METRO NY / NJ Pediatric
Board Review Course
Pediatric Nephrology
May, 2010
Leonard G. Feld MD PhD
Levine Children’s Hospital
Charlotte, NC
March 17, 2005
March 17, 2005
For the Exam
Fluid and Electrolyte Metabolism
A.
Composition of body fluids -Intracellular,
extracellular, Electrolytes (sodium,
potassium, chloride), Protein
B.
Acid-base physiology -Normal mechanisms
and regulation, Acidosis, alkalosis
C.
Electrolyte abnormalities - Sodium –
Hypernatremia; Hyponatremia; Potassium
Hyperkalemia; Hypokalemia; Chloride
imbalance
D.
Disease states, specific therapy - Pyloric
stenosis, gastroenteritis, acute renal failure,
shock, SIADH, Cystic fibrosis, Dehydration,
Hyperosmolar non-ketotic coma
March 17, 2005
For the Exam
Renal Disorders
A.
Normal function, proteinuria, hematuria, persistent microscopic hematuria,
causes of gross and microscopic hematuria, nonhematogenous etiology of red
urine,dysuria,
B.
Incontinence - Nocturnal, functional, daytime incontinence,
C.
Congenital - Renal dysplasia, unilateral multicystic dysplastic kidney,
autosomal dominant polycystic kidney disease, autosomal recessive polycystic
kidney disease, Juvenile nephronophthisis, Renal agenesis
D.
Abnormalities of the collecting system, kidney, and bladder – Hydronephrosis,
Hydroureter and megaureter, Ureterocele, Vesicoureteral reflux,
E.
Abnormalities of the urethra - Posterior urethral valves, Urethral stricture
F.
Hereditary nephropathy - Familial nephritis, Congenital nephrotic syndrome
G.
Acquired - Infection of the urinary tract (Pyelonephritis, Cystitis), acute
glomerulonephritis, Nephrotic syndrome, Hemolytic-uremic syndrome,
Henoch-Schoenlein purpura,IgA nephropathy
H.
Renal failure - Prerenal failure, Intrinsic renal failure , chronic renal failure,
I.
Other - Trauma, renal injuries, Urethral injury, Toxins, Renal stones, Renal
tubular acidosis, Hereditary conditions with renal manifestations, Nephrogenic
diabetes, insipidus, Cystinosis
J.
Hypertension – General, Renal, Vascular, Adrenal, Pheochromocytoma,
Cushing syndrome, Miscellaneous causes, Essential hypertension,
Administration of drugs, Traction on legs
March 17, 2005
Outline
• Fluid and Electrolyte abnormalities
–
–
–
–
Maintenance
Dehydration
Electrolyte Disturbances
Acid Base Problems
• Renal
–
–
–
–
–
March 17, 2005
Hematuria
Proteinuria
Hypertension
Urinary tract infections
Glomerulonephritis
Fluids and Electrolytes
March 17, 2005
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
March 17, 2005
Plasma
¼ of ECF
INTRACELLULAR FLUID (ICF)
0.4 x BW
Clinical Assessment
Fluid
Deficit
Clinical
Status
Clinical
Assessment
Mild
( 5%)
50 cc/kg
Compensated
Moderate
(10%)
100 cc/kg
Decompensated Very dry mucosa, < skin
turgor, sunken eyes, deep
resp, weak pulses, cool
extremities, oliguria
Severe
(15%)
150 cc/kg
Shock
March 17, 2005
Thirsty, HR, Normal BP
tears, slightly dry mucosa,
alert/restless, [urine]
Intense thirst,  BP, cap
refill > 3 sec, weak pulses,
apnea/rapid breathing,
coma, anuria
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
March 17, 2005
Fluid and Calories
• Kidney losses is about 45-75 mL/100 calories
expended;
• Sweat losses usually 0;
• Stool losses is about 5-10 mL / 100 calories
expended,
• Insensible losses (skin ~ 30 mL + Respiratory ~
15 mL ) is about 45 mL/100 calories expended
SO - 100 mL of total daily water losses = 100
calories expended per day or 1 mL = 1 calorie.
March 17, 2005
Defcit
Type of Dehydration
based on serum [Na] in
mEq/L
Water
Sodium
(mL/kg)
(mEq/kg)
Potassium
(mEq/kg)
Isonatremic [Na] 130-150
100-120
8-10
8-10
Hyponatremic [Na] < 130
100-120
10-12
8-10
Hypernatremic [Na] > 150
100-120
2-4
0-4
March 17, 2005
Case 1 Dehydration
A four month-old infant presents to her pediatrician with a four to
five day history of low grade fever (38-38.5oC), numerous
watery diarrhea and decreased activity.
Since the child refused to take her usual breast milk volume or
solid foods, the mother and grandmother substituted noncarbonated soda (Coca-cola, ginger ale, apple juice or orange
juice will have ~550-700 mOsm/kg H2O) with less than 5 mEq/L
of sodium), and “sweet” (sugar added) iced tea.
Over the last 12 hours there were a few episodes of emesis and
there were less wet diapers.
March 17, 2005
On examination the child was lethargic, dry mucous
membranes, no tears, sunken eyeballs, and reduced skin
turgor.
Vitals signs were the following: Blood pressure 74/43 mmHg;
Temperature of 38oC, respiratory rate of 36 per minute and
pulse of 175 beats per minute. The weight was 6 kg. Weight at
the time of her immunization 7 days ago was 6.6 kg.
There were no other significant findings.
With the magnitude of dehydration and lethargy, the decision
by the clinician was to initiate parenteral fluid replacement
rather than oral rehydration therapy. The child was admitted to
the hospital with diagnosis of dehydration. On admission the
laboratory studies were as follows:
March 17, 2005
Sodium 124 mEq/L, chloride 94 mEq/L, potassium 4 mEq/L
bicarbonate (or total COs) was 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%
Urinalysis/ chemistries: specific gravity of 1.030, trace
protein, no blood or glucose, small ketones; urine creatinine 40
mg/dL and sodium 15 mEq/L;
Fractional excretion of sodium (FENa)
( [urine sodium x serum creatinine]/ [serum sodium x urine
creatinine] x 100%) =
([15 mEq/L x 0.8 mg/dL] / [129 mEq/L x 40 mg/dL]) = 0.23%
Normal values for FENa = ~ 1-2%; decreased renal perfusion
(dehydration, decreased intravascular volume) < 1%
March 17, 2005
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
March 17, 2005
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
March 17, 2005
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. 0.9% isotonic saline + 40 mEq KCl /L
D. 5% dextrose + 40 mEq KCl /L
E. 5% dextrose + 0.2% isotonic saline
March 17, 2005
Assessment
The information suggest hyponatremic
dehydration secondary to extrarenal losses from
diarrhea with administration by the family of hypotonic or
dilute fluids.
The child has lost proportionally more sodium than
water or a relatively hypertonic fluid loss. The result is a
lower extracellular fluid osmolality compared to the
intracellular fluid osmolality. The magnitude of the
dehydration is about 10% or moderate to severe. The
pre-illness weight was 6.6 kg with a current weight of 6
kg or a 0.6 kg loss over the last week.
March 17, 2005
Oral Rehydration
The decision by the clinician was to initiate
parenteral fluid replacement rather than oral
rehydration therapy. The relative
contraindications for oral rehydration
therapy would include a young infant less
than 3-4 months of age, the presence of
impending shock or markedly impaired
perfusion (increased capillary refill
time/decreased skin turgor), inability to
consume oral fluids due to intractable
vomiting, marked irritability or
lethargy/unresponsiveness or the judgment
of the clinician.
March 17, 2005
Therapeutic Plan
1 Volume, Deficit, Electrolyte Calculations
Phases
emergent or acute phase – isotonic fluid infusion
over about one hour;
replacement phase – over 24 hrs unless there are
on-going losses which are not replaced
adequately in the first day of treatment;
maintenance phase- day 2 continuing to home
management.
March 17, 2005
Emergent Phase
Emergent or acute phase
• Over about one hour - reestablish circulatory volume to prevent
prolonged loss of perfusion to the key organs such as kidney, brain,
gastrointestinal tract, etc.
• Fluid choices would be isotonic (0.9%) saline (normal saline) or
another isotonic /hypertonic solution such as 5% albumin, Ringer’s
lactate, or a plasma preparation.
With the availability of isotonic saline, this is the usual fluid choice.
Weight (kg) x fluid bolus of 20 mL/kg over 30 -60 minutes.
(If the patient was in shock fluid delivery more rapid infusion to
prevent organ failure.)
6 kg x 20 mL = 120 mL over 30-60 minutes.
only replaces 20% of the losses [total losses 600 ml]
March 17, 2005
Approach
For this 6.6 kg infant
Maintenance requirements for 24 hours
Water
Sodium
Potassium
March 17, 2005
100 mL / kg x 6.6 kg = 660 mL
3 mEq / 100 mL x 660 mL = 20 mEq
2 mEq / 100 mL x 660 mL = 13 mEq
Approach 1
Type of Dehydration*
based on serum [Na] in mEq/L
Water (mL/kg)
Sodium (mEq/kg)
Potassium (mEq/kg)
Isonatremic [Na] 130-150
100-120
8-10
8-10
Hyponatremic [Na] < 130
100-120
10-12
8-10
Hypernatremic [Na] > 150
100-120
2-4
0-4
•Isonatremic dehydration is the most common accounting for 70-80% of infants and children;
•hypernatremic dehydration accounts for about 15%, and
•hyponatremic dehydration for about 5-10% of cases.
For this 6 kg infant with hyponatremic dehydration at 10%
Deficits for 24 hours
Water Pre-illness weight – Illness weight = 6.6 – 6 kg = 0.6 kg = 600 mL
Sodium
10 mEq x 6.6 kg = 66 mEq
Potassium
8 mEq x 6.6 kg = 53 mEq
Total First 24 hours Requirements
The total amount of maintenance and deficit amounts are given 50% over
the first 8 hours and the remainder over the next 16 hours.
March 17, 2005
Approach
For this 6.6 kg infant
Maintenance requirements for 24 hours
Water
100 mL / kg x 6.6 kg = 660 mL
Sodium
3 mEq / 100 mL x 660 mL = 20 mEq
Potassium
2 mEq / 100 mL x 660 mL = 13 mEq
For this 6 kg infant with hyponatremic dehydration at 10%
Deficits for 24 hours
Water Pre-illness weight – Illness weight = 6.6 – 6 kg = 0.6 kg =
600 mL
Sodium
10 mEq x 6.6 kg = 66 mEq
Potassium
8 mEq x 6.6 kg = 53 mEq
March 17, 2005
Component of Therapy
Water
Sodium
Potassium
Hourly Rate
Round number
up or down to
the nearest 5
increment
Acute Phase
120
18 (154mEq/L x
0.12 L)
0
Entire amount
over 20-60 min
Maintenance
660
20
13
Deficit
600
66
53
TOTAL
1280
104
66
Emergent Phase Therapy
(120)
(18)
FINAL THERAPY
Hrs 1- 8
Hrs 9-24
1160
580
580
86
43
43
Ongoing losses of diarrhea
of vomiting*
March 17, 2005
66
33
33
72 mL / hr
36 mL / hr
Closing thoughts
Gastrointestinal losses tend to resolve or decrease significantly following IV
therapy. If it does continue these losses will need to be added to the ongoing
loss
For each liter of IV solution there would be 43 mEq / 0.58 L = ~75 mEq Per Liter
Fluid selection – 5% dextrose + 0.45% isotonic saline + 40 mEq KCl /L
Potassium concentration is ~ 30- 40 mEq/L (it should not exceed 40 mEq/L without close
intensive care monitoring).
Some recommend 20-25 mEq/L - potassium stores will be replenished when the
child restart oral feeds.
The 5% dextrose provides 50 grams of carbohydrate per liter of 50 grams x ~ 4
calories per gram = 200 calories. This would be about 20% of the daily caloric
intake which is sufficient to prevent protein breakdown over a short treatment
period (less than one week).
March 17, 2005
Case 2
A ten month-old infant presents to the pediatric emergency room
with a generalized tonic clonic seizure. The child had a fever to
39-400C for the past 24-36 hours, lethargy, vomiting, decreased
oral intake, less wet diapers.
The child did not receive Prevnar (pneumococcal vaccine).
On exam - ill and irritable resisting any movement, VS: BP
94/58mmHg; Temperature of 39oC, respiratory rate of 40; pulse
175 beats. The weight 10 kg. There were no focal neurological
findings. The impression was meningitis, probable pneumococcal
and hyponatremia.
March 17, 2005
On admission labs:
Sodium 126 mEq/L, chloride 95 mEq/L, potassium 4 mEq/L
Bicarbonate (or total COs) 19 mEq/L Serum creatinine 0.3 mg/dL blood
urea nitrogen 6 mg/dL, uric acid of 2.4 mg/dL, blood glucose 85 mg/dL;
WBC 26,000 /mm3 with 255 immature cells (bands). LP protein 140
mg/dL, glucose 30 mg/dL and 2000 leukocytes /mm3 with more than 80%
PMNs. Blood and urine culture pending. Serum osmolality 262 mOsm/kg
[2 x serum sodium + glucose/18 + BUN/1.8 = 252 + 5 + 4 = 261].
Urinalysis/ chemistries: specific gravity of 1.018 (estimated osmolality
= 720 mOsm/kg), no blood, protein or glucose, small ketones; urine
sodium 100 mEq/L, urine creatinine 15 mg/dL; fractional sodium excretion
(FENa) – 1.6 %
March 17, 2005
Question 2: What is the most likely
diagnosis for the Hyponatremia
A.
B.
C.
D.
Diabetes Insipidus
Water Intoxication
Thyroid insufficiency
Syndrome of inappropriate
antidiuretic hormone secretion
E. Glucocorticoid insufficiency
March 17, 2005
Causes of SIADH
Tumors
Bronchogenic
AdenoCa Duodenum
AdenoCa Pancreas
Ca Of Ureter
Hodgkin's
Thymoma
Acute Leukemia
Lymphosarcoma
Histiocytic
Lymphoma
March 17, 2005
Chest Disorders
Infection
Tb
Bacterial
Mycoplasma
Viral
Fungal
PositivePressure Ventilation
Dec Left Atrial Pressure
Pneumothorax
Atelectasis
Asthma
Cystic fibrosis
Mitral Valve
Commissurotomy
PDA Ligation
Malignancy
CNS Disorders
Infection / Inflammatory
TB Meningitis
Bacterial Meningitis
Encephalitis
Head Trauma
Subarachnoid hemorrhage
Hypoxia-Ischemia
Acute Psychosis
Brain Tumor / Mass Lesions
Miscellaneous
Guillain-Barré syndrome
Spinal Cord lesions
VA Shunt Obstruction
/ hydrocephalus
AcuteIntermittent Porphyria
Cavernou Sinus Thrombosis
Stress / Extensive Exercise
(running a marathon, etc.)
Idiopathic
Drugs
Adenine
Arabinoside
Amitriptyline
Barbiturates
Carbamazepine
Chlorpropamide
Clofibrate
Colchicine
Diuretics
Fluphenazine
Isoproterenol
Morphine
Nicotine
Tricyclics
Vinblastine
Vincristine
Criteria
1)
2)
3)
4)
5)
March 17, 2005
Hypotonic hyponatremia.
Inappropriate urine osmolality compared to plasma
osmolality. In patients with an medical condition
associated with the occurrence of SIADH, a urine
osmolality greater than maximal dilution (75-125
mosm/L) and a low plasma osmolality is “inappropriate”
to state of water balance.
Absence of thyroid, adrenal, cardiac, or renal disease.
Absence of volume contraction.
High urinary sodium concentration (increased FENa).
Information suggest meningitis with SIADH.
Neurological findings with hyponatremia suggests this
diagnosis.
No evidence of volume depletion or expansion/excess of the
extracellular fluid compartment.
Hyponatremia with a decreased serum osmolality (effective
osmolality/tonicity) with a urine osmolality which is not
maximally dilute (< ~125 mOsm/kg) without evidence of renal,
thyroid or adrenal disease is consistent with SIADH.
Additional info: low serum uric acid and BUN in the face of
clinical euvolemia, elevated FENa (> 1%) – inconsistent with
hypovolemia when the FENa should be < 1%, lack of evidence
of diuretic use, pseudohyponatremia (secondary to increased
plasma proteins or lipids) or hypertonic hyponatremia
(hyperglycemia or mannitol infusions).
March 17, 2005
KEY POINTS ON SIADH
•
SIADH will not resolve until the underlying disease process has significantly
improved or resolved (treatment of meningitis will not be discussed).
The approach is a multi-step process.
•
Assess - Acute presentation (neurological manifestations such as coma,
encephalopathy, seizures).
If symptomatic presentation - increase the serum sodium concentration /
serum osmolality.
• Increase the serum sodium by 10 mEq/L or the serum osmolality by 20
mOsm/kg
(10 mOsm from sodium and 10 mOsm from chloride) with the use of
hypertonic or 3% saline (513 mEq/L of sodium or ~ 0.5 mEq/mL).
•
Regardless of the approach, when the symptoms are improved the 3%
infusion should be discontinued.
March 17, 2005
For sodium correction = 10 mEq/kg Na x body weight (BW) x 0.6
(distribution factor for sodium) = 6 BW = # of mEq to be infused.
Since there is 0.5 mEq Na/mL or 1 mEq per 2 mL, the amount of 3%
saline to be infused over about 60-90 minutes would be 2mL/mEq
x 6 mEq X BW = 12 BW.
If the symptoms are absent or mild – asymptomatic presentation,
lower infusion rate of 0.5 to 2 mL per kg of body weight may be used which
will increase the serum sodium from 0.5-2 mEq/L per hour. Some select
isotonic saline in asymptomatic patients for patients with a serum sodium
above 123-125 mEq/L.
IN EITHER CASE, the serum sodium should be monitored every 2-3
hours to prevent overcorrection of the serum sodium concentration.
The maximum serum Na correction per 24 hours should not exceed 10
mEq/L (some clinicians limit the increase to 8 mEq/L per 24 hours).
March 17, 2005
Case 3
A six month-old infant presents to her pediatrician in December with a
four day history of fever (up to 40oC), along with mild upper respiratory
symptoms. On the evening and night prior to presentation she began
to have diarrhea and emesis with cessation of formula and solid foods
The child had a wet diaper this morning.
On exam the child appeared quiet but became irritable during the
exam, mucous membranes were mildly dry, and the skin felt doughy.
Vitals signs were the following: Blood pressure 85/58 mmHg;
Temperature of 39oC, respiratory rate 40 and pulse 175. Weight 7.5 kg.
A previous weight about two weeks ago was 8.4 kg. There were no
other significant findings and the child appears to have good turgor
and skin elasticity.
March 17, 2005
Question 3: What is the percent of
dehydration?
A.
B.
C.
D.
E.
3-5%
6-9%
0%
10%
15%
March 17, 2005
With the magnitude of dehydration, high fever and irritability, the
decision by the clinician was to initiate parenteral fluid replacement rather
than oral rehydration therapy. The child was admitted to the hospital with
diagnosis of dehydration.
On admission the laboratory studies were as follows:
Sodium 162 mEq/L , chloride 126 mEq/L, potassium 4 mEq/L
Bicarbonate (or total CO2) was 12 mEq/L Serum creatinine 1 mg/dL, blood
urea nitrogen 29 mg/dL, blood glucose 85 mg/dL; complete blood count
was normal
Urinalysis/ chemistries: specific gravity of 1.030, no blood, protein or
glucose, small ketones; urine creatinine 30 mg/dL and sodium 30 mEq/L;
Fractional excretion of sodium (FENa)
( [urine sodium x serum creatinine]/ [serum sodium x urine creatinine]
x 100%) =
([30 mEq/L x 1 mg/dL] / [161 mEq/L x 30 mg/dL]) = 0.62%
Normal values for FENa = ~ 1-2%; decreased renal perfusion
(dehydration, decreased intravascular volume) < 1%
March 17, 2005
Information suggest hypernatremic dehydration.
In many cases there is extrarenal losses from diarrhea and vomiting with predisposing
factors being young age, fever, curtailment of oral intake and possibly, high solute
fluids such as concentrated or improper preparation of formula or other fluid with a
high sodium content.
Child lost proportionally more water than sodium or a relatively hypotonic fluid loss.
The result is higher extracellular fluid osmolality which results in a fluid shift from the
ICF to ECF. This provides for better organ perfusion compared to iso- or hyponatremic
dehydration of comparable degrees.
The child on exam appears better perfused and provides a history of urine output rather
than oliguria. This may lead to an underestimate of the degree of dehydration. In this
case the magnitude of the dehydration is about 10% or moderate.
The pre-illness weight was ~ 8.3 kg with a current weight of 7.5 kg or a 0.8 kg loss over
last week.
March 17, 2005
The decision by the clinician was to initiate parenteral
fluid replacement rather than oral rehydration therapy.
The relative contraindications for oral rehydration
therapy would include a young infant less than 3-4
months of age, the presence of impending shock or
markedly impaired perfusion (increased capillary refill –
turgor), inability to consume oral fluids due to intractable
vomiting, marked irritability or lethargy/
unresponsiveness or the judgment of the clinician.
March 17, 2005
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
March 17, 2005
0
NORMAL ICF
Therapy
Traditionally, treatment has been divided into three
phases.
However in hypernatremic dehydration,
the hyperosmolality results in the formation of idiogenic
osmols (organic and inorganic) such as taurine, glutamate,
glutamine, urea, inositol within the brain cells to assist in
maintaining osmotic equilibrium between the two fluid
compartments.
If the adjustment in osmolality (lowering) occurs to quickly
in the extracellular compartment , the osmotic changes will
result in the brain cells to swell with resultant neurologic
manifestations such as hemorrhage.
March 17, 2005
Emergency / acute phase
This may need to be prolonged in cases of more significant
volume depletion:
In some cases of hypernatremic dehydration emergent phase not
necessary. If there are significant findings of decreased perfusion or
hypotension, then therapy would be reasonable.
Otherwise the process is for a slow restoration of the serum
sodium concentration to allow the idiogenic osmols to dissipate over a
few days.
Similar to other forms of dehydration, if it is necessary to
reestablish circulatory volume to prevent prolonged loss of perfusion
to the key organs;
the fluid choices would be isotonic (0.9%) saline (normal saline) or
another isotonic /hypertonic solution
March 17, 2005
Acute – Repletion/ Replacement /Restoration Phase
Over 48 hours;
daily fluid/electrolyte maintenance requirements and deficit calculation are
derived from standard estimates.
For hypernatremic dehydration there are two basic rules –
slow correction and close monitoring.
1.
serum sodium concentration should not be reduced by more than
about 10 mEq per day. Correct the patient over 48 hours for a serum
sodium concentration of less than 165 mEq/L; correct the patient over 72
hours for values above 165 mEq/L
2.
Maintenance fluid / electrolyte calculations for 24 hours: Since the
patient has a serum sodium concentration of 161, the correction is over 2
days so 2 days of maintenance fluids needs to added to the total fluid
requirements for 48 hours.
March 17, 2005
1.Total 48 hours Requirements
The total amount of maintenance (2 days) and deficit amounts are given equally over the
48 hour period with frequent monitoring of electrolytes in order to adjust the intravenous
rate or sodium concentration based on the rate of decline of the serum sodium
concentration.
Water
Sodium
Potassium
Maintenance – 2
days
1660
50
34
Deficit
800
33
17
2460
83
51
Component of
Therapy
Hourly
Rate
Round
number
up or
down to
the
nearest 5
increment
Ongoing losses
of diarrhea of
vomiting*
TOTAL
March 17, 2005
50 mL /
hr
Fluid selection – 5% dextrose + ¼ isotonic saline (~3040 mEq/L of Na) + 20 mEq KCl /L
Generally the final solution potassium concentration is
about 20 mEq/L, it should not exceed 40 mEq/L without
close intensive care monitoring. The 5% dextrose
provides 50 grams of carbohydrate per liter of 50 grams
x ~ 4 calories per gram = 200 calories. This would be
about 20% of the daily caloric intake which is sufficient
to prevent protein breakdown over a short treatment
period (less than one week).
March 17, 2005
Case 4
A 4 year old was referred for evaluation for short
stature. The primary care physician has followed
the patient since birth. The child is below the 5th
% ile for height and the 10th %ile for weight. The
child has a normal physical examination and no
prior illnesses or hospitalizations.
Initial studies show a urine pH of 6.7, negative for
glucose, ketones, blood and protein. No crystals,
bacteria or casts.
Serum values: Na – 140 mEq/L, K - 4 mEq/L, Cl
– 110 mEq/L, Bicarbonate 17 mEq/L, glucose 80
March 17, 2005
Case 3: The most likely diagnosis
with this presentation is
A.
B.
C.
D.
E.
Fanconi’s syndrome
Chronic kidney failure
Renal tubular acidosis
Bartter’s syndrome
Gitelman’s syndrome
March 17, 2005
Serum Anion Gap
• Anion gap (AG, mEq/L) = (Na+)– (Cl- +
HCO3-)
• Normal is 8 to 16
March 17, 2005
Causes of Metabolic Acidosis by type of
Anion Gap
Normal Anion Gap (Hyperchloremic)
Elevated Anion Gap
Renal (loss of bicarbonate)
Renal Tubular Acidosis – Type 1 (Distal) -,
2 (Proximal) and 4 (mineralcorticoid) –
See table 5 below)
Renal Failure (Early)
Carbonic Anhydrase Inhibitors – Acetazolamide
Potassium sparing diuretics
Mineralocorticoid deficiency
Renal Failure – acute and chronic
Gastrointestinal (loss of bicarbonate)
Diarrhea, Drainage (small bowel, pancreatic,
biliary, fistula, etc), anion exchange resins
Poisoning - carbon monoxide or
cyanide
Circulatory Failure / Tissue Hypoxia
Miscellaneous
Rapid intravenous expansion with bicarbonate or
isotonic/hypertonic solutions
Recovery from Ketoacidosis
Post-hypocapnia
Exogenous chloride administration
(CaCl2, MgCl2, Arginine HCl, HCl)
Hyperalimentation
Lactic Acidosis – hypoxia, glycogen
storage disease (type 1), pancreatitis,
leukemia, seizures
Ketoacidosis – diabetes mellitus,
starvation
Ingestions or overdose – Ethanol,
methanol, ethylene glycol, salicylate,
isoniazid
Inborn errors in metabolism, organic
acidosis
Paraldehyde – organic anions
March 17, 2005
Electrolyte disturbances: RTA
• Metabolic acidosis
– Normal anion gap -- hyperchloremic
• Diarrhea
• RTA
– High anion gap -- normochloremic
• MUDPIES or KUSSMAUL
• Key entities:
–
–
–
–
–
March 17, 2005
DKA
Lactic acidosis
Uremia
Metabolic disease
Toxins
Evaluation of Metabolic Acidosis
Classification and Diagnosis of Metabolic Acidosis
Measure serum anion gap
HIGH
NORMAL
Calculate osmolal gap
Calculate urine
anion gap
Cl > Na + K
HIGH
Cl < Na + K
NORMAL
Urine pH
Ethylene glycol
Methanol
March 17, 2005
Alcoholic ketoacidosis
Diabetic ketoacidosis
D-lactic acidosis
Lactic anion acidosis
Methylmalonic acidosis
Pyroglutamic acidosis
Salicylates
Starvation ketoacidosis
Proximal Renal
Tubular Acidosis
(type II)
Acetazolamide
administration
Intestinal HCO3losses (diarrhea)
Exogenous acid
administration
Total parenteral
nutrition
Ureterosigmoidosto
my
Rectouretheral
fistula
> 5.8
< 5.8
RTA
(type IV)
Serum K
Low
High
Distal RTA
(type I)
Hyperkalemic
Distal RTA
Patient
• Repeat urine pH showed a pH of 6.5,
venous blood gas had a pH of 7.28,
bicarbonate of 15 mEq/L, Pco2 was 34,
serum creatinine was 0.4 mEq/L, BUN of
6, urine calcium to creatinine ratio was 1.1
(increased)
March 17, 2005
Features of Renal Tubular Acidosis in
Childhood
Type I
(Distal)
Type II
(Proximal)
Type IV
(Hyperkalemic)
>5.5
<5.5
<5.5
Urine anion gap
Positive
Negative
Positive
FEHCO3- at normal serum HCO3
<15%*
>15%
<15%
Serum potassium
Normal or low
Normal or low
Increased
Calcium excretion
Increased
Normal or ↑
Normal (?)
Nephrocalcinosis
Common
Rare
Absent
Associated tubular defects
Rare
Common
Rare
Rickets
Rare
Common
Absent
Daily alkali requirement
(mEq/kg/day)
1-4*
10-15
2-3
No
Yes
No
Features
Urine pH during acidosis
Potassium supplementation
March 17, 2005
Electrolyte disorders: Fanconi’s
Fanconi’s
Syndrome
Complete proximal
tubule dysfunction
RTA
March 17, 2005
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
March 17, 2005
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
March 17, 2005
RENAL
March 17, 2005
March 17, 2005Trying
to think about pediatric kidney disease - nephWHAT
Hematuria
Case 5: Susan is an 8 year old noted on
routine exam to have moderate hematuria
on dipstick. She has an unremarkable
past medical history. Family history is
negative in the parents and siblings for
any renal disease. History of hematuria is
unknown. A repeat urine in one week is
still positive and a urine culture showed
no growth.
March 17, 2005
Question 5: 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 one year
March 17, 2005
• Repeat a first AM void following restricted
activity , perform a microscopic on a fresh urine
• Check the family members
• 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
• Caveat - Family anxiety because of the
connotation of blood and cancer in adults.
March 17, 2005
Classification of Hematuria
• Microscopic (vast majority of the cases)
–
–
Transient
Persistent
• Macroscopic (urologic / renal disorders)
–
–
Transient
Persistent (> 2 weeks)
• Persistent microscopic/ Transient
macroscopic
–
IgA or Berger’s; benign recurrent hematuria
March 17, 2005
Glomerular v. Non-glomerular bleeding
• Glomerular
– oliguria, edema, hypertension, proteinuria, anemia
• Non-glomerular
–
dysuria, frequency, polyuria, pain or colic, hx
exercise
–
crystals on microscopic
–
mass on exam
–
medication history - sulfas, aspirin, diuretics
March 17, 2005
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
March 17, 2005
Initial evaluation of the patient with hematuria
• All patients: Serum creatinine, kidney and bladder
ultrasound, urine calcium to creatinine ratio
• 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
March 17, 2005
Pearls for Hematuria
• Hematuria is 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.
March 17, 2005
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.
March 17, 2005
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
is hypercalciuria, SS trait, or thin basement
membrane disease.
• Cysto is rarely helpful
March 17, 2005
Case 6: 7 year old boy developed gross tea colored
hematuria after a sore throat and upper respiratory infection.
No urinary symptoms but urine output was decreased. He
complained of mild diffuse lower abdominal pain. There is no
fever, rash or joint complaints. Past med history was
unremarkable but had intermittent headaches for two years.
On exam he was well (afebrile) with a BP of 95/65
mHg, no edema, some suprapubic tenderness and red
tympanic membranes. The mother thinks that a similar
episode occur on vacation a few months ago.
Urinalysis shows 20 RBCs/hpf, 5-10 WBCs, 100
mg/dL of protein, rare cellular and hyaline casts. Serum
creatinine is 0.8 mg/dL, C3 100 (normal).
March 17, 2005
Question 6: 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
March 17, 2005
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
March 17, 2005
Acute
Glomerulonephritis
Low Complement
Normal Complement
Systemic diseases
Systemic diseases
SLE
Subacute Bact Endocarditis
Shunt nephritis
Essential mixed cryoglobulinemia
Visceral abscess
Polyarteritis nodsa
Hypersensitivity vasculitis
Wegener’s
HSP
Goodpasture’s
Renal diseases
Acute proliferative GN
Membranoproliferative GN
Renal diseases
IGA
RPGN Anti-GBM, immune complex GN
Serologic evidence of antecedent strep infection
(ASO, anti-Dnase B, streptozyme
Positive
Negative
Lupus
Essential mixed cryoglobulinemia
Shunt nephritis
Visceral abscess
MPGN
Non-strep infection
PSAGN
Strep endocarditis
Y
E
S
Clinical evidence to
support endocarditis
Blood cultures
Echocardiogram
March 17, 2005
NO
Treat PSAGN
Glomerular
Non-glomerular
Urinalysis
Dysmorphic RBC
Cellular casts
Brown/tea color
Bright red
Clots
Crystals
Protein
+
+
++
+
+
+
++
+
+
-
History
Family Hx of ESRD
Systemic disease
Nephrolithiasis
Trauma
Symptomatic vomiting
+
+
-
+
+
+
Physical
Hypertension
Systemic signs
Edema
Abdominal mass
Genital bruising
++
+
+
-
+
+
+
March 17, 2005
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.
March
17, 2005
Question 7
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 intravenous pyelogram
C. Obtain a voiding cystourethrogram
D. Perform a CBC in the office
E. Order an ASO titer
March 17, 2005
Question 8
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 an intravenous pyelogram and
VCUG
March 17, 2005
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
March 17, 2005
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)
March 17, 2005
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
March 17, 2005
Please try to
Wait until the
Lecture is
over
We are
talking about
the kidneys
March 17, 2005
Proteinuria
Case 9: 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.
March 17, 2005
Question 9: 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
March 17, 2005
What does Orthostatic Proteinuria
mean?
Protein
Excretion
Threshold of Detection
Normal
March 17, 2005
Orthostatic
Recumbant
Erect
• 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 workup is generally required, although no
indemnification from subsequent renal disease.
• Caveat - Family anxiety because of the
connotation of protein and friends told them
about kidney failure.
March 17, 2005
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
March 17, 2005
Question 10
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
appropriate tests include all the following
except.
A. Urinalysis
B. Blood tests for total protein and albumin
C. Serum creatinine
D. Sedimentation rate
E. Serum complement (C3)
March 17, 2005
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
March 17, 2005
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
March 17, 2005
Nephrotic Syndrome - RX
Corticosteroid treatment
• Induction therapy:
–
–
•
Maintenance therapy (following above induction therapy)
–
–
•
Exclude active infection or other contraindications prior to steroid therapy.
Oral prednisone or prednisolone at 60 mg/m2/d (~2 mg/kg/d) daily for 4 weeks.
Oral prednisone or prednisolone at 40 mg/m2 (or ~1.5 mg/kg) given as a single dose
on alternate days for 4 weeks.
NOTE: Some nephrologists recommend daily induction steroid treatment for 6 weeks,
followed by alternate day maintenance therapy for another 6 weeks.
Relapse therapy
–
–
For infrequent relapses, Prednisone 60 mg/m2/d (~2 mg/kg/d) given as a single
morning dose until proteinuria has resolved for at least 3days.
Following remission of proteinuria, prednisone is reduced to 40 mg/m2 (or ~1.5 mg/kg)
given as a single dose on alternate days for 4 weeks. Prednisone may then be
discontinued or a tapering regimen.
Frequently relapsing nephrotic syndrome is defined as steroid-sensitive nephrotic
syndrome with 2 or more relapses within 6 months or more than 3 relapses
within a 12-month period.
March 17, 2005
Hypertension
March 17, 2005
Hypertension
Case 11: 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.
March 17, 2005
Question 11: What is the most appropriate
initial testing for this child?
A. Renal mag-3 flow scan
B. Electrolytes, BUN, Creatinine,
Bicarbonate
C. Renal Sonogram with doppler
D. Urinary screening for drugs
E. 24 hour urine for catecholamines
March 17, 2005
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
March 17, 2005
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
March 17, 2005
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
March 17, 2005
Indications for Treatment
•
•
•
•
•
Symptomatic hypertension
Secondary hypertension
Hypertensive target-organ damage
Diabetes (types 1 and 2)
Persistent hypertension despite
nonpharmacologic measures
March 17, 2005
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.
March 17, 2005
Urinary Tract
Infections
March 17, 2005
Case History
• 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. dUrinalysis shows hematuria,
30 mg/dL of protein, leukocyte esterase
and positive nitrite. Urine culture is
obtained.
Feld - 10/98
100
Question 12: What is the most likely bacterial
cause of her urinary tract infection?
A.
B.
C.
D.
E.
Proteus mirabilis
E. coli
Coagulase negative Staphlococus
Alpha hemolytic Streptococcus
Klebsiella pneumoniae
March 17, 2005
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%
Feld - 10/98
102
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
Feld - 10/98
103
Diagnosis
• Leukocyte test and nitrate test
• Urine culture > 40-50,000 CFU/mL
• Pyuria - not on recurrent UTIs
Feld - 10/98
104
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
Feld - 10/98
105
Radiological Evaluation
• Renal ultrasound - anatomy, size, location,
echogenicity
• DMSA (2nd choice glucoheptanate SGH) - cortical integrity, photopenic regions,
differential function, abscess
• CT scan - abscess
• VCUG - standard for first UTI; radionuclide
for follow-up or siblings
• IVP - NO WAY
Feld - 10/98
106
Grades of Reflux
Feld - 10/98
107
Reflux Recommendations
“the simple way”
• GRADES
I - III
Antibiotics
• GRADES
IV - V
Surgery
Feld - 10/98
108
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)
Feld - 10/98
109
Question 13: 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.
Feld - 10/98
110
Question 13: 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 and VCUG
Perform urodynamics and flow studies
Repeat urine culture in 3 months
March 17, 2005
The Suggested Answers
• What are your concerns?
– Voiding history
• Radiographic studies
– ultrasound and VCUG
• Follow-up (no reflux)
– cultures every month for three months,
then every other month for six months
( every 4 months)
• Follow-up (reflux) - antibiotics
Feld - 10/98
112
Glomerulonephritis / Acute
renal failure
March 17, 2005
Case History
• A 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. On examination the child is pale
and is unable to void. His laboratory testing in
your office shows a WBC of 26,000,
hemoglobin of 8 g/dL, platelets 98,000,
Serum creatinine of 1 mg/dL, BUN 54 mg/dL,
urinalysis with large blood, 100 mg/dL of
protein.
Feld - 10/98
114
Question 14: What is the most
likely diagnosis?
A.
B.
C.
D.
E.
Henoch Schoenlein Purpura
Post streptococcal glomerulonephritis
IgA nephropathy
Acute pyelonephritis
Hemolytic uremic syndrome
March 17, 2005
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
March 17, 2005
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
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Toxic megacolon
Rectal prolapse
Colonic gangrene
Intussusceptions
Perforation
Strictures
Mimic appendicitis, IBD
March 17, 2005
Thank you
GOOD LUCK
March 17, 2005
Supplement 1
• Acute renal failure
• Chronic renal failure
• More Fluids & Electrolytes
• Tubular disorders
• Cystic kidney disease
March 17, 2005
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
March 17, 2005
ARF: Diagnosis
Pre-renal
AGN
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
March 17, 2005
ATN
Obstruction
ARF: Diagnosis
• AGN
– PSAGN
– HSP
– SLE
– MPGN
– Wegener’s
March 17, 2005
ARF: Diagnosis
• ATN
– Unreversed pre-renal azotemia
– Nephrotoxic meds
– Contrast agents
– High calcium, uric acid, phosphate
– Rhabdomyolysis (myoglobin)
– Intravascular hemolysis (hemoglobin)
March 17, 2005
ARF: Diagnosis
• Obstructive uropathy
– PUV
– Prune belly
– Vesicoureteric reflux
– Neurogenic bladder (myelomeningocele)
– Megacystis/megaureter
– Secondary: stones, fibrosis
• Effect of age and gender
March 17, 2005
ARF: Testing
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Key labs: BUN, creatinine, K
EKG
CXRay
Renal ultrasound
Specific blood tests based on underlying
condition
March 17, 2005
ARF: Management
• Urgent issues
– Potassium
• Calcium
• Glucose/insulin
• NOT bicarbonate
– Blood pressure: parenteral therapy
• Labetalol
• Nitroprusside
– ECF volume
March 17, 2005
ARF: Conservative
Management
• Potassium
– Diet restriction
– Kayexalate
• Blood pressure
– IV/PO meds
• ECF volume
– Na restriction
– Diuretic use – need for furosemide
March 17, 2005
ARF: Pearls
• Pre-renal azotemia and AGN are similar
• ATN and post-renal failure are similar
• Potassium kills first in ARF
March 17, 2005
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
March 17, 2005
CKD: Common features
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Impact on growth
Impact on bone: osteodystrophy
Impact on puberty
Impact on development – social and
cognitive
March 17, 2005
CKD: Causes
• Non-glomerular
– Hypoplasia/dysplasia
– Reflux nephropathy
– Obstructive uropathy
• PUV
• Prune Belly
• Neurogenic bladder
March 17, 2005
CKD: Clinical manifestations
• Growth failure
– Dependent on age of onset
– Dependent on level of GFR
• UTIs
– Pyelonephritis
• Electrolyte abnormalities
– Pseudohypoaldosteronism
– Nephrogenic DI
•MarchNeurocognitive
disability
17, 2005
CKD: Causes
• Glomerular
– FSGS
– HUS
– SLE
– Membranoproliferative MPGN)
– Alport
– IgA Nephropathy
– Membranous nephropathy
– NOT diabetic or hypertensive nephropathy
March 17, 2005
CKD: Clinical manifestations
• Growth failure
– Dependent on age of onset
• Hypertension
– Role of ECF volume and PRA
• Electrolyte abnormalities
– Acute
– Hyperkalemia
• Edema
•MarchSigns
17, 2005 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
March 17, 2005
CRF: Management
• Nutritional supplementations
– CHO deficiency
• Protein restriction
– Impact on growth
– Effect in more advanced CKD
• BP control
– Disease progression
– ACEI/ARB
March 17, 2005
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
March 17, 2005
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
March 17, 2005
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
March 17, 2005
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
March 17, 2005