
Red Cells
Hematuria
Supernatant Red without
Red Cells
Hemoglobinuria*
Myoglobinuria
* Hemoglobinuria will have
a red or pink hue to the
serum
NOTE: If there is no red sediment, no RBCs
and a clear supernatant, consider other
causes such as urates, bile pigments,
beets, porphyria, some medications, etc.
Question 4
On routine physical examination, an 8-yearold boy is found to have microscopic
hematuria. The first step in your
evaluation should be.
A. Examine the urine sediment
B. Order an renal ultrasound
C. Obtain a voiding cystourethrogram
D. Perform a CBC in the office
E. Order an ASO titer and C3
Question 5
An 8-year-old boy presents with tea colored
urine. He has very mild edema. History of
strep infection about 2 weeks ago. The
work-up should include all the following
except.
A. Complement studies
B. Serum creatinine
C. Urinalysis for protein
D. Monitor blood pressure and urine output
E. Obtain a renal ultrasound
Acute glomerulonephritis: clinical
• May be clinically asymptomatic (? 90%)
with low C3 and hematuria
• Usually within 3 weeks after strep infection
– mean about 10 days
• Periorbital, peripheral edema
• Hematuria - coke-colored, tea-colored,
reddish/brown
• Nonspecific findings such as abdominal
pain, malaise, anorexia, headaches, pallor
Acute glomerulonephritis: DD
• Acute Poststreptococcal glomerulonephritis
(PSAGN) – most common
• Acute Postinfectious or nonstreptococcal
postinfectious glomlerulonephritis 9AIAGN)
– Bacterial: endocarditis (low C3), shunt nephritis (low
C3), pneumococcal pneumonia, etc.
– Viral: hepatitis B, infectious mononucleosis, varicella,
etc,
– Parasites:
• Other: SLE (low C3), membranoproliferative GN
(low C3), hyperthyroidism, HSP (nl C3)
Acute glomerulonephritis:
evaluation/ treatment
• Evaluation
–
–
–
–
ASO, C3, C4
Renal function
Evaluation for hypertension and oliguria
Magnitude of proteinuria
• RX – supportive
– Admission for hypertension, oliguria, impaired renal
function, nephrotic syndrome
• Prognosis: C3 normalizes by 12 weeks,
hypertension and other abnormalities resolve by
2-3 months, hematuria may persist for 6-24 mo
Proteinuria
Case 6: John is an 12 year old noted on a
basketball team physical to have 2+
protein on dipstick. There are no recent
illnesses. He has an unremarkable past
medical history and he is not taking any
medications. Family history is negative in
the parents and siblings for any renal
disease.
Question 6: Which of the following
is the best approach?
A.
B.
C.
D.
E.
Obtain a 1st AM urine for protein
Perform a complete biochemical profile
Obtain a C3, ASO and ANA
Refer for a renal biopsy
Schedule a renal sonogram and VCUG
What does Orthostatic Proteinuria
mean?
Protein
Excretion
Threshold of Detection
Normal
Orthostatic
Recumbant
Erect
More on Proteinuria
• Repeat a first AM void following restricted
activity, perform a microscopic on a fresh
urine; also an alkaline pH may give a false
positive result
• If there is still protein perform a more
formal orthostatic test. If orthostatic, no
further work-up is generally required,
although no indemnification from
subsequent renal disease.
Causes of Proteinuria
• Transient
–
fever, emotional stress, exercise, extreme cold,
abdominal surgery, CHF, infusion of epinephrine
• Orthostatic
–
Transient or fixed / reproducible
• Persistent
–
–
–
Glomerular disease: MCNS, FSGS, MPGN, MN
Systemic:
SLE, HSP, SBE, Shunt infections
Interstitial:
reflux nephropathy, AIN, hypoplasia,
hydronephrosis, PKD
Question 7
A four-year boy presents with a 5-day history of
swollen eyes and “larger ankles”. On exam he
has periorbital and pretibial edema. The most
likely cause of nephrotic syndrome would be?
A. Systemic lupus erythematosus
B. Hemolytic uremic syndrome
C. Minimal change nephrotic syndrome
D. Membranous nephropathy
E. Membranoproliferative glomerulonephritis
Definitions (Pearl)
• Urine protein to creatinine ratio
–
–
–
Normal:
Mild to moderate:
Heavy or severe:
< 0.2 (< 0.15 adolescents)
0.2 to 1.0
> 1.0
• Persistent proteinuria: present both in the
recumbent and the upright posture; even in this
situation, proteinuira is less during recumbency
Nephrotic Syndrome
• Primary Nephrotic Syndrome:
– Minimal change disease (~75%) – mean age 4 yrs
• No hematuria, nl C3, no hypertension, nl creatinine
– Membranoproliferative GN (~ 5-10%)
– FSGS (5-10%)
– Proliferative GN, Mesangial proliferation
– Membranous nephropathy
• Secondary Nephrotic Syndrome:
– SLE, HSP, diabetes mellitus, HIV, vasculitis, malignancy
(lymphoma, leukemia), drugs (heroin, inteferon, lithium),
infections (toxo, CMV, syphilis, hepatitis B and C)etc.
• Congenital/Infantile Nephrotic Syndrome:
– Finnish-type congenital nephrotic syndrome,Denys-Drash
syndrome
– Diffuse mesangial sclerosis, Nail-patella syndrome
Nephrotic Syndrome - RX
Corticosteroid treatment
• Induction therapy: Exclude active infection or other
contraindications prior to steroid therapy.
– Oral prednisone- 60 mg/m2/d (~2 mg/kg/d) daily for 4 -6 wks.
– Oral prednisone at 40 mg/m2 (or ~1.5 mg/kg) given as a
single dose on alternate days for 4 -6 wks.
• Relapse therapy - For infrequent relapses,
– Prednisone 60 mg/m2/d (~2 mg/kg/d) as single AM dose
until proteinuria resolved for at least 3 -4 days.
– Following remission of proteinuria, prednisone reduced to
40 mg/m2 (or ~1.5 mg/kg) given as a single AM dose on
alternate days for 4 weeks. Prednisone may then be
discontinued or a tapering regimen.
Frequently relapsing nephrotic syndrome is steroid-sensitive
nephrotic syndrome with 2 or more relapses within 6 mos or
more than 3 relapses within a 12-mo period.
Hypertension
Hypertension
Question 8: David is a 10 year old boy first noted
to have an elevated blood pressure of 123/85
during a annual physical examination. Pt has a
long history of learning and behavioral issues.
He has a previous history of headaches that
were evaluated with a CT scan of the brain and
sinuses. On following evaluation in one week,
his BP is126/86 mmHg with a weight > 99%ile
for age and a height at ~50th %ile.
Question 8: What is the most appropriate initial
testing for this child?
A. Renal mag-3 flow scan
B. Electrolytes, BUN, Creatinine,
Bicarbonate, glucose
C. Renal Sonogram with doppler
D. Urinary screening for drugs
E. 24 hour urine for catecholamines
BP Classification
Grade of hypertension
Definition
Appropriate next step
“White-coat” hypertension
BP levels >95th percentile in a
physician's office or clinic, but
normotensive outside a clinical
setting
Readings may be obtained at home with
appropriate family training or with the
assistance of a school nurse, or with the
use of ambulatory BP monitoring
(ABPM)
Normal
< 90th %ile
Pre-hypertension
>120/80 mm Hg should be
considered pre-hypertensive or
90-95%ile
Additional readings may be obtained at
home with appropriate family training
or with the assistance of a school nurse
Stage I hypertension
95th -99th %ile + 5 mmHg
Organize a diagnostic evaluation in a
non-urgent, phased approach
Stage II hypertension
Average SBP or DBP that is >5 mm
Hg higher than the 99th percentile
Organize a diagnostic evaluation over a
short period of time in conjunction with
pharmacological treatment
Hypertensive urgency and
emergency
Average SBP or DBP that is >5 mm
Hg higher than the 95th percentile,
along with clinical signs or
symptoms
Hospitalization and treatment to lower
the blood pressure
Estimate of Hypertension
Estimate without height adjustment
1. If systolic BP equals or exceeds
100 + 2 times pt age in yrs
2. If diastolic BP equals or exceeds
70 + pt age in yrs
Estimate with height adjustment
1. If systolic BP at 95th %tile for age and sex
Add 4 mmHg to the value at the 50th %tile
2. If diastolic BP at 95th %tile for height
Add 2 mmHg to the value at the 50th %tile
Evaluation of Hypertension
Historical
Information
Physical
Examination
Neonatal history
Family history
Dietary history
Risk Factors (smoking, alcohol use,
drug use)
Non-specific / specific symtomatology
Review of Systems - sleep and exercise
patterns, etc.
Vital signs
(including extremities)
Height/Weight
Specific attention to organ systems cardiac, eye, abdominal or other
bruits, etc.
Consider ambulatory blood pressure
monitor
Evaluation Phase 1
CBC, urinalysis, urine culture, electrolytes, BUN, creatinine,
thyroid studies, uric acid
plasma renin, lipid profile, echocardiogram, renal ultrasound
with duplex doppler
Evaluation Phase 2
Selected studies based on magnitude of the hypertension and/
or other clinical /laboratory findings
Renal flow scan (MAG 3)
CT Angiography (CTA)
MRA (may not provide adequate evaluation for
peripheral renal vascular lesions)
Renal arteriography with renal vein sampling
Plasma / urine catecholamines and/or steroid concentrations
Indications for Treatment
•
•
•
•
•
Symptomatic hypertension
Secondary hypertension
Hypertensive target-organ damage
Diabetes (types 1 and 2)
Persistent hypertension despite
nonpharmacologic measures
Pharmacologic Therapy
for Childhood Hypertension
• The goal for antihypertensive treatment in
children should be reduction of BP to
<95th percentile, unless concurrent
conditions are present. In that case, BP
should be lowered to <90th percentile.
• Severe, symptomatic hypertension should
be treated with intravenous
antihypertensive drugs.
Urinary Tract
Infections
Case 9
• A 4 mo old girl presents with low grade
fever, mid-lower abdominal pain and
nighttime-incontinence. She is not
eating well. Prior visits she had normal
blood pressure, urinalysis and excellent
growth. Urinalysis shows hematuria, 30
mg/dL of protein, leukocyte esterase
and positive nitrite. Urine culture is
obtained.
53
Question 9: What is the most likely bacterial cause
of her urinary tract infection?
A.
B.
C.
D.
E.
Proteus mirabilis
E. coli
Coagulase positive Staphlococus
Alpha hemolytic Streptococcus
Klebsiella pneumoniae
Bacteriology /Pathogenesis UTI - 1
• Most Common - E. Coli, coliforms
• Virulence Factors
• adherence to uroepithelium by P-fimbriae
• endotoxin release
• Pyelo vs cystitis - 80 to 20%
55
Bacteriology /Pathogenesis UTI 2
• Perineal / urethral factors
– uncircumcised - 10-20x risk
– ? Urethral caliber (infant girls)
– other myths such as bubble bath, wiping
techniques
• Low Urinary factors
– dysfunctional voiding ; constipation
• Other - indwelling catheters, congenital
anomalies, Vesicoureteral reflux, sexual
activity
56
Diagnosis
• Leukocyte test and nitrite test
• Urine culture > 40-50,000 CFU/mL
• Pyuria - not on recurrent UTIs
57
Clinical Issues
• Lower tract - frequency, urgency,
enuresis, dysuria
• Upper tract - fever - nearly all in boys
under 1 year of age; females peak in
first year but still significant through the
first decade
• Asymptomatic bacteriuria - low risk
58
Radiological Evaluation
• Renal ultrasound - anatomy, size, location,
echogenicity
• DMSA (2nd choice glucoheptanate SGH) - cortical integrity, photopenic regions,
differential function, abscess
• CT scan - abscess
• VCUG – not the current standard for first
UTI; radionuclide for follow-up or siblings
• IVP - NO WAY
59
AAP SEPT 2011
Practice guidelines
• DX: Urinalysis with pyruria and culture with
50,000 col/ml single organism by SPA or cath
• Treat for 7-14 days
• Ultrasound for all with febrile UTI
• VCUG only with abnl Ultrasound, or other
findings to suggest atypical or complex issues
• VCUG – after 2nd febrile UTI
• No Abx prophylaxis unless VUR grade V
Grades of Reflux
61
Reflux Recommendations
“the simple way”
• GRADES
I - III
Antibiotics
• GRADES
IV - V
Surgery
• Although endoscopic approach is gaining
favor over open reimplantation
62
Treatment
• Oral
– SMX-TMP, Amoxicillin/Clavulanate
– Cefuroxime, cefprozil, cefixime, cefprodoxime
• Parenteral
– Neoates: Ampicillin / Gentamicin
– Older Children:
• Advanced level cephalosporin
• Beta lactam + beta lactamase inhibitor
• Aminoglycoside (+ ampicillin)
63
Case10: Case History
• A 12 mo old girl is diagnosed with the
first febrile UTI. She is not eating well.
UA shows pyuria and bacteria. Urine
culture is obtained and shows >
100,000 colonies of E. Coli. Antibiotics
are given.
64
Question 10: What is the most
appropriate next step?
A.
B.
C.
D.
E.
Perform a DMSA renal scan
Refer to urology for cystoscopy
Perform a renal sonogram
Perform urodynamics and flow studies
Repeat urine culture in 3 months
Glomerulonephritis / Acute
renal failure
Case 11
• 3 year old boy was attending summer camp.
• Five days later he presents with diarrhea,
abdominal pain and appear pale.
• His mother finds out that there was cook out
at camp.
• EXAM- child is pale & unable to void. LABS
WBC 26,000, hemoglobin 8 g/dL, platelets
98,000, Serum creatinine 1 mg/dL, BUN 54
mg/dL, urinalysis - large blood, 100 mg/dL of
protein.
67
Question 11: What is the most
likely diagnosis?
A.
B.
C.
D.
E.
Henoch Schoenlein Purpura
Post streptococcal glomerulonephritis
IgA nephropathy
Acute pyelonephritis
Hemolytic uremic syndrome
Clinical prodrome
• Diarrhea prodrome 1-15 days
• Abdominal pain – may be confused with
ulcerative colitis, appendicitis, rectal
prolapse, intussusception
• Pallor
• Irritability, restlessnes
• Edema – after rehydration
• Oliguria/anuria
HUS: Clinical manifestations
•
•
•
•
•
•
Thrombocytopenia
Hemolytic anemia
Renal failure
Neurologic (irritability, seizure, CVA)
Pancreatitis (IDDM) and colitis
Hypertension
HUS: Pathogenesis
• Endothelial cell damage occurs secondary
to toxin injury via binding to glycolipid
receptor or lipopolysaccharide absorption.
HUS: Differential diagnosis
• Other forms of acute Glomerulonephritis /
renal failure
• Vasculitis
• Urosepsis
• Renal vein thrombosis
• Coagulopathy (DIC)
Conservative management
• Fluid restriction to <insensible losses plus
urine output
• Foley catheter – limit to 24-48 hrs
• Blood transfusion / platelets
• Routine use of antibiotics controversial
• Diuretics
• Nutrition
Surgical Complications
•
•
•
•
•
•
•
Toxic megacolon
Rectal prolapse
Colonic gangrene
Intussusceptions
Perforation
Strictures
Mimic appendicitis, IBD
BONUS
A 6 year old boy presents with recurrent episodes of
brownish urine that developed coincidental with URIs. His
urinalysis during the episodes reveals red blood cell casts
and small protein. His complement levels are normal. His
hepatitis B screen is normal. The MOST likely diagnosis is:
1.Post Strep AGN
2.IgA nephropathy
3.Membranoproliferative glomerulonephritis
4.Membranous nephropathy
5.Wegener’s granulomatosis
SOME QUICKIES
• Unilateral multicystic dysplastic kidney – MOST COMMOM CAUSE
OF ABDOMINAL MASS IN NEWBORN
– ULTRASOUND AND VCUG to DETERMINE CONTRALATERAL
DISEASE
• Polycystic Kidney Disease
– Autosomal recessive – bilateral enlarged kidneys with microcysts
(Potter’s – pulmonary hypoplasia); overtime – liver fibrosis and
failure
– Autosomal dominant – MOST COMMON INHERITED KIDNEY
DISEASE; bilateral enlarged kidneys with MACROCYSTS;
association with cerebral aneurysm
• Hydronephrosis
– Usually obstruction; Ultrasound may show enlarged kidney
without hydroureter
• Posterior urethral valves –
– MOST COMMON CAUSE of OBSTRUCTIVE UROPATHY IN MALES; remember poor
urinary stream and palpable bladder
• Vesicoureteral reflux
– Grades from I to V; VCUG diagnoses REFLUX, Radionuclide (DMSA)
scans detect scars ; Surgery for grades IV to V (in general)
• UTIs
– E. coli most common followed by Klebsiella, Proteus. Males over 1
also have E. Coli then Proteus, Staph
– Females > males; greater in uncircumcised; remember constipation
may increase incidence of UTIs
– DX – culture, cath or mid stream; UA – positive nitrites and
leukocytes
– 1st febrile UTI – ultrasound ; VUCG for girls with more than 2 UTI in 6
months; all males
• Hematuria
– Rule out hemoglobin and myoglobin
– Brown urine – glomerular – look for red cell casts
– Lower tract – gross red (possible at end of stream), no casts,
possible clots
– Rule out hypercalciuria – spot ratio
– Common diseases
• IgA – gross hematuria with respiratory or GI illness
• Post Strep AGN – follows throat or skin infection by 10-21 days,
Low C3 but recovers by 8-12 weeks, maybe increased ASO titer
• HUS – E. coli – 0157:H7 – MOST COMMON CAUSE OF
ACUTE RENAL FAILURE; low platelet count and
microangiopathic hemolytic anemia (schistocytes; coombs
negative)– cause undercooked meat or unpasteurized milk
• Proteinuria
– Rule out Orthostatic Proteinuria; urine protein to creatinine ratio –
abnormal above 0.2 from AM specimen
– Nephrotic syndrome – ratio greater than 2 or more the 40 mg/m2/hr
of protein
• Minimal change – steroid responsive is MOST COMMON
• Usually 2- 6 yrs with mean of 4 yrs; remember edema is
dependent - first eyes than later in day to the legs.
• Treatment – prednisone – 60 mg/m2/day for 4-6 weeks followed
by alternate day steroids for 4-6 weeks.
• Tubular entities
– Diabetes insipidus
• X linked or secondary to ADH resistance
• Look for dilute urine in face of hypernatremia
• Water deprivation test then give IV or intranasal vasopressin
– Renal tubular acidosis – normal anion gap – hyperchloremic
metabolic acidosis
• Proximal or Type II – bicarbonate wasting
– Failure to thrive
– pH < 5.5
– Serum bicarbonate usually less than 18
– Remember FANCONI syndrome is RTA = glycosuria,
phosphaturia, and amino aciduria.
– Treated with bicarbonate
– Distal or Type I – impaired distal acidification; pH > 5.5; may have
hypokalemia and hypercalciuria
– Look for polyuria, vomiting, nephrolithiasis
– Treated with bicarbonate – low dose compared to proximal
– Bartter syndrome
• Hypochloremic metabolic ALKALOSIS; hypokalemia.
• Look for polyuria, failure to thrive, low serum chloride and low
potassium
– Kidney Stones
• Imaging of choice – spinal CT.
• Most stones are radiopaque since they contain calcium. Nonradiopaque are uric acid stones.
• Cystinuria – increased urinary excretion of dibasic amino acids
• Acute kidney injury (failure)
– Evaluation to determine – prerenal (perfusion);
renal (intrinsic) or post renal (obstruction)
• Chronic kidney disease
– Key items – anemia, growth failure, renal
osteodystrophy
– Options – dialysis and preferred renal
transplantation
For the Exam
• High frequency sensorineural hearing loss, ocular and renal
disease – think Alport syndrome – most cases are X-linked
• Neurofibromatosis – renal abnormality is renal artery stenosis
causing hypertension
• Nail patella syndrome – nephrotic syndrome
• Turner syndrome – Horseshoe kidney
• Tuberous sclerosis – angiomyolioma and polycystic kidney,
hypertension
• Congenital hepatic fibrosis – autosomal recessive polycystic
kidney disease
• Multicystic dysplastic kidney – non-functioning renal tissue check contralateral kidney for abnormalities – may be
associated with other conditions such a VATER, CHARGE,
• Mesoblastic nephroma – most common renal mass in
neonates
For the Exam
• Hematuria – rarely a cause of anemia; check complements, spot
urine calcium to creatinine ratio
• Isolated microscopic hematuria does not require an extensive
medical and imaging evaluation.
• Gross hematuria may be a tip for Wilms Tumor and require renal
imaging;
– If suspect renal stone – spiral CT is best (sonogram and plain xray may be first test in ED). If pt with a fever and a stone – think
Proteus
– If sickle cell trait or disease need imaging test – ultrasound and
possible IVP or CT. Could be papillary necrosis.
• Urethrorrhagia– painless hematuria in males– red blood spots on
underwear
• Painful hematuria – stones, infections or other urological disease
For the Exam
• First morning urine is best to assess concentrating ability,
exercise induced hematuria and orthostatic proteinuria
• Normal urinary protein is < 0.2 (ratio), < 4 mg/m2/hr; nephrotic
> 40 mg/m2/hr or ratio > 2.
• Fractional excretion of sodium - dehydration < 1; acute renal
injury > 2-3
• Hypertension by age
– Newborn and infants – think umbilical catheter, artery or
vein thrombosis, coarctation
– Preschool – think renal, renal artery stenosis or coarctation
– School age – think renal renal artery stenosis, essential
– Adolescence – think – essential, obesity, renal or drugs.
For the Exam
•
Renal Diseases
– Acute glomerulonephritis: Post strep, low C3 – hospitalization for
hyperkalemia, fluid overload or hypertension. C3 resolves by 12
weeks.
– IgA – macroscopic or microscopic hematuria, normal C3
– HSP – normal C3 and platelet count are normal; skin - purpuric
papules and may start on lower extremities or other parts of the
body including ears, genitalia; GI – may precede rash;
intussusception common; renal and joints (arthritis/arthralgias) –
they can occur in any order; causes – infections, medications,
vaccinations; REMEMBER DIFFENTIAL RENAL DIAGNOSIS
includes Post StrepAND FOR PURPURA – Sepsis,
Meningococcemia.
– Membranoproliferative – Low C3 and C4 in Type 1; only C3 low in
Type 2 and 3. Differential is Lupus and Post Strep due to low C3.
Treatment is alternate day corticosteroids
For the Exam
– Nephrotic Syndrome – minimal change; normal C3; steroid
responsive in majority of cases; causes – idiopathic, drugs,
allergies, tumors (Hodgkin and non-Hodgkin), infections.
Infection potential while on corticosteroids, BEWARE NOT TO
GIVE LIVE VIRAL VACCINES - see REDBOOK
– Focal Segmental Glomerulosclerosis – normal C3; usually a
steroid unresponsive form of Nephrotic syndrome; usually
idiopathic and an unremarkable (non-nephritic) urinary sediment
(no red cell casts or white cells); can be inherited; usually older
patients compared to Minimal change.
– Membranous Nephropathy – older age than minimal change,
may be history of hepatitis, unremarkable (non-nephritic) urinary
sediment (no red cell casts or white cells); forms of
membranous can occur in LUPUS.
For the Exam
• HUS – associated with Shiga Toxin (old term is
diarrheal or typical) or S. Pneumoniae infections;
can be idiopathic or hereditary; Hemolytic anemia
with fragmentation of RBCs, thrombocytopenia and
acute kidney failure. Poor prognosis – older age,
non-shiga toxin HUS which is often associated with
complement mutations
For the Exam
• Polycystic Kidney Disease
– Autosomal recessive – kidney and liver (congenital hepatic
fibrosis) – think esophageal varices in later life. Potter’s facies,
present in newborn period with large masses; maybe have
oliguria, RDS. On ultrasound have increased echogenicity and
loss of corticomedullary differentiation. DIFFERENTIAL
includes Autosomal dominant, congenital nephrotic syndrome,
glomerulocystic disease
– Autosomal dominant – chromosome 16 mutation, may present
with hypertension, gross hematuria, or as an incidental finding
on ultrasound. MAY have hepatic, pancreatic and genital organ
involvement; mitral valve prolapse and cerebral aneurysm
(family association).
• Prenatal ultrasound can detect hydronephrosis, renal agenesis,
oligohydramnios and polyhydramnios, cystic kidney disease.
For the Exam
• Nocturnal enuresis
– Recurrence of bed wetting after a period of
toilet training – obtain a UA to rule out UTI
– Treatment options for primary enuresis
include
• No intervention
• There is progression resolution with age – about
15% each year during school age.
• Alarm have good long term success
• DDAVP is a consideration under special
circumstances
ANSWERS TO THE CONTENT
SPECIFICATIONS
• Fluid and electrolyte
• Nephrology
[email protected]
SUBJECT LINE: NYNJ PEDS
Outline – Part 2
• Acute renal failure
• Chronic renal failure
• More Fluids & Electrolytes
• Tubular disorders
• Cystic kidney disease
SCENARIO
A 6 year boy is diagnosed as having ALL. He is started on
chemotherapy and his white blood cell count drops
precipitously. The child is discharged and the family is
encouraged. However, after two days at home he spikes a
temperature to 39 C. The parents contact the heme/ onc
fellow who tells them to come to the hospital immediately.
On arrival to the ER, the child is a bit lethargic. His BP is
60/40.
What is the most important first step in the management of
this child?
What are the most useful diagnostic tests?
What are the possible causes of his condition?
How should his condition be treated?
Acute Renal Failure (ARF) vs
Pre-renal Azotemia
• Key maneuver is restore RBF to
distinguish reversible pre-renal state from
short-term irreversible
• Options
– Bolus infusion of crystalloid solutions
– Infusion of albumin
– Administration of pressors
– Administration of antagonists of clinical
condition as in anaphylaxis
ARF: Diagnosis
Pre-renal
AGN
ATN
Obstruction
UA
Marginal
value
Key
RTEC
RBC casts
Marginal value
SG
>1.020
>1.020
1.0081.012
1.008-1.012
UNa
<20
<20
>40
>40
FENA
<1%
<1%
>1%
>1%
Uosm
>400
>400
200-400
200-400
ARF: Diagnosis
• AGN
– PSAGN
– HSP
– SLE
– MPGN
– Wegener’s
ARF: Diagnosis
• ATN
– Unreversed pre-renal azotemia
– Nephrotoxic meds
– Contrast agents
– High calcium, uric acid, phosphate
– Rhabdomyolysis (myoglobin)
– Intravascular hemolysis (hemoglobin)
ARF: Diagnosis
• Obstructive uropathy
– PUV
– Prune belly
– Vesicoureteric reflux
– Neurogenic bladder (myelomeningocele)
– Megacystis/megaureter
– Secondary: stones, fibrosis
• Effect of age and gender
ARF: Testing
•
•
•
•
•
Key labs: BUN, creatinine, K
EKG
CXRay
Renal ultrasound
Specific blood tests based on underlying
condition
ARF: Management
• Urgent issues
– Potassium
• Calcium
• Glucose/insulin
• NOT bicarbonate
– Blood pressure: parenteral therapy
• Labetalol
• Nitroprusside
– ECF volume
ARF: Conservative
Management
• Potassium
– Diet restriction
– Kayexalate
• Blood pressure
– IV/PO meds
• ECF volume
– Na restriction
– Diuretic use – need for furosemide
ARF: Indications for Dialysis
•
•
•
•
Refractory hyperkalemia
Refractory hypertension
Symptomatic ECF volume overload
Symptomatic azotemia
– Infection
– Bleeding
– CNS changes
ARF: Pearls
• Pre-renal azotemia and AGN are similar
• ATN and post-renal failure are similar
• Potassium kills first in ARF
SCENARIO
A 6 year boy is seen at a routine physical examination.
Although he has no specific complaints, his mother says he
has been very listless and his appetite is very poor. He has
not been playing well with his friends in play group. Although
he is toilet trained he seems to be having more accidents
during the night.
On examination, he looks a bit pale and tired. His height has
fallen from the 50% at his last visit 18 months ago to 10%. His
BP is 106/62 mm Hg.
What is the most important first step in the diagnosing this
child’s problems?
What are the likely causes his condition?
How should his condition be treated?
CKD: Diagnosis
• Stages
– CKD I: renal injury GFR >90
– CKD II: GFR 60-90
– CKD III: GFR 30-60
– CKD IV:GFR 15-30
– CKD V: ESRD
CKD: Common features
•
•
•
•
Impact on growth
Impact on bone: osteodystrophy
Impact on puberty
Impact on development – social and
cognitive
CKD: Causes
• Non-glomerular
– Hypoplasia/dysplasia
– Reflux nephropathy
– Obstructive uropathy
• PUV
• Prune Belly
• Neurogenic bladder
CKD: Clinical manifestations
• Growth failure
– Dependent on age of onset
– Dependent on level of GFR
• UTIs
– Pyelonephritis
• Electrolyte abnormalities
– Pseudohypoaldosteronism
– Nephrogenic DI
• Neurocognitive disability
CKD: Diagnosis
• Structural assessment
• Imaging studies
– US
– VCUG: dye vs radioisotope
– DMSA scan
– Retrograde studies, etc
CKD: Diagnosis
ARF
Younger child, abd mass, UTI
UA
WBC, impaired concentration
US, VCUG, DMSA
Retrograde studies
Cystoscopy, urodynamics
SCENARIO
A 15 year old girl comes to the clinic because she has not had
her period for the last 8 months. She feels tired all the time at
home school and is having a hard time concentrating in
school.
She is not taking any medications except for occasional
NSAIDs for headaches and some vitamins. Her parents are in
good health.
On examination, her height and weight are normal. Her BP is
162/98 mm Hg. She is pale and has a mild amount of edema
in both legs. She has no rash or arthritis.
What is the most important first step in diagnosing this
adolescent’s problem?
What are the most likely causes?
How should her condition be treated?
CKD: Causes
• Glomerular
– FSGS
– HUS
– SLE
– Membranoproliferative MPGN)
– Alport
– IgA Nephropathy
– Membranous nephropathy
– NOT diabetic or hypertensive nephropathy
CKD: Clinical manifestations
• Growth failure
– Dependent on age of onset
• Hypertension
– Role of ECF volume and PRA
• Electrolyte abnormalities
– Acute
– Hyperkalemia
• Edema
• Signs of underlying disease
CKD: Diagnosis
• Low value of radiology tests
• Blood tests
– C3, C4, CH50
– ASLO
– ANA, dsDNA, Ro, La, Sm
– ANCA
– Anti-GBM
– Renal biopsy
CRF: Management
• Nutritional supplementations
– CHO deficiency
• Protein restriction
– Impact on growth
– Effect in more advanced CKD
• BP control
– Disease progression
– ACEI/ARB
CRF: Management
• Interference with renin-angiotensin
aldosterone axis
– Safety of ACEI even with advanced CKD
– Role of combined ACEI/ARB
– Effect of aldosterone antagonists
• Safety issues
– Hyperkalemia
– Reduction in GFR
CRF: Management
• Endocrine treatments
– rhGH
• Doubles growth velocity
• Minimal risk of progression
– Erythropoietin
• Nearly always effective
• Antibody induced pure red cell aplasia
– Calcitriol
• IV route
• More selective agents
CRF: Pearls
• Chronic glomerular diseases have oliguria
vs chronic tubular diseases which can
have polyuria and sodium loss
– Nocturia and enuresis may indicate CRF
• Severity of growth failure and
neurocognitive deficits are inversely
related to age of onset of CRF
CRF: More pearls
• Most important feature of nutritional
support is to correct low caloric intake
• Medication doses need to be adjusted as
GFR declines
• Almost no form of CRF is a
contraindication to transplant
SCENARIO
A 10-day male infant presents with a history of irritability,
low grade fever, emesis and diarrhea. Prenatal and family
history is non-contributory. On examination the infant is
irritable, temp is 38°C, has mottled skin and a capillary
refill of 4 sec. The systolic blood pressure is barely
palpable and the pulse is 195 beats/min. The anterior
fontanelle is flat.
Hemoglobin
18 g/dl
White cell count
30,000
Platelets
280,000
What are key features in the history and examination?
What studies would you perform?
What is your initial therapy?
What is your initial diagnosis (es)?
Electrolyte Disorders: Sodium
• KEY function of Na+
– ECF cation
– Maintenance of intravascular compartment
• Disturbances in ECF volume are
secondary to disturbances in Na+ balance
• ECF volume assessment is clinical
– Reduced – see dehydration above
– Increased – pulmonary and/or peripheral
edema
March 17, 2005
Electrolyte disorders: Sodium
Assess ECF
Measure serum Na
High ECF
Normal ECF
Low ECF
Electrolyte Disorders: Sodium
•
•
•
•
History
Source of Na loss
Change in body weight
Renal response to low ECGF volume
– Oliguria
– Reduced urine Na+
– Reduced FENA
March 17, 2005
Electrolyte disorders: Sodium
120
100
80
ICF
ECF
60
40
20
0
Normal
Hypo
Hyper
Electrolyte disorders: Sodium
• Hypernatremia
– Risk factors
•
•
•
•
Breast feeding
Feeding errors
Impaired thirst
Impaired access to water
– Presentation
• Irritability, seizures
– Treatment
• SLOW
• HYPOTONIC FLUIDS – 1/5 NS
Electrolyte disorders: Sodium
• Hyponatremia
– Risk factors
•
•
•
•
•
Feeding errors (Keating)
Salmonella diarrhea
Increased extra-renal salt loss
Pain, anesthesia, post-operative picture
Female gender
– Presentation
• Lethargy, seizures
– Treatment
• ?SLOW
• Correction 25 mmol/L OR 130 mmol/L over initial 48 hr
Electrolyte disorders: Sodium
• Bad outcomes
• Brain
– Hemorrhage and cerebral edema in
hypernatremia
– Osmotic demyelinating syndrome and acute CNS
deterioration in Hyponatremia
• DKA
– ?Hyponatremia (100 glucose mg/dl  1.6 Na meq/l)
– Comparison to hypernatremia
SCENARIO
A 4-week old infant presents with a history of irritability, low
grade fever and poor feeding. Prenatal and family history is
non-contributory. On examination the infant is irritable,
temp is 37°C, has dark skin and a capillary refill of 4 sec.
The systolic blood pressure is barely palpable and the
pulse is 195 beats/min. The anterior fontanelle is sunken.
Hemoglobin
18 g/dl
White cell count
30,000
Platelets
280,000
What are key features in the history and examination?
What studies would you perform?
What is your initial therapy?
What is your initial diagnosis (es)?
Electrolyte Disorders: Potassium
• KEY function of K+
– ICF cation
– Transmembrane potential, secretion,
neuromechanical coupling
• Disturbances in K+ reflect sudden
changes in serum concentration and
transmembrane ratio
• Assessment is linked to cardiac impact of
abnormal K+ concentration
Electrolyte disorders: Potassium
• Regulatory organs
– Kidney secretion
• Na+
• Urine flow rate
– Adrenal
• Aldosterone
– GI tract
• Transmembrane
–
–
–
–
pH
Osmolality
Beta adrenergics
Insulin
• Diet
Potassium
• Key tests
– BUN, Cr, Na, K, bicarbonate
– Urine K useless
– Urine Na/K ratio
– Hormones
• PRA
• Aldosterone
Electrolyte disorders: Potassium
• Hyperkalemia
– EKG
• Peaked T waves
– Treatment
•
•
•
•
•
Calcium infusion
Glucose/insulin
NOT Bicarbonate
Kayexalate
DIALYSIS
Hyperkalemia: differential diagnosis
• No real disease
– Increase cells: WBC, polycythemia, thrombocytosis,
crush injury
– Transmembrane
• Renal
– ARF
– CRF
– Liddle’s
• Adrenal
– Adrenal failure
– Congenital adrenal hyperplasia – ambiguous genitalia
– Isolated renin abnormalities
Hyperkalemia: Work-up
•
•
•
•
BUN, creatinine, Na, K, Bicarbonate
PRA
Aldosterone
Urinary Na/K ratio
Electrolyte disorders: Potassium
• Hypokalemia
– EKG
• U waves
– Treatment
• Restore ECF volume to 2hyperaldosteronism
• PO potassium
– Limitations: tolerance
• IV potassium
– Limitation: 0.3 meq/kg/hr
– Central vs peripheral IV
Hyperkalemia: differential diagnosis
• Systemic
– Malnutrition
• Adrenal
– Adrenal overactivity
– Congenital adrenal hyperplasia
– Primary renin abnormalities
• Renal
– DKA
– Osmotic diuresis
SCENARIO
A 15 month child presents with a history of poor feeding
and impaired growth. Prenatal and family history is noncontributory. On examination the infant’s height and
weight are below the 5th percentile. The systolic blood
pressure is 102 and the pulse is 110. The rest of the
examination is normal.
Na
138
Cl
114
Bicarbonate
16
What are key features in the history and examination?
What studies would you perform?
What is your initial therapy?
What is your initial diagnosis (es)?
Electrolyte disorders: acid-base
Acid load
Acute
Chronic-Kidney
Proximal
Chronic-Kidney
Distal
Lung
Reclaim filtered
bicarbonate
Regenerate
Titrated bicarbonate
Large frequent
doses
1-3 mmol/kg/day
Electrolyte disorders
• Anion gap
• [Na] – {[Cl] + [HCO3]}
• Normal value: 4-12
• Impact of serum albumin
March 17, 2005
Electrolyte disturbances: RTA
• Metabolic acidosis
– Normal anion gap -- hyperchloremic
• Diarrhea
• RTA
– High anion gap -- normochloremic
• MUDPIES or KUSSMAUL
• Key entities:
–
–
–
–
–
DKA
Lactic acidosis
Uremia
Metabolic disease
Toxins
Electrolyte disturbances: RTA
• Proximal
– Low K
– Primary
– Secondary
•
•
•
•
Glycogen storage
Wilson’s, fructose intolerance, tyrosinemia
PTH, Vitamin D
Cystinosis
Electrolyte disturbances: RTA
• Distal
– Primary
– Secondary
• Transplant rejection
• Drugs: amphotericin, cisplatinum
• Collagen vascular disease
Electrolyte disorders: RTA
• Assessment
– SMAC: Cl– VBG: Bicarbonate
– Urine: calcium, citrate
– Urine anion gap: unmeasured cation (NH4+)
– Xrays
Electrolyte disturbances: RTA
• Treatment
• Proximal
– Higher doses of bicarbonate
– More frequent dosing
– Exacerbation of hypokalemia with Rx
• Distal
– 1-3 mmol/kg varying with age and diet
– 3 doses
– Stabilization of K with Rx
Electrolyte disorders: Fanconi’s
Fanconi’s
Syndrome
Complete proximal
tubule dysfunction
RTA
Glycosuria
Phosphaturia
TRP
Amino
Aciduria
Electrolyte disorders: metabolic
alkalosis
• Extrarenal/GI loss of K
– CF
• Vomiting
– NG suction
– Pyloric stenosis
• Distal GI loss of bicarbonate
– Chloride diarrhea
• Renal
– Bartter’s
– Gitelman’s
– Apparent mineralocorticoid excess (AME)/licorice
Electrolyte disorders: DI
• Central
• Nephrogenic
• Risk of CNS disease
– 1/12 (1/3 X ¼) of loss from ECF
– Limited access to water
– Altered thirst
Electrolyte disorders: DI
• Central
– AVP replacement
• Nephrogenic
– Adequate water intake
– Low solute diet
– Hydrochlorothiazide
Electrolytes: Pearls
There are three pure renal causes of FTT –
azotemia, DI, and RTA
RTA causes hyperchloremic acidosis
Bartter’s and Gitelman’s differ in calcium
excretion – high in former low in latter
Thank you
GOOD LUCK