Tea-colored Urine
HISTORY OF PRESENT ILLNESS
Facial swelling
No fever
No oliguria
Consulted at a PMD but no medications
given.
Patient was advised to seek consult at
our institution but did not comply
days PTA
HISTORY OF PRESENT ILLNESS
Facial swelling
Bipedal edema
Tea colored urine
Consulted at a PMD
Advised for admission at our
institution but refused
day PTA
HISTORY OF PRESENT ILLNESS
Few hours PTA
Persistence of above signs and symptoms
Decreased urine output
Patient was brought to our institution hence
admitted
D
(+) ATP : Oct 23, 2018
(+) healed pyodermal lesions
(-) asthma
(-) heart disease
(-) diabetes
PAST MEDICAL HISTORY
1st word
• Mama, 8 months
✔7m ✔8m ✔10m ✔1y
Toilet-trained
• 3 years
PAST MEDICAL HISTORY
IMMUNIZATION HISTORY
PULMONARY CARDIOVASCULAR
(-) Cough (-) Cyanosis
(-) DOB (-) palpitations
REVIEW OF SYSTEMS
MUSCULOSKELETAL
(-) muscular pain
(-) numbness
(-) paresthesia
General Awake, Conscious, Coherent,
NICRD
Vital Signs BP: 160/80
HR: 85
RR: 21
Temp. : 36.8 C
Weight: 18 kg
Ht: 131 cm
Skin No pallor, No cyanosis, No Jaundice
HEENT Anicteric Sclerae, Pink Palpebral Conjunctiva, With
Facial Edema, No TPC, No CLAD
Medication
Upper Tract Lower Tract
intake
Common in males
Edema
Characterized by
purpuric rash, arthritis
and abdominal pain.
Rule In Rule Out
Hematuria Arthritis
Edema
Hypertension
Occur in 1% of boys & 1-3
% of girls
M>F during 1st year of life
3 basic Forms:
Pyelonephritis
Cystitis
Asymptomatic Becteuria
Rule in Rule Out
Hematuria Fever
Dysuria/Frequency/Urgency
Strong smelling urine
Abdominal/flank pain
Classic example of the acute
nephritic syndrome
History of ATP
Hematuria
Edema
Hypertension
Decreased Urine
Frequency
S O A P
(+) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored urine cardiorespiratory distress GLOMERULONE Limit fluid intake 133 cc/hr
(+) decreased Vital signs: PHRITIS Insert heplock
frequency in BP: 160/100 Wt: 18 kg Diagnostics:
urination CR: 85 Ht: 131 cm CBC with pc
RR: 20 BSA: 0.8 m2 Urinalysis with RBC
T: 36.8 morphology
No pallor, no jaundice BUN, Crea
(+) Facial edema, anicteric sclerae, C3, ASO Titer
pink palpebral conjunctivae, (-) CLAD Na, K, Cl
Symmetrical chest expansion, (-) Chest xray-PA/Lat
retractions, clear breath sounds Therapeutics:
Adynamic precordium, normal rate, Furosemide 20 mg/IV now
regular rhythm, PMI at 4th ICS LMCL, (-) BP: 130/90 Another
murmur Furosemide 20 mg/IV
Flabby, normoactive bowel sounds, soft 120/70 Furosemide 20
Grossly male, (-) scrotal edema mg/IV q6
(+) Healed pyodermal lesions, (+) (200T) Pen G
Bipedal edema, full and equal pulses (10) Paracetamol
GCS 15 Amlodipine 2.5 mg/tab OD
CBC URINALYSIS
Color Amber
Hgb 97 L
Transparency Turbid
Hct 0.30 L
pH 6.5
RBC 4.21 L
SG 1.025
Plt 444 H
Protein +++
MCV 70 L
Glucose Negative
MCH 23 L
Ketone Negative
MCHC 329
Blood +++
WBC 11.6 H
Neutro 50.4 Bilirubin Negative
Lymph 33.8 Urobilinogen NORMAL
Mono 5.9
Eos 9.5 H Nitrite Negative
Baso 0.4 Leukocytes Negative
WBC 143
RBC 93
Epith cells 16
Hyaline cast 42
Bacteria 22
RBC Morphology Creatinine 52.1 L
BUN 3.4
60% Normal RBCs
Na 148.5
40% Dysmorphic RBCs
K 4.45
Cl 109.8
C3 0.246 L
ASO Titer 6400 IU/ml H
S O A P
(+) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored cardiorespiratory distress GLOMERULONEPHR Limit fluid intake 133 cc/hr
urine Vital signs: ITIS Maintain heplock
BP: 110/70 Diagnostics:
CR: 92 TPAG
RR: 20 Lipid profile
T: 37.1 Therapeutics:
No pallor, no jaundice Furosemide 20 mg/IV q6
(+) Facial edema, anicteric sclerae, pink (200T) Pen G
palpebral conjunctivae, (-) CLAD (10) Paracetamol
Symmetrical chest expansion, (-) Amlodipine 2.5 mg/tab OD
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (+)
Bipedal edema, full and equal pulses
GCS 15
UO: 1.9cc/kg/hr
S O A P
(-) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored cardiorespiratory distress GLOMERULONEPHR Limit fluid intake 260 cc/hr
urine Vital signs: ITIS Maintain heplock
BP: 100/70
CR: 89 Therapeutics:
RR: 20 Furosemide 20 mg/IV q8
T: 36.8 (200T) Pen G
No pallor, no jaundice (10) Paracetamol
Anicteric sclerae, pink palpebral Amlodipine 2.5 mg/tab OD
conjunctivae, (-) CLAD
Symmetrical chest expansion, (-)
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (+)
Bipedal edema, full and equal pulses
GCS 15
UO:1.5cc/kg/hr
TPAG
Total protein 74.47
Albumin 30.62 L
Globulin 43.85 H
A/G Ratio 0.69 L
S O A P
(-) tea- Awake, conscious, coherent, not in ACUTE MGH
colored cardiorespiratory distress GLOMERULONEPHR
urine Vital signs: ITIS Home meds:
BP: 90/60 1. Amoxicillin 250mg/5ml,
CR: 90 4 ml TID x 7 days
RR: 20 2. Amlodipine 2.5 mg/tab
T: 36.7 OD x 5 days
No pallor, no jaundice
Anicteric sclerae, pink palpebral Low salt, low fat diet
conjunctivae, (-) CLAD Follow up on Nov. 12,2018
Symmetrical chest expansion, (-)
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (-)
Bipedal edema, full and equal pulses
GCS 15
UO:1.5cc/kg/hr
The kidneys preserve homeostasis through:
maintain fluid and electrolyte balance
excrete metabolic waste products through glomerular filtration and
tubular secretion
generate energy (gluconeogenesis)
Produce important endocrine hormones (renin, vitamin D
metabolites, erythropoietin
Fetal urine production contributes to amniotic fluid volume,
lung maturation, and somatic development.
Congenital renal disorders may be associated with
reduced (oligohydramnios) or increased amniotic fluid
volume (polyhydramnios).
Pulmonaryhypoplasia and fetal maldevelopment of the face
and extremities may result from insufficient amniotic fluid.
Risk factors for renal disease can be detected by a
careful history.
A detailed family history may identify hereditary
renal conditions. Poor growth and/or feeding,
abnormal fluid intake and/or output may indicate
underlying renal dysfunction.
Laboratory Result
Examination
Urinalysis with RBC May demonstrate RBCs, RBC casts, Proteinuria, PMNs, or dysmorphic
morphology RBCs particularly acanthocytes
Proteinuria normalizes 4-6 wks after onset
Microscopic hematuria may persists for 1-2 yrs after initial
presentation
CBC Mild normochromic anemia may be present from hemodilution and
low grade hemolysis
Serum C3 Reduced in acute phase and returns to normal 6 to 8 wks after onset
ASO Titer Increased after pharyngeal infection rarely increases in strep skin
infection
Anti-Dnase B Documents Recent Strep Skin infection
Serum Electrolytes To correct any electrolyte abnormalities
BUN and Creatinine Renal function tests
Chest X-ray Pulmonary Edema
Renal Biopsy Persistent microscopic hematuria
Children with recurrent gross hematuria with dec. renal function,
proteinuria or HTN.
Genetic disorder- mutation
Immunologic disorder- histopathologic
Perfusion disorder
coagulation disorders.
Proliferation
Sclerosis
Tubulointerstitial fibrosis
Criteria INS APSGN
Age 1-10 y/o 3-15 y/o
Sex M> F M=F
Edema Generalized Localized
Gross Hematuria (-) +++
Oliguria ++ +++
Preceding Infection +/- +
Phases - +
Criteria INS APSGN
Congestion +/- +
Pleural effusion + -
Small amounts of protein are found in the urine of
healthy children (<4 mg/m2/hour or UPr/Cr <0.2).
Endostreptosin Ag
Lipoteichoic acid & previously planted in
polysaccharide Ag in glomeruli
the circulation
Immune IC Induce Ab
Granular
response: production:
Ag Ab – Ag
deposition Ab – Ag
pattern
excess complex in circ. in immunofluor
complex in
ence
glomeruli glomeruli
microscopy
AG IC deposition in
EXCESS glomeruli
Proliferation and
C3 convertase
swelling of parietal
Few days to enzyme
epithelial,
weeks: additional formation: C3
endothelial &
Ab enter cleavage
mesangial cells
circulation
Ag ultimately C3
removed from fragmentation,
Decrease
circulation Complement
activation C3
Glomerulonephri Chemotaxis:
tis subsides leukocytic Injury to
infiltration and capillary walls
degranulation
INJURY TO
CAPILLARY WALLS
Escape of Albumin/Protein
RBC Inc permeability leakage
Albuminuria/protein
uria
hematuria Dec oncotic
pressure
Accumulation of
Tea colored
fluid in interstitial
urine spaces
edema
Proliferation and INCREASE
swelling of parietal GLOMERULAR Stretched renal
epithelial, endothelial SIZE capsule
& mesangial cells
Narrowing of
glomerular
capillary lumen Flank pain
Reciprocal Enhanced Na
Fluid retention reabsorption
hypertensi
Hypervolemi Na
on
a retention
Oliguric Phase
- acute salt and water overload and
related and complications as
hypertensive encephalopathy, renal
failure and CHF.
Diuretic Phase
spontaneous voiding or sudden volume
increments with diuretic agents.
unrecognized hypovolemia that ensues can
cause serious electrolyte disturbances or even
shock.
BP normalizes and the child starts feeling better.
Immediate convalescent periods.
most hospitalized children are ready for discharge.
Except perhaps for residual gross or significant
microscopic hematuria, all alarming indices seen in
the oliguric period are gone,
Serial urinalyses will still show proteinuria, micro-
hematuria and casts, findings which may persist for
a few months to even a year notwithstanding
excellent clinical recovery
acute phase
resolves w/in 6–8 wks
urinary protein excretion & HPN
usually normalize by 4–6 wks
after onset
persistent microscopic hematuria
1–2 yr after initial presentation
MANAGEMENT
Ambulation + -
Prednisone +++ -
Diuretics +/- ++
Albumin + -
Hyperlipidemia
promotes increased atherosclerotic vascular disease
Most children with NS eventually go into remission.
80% of children with MCNS experience NS relapse(heavy proteinuria that persists
for 3 or more consecutive days)
Transient (up to 3 days) proteinuria may occur with intercurrent infection in
children with MCNS and is not considered a relapse.
effective for true relapse.
Steroid-responsive patients have little risk of chronic renal failure.
Patients with FSGS may initially respond to steroids but later develop resistance.
Many children with FSGS
progress to end-stage kidney failure
Recurrence of FSGS occurs in 30% of children who undergo renal transplantation.
In typical cases, the gross hematuria, proteinuria, and edema decline quickly (in 5
to 10 days).
Microscopic hematuria may persist for months or even years; over 95% of children
recover completely with no longterm sequelae.
Children with IgA nephropathy and other forms of chronic GN have a greater risk
of progression to ESRD.
The prognosis for renal recovery in chronic GN and in RPGN is variable and
related to the underlying disorder and disease severity.
The presence of persistent, heavy proteinuria, hypertension, decreased kidney
function, and severe glomerular lesions on
biopsy is associated with poor outcomes.
idiopathic isolated asymptomatic microscopic hematuria or suspected thin
basement membrane disease typically have an excellent renal prognosis.
Long-term follow-up, including yearly urinalysis (to rule out proteinuria) and blood
pressure, is required to exclude progressive forms of renal disease