[PEDIATRICS 3A] Nephrology A

Lecturer: Joselito C. Matheus, MD

Transcriber: Patrick Angelo R. Bautista February 2020


References and Legends Table 509-1 Other Causes of Red Urine
• {⏯} Recordings + {💻} Powerpoint + {📕} Lecture Guide and Manual HEME POSITIVE
• {📖} Nelson Textbook of Pediatrics 20th Ed Hemoglobin
Myoglobin
• {📌} Transcriber’s Note
HEME NEGATIVE
Dyes (Vegetable / Fruit)
Table of Contents Drugs
Beets
Chloroquine
I. Hematuria 1 Blackberries
Deferoxamine
II. Post-Infectious (Streptococcal) Glomerulonephritis 2 Food and candy coloring
Ibuprofen
III. Proteinuria and Nephrotic Syndrome 3 Rhubarb
Iron sorbitol
IV. Urinary Tract Infection 6 Metronidazole
Metabolites
V. IGA Nephropathy 9 Nitrofurantoin
Homogentisic acid
VI. Henoch-Schonlein Purpura (HSP) Nephritis 9 Phenazopyridine (Pyridium)
Melanin
VII. Renal Venous Thrombosis 10 Pholphthalein
Methemoglobin
11 Phenothiazines
VIII. Wilms Tumor (Nephroblastoma) Porphyrin
Rifampin
IX. Reading Assignment: SLE, HUS, Interstitial Nephritis 12 Tyrosinosis
Salicylates
X. Compiled Samplex 14 Urates
Sulfasalazine
Table 509-2 Causes of Hematuria in Children
I. HEMATURIA {📖 509} UPPER URINARY TRACT DISEASE
• Gross Hematuria Isolated renal disease
Immunoglobulin (Ig) A nephropathy (Berger disease)
9 Bright red color; or brown, tea, coffee or cola-colored urine or
Alport syndrome (hereditary nephritis)
presence of clots in the urine Thin glomerular basement membrane nephropathy
§ Bright red urine – post glomerular Postinfectious GN (Poststreptococcal GN) *
§ Tea-colored urine – glomerular Membranous nephropathy
• Microscopic / Significant Hematuria Membranoproliferative GN*
9 Diagnosed through microscopy; >5 RBCs/hpf* on >2 occasions Rapidly progressive GN
9 {⏯} Range: >3 to >5 RBC/hpf Focal segmental glomerulosclerosis
Anti–glomerular basement membrane disease
§ Lower cut-off implication (>3): you will be screening for
Multisystem disease
more people and getting work-up for patient that is normal Systemic lupus erythematosus nephritis*
§ Higher cut-off implication (>5): less people screened, Henoch-Schönlein purpura nephritis
possibly miss patients who may have significant hematuria. Granulomatosis with polyangiitis (formerly Wegener granulomatosis)
• Persistent Hematuria Polyarteritis nodosa
9 Significant hematuria by dipstick test or microscopy in 3 Goodpasture syndrome
separate occasions over a span of 2-3 weeks Hemolytic-uremic syndrome
Sickle cell glomerulopathy
9 {⏯} 3 urinalyses are usually not required. 1 is enough if:
HIV nephropathy
§ (+) microscopic evidence of hematuria Tubulointerstitial disease
§ Patient is already passing out tea-colored urine Pyelonephritis Interstitial nephritis
• Tea-colored or cola-colored urine may be due to: Papillary necrosis
9 Hemoglobinuria – due to diseases causing hemolysis and the Acute tubular necrosis
subsequent release of hemoglobin Vascular
9 Myoglobinuria – due to muscle injuries like crushing injuries, Arterial or venous thrombosis
Malformations (aneurysms, hemangiomas)
sudden and excessive use of specific muscle groups causing
Nutcracker syndrome
muscle injury and some are due to medications. Hemoglobinopathy (sickle cell trait/disease)
• Dipstick / Test strips Crystalluria
9 Can detect 5-10 intact RBCs/uL or 2-5 RBC/hpf Anatomic
9 If it falls under the 5 RBC cut-off, it may or may not be Hydronephrosis
significant, so you have to redo the test. Cystic-syndromic kidney disease
9 Note: test strips (qualitative) should be correlated with Polycystic kidney disease
Multicystic dysplasia
microscopic findings (quantitative)
Tumor (Wilms, rhabdomyosarcoma, angiomyolipoma, medullary Ca)
Trauma
LOWER URINARY TRACT DISEASE
Inflammation (infectious and noninfectious) Cystitis
Urethritis
Urolithiasis
Trauma
Coagulopathy
Heavy exercise
Bladder tumor
Factitious syndrome, factitious syndrome by proxy†
*Denotes glomerulonephritides presenting with hypocomplementemia.
†Formerly Munchausen syndrome and Munchausen syndrome by proxy.

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II. POST-INFECTIOUS GN {📖 511}
• Umbrella term; may be bacterial, viral, protozoan
9 Most common cause is GABHS
9 Other organisms: staphylococcus, salmonella, measles,
mumps, chickenpox, malaria
• PIGN is characterized by a previous infection prior to onset of
nephritic syndrome
• Immune complex reaction leading to nephritis
Infection ➡ Latent Period ➡ Nephritic Syndrome
Latent period:
• Analogous to an incubation period
• Variable; <1 week to 6 weeks
9 Average: 10-14 days for post-strep GN
Acute Post-Streptococcal Glomerulonephritis
• Classic example of the acute nephritic syndrome characterized
by the sudden onset of:
9 Gross hematuria, edema, hypertension, renal insufficiency
PSGN: Etiology
• APSGN follows infection of the throat or skin by certain
“nephritogenic” strains of GABHS.
• PSGN commonly follows:
9 Strep pharyngitis during cold-weather months
§ Serotypes: 1, 3, 4, 12, 25, 49
9 Skin infections/ pyoderma during warm-weather months
§ Serotypes: 2, 49, 55, 57, 60
Note: If the question is what is the etiology of PSGN, the answer
is immune complex reaction.
Group A Beta hemolytic strep is responsible for the infection prior
but the development of PSGN is due to immune complex.
PSGN: Pathogenesis
Theories on Renal Injury: Immune mediated
• Trapping of circulating immune complexes in the glomeruli
• Molecular mimicry between streptococcal and renal antigens
• In-situ immune complex formation between anti-streptococcal
antibodies and glomerular planted antigen
• Direct complement activation by streptococcal antigens deposited
in the glomeruli
PSGN: Clinical Manifestations of Acute PSGN {💻+📖}
Symptom % 9 Serum CH50 – commonly depressed
Hematuria 100
Proteinuria 80
Edema 90
Hypertension 60-80
Oliguria 10-50
Dyspnea, Heart Failure <5
Nephrotic proteinuria 4 9 Indicated in those with signs of heart failure or respiratory
Azotemia 25-40
Early mortality <1
• Most common in children ages 5-12 years
9 Uncommon before the age of 3 years.
• The typical patient develops an acute nephritic syndrome:
9 1-2 weeks after a streptococcal pharyngitis or
9 3-6 weeks after a streptococcal pyoderma
• The history of a specific infection may be absent, because
symptoms may have been mild or have resolved without patients
receiving specific treatment or seeking the care of a medical
provider.
• The severity of kidney involvement varies from asymptomatic
microscopic hematuria with normal renal function to gross
hematuria with acute renal failure.
• Depending on the severity of renal involvement, patients can
develop various degrees of edema, hypertension, and oliguria.
• Patients are at risk for developing:
9 Encephalopathy and/or heart failure secondary to
hypertension or hypervolemia.
• Hypertensive encephalopathy
9 Considered in patients with: blurred vision, severe headaches,
altered mental status, new seizures.
• Symptoms of Pulmonary Edema and Heart Failure
9 Respiratory distress, orthopnea, cough
• Peripheral edema from salt and water retention
• Nephrotic syndrome
• Nonspecific symptoms:
9 Malaise, lethargy, abdominal pain, flank pain
• Atypical presentations:
9 Subclinical disease, severe symptoms but an absence of initial
urinary abnormalities, purpuric rash
• The acute phase generally resolves within 6-8 wk.
• Although urinary protein excretion and hypertension usually
normalize by 4-6 wk after onset, persistent microscopic hematuria
can persist for 1-2 years after the initial presentation.
PSGN: Diagnosis {💻+📖+📕}
• Urinalysis
9 Gross or microscopic hematuria
2
9 Proteinuria (cut-off for nephritic: <40 mg/m /hr)
2
§ >40 mg/m /hr is nephrotic
• Complete blood count
9 Mild normochromic anemia may be present from
hemodilution and low-grade hemolysis.
+
• Serum electrolytes (Na, K, Ca, P, H )
+
9 Hypo-Na, hyper-K, hypo-Ca, hyper-P, increased H
• Acid-base balance (case to case basis): metabolic acidosis
• Renal function test
9 BUN/Creatinine, eGFR
§ Compute using Schwartz Formula: eGFR = kL/PCr
§ k = constant; L = height; PCr = plasma creatinine
• ASO, neuraminidase, DNAse test
9 Antistreptolysin O (ASO) titer – commonly ↑ after a
pharyngeal infection but rarely ↑ after strep skin infections.
9 Anti-deoxyribonuclease (DNAse) B level – best single
antibody titer to document cutaneous streptococcal infection
• Throat swab/ culture
• Skin lesion discharge culture
• Serum C3, C4
9 Serum C3 level – significantly reduced in >90% of patients in
the acute phase, and returns to normal 6-8 wk after onset
9 Serum C4 – most often normal, or only mildly depressed
• Magnetic Resonance Imaging of the brain
9 Indicated in patients with severe neurologic symptoms
9 Can demonstrate posterior reversible encephalopathy
syndrome in the parietooccipital areas on T2-weighted images
• Chest X-ray
distress, or physical exam findings of a heart gallop, decreased
breath sounds, rales, or hypoxemia.
Essential for Diagnosis
• Identification of the primary infection (History)
• Establish presence of latent period (History)
• Appearance of signs and symptoms of nephritis (History + PE)
• Evidence of previous or ongoing strep infection (Laboratory)
Majority of cases – good prognosis and asymptomatic in nature
PSGN: Complications
• Volume overload
• Renal failure
• Electrolyte imbalance
• Hypertensive Crisis / Hypertensive Encephalopathy
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PSGN: Treatment {💻+📕} • Dialysis – seldom used

• Primarily supportive
• Penicillin for 10 days – drug of choice*
9 To completely eradicate remaining organism
9 Alternatives:
ST ND
§ Amoxicillin, 1 / 2 gen Cephalosporins, Macrolides
• Maintain Homeostasis – fluid and electrolytes
9 Regulation of Fluid – prevent fluid overload
§ Diuretics: Furosemide 1-2 mg/kg/dose
§ Fluid Restriction:
(BSA x Insensible H2O loss + Urine Output) / 2
• Anti-hypertensives
9 Hypertension >95% for age and height
9 Use appropriate size of cuff
• Diuretics, CCB, ACEi / ARBs, Vasodilators
9 Peritoneal Dialysis or Hemodialysis
9 Indication: progressive increase in BUN and creatinine
especially with uremic signs and symptoms, intractable
hypertension or intractable hyperkalemia
PSGN: Prognosis {💻+📕}
• Good, >90% recover without long term sequelae
• Natural History of PSGN
9 Oliguric phase – presence of nephritic s/sx (2 wks)
9 Diuretic phase – ↑ urine output, nephritic s/sx subside (2 wks)
9 Resolution phase – improvement in urinalysis findings
(proteinuria, hematuria decreasing in intensity until normal), C3
normalizes in 4-6 wks

III. PROTEINURIA and NEPHROTIC SYNDROME {📖 523-527}

Proteinuria {📖} 9 Podocyte Functions:

• Classified as either benign or pathologic; Classified as
glomerular or tubular proteinuria
• Normal protein excretion is defined as ≤4 mg/m2/hr
• Abnormal proteinuria is defined as excretion of 4-40 mg/m2/hr
• Nephrotic-range proteinuria is defined as >40 mg/m2/hr
Nephrotic Syndrome {💻+📖}
• Clinical manifestation of glomerular diseases associated with
heavy (nephrotic-range) proteinuria
2
9 *Proteinuria >3.5 g/24hr or >40 mg/m /hr
9 *Urine protein:creatinine ratio >2
• Triad of clinical findings associated with nephrotic syndrome:
1. Hypoalbuminemia (≤2.5 g/dL)
2. Edema
3. Hyperlipidemia (cholesterol >200 mg/dL)
• Responsive to corticosteroid therapy
NS: Pathogenesis: Role of a Podocyte
• The underlying abnormality in nephrotic syndrome is an
increased permeability of the glomerular capillary wall, which
leads to massive proteinuria and hypoalbuminemia.
§ Structural support of the capillary loop
§ Major component of glomerular filtration barrier to proteins
§ Synthesis and repair of glomerular basement membrane
• Foot processes
9 Extensions of the podocyte that terminate on the glomerular
basement membrane.
9 Interdigitate with those from adjacent podocytes and are
connected by a slit called the slit diaphragm.
• Slit diaphragm
9 One of the major impediments to protein permeability across
the glomerular capillary wall.
9 Not simple passive filters—they consist of numerous proteins
that contribute to complex signaling pathways and play an
important role in podocyte function.
9 Important component proteins of the slit diaphragm:
§ Nephrin, podocin, CD2AP, α-actinin 4
• Podocyte injury or genetic mutations of genes producing
podocyte proteins may cause nephrotic-range proteinuria.
• In idiopathic, hereditary, and secondary forms of nephrotic
syndrome, there are immune and nonimmune insults to the
podocyte that lead to:
9 Foot process effacement of the podocyte

• Podocyte 9 Decrease in number of functional podocytes

9 Plays a crucial role in the development of proteinuria and 9 Altered slit diaphragm integrity

progression of glomerulosclerosis. • The end result is increased protein “leakiness” across the
9 A highly differentiated epithelial cell located on the outside of glomerular capillary wall into the urinary space.
the glomerular capillary loop.

Table 526-1 Causes of Proteinuria

TRANSIENT PROTEINURIA GLOMERULAR DISEASES WITH PROTEINURIA AS A PROMINENT FEATURE
Fever Acute postinfectious glomerulonephritis (streptococcal, endocarditis,
Exercise hepatitis B or C virus, HIV)
Dehydration Immunoglobulin A nephropathy
Cold exposure Henoch-Schönlein purpura nephritis
Congestive heart failure Lupus nephritis
Seizure Serum sickness
Stress Alport syndrome
ORTHOSTATIC (POSTURAL) PROTEINURIA Vasculitic disorders
GLOMERULAR DISEASES CHARACTERIZED BY ISOLATED PROTEINURIA Reflux nephropathy
Idiopathic (minimal change) nephrotic syndrome TUBULAR DISEASES
Focal segmental glomerulosclerosis Cystinosis
Mesangial proliferative glomerulonephritis Wilson disease
Membranous nephropathy Lowe syndrome
Membranoproliferative glomerulonephritis Dent disease (X-linked recessive nephrolithiasis)
Amyloidosis Galactosemia
Diabetic nephropathy Tubulointerstitial nephritis
Sickle cell nephropathy Acute tubular necrosis
Renal dysplasia
Polycystic kidney disease
Reflux nephropathy
Drugs (penicillamine, lithium, NSAID)
Heavy metals (lead, gold, mercury)

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Table 523-1 Methods Available to Test for Proteinuria

METHOD INDICATIONS NORMAL RANGE COMMENTS
Dipstick testing Routine screening for proteinuria Negative or trace in a concentrated False-positive test can occur if urine
performed in the office urine specimen (spgr: ≥1.020) is very alkaline (pH > 8.0) or very
concentrated (spgr: >1.025)
24 hr urine for protein and Quantitation of proteinuria (as well <100 mg/m2/24 hr or <150 mg/24 hr More accurate than spot urine
creatinine* excretion as creatinine clearances) in a documented 24 hr collection analysis; inconvenient for patient;
limited use in pediatric practice
Spot urine for protein/creatinine Semiquantitative assessment of <0.2 mg protein/mg creatinine in Simplest method to quantitate
ratio—preferably on first morning proteinuria children >2 yr old proteinuria; less accurate than
urine specimen <0.5 mg protein/mg creatinine in measuring 24 hr proteinuria
those 6–24 mo old
Microalbuminuria Assess risk of progressive <30 mg urine albumin per gram of Therapy should be intensified in
glomerulopathy in patients with creatinine on first morning urine diabetics with microalbuminuria
diabetes mellitus
*Note that in a 24 hr urine specimen, the creatinine content should be measured to determine whether the specimen is truly a 24 hr collection. The amount of
creatinine in a 24 hr specimen can be estimated as follows: females, 15-20 mg/kg; males, 20-25 mg/kg.

Table 527-2 Summary of Primary Renal Diseases That Manifest as Idiopathic Nephrotic Syndrome
FEATURES MINIMAL CHANGE FOCAL SEGMENTAL MEMBRANOUS MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
NEPHROTIC SYNDROME GLOMERULOSCLEROSIS NEPHROPATHY Type I Type II
DEMOGRAPHICS
Age (years) 2-6, some adults 2-10, some adults 40-50 5-15 5-15
Sex 2:1 male 1.3:1 male 2:1 male Male-female Male-female
CLINICAL MANIFESTATIONS
Nephrotic syndrome 100% 90% 80% 60% * 60% *
Asymptomatic 0 10% 20% 40% 40%
proteinuria
Hematuria (microscopic 10-20% 60-80% 60% 80% 80%
or gross)
Hypertension 10% 20% early Infrequent 35% 35%
Rate of progression to Does not progress 10 yr 50% in 10-20 yr 10-20 yr 5-15 yr
renal failure
Associated conditions Usually none HIV, heroin use, sickle Renal vein thrombosis; None Partial lipodystrophy
cell disease, reflux medications; SLE;
nephropathy hepatitides B, C;
lymphoma; tumors
GENETICS
None except in Podocin, α-actinin 4, None None None
congenital TRPC6 channel, INF-
nephrotic syndrome 2, MYH-9
LABORATORY FINDINGS
Manifestations of Manifestations of Manifestations of Low complement Normal complement
nephrotic syndrome nephrotic syndrome nephrotic syndrome levels—C1, C4, C3- levels—C1, C4, low
↑ BUN in 15-30% ↑ BUN in 20-40% Normal complement C9 C3-C9
Normal complement Normal complement levels
levels levels
RENAL PATHOLOGY
Light microscopy Normal Focal sclerotic lesions Thickened GBM, spikes Thickened GBM, Lobulation
proliferation
Immunofluorescence Negative IgM, C3 in lesions Fine granular IgG, C3 Granular IgG, C3 C3 only
Electron microscopy Foot process fusion Foot process fusion Subepithelial deposits Mesangial and Dense deposits
subendothelial
deposits
REMISSION ACHIEVED AFTER 8 WEEKS OF ORAL CORTICOSTEROID THERAPY
90% 15-20% Resistant Not established/ Not established/
resistant resistant
*Approximate frequency as a cause of idiopathic nephrotic syndrome. Approximately 10% of cases of adult nephrotic syndrome are a result of various diseases
that usually manifest as acute glomerulonephritis.

Histologic Dx (Primary Disease) in Renal Biopsies of 521 children NS: Clinical Features
Minimal Change Nephrotic Syndrome 77.1% Clinical Hallmark of Nephrotic Syndrome is Edema Formation
Focal Segmental Glomerulonephritis 7.9%
Membranoproliferative Glomerulonephritis 6.2%
Others (membranous GN, mesangial GN) 8.8%
• Note: those in red show progressive disease despite treatment
and eventually leads to End-Stage Renal Disease.

Responsiveness to Steroid Treatment

• Minimal Change Nephrotic Syndrome – most sensitive
9 Sensitivity of 93.1%
9 Specificity of 72.2%
Classic Symptoms:
Clinical Classification of Childhood NS • Periorbital edema, taut skin, scrotal edema, pitting pedal edema
• Secondary (10%)
9 Related to systemic disease, drug, toxin, allergen, APSGN
Edema
• Most common presenting sx of children with Nephrotic syndrome
• Congenital Nephrotic Syndrome 2
• Massive proteinuria (>40 mg/m /hr)
• Asymmetric and dependent (influenced by gravity)

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Proteinuria (Albuminuria) Note: For steroid sensitive nephrotic syndrome, majority will undergo
• Dipstick: 4+ albumin diuresis within 5-10 days after starting steroid treatment. Although
• Protein/Crea ratio: random urine sample – screening test only diuretics may be used to manage edema, caution has to be observed
9 >200 mg/mmol or >2 mg/dL in its use because the patient may already be in a state of volume
• 24-hour urine albumin determination: Gold standard contraction that will be aggravated by diuretic use.
2
9 Through body surface area: >40 mg/m /hr
9 Through weight: >50 mg/kg/day Other Medications
• Antacids: usually not necessary
NS: Investigation of Initial Presentation • Calcium Carbonate: for prolonged steroid use (>3 months)
• Hyperlipidemia medications: not usually required for steroid
• CBC with platelet count
sensitive NS
9 ↑ WBC – infection
• Isoniazid: for 6 months for Mantoux positive only
9 ↑ hematocrit, thrombocytosis - intravascular vol. contraction
• TB disease: treated with standard therapy
• Serum creatinine, cholesterol, TPAG
• Urinalysis
Natural Course of Steroid Sensitive NS (Minimal Change Disease)
• 24-hour creatinine clearance / eGFR
• Renal Ultrasound: Not mandatory; only if entertaining differentials • 80% will have one or more relapses
• Others: • 50% will either have frequent relapses or be steroid dependent
9 C3 (depends on the clinical features) – prognostic indicator • Increasing age = Decreasing incidence of relapses
§ Minimal change disease = normal C3 9 Frequency of relapses decrease with time with:
§ Primary type: Membranous proliferative disease = ↓ C3 § 50- 70% being relapse-free after 5 years
9 Hepatitis B Screening § 85% relapse-free at 10 years
9 Tuberculin test • Early relapse after initial treatment and short duration of remission
increase risks for subsequent relapse.
Secondary Nephrotic Syndrome • Patients with frequent relapses during childhood are more likely to
• Systemic disease with renal manifestations have disease persisting into adulthood.
• Supporting laboratory exams exist for the primary disease
9 Ex. SLE with (+) tests for ANA, anti-DNAse, anti-Sm NS: Complications
• Thrombosis
NS: Current Treatment 9 Correction of hypovolemia and hemoconcentration
• International Study of Kidney Disease in Children (ISKDC) 9 Anticoagulation for thromboembolic episodes and those at risk
• Arbeitsgemeinschaft fur Padiatrische Nephrologie (APN) • Hypovolemia (Shock)
2
• DOC: Prednisone 60 mg/m → 40 mg/m
2 9 Abdominal pain, oliguria, cold peripheries, poor pulse volume,
hypotension, hemoconcentration, usually minimal edema
Steroid Treatment Regimen: ISKDC vs. APN 9 20-25% salt poor albumin 0.5-1.0g/kg/dose over 1-2 hr infusion
• ISKDC: 8 weeks (4 weeks daily, 4 weeks alternate days) 9 Furosemide 1-2 mg/kg/dose
9 2 months intensive treatment • Hyperlipidemia
ST
§ 1 half (4 weeks daily): 60 mg/m
2 9 Dietary advice
ND
§ 2 half (4 weeks alternate): 40 mg/m
2 9 HMG-CoA reductase inhibitors are effective but experience is
• APN: 12 weeks* (6 weeks daily, 6 weeks alternate days) still limited (not usually necessary if responsive to steroids)
9 Superior than ISKDC regimen 9 ↑ risk for CVD for Non-Minimal Change Disease (NMCD) with
9 3 months intensive treatment persistently heavy proteinuria and ↑ VLDL and LDL
ST 2
§ 1 half (6 weeks daily): 60 mg/m * • Infection
ND
§ 2 half (6 weeks alternate): 40 mg/m
2 9 Relapses with complaint of abdominal pain
9 Primary peritonitis
Steroid Response § Cover for both gram (+) and (-) until cultures are available
Remission Proteinuria and edema subsides with 3 § Prophylactic oral penicillin 125-250 mg BID in an
consecutive (-) proteinuria (dipstick) edematous child
Frequent Relapse 2-3 relapses in 6 months § Streptococcus pneumoniae is most common agent
3-4 relapses in a year causing peritonitis and septicemia
Infrequent Relapse 1-2 relapses in a year
Steroid Dependent (+) remission but with relapses after tapering NS: Immunization
steroids • Live vaccines (measles, polio boosters) not given to patients on
Steroid Resistant Still unresponsive after giving intensive course corticosteroids; can be given 4 weeks after cessation of treatment
• Killed vaccine may be given anytime
Steroid-Sensitive Nephrotic Syndrome Diet • 23-polyvalent pneumococcal polysaccharide vaccine
• Balanced diet 9 Given especially if prone to S. pneumoniae infections (relapses
• Protein at 1.5-2.5 g/kg for patients with persistent proteinuria associated with URTI)
9 For growth and nitrogen balance 9 >2 years old
9 High protein diets >2.5 g/kg worsens renal symptoms 9 Variable response
• Salt restriction: 1-2 g/day (no added salt) 9 Loss of antibody titer over time
• Ensure physical activity and prevent excessive weight gain • PVC 13
• Education regarding effects of high dose steroids: • Influenza A
9 Voracious appetite, central obesity, fluid retention, 9 Adequate Ab titer maintained at 6 months post-vaccination
hypertension, diabetes mellitus, cataract • Susceptible Nephrotics
9 Varicella exposure
Edema Treatment § Zoster immunoglobulin within 72 hours from exposure
• Diuresis from treatment within 5-10 days § Acyclovir, if varicella develops
• Oral furosemide 1-3 mg/kg daily 9 Measles exposure
9 For persistent edema and weight gain of 7-10% § Gamma globulin
• Spironolactone 2-4 mg/kg daily
9 For patients with prolonged and high dose furosemide NS: Prognosis
requirements.
• Overall good prognosis for Minimal Change
• Albumin transfusion (1-2 g/kg) – should be done first before
• Guarded prognosis for other primary types (MPGN, FSGS)
diuresis to increase oncotic pressure.

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IV. URINARY TRACT INFECTION {📖 538}

Other Risk Factors
• Congenital Functional Problems
UTI: Prevalence and Etiology 9 Important concern for these may cause recurrent UTI
• Prevalence of UTIs varies with age • Immune System of the Patient
9 During 1st yr of life – M:F ratio is 2.8-5.4: 1 9 Could be due to increase virulence and decrease in the

9 Beyond 1-2 yrs – female preponderance; M:F ratio 1:10.

defense mechanism of the patient
• Circumcision
9 In boys: most UTIs occur during the 1st yr of life; much more
9 Risk of complications outweighed the benefits in boys without
common in uncircumcised boys
UTI, but in boys with previous UTI or high grade VUR (III- V),
9 In girls: the first UTI usually occurs by the age of 5 yrs, with
the benefits outweighed the risks.
peaks during infancy and toilet training.
9 Circumcision of the male infant with VUR may be considered
• Etiology
based on an ↑ risk of UTI in boys who are not circumcised.
9 Females: E. coli (75-90%), Klebsiella, Proteus
• Bladder Bowel Dysfunction (BBD)
9 Males: E. coli, Proteus, Gram (+) 9 The risk of febrile UTI in children with VUR on continuous
9 Both Sexes: S. saprophyticus, Enterococcus antibiotic prophylaxis is greater in patients with BBD compared
9 Adenovirus, other virus – cystitis with gross hematuria with those without BBD
• Epidemiology: {💻} 9 BBD Risk Factors
9 By the age of 7 years, 8.4% of girls and 1.7% of boys has had § Day time urinary incontinence
one or more symptomatic UITs § Squatting and other holding maneuvers (Sphincter control,
9 UTI is most common in the first year of life with boys having children seating on heel, etc.)
more UTI that girls in the first 6 months of life. § Prolonged or fractionated voiding
§ ↑ Residual volumes (pre- vs. post-voiding bladder US)
UTI: Risk Factors § Constipation – directly related to UTI
§ Fecal soiling
Table 538-1 Risk Factors for Urinary Tract Infection
9 BBD Intervention
Female gender Tight clothing (underwear)
Uncircumcised male Pinworm infestation § Increasing fluid intake
Vesicoureteral reflux * Constipation § Regular or timed voiding (e.g. every 3 hours even if they
Toilet training Bacteria with P fimbriae don’t feel urgency to void)
Voiding dysfunction Anatomic abnormality (labial § Relaxation measures to avoid holding maneuvers
Obstructive uropathy adhesion) § Prevention and treatment of constipation
Urethral instrumentation Neuropathic bladder § Use of bladder and bowel diaries to assess progress
Wiping from back to front in girls Sexual activity
Bubble bath? Pregnancy
*Risk increased for clinical pyelonephritis, not cystitis
UTI: Common Uropathogens / Etiologic Agents
• Predominant organisms are gram (-) organisms:
Independent Risk Factors for Recurrence are: 9 E. coli – 70% of UTI
• Age below 6 months at first UTI 9 Others: Proteus mirabilis, Klebsiella, Enterobacter,
• Age 3-5 years Pseudomonas aeruginosa, Enterococcus
• Vesicoureteral reflex grades III, IV, V • Proteus vulgaris: for uncircumcised boys
• S. saprophyticus: acute UTI in adolescent girls

UTI: Pathogenesis
• Ascending infection
• Periurethral area contains bowel bacteria
• This is caused predominantly of E. coli in girls, and after the first 6
months of life, Proteus in boys
• In older children, gram negative bacteria colonize the periurethral
area and precedes the development of UTI
• The change from normal flora may be induced by a course of a
broad-spectrum antibiotics causing an infection
Grading of vesicoureteral reflux:
Grade I: VUR into a non-dilated ureter. Bacterial Virulence Factors Host Response to UTI
Grade II: VUR into the upper collecting system without dilation. • E. coli strains express surface • Innate host immune system
Grade III: VUR into dilated ureter and/or blunting of calyceal fornices. fimbriae (P fimbriae) • Cytokine production
Grade IV: VUR into a grossly dilated ureter. • Flagella mediated motility • Neutrophil recruitment to kill
Grade V: massive VUR, with significant ureteral dilation and tortuosity • Lipopolysaccharide production bacteria
and loss of the papillary impression. • Capsular polysaccharide • IL-6
• Hemolysins • IL-8 causes an increase in
Host Factors • E. coli compete with host cells neutrophil migration and
for nutrients including Iron activation resulting in pyuria
• Constipation – directly related to UTI
Aerobactin which is a high
• Infrequent urination affinity iron binding protein
• Flushing mechanism of urine helps in getting rid of bacteria
• Associated with holding or postponing urination UTI: Clinical Manifestations and Classification
• Normal urination in neonates is 8-12x; voids every feeding
• Immune system
3 Basic Forms of UTI
a. Pyelonephritis – involvement of the renal parenchyma
• Congenital/functional problems: may cause recurrent UTI
9 Characterized by any or all of the following:
§ Abdominal, back, or flank pain
Bacterial Virulence Factors
§ Fever – may be the only manifestation at times
• Ability to adapt
§ Malaise
• Fimbriae
§ Nausea, vomiting
§ Diarrhea (occasionally)
9 Newborns – non-specific signs and symptoms
§ Poor feeding, irritability, jaundice, weight loss
9 Pyelitis – term when no renal parenchyma involved
9 Pyelonephritic scarring – renal injury due to pyelonephritis

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b. Cystitis – involvement of the bladder Criteria for the Diagnosis of UTI by Urine Culture
9 Dysuria, urgency, frequency, suprapubic pain, incontinence, Method of Collection Colony Count Probability of Infection
9 Malodorous urine – not specific for a UTI Suprapubic aspirate Any number >99%
9 Does not cause fever and does not result in renal injury Catheter ≥10,000 95%
Clean void ≥100,000
c. Asymptomatic Bacteriuria Boy 1 specimen Infection unlikely
9 Positive urine culture without any manifestations of infection
9 Most common in girls Girl 1 specimen 80%
9 Benign condition 2 specimens 90%
9 Does not cause renal injury except in pregnants
What may cause a false-negative culture:
• Focal Pyelonephritis (Nephronia) and Renal abscess
• Had already taken antibiotic medication
9 Less common forms
• Double voided urine sample
• Diluted urine
Clinical Presentation
• The most useful indicators of UTI in infants aged <24 months are:
UTI: Imaging Studies
9 Fever above 40 degrees
9 Previous history of UTI • To detect: Obstructive lesions, VUR, Kidney damage
9 Fever for more than 24 hours • Indications:
9 Suprapubic tenderness 9 Any complicated UTI (>3 months, congenital abnormalities)
9 Ill appearance 9 Acute pyelonephritis
9 No other source of fever 9 Bacteriuria before 1 year of age
9 Uncircumcised in boys 9 Hypertension
9 Combined predictors of fever exceeding 39°C for >48 hours 9 Abdominal mass
without another source of fever were more useful than 9 Decreased renal concentrating ability
individual findings. 9 Recurrent cystitis in boys
9 The presence of abdominal pain, back pain, dysuria, frequency 9 Covert bacteriuria
and new onset incontinence increases the likelihood of a UTI in 9 Posterior midline anomaly (lumbosacral meningocele)
older children.
Ultrasound
Clinical Manifestations (varies with age) • Non-invasive
• Febrile children <5 years old (preschool-toddler) • Identify structural abnormalities
9 Fever above 38 degrees 9 Obstruction
9 Looking unwell 9 Differences in kidney size
9 Urinary symptoms (inc. frequency, urgency, dysuria) 9 Kidney damage
9 Reduced fluid intake • Post-voidal ultrasound – to check for urinary retention
• Neonates: • KUB (kidneys, ureters, urinary bladder)
9 Lethargy, Poor feeding, Jaundice 9 *First imaging study performed for a diagnosed case of UTI
9 Fever or no fever in combination of the presentation above 9 Normal kidney is vascular, same echogenicity with liver
9 UTI in neonates presents non-specific clinical symptoms and 9 Kidney whiter than liver (hyperechoic) indicates renal
sometimes with similar manifestation with sepsis* parenchymal disease

UTI: Laboratory Diagnosis DMSA Scan (dimercaptosuccinic acid)

• In identifying acute parenchymal injury following UTI
Urinary Sample Collection
9 Sensitivity of 86% | Specificity of 91%
• “The diagnosis of UTI will start with Urinalysis. It is very important
• Most sensitive investigation for acute and chronic kidney damage
not just to get any urine sample, but to get a quality urine sample.”
• Cannot differentiate damage due to UTI and congenital causes
9 Clean voided samples (common)
• Detects:
9 Catheterized sample
9 Scars after pyelonephritis
9 Suprapubic sample
9 Renal agenesis
• Dipstick testing of urine for WBC esterase and nitrite or urinary
9 Ectopic kidney
microscopy for pyuria or bacteria cannot replace urine culture
• Static renal exam; specific to the cortex
for the diagnosis of UTI.
• *Pyuria (pus / WBC in urine) – least reliable indicator for UTI
VCUG (voiding cystourethrogram)
• For high-risk patients
Sensitivity and Specificity of Components of Urinalysis
• Reference standard for identifying vesicoureteral reflex (VUR)
Test Sensitivity Specificity
• Provides information on the bladder and urethra
WBC Esterase 83% 78%
Nitrite Test 53% 98%
WBC Esterase and Nitrite 93% 72%
Microscopy: WBC >5/hpf 73% 81%
Microscopy: Bacteria 81% 83%
WBC Esterase, Nitrite, 99.8% 70%
Microscopy positive

Diagnosis Based on Urine Culture: gold standard*

• Freshly voided urine sample: >100,000 CFU/mL of a single
(gram-negative) bacterial species
• Catheter specimen: >10,000 CFU/mL
• Suprapubic aspiration: any bacterial growth Figure 538-5 (left) Dimercaptosuccinic acid renal scan showing bilateral
photopenic areas indicating acute pyelonephritis and renal scarring. LPO, left
• If the culture shows >50,000 colonies of a single pathogen posterior oblique; RPO, right posterior oblique.
(suprapubic / catheter sample), or if there are 10,000 colonies and
the child is symptomatic, the child is considered to have UTI Figure 538-6 (right) Intrarenal reflux. Voiding cystourethrogram in an infant boy
with a past history of a urinary tract infection. Note the right vesicoureteral
• In a bag sample (wee bag), if the urinalysis result is positive, the
reflux with ureteral dilation, with opacification of the renal parenchyma
patient is symptomatic, and there is a single organism cultured with a
representing intrarenal reflux.
colony count >100,000, there is a presumed UTI.

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Controversies Surrounding Renal Imaging Sensitivity Specificity Cut-Off

• Children with VUR have 1.5x damage seen in DMSA Procalcitonin 71% 72% 0.5 ng/mL
• Half of children without VUR also have changes CRP 87% 41% 20 mg/L
• Systematic review of 13 studies showed that DMSA is a poor WBC 63% 55% 15,000/mm3
predictor of dilating VUR Even if they are said to be indicators of UTI. In reality, they cannot
• VCUG and DMSA scans are associated with significant radiation differentiate Upper from Lower unless coupled with a positive DMSA
exposure
• Lower Urinary Tract Infection: urethra, urinary bladder
Top to Bottom vs. Retrograde Studies First 9 Considered as uncomplicated infection
• National Institute of Health and Care Excellence (NICE) • Upper Urinary Tract Infection: ureter, kidneys
9 Uncomplicated first UTI of children >6 months require no 9 Considered as complicated infection
investigation
• AAP and ISPN Guidelines UTI: Treatment
9 All infants 2 -24 months with febrile UTIs should undergo • Risk of kidney damage on DMSA scan 6 -12 months after UTI
ultrasound shows no significant difference between oral antibiotics for 10-14
• All guidelines do not recommend routine VCUG & DMSA unless: days vs IV meds for 3-4 days followed by oral antibiotics vs IV
9 Ultrasound is abnormal antibiotics for 7-14 days. (Not included in the study are 1-3 months
9 Child is seriously ill old neonates)
9 Fails to respond rapidly to antibiotics • Majority of children may be treated with oral antibiotics or short
9 Recurrent infection course IV antibiotics followed by oral antibiotics

Continuous Antibiotic as Prophylaxis

• RCT’s found no difference in the efficacy of antibiotics in
preventing UTI between children with and without VUR or between
mild and severe VUR

Which Antibiotics to Use? Depends on the Organism

• on the basis of resistance patterns:
9 >50% are resistant to ampicillin
st
• Retrograde: start with VCUG first 9 30% resistant to trimethoprim and 1 gen cephalosporins
rd
9 If (+) Reflux: DMSA 9 Amoxicillin-clavulanate and to 3 gen cephalosporins are also
9 If Normal: No work up increasing due to ESBL producing E. coli
9 If (+) Hydronephrosis: MAG-3 Lasix, Renogram (MR Urogram) • Identify organism but while waiting for the result, give empirical
• Top to Bottom: Starts from a renal scan (DMSA) proceed to other treatment based on most common pathogen for the age group.
investigation depending on the result of the scan:
9 If (+) Cortical defect (pyelonephritis): proceed to VCUG Other Therapies
9 If normal: no work up done; If recurrent febrile UTI: do VCUG • Cranberry
9 If (+) Central photopenia (hydronephrosis): do sonogram 9 Inhibits the P fimbriae of E. coli preventing it from adhering to
uroepithelial cells → E. coli can be easily flushed out
Localization of UTI • Probiotics
• Standard for acute pyelonephritis is acute parenchymal damage 9 In vitro studies show bactericidal effects
on DMSA scan 9 RCTs: no significant data that proves its advantages
• Increased levels of: Procalcitonin, CRP, WBC • Vaccines
• Metanalysis of 18 studies of children with febrile UTI: 9 In adults: immunostimulants are beneficial
9 61% positive for DMSA 9 In pediatrics: no study to support
9 increase level of Procalcitonin, CRP, WBC count

Table 538-3 Guideline Recommendations for Diagnostic Evaluation Following a Febrile Urinary Tract Infection in Infants
GUIDELINE ULTRASONOGRAPHY VCUG LATE DMSA SCAN
National Institute for Health and (see Table 538-4)
Care Excellence (NICE)*
American Academy of Pediatrics Yes If abnormal ultrasonogram No
Italian Society for Paediatric Yes If abnormal ultrasonogram or if risk If abnormal ultrasonogram or VUR
Nephrology (ISPN) factors are present†
* Upper urinary tract dilation on ultrasonography, poor urinary flow, infection with organism other than E. coli, or family history of vesicoureteral reflux.
† Abnormal antenatal ultrasonogram of fetal urinary tract, family history of reflux, septicemia, renal failure, age younger than 6 mo in a male infant, likely family
noncompliance, incomplete bladder emptying, no clinical response to appropriate antibiotic therapy within 72 hr, or infection with organism other than E. coli.

Table 538-3 Guideline Recommendations for Diagnostic Evaluation Following a Febrile Urinary Tract Infection in Infants
Type of Infection
CHILD AGE AND TESTS RESPONDS WELL TO TX WITHIN 48 HR ATYPICAL INFECTION RECURRENT INFECTION
CHILDREN YOUNGER THAN 6 MO OLD
Ultrasound scan during acute infection No Yes Yes
Ultrasound scan within 6 wk of infection Yes No No
DMSA scan 4-6 mo after acute infection No Yes Yes
Micturating cystograms Consider if ultrasound scan abnormal Yes Yes
CHILDREN 6 MO-3 YR OLD
Ultrasound scan during acute infection No Yes No
Ultrasound scan within 6 wk of infection No No Yes
DMSA scan 4-6 mo after acute infection No Yes Yes
Micturating cystograms No Not routine, consider if dilation on ultrasound, poor urine flow, non–E. coli
infection, or family history of vesicoureteric reflux
CHILDREN OLDER THAN AGE 3 YR
Ultrasound scan during acute infection No Yes No
Ultrasound scan within 6 wk of infection No No Yes
DMSA scan 4-6 mo after acute infection No Yes Yes
Micturating cystograms No No No

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V. ISOLATED GLOMERULAR DISEASES WITH • Prophylactic antibiotics and tonsillectomy have no proven benefit.
• Renal transplantation (no absolute cure) or dialysis
RECURRENT HEMATURIA {📖 510} • Allograft loss caused by IgA nephropathy in 15-30% of patients
1. IgA Nephropathy (Berger) {📖 510.1} causes recurrence.
• Most common chronic glomerular disease worldwide
• Benign hematuria without systemic manifestations
2. Alport Syndrome {📖 510.2}
• Characterized by a predominance of IgA within mesangial • Aka hereditary nephritis
deposits of the glomerulus • Genetically heterogeneous disease caused by mutations in the
• Initially presents with significant microscopic hematuria without genes coding for type IV collagen, a major component of
HTN or edema. basement membranes
9 HTN and edema occurs only as disease progresses. • Clinical Manifestations:
• Natural history: 9 Asymptomatic microscopic hematuria
9 Initial and persistent microscopic hematuria, then 9 Single or recurrent episodes of gross hematuria commonly
9 Gross hematuria, then
occurring 1-2 days after an upper respiratory infection (50%)
9 Eventually disappears, with URTI
9 Proteinuria in boys; may be absent, mild, intermittent in girls.
• An immune complex disease caused by abnormalities in IgA 9 Progressive proteinuria
• Familial clustering =? genetic factors
9 Bilateral sensorineural hearing loss
• Genome-wide linkage analysis: 6q22-23
9 Ocular abnormalities: anterior lenticonus (extrusion of the
• Other diseases with prominent IgA mesangial deposition
9 Rheumatic Arthritis (RA)
central portion of the lens into the anterior chamber), macular
9 Ankylosing Spondylitis (AS)
flecks, and corneal erosions.
9 Reiter syndrome (arthritis, urethritis, bilateral conjunctivitis) 9 Leiomyomatosis of the esophagus, tracheobronchial tree, and

9 Hepatic cirrhosis female genitals in association with platelet abnormalities: rare

IgA N: Clinical and Laboratory Manifestations 3. Thin Basement Membrane Disease {📖 510.2}
• Seen more often in male than in female patients. • Presence of persistent microscopic hematuria and isolated
• Westerners present with gross hematuria; Asians (Japan) thinning of the GBM (and, occasionally, tubular basement
present with microscopic hematuria and/or proteinuria membranes) on electron microscopy.
• Other types of Presentation: • Microscopic hematuria is often initially observed during child-
9 Acute Nephritic; Acute Nephrotic; Combined Nephritic- hood and may be intermittent.
Nephrotic syndrome (sig. proteinuria and hematuria) • Episodic gross hematuria can also be present, particularly after a
• Gross hematuria may occur in association with URTI or GI
respiratory illness.
infection, and may be associated with loin pain.
• Benign Familial Hematuria
9 Often occurs within 1-2 days of onset of the infection, in
9 Isolated hematuria in multiple family members without renal
contrast to the longer latency period of PSGN
dysfunction
• IgA nephropathy: Gross hematuria may recur.
9 Although most of these patients will not undergo renal biopsy,
9 PSGN: Gross hematuria does not recur.
it is often presumed that the underlying pathology is TBMD.
• Proteinuria is frequently in the nephritic range (<1000 mg/24hr) in
patients with asymptomatic, microscopic hematuria. • Heterozygous mutations in the COL4A3 and COL4A4 genes,
• Mild to moderate hypertension which encode the α3 and α4 chains of type IV collagen present in
9 Most often seen in patients with nephritic/nephrotic syndrome, the GBM, result in TBMD.
but rarely severe enough to result in hypertensive emergencies • Rare cases of TBMD progress, and such patients develop
• IgA Nephropathy: Normal serum C3 significant proteinuria, hypertension, or renal insufficiency.
9 PSGN: Decreased C3
• Serum IgA have no diagnostic value VI. HSP (Henoch-Schonlein Purpura) NEPHRITIS {📖 515}
9 Only elevated in 15% of patients.
• IgA Nephropathy with systemic manifestations
• Progressive disease develops in 20-30% of children at 15-20 years
• Also referred to as Anaphylactoid Purpura
after onset. • Small vessel vasculitis characterized by a tetrad of*
1. Purpuric rash
IgA N: Prognosis § Palpable purpura, symmetrical, in gravity-dependent areas
Good • Isolated hematuria (lower extremities) or pressure points (buttocks)
• Isolated proteinuria § Greater than macule; >1cm; elevated
Poor • Persistent hypertension § Red, becomes purplish, to yellow-brown, then disappears
• Diminished renal function 2. Arthritis
• Heavy or prolonged proteinuria § Big joints (wrist, elbow, knees, ankle)
• Combination
§ Signs of inflammation (rubor, calor, dolor, tumor, functio laesa)
Worse • Diffuse mesangial proliferation
§ DDx: SLE/ RA/ Septic arthritis/ JRA (small joints, primarily)
(>5-8 mesangial cells affected)
3. Abdominal pain
• Extensive glomerular crescents (also seen in RPGN)
§ Primary peritonitis
• Glomerulosclerosis
§ Can present as an acute abdomen; mistaken for appendicitis
• Tubulointerstitial changes – inflammation, fibrosis
(chronic indicator) 4. Glomerulonephritis

IgA N: Treatment – No Drug of Choice HSP Nephritis and IgA Nephropathy have identical findings,
• Proper BP control
except that systemic findings are only found in HSP.
• Fish oil – with anti-inflammatory omega-3 FA
9 Decrease rate of renal progression HSP N: Pathogenesis
• Immunosuppressive therapy with corticosteroids or more • Remains unknown
intensive multidrug regimens (i.e. cyclophosphamide) may be • Appear to be mediated by the formation of immune complexes
beneficial in some patients containing polymeric IgA1 within capillaries of the skin, intestines,
• ACEI and ARBS and glomerulus
9 Still under study concerning reduction of proteinuria and
retarding renal progression

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HSP N: Diagnosis RVT: Clinical Manifestations

• Non-specific: based on clinical findings
9 Gross hematuria: 20-30%
9 Isolated microscopic hematuria
9 Hematuria and proteinuria
9 Acute nephritic signs and symptoms
9 Nephrotic signs and symptoms
9 Renal insufficiency
• Specific
9 Renal manifestations occurring up to *12 weeks after initial
presentation
Ureteritis
• Uncommon urologic manifestation RVT: Diagnosis
• Associated with loin pain and renal colic
• Usually seen in children <5 years
• Frequently leads to ureteral stenosis and strictures, causing
hydronephrosis that requires surgical correction
HSP N: Treatment
• There are no controlled data demonstrating that steroids, cytotoxic
agents, or anticoagulants alter the course of HSP nephritis.
• Uncontrolled studies suggest:
9 Potential value of high-dose steroids, tacrolimus, cytotoxic
therapy (cyclophosphamide, azathioprine) in patients with
crescentic GN or significant proteinuria. RVT: Differential Diagnosis
9 Additional dipyridamole and/or heparin/warfarin may provide
added benefit.
HSP N: Prognosis
• Generally favorable
• Signs & symptoms may continue for several months, especially GN
• Risk of chronic renal insufficiency is 2-5%
• Presentation with isolated microscopic hematuria alone carries
the best prognosis
• Acute nephritic syndrome and Nephrotic syndrome carries the
highest risk of developing chronic renal failure.
• The development of RVT is classically heralded by:
9 Sudden onset of gross hematuria
9 Unilateral or bilateral flank masses
• However, patients can also present with any combination of:
9 Microscopic hematuria
9 Flank pain
9 Hypertension
9 Microangiopathic hemolytic anemia with thrombocytopenia
9 Oliguria
• RVT is usually unilateral
9 Bilateral RVT results in acute renal failure
• Suggested by the development of hematuria and flank masses in
patients seen in the high-risk clinical settings or with the
predisposing clinical features noted above.
• CBC: microangiopathic hemolytic anemia, thrombocytopenia
• Ultrasonography: marked renal enlargement
• Radionuclide studies: reveal little or no renal function in the
affected kidney(s)
• Doppler flow studies of IVC and renal vein confirm the diagnosis.
• Contrast studies: should be avoided to minimize the risk of
further vascular damage.
• Includes other causes of hematuria that are associated with rapid
development of microangiopathic hemolytic anemia or
enlargement of the kidney(s).
9 Hemolytic uremic syndrome
9 Hydronephrosis
9 Polycystic kidney disease
9 Wilms tumor
9 Renal abscess
9 Hematoma
• All patients should be evaluated for congenital and acquired
hypercoagulable states.

VII. RENAL VENOUS THROMBOSIS {📖 519.7} RVT: Treatment

RVT: Epidemiology
Renal vein thrombosis (RVT) occurs in 2 distinct clinical settings:
1. In newborns and infants*, RVT is commonly associated with:
9 Asphyxia
9 Dehydration
9 Shock
9 Sepsis
9 Congenital hypercoagulable states
9 Maternal diabetes
2. In older children*, RVT is seen in patients with:
9 Nephrotic syndrome
9 Cyanotic heart disease
9 Inherited hypercoagulable states
9 Sepsis
9 Following kidney transplantation
9 Following exposure to angiographic contrast agents
RVT: Pathogenesis
• RVT begins in the intrarenal venous circulation and can then
extend to the main renal vein and even the inferior vena cava.
• Thrombus formation is mediated by endothelial cell injury
resulting from hypoxia, endotoxin, or contrast media.
• Other contributing factors include:
9 Hypercoagulability
§ Nephrotic syndrome, factor V Leiden deficiency
9 Hypovolemia and decreased venous blood flow
§ Septic shock, dehydration, nephrotic syndrome
9 Intravascular sludging
§ Polycythemia
• Aggressive supportive intensive care
9 Correction of fluid and electrolyte imbalance
9 Treatment of renal insufficiency
• Anticoagulation or thrombolysis remain controversial
9 Streptokinase
9 Urokinase
9 Recombinant t-PA
9 Difficult in patients with sepsis and deranged coagulation
• Surgical thrombectomy – indicated for thrombosis of the IVC
• Nephrectomy – for children with severe hypertension secondary
to RVT who are refractory to antihypertensive medications
RVT: Prognosis
• Perinatal mortality from RVT has decreased significantly due to
intensive support.
• Partial or complete renal atrophy is a common sequela of RVT in
the neonate, leading to an increased risk of renal insufficiency,
renal tubular dysfunction, and systemic hypertension.
• These complications are also seen in older children.
• However, recovery of renal function is common in older children
with RVT resulting from nephrotic syndrome or cyanotic heart
disease with correction of the underlying etiology.
• RVT during neonatal period requires follow-up for life because of
early onset hypertension.

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VIII. WILMS TUMOR/NEPHROBLASTOMA {📖 499} WT: Treatment

• Surgery
• Complex mixed embryonal neoplasm of the kidney
• Patency of the IVC should be established prior to resection
• Composed of 3 elements:
• If IVC not patent: chemotherapy should be administered
9 Blastema
9 Epithelia
9 Stroma
Chemotherapy Guidelines
S1, S2 with favorable • Vincristine
• 8 cases/million children <15 years of age
histology • Dactinomycin
• Peak: 2-5 years of age S3 with • Radiation in tumor
• Second most common malignant abdominal tumor in childhood favorable histology bed
• May arise in one or both kidneys • Radiation to sites of
9 One side may be bigger than the other
S4 with
• Vincristine known disease,
favorable histology
• The incidence of a bilateral Wilms is 7%. • Dactinomycin particularly the lungs
• May be associated with the following: • Doxorubicin • Surgical resection
9 Hemihypertrophy – one side is bigger, very obvious S4 with may be considered,
9 Aniridia – absence of iris, unilateral or bilateral tumor in the liver as opposed to
radiation
9 Other congenital anomalies, usually of GUT
Genitourinary Anomalies – most commonly associated S4, resistant tumors
• Consider surgical resection and alternate or
with chemo or
§ Hypoplasia (small kidney, few glomeruli) investigational chemotherapy and alternate or
radiation failure;
§ Fusion (horseshoe kidney) investigational chemotherapy
recurring tumors
§ Ectopia (not in renal fossa), 2 kidneys on the same side
• Radiation to tumor
§ Duplication of the collecting systems (hydronephrosis at • Vincristine bed and sites of
the upper portion of the system) Unfavorable • Dactinomycin established
§ Hypospadias histology • Doxorubicin metastasis
ª Mild: meatus displaced at apex • Cyclophosphamide • More aggressive
ª Moderate: at the middle treatment
ª Severe: at the perianal area
• Chemotherapy is administered
§ Cryptorchidism Wilms tumor
• Diagnosis established by percutaneous needle
9 Variety of syndromes
not operable
biopsy
§ WAGR syndrome
§ Denys-Drash syndrome • Chemo identical to
§ Beckwith-Wiedemann syndrome
Bilateral Wilms that employed in • Surgical extirpation
tumor inoperable tumors after chemotherapy
§ Pearlman syndrome
utilized
§ Sotos syndrome
§ Neurofibromatosis (von Recklinghausen disease)
§ von Willebrand disease
Chemotherapy Guidelines
• Chemotherapy is administered for all Wilms tumors that appear
• Majority are sporadic - 1-2% are familial, AD
• Familial cases are associated with diagnosis at an earlier age inoperable.
• Diagnosis is established by percutaneous needle biopsy.
• Increased frequency of bilateral disease
• Chemotherapy for bilateral Wilms tumor is identical to that
• Congenital absences are usually absent
• Not associated with Wilms tumor gene (WT1) employed for inoperable tumors and is utilized to render the tumor
amenable to surgical extirpation.
WT: Clinical Manifestations
Table 499-4 Staging of Wilms Tumor
• Abdominal mass - approached as malignant mass Stage I Tumor confined to the kidney and completely resected.
9 Smooth, firm Renal capsule or sinus vessels not involved. Tumor not
9 Occasionally cross the midline ruptured or biopsied. Regional LN examined and negative.
• Abdominal pain, vomiting Stage II Tumor extends beyond the kidney but is completely resected
• Hematuria with negative margins and lymph nodes. At least 1 of the
following has occurred: (a) penetration of renal capsule,
• Hypertension
(b) invasion of renal sinus vessels.
Histology Stage III Residual tumor present following surgery confined to the
Favorable Unfavorable abdomen, including gross or microscopic tumor; spillage
of tumor preoperatively or intraoperatively; biopsy prior to
• Conventional form • Markedly large nuclei
nephrectomy, regional LN metastases; tumor implants on
characterized by blastema, • Hyperchromatism and multipolar the peritoneal surface; extension of tumor thrombus into
epithelia, stromal elements figures of nuclei the IVC including thoracic vena cava and heart.
• Devoid of ectopia, anaplasia • Areas of anaplasia may be focal Stage IV Hematogenous metastases (lung, liver, bone, brain, etc.) or
or diffuse; predict higher rates of LN metastases outside the abdominopelvic region.
tumor relapse and death Stage V Bilateral renal involvement by tumor.
• Clear cell sarcoma is a subtype
of the unfavorable form and WT: Prognostic Factor
usually metastasizes to the bone
• Major prognostic factors are tumor size, stage and histology
• Prognosis is worse with:
WT: Diagnosis
9 Large tumor (>500 g)
• Abdominal mass: urgent nature of the condition
9 Advanced stage (S3, S4)
• Complete PE, CBC
9 Unfavorable histological type
• Liver and Kidney FT’s
• Wilms tumor constitutes a paradigm of successful multidisciplinary
• Specific tumor markers
treatment; >60% of patients with all stages generally survive.
• Flat plate of the abdomen
• Stages I-III have a cure rate varying from 88-98%.
• Ultrasonography: often used
• CT/MRI
• Chest X-ray: detection of metastasis, useful for pre-op

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IX. READING ASSIGNMENTS SLE GN: Treatment

• Pediatric specialist required
1. SLE Nephritis {📖 514} • Immunosuppressive tx → establish clinical & serologic remission
• Characterized by: 9 Normalization of anti-DNA, C3 and C4 levels

9 Fever, weight loss, rash, hematologic abnormalities, arthritis,

• Initial: Prednisone (1-2 mg/kg/day) in 2-3 divided doses
9 Tapered over 4-6 months, 4-6 week after remission
and involvement in the heart, lungs CNS and kidneys
• Majority are adolescent females • More severe forms (III, IV) – 6 months IV Cyclophosphamide at
500 -1000 mg/m2
9 Followed by every 3 months for 18 months
WHO Classification
• Class I, II – steroid sparing agent Azathioprine (1.5-2.0 mg/kg OD)
Class I Nephritis No histologic abnormality
Class II Nephritis Glomeruli with mesangial deposits • Mild – Mycophenolate mofetil
(mesangial lupus nephritis) with Ig & Complement • Refractory Class IV – Rituximab, a chimeric monoclonal Ab
Class IIA Mild mesangial hypercellularity specific for human CD20
Class IIB Moderate mesangial hypercellularity
and ↑ matrix SLE GN: Prognosis
Class III Nephritis Almost all glomeruli • Aggressive immunotherapy → improved prognosis
(focal segmental lupus GN) • Mesangial deposits • Renal survival without dialysis in 80% after 10 years
• Subendothelial deposits between • Highest risk for ESRD – diffuse proliferative class IV
endothelial cells and glomerular • Risks of treatment
basement membrane 9 Chronic immunosuppressive treatment
Occasional 9 Chronic steroid treatment: osteoporosis, obesity, HPN, DN
• Capillary wall necrosis, crescent
9 Cyclophosphamide (>20g): high risk of malignancy of infertility
formation, and sclerosis
Class IV Nephritis All glomeruli
(diffuse proliferative lupus • Significant mesangial deposits 2. Hemolytic Uremic Syndrome {📖 518}
nephritis) • Subendothelial deposits of Ig • Most common cause of acute RF in young children
most common and most and complement • Classic triad
severe • Mesangial proliferation 9 Microangiopathic hemolytic anemia
Frequently 9 Thrombocytopenia
• Capillary walls thickened,
9 Uremia
secondary to subendothelial
• Features common to TTP except latter (TTP) tends to occur in
deposits (wire loop lesion) often
necrosis, crescent formation, and young adult women as relapsing illness with fever, serious CNS
scarring involvement and thrombocytopenia
Class V Nephritis Resembles idiopathic membranous
(membranous lupus nephritis) glomerulopathy, except for presence HUS: Etiology
least common of mild to moderate mesangial Typical HUS • Acute enteritis with diarrhea caused by Shiga-like
proliferation (post-diarrheal) verotoxin-producing E. coli O157:H7 – 80%
• Shigella and less commonly:
SLE GN: Pathology 9 Salmonella, campylobacter, Streptococcus
pneumonia, Bartonella
• Clinical manifestations are mediated by immune complexes
9 Coxsackie, echovirus, influenza, varicella,
• Aberrations in both B- and T-cell function
HIV, EBV
• WHO classification based on light microscopy +
Atypical HUS • UTI due to Shiga toxin-producing E. Coli
immunofluorescence + electron microscopy features • Post-infectious outside GIT (Strep pneumoniae)
9 Transformation from one class to another is common
• Oral contraceptives, mitomycine or cyclosporine,
9 Likely to occur in inadequately treated patients ganciclovir, crack cocaine, quinine
• Exposure to pyran copolymer
SLE GN: Clinical Manifestations • Familial occurrence – no diarrhea, autosomal
• Clinical evidence in 30 -70% of children recessive or autosomal dominant
9 Kidney disease is one of the most common features of SLE in 9 Mutation in complement component H
childhood, may even be the only one 9 Complete deficiency of von Willebrand factor
• Milder forms (all class II, some class III) metalloprotease and membrane cofactor
9 Hematuria
protein
• Rare association:
9 Normal renal function
9 SLE, malignant hypertension, preeclampsia,
9 Proteinuria of <1 g/24h
post-partum renal failure, radiation nephritis
• Some class II, all class IV
9 Hematuria and proteinuria
HUS: Pathology
9 Reduced renal function
9 Nephrotic syndrome • Initial glomerular changes due to subendothelial and mesangial
9 Acute renal failure deposition of granular, amorphous, material of unknown origin
• Class IV can rarely have normal urinalysis 9 Thickening of capillary walls
• Class V: Nephrotic Syndrome 9 Narrowing of capillary lumens
9 Widening of mesangium
SLE GN: Diagnosis • Fibrin thrombi in glomerular capillaries/ arterioles → cortical
necrosis
• Circulating ANAs – suggestive
• Severe – partial or total sclerosis, ischemia, concentric intimal
• Ab to native dsDNA – confirmatory
proliferation → vascular occlusion
• C3, C4 depressed
• Renal biopsy if no clear correlation between clinical manifestations
HUS: Pathogenesis
and severity of renal involvement
• Results guide immunosuppressive treatment • Endothelial cell injury
• Localized clotting in the kidney capillaries/ arterioles
9 DIC is unusual; Low C3 in non-diarrheal forms
• RBC damage → Microangiopathic anemia
• Intrarenal and diffuse microvascular platelet adhesion/ damage →
Thrombocytopenia

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HUS: Clinical Manifestations
• Most common in children <4 years old
• Onset usually preceded by gastroenteritis characterized by
fever, vomiting, abdominal pain, and diarrhea (watery → bloody)
9 Less common: URTI
• 5-10 days later: sudden onset of pallor, irritability, weakness,
lethargy, oliguria
• PE: dehydration, edema, petechiae, hepatosplenomegaly, and
marked irritability
HUS: Diagnosis and Differentials
• Clinical findings – always consider HUS in pediatric ARF
• Differentials:
9 SLE and malignant hypertension
9 Bilateral RVT (differentiate by Doppler)
Complete Blood Count (CBC)
• Hgb: 5-9 g/dL; ↑ plasma Hgb, ↓ plasma haptoglobin
• PBS: helmet cells, burr cells, fragmented RBCs
• Reticulocyte: moderately elevated
• (-) Coombs test
• Significant leukocytosis: usually > 3-,000/ mm3
• Thrombocytopenia (90%): 20,000 100,000/ mm3
• Normal PTT and PT (no vitamin K deficiency)
Acute Renal Injury
• Varies: mild RI to acute oliguric or anuric RF requiring dialysis
9 Elevated creatinine level
• Urinalysis: surprisingly mild
9 Low-grade microscopic hematuria and proteinuria
Imaging
• Barium contrast studies:
9 colonic spasms, transient early filling defects
• Radio: colitis “thumb-printing”
Case Classification (CDC)
• Confirmed
9 Acute illness diagnosis as HUS or TTP meeting lab criteria with
history of acute or bloody diarrhea in past 3 weeks
• Probable
9 Meeting laboratory criteria with no clear history of acute or
bloody diarrhea in past 3 weeks or
9 Onset within 3 weeks after acute or bloody diarrhea and meets
the laboratory criteria except that microangiopathic changes
are not confirmed
HUS: Complications
• Anemia, acidosis, hyperkalemia, fluid overload, HF, HTN, uremia
• Extra-renal (life-threatening)
9 CNS: irritability, seizures, infarcts of BG and CC, cortical
blindness, coma
9 GIT: Ischemic or inflammatory colitis, intestinal perforation,
intussusception and hepatitis
9 Pancreas: Focal necrosis → acute pancreatitis, glucose
intolerance, insulin – dependent DM, High lipase
9 Heart: Pericarditis, myocardial dysfunction, arrhythmias
9 Other: Skin necrosis, parotitis, adrenal dysfunction,
rhabdomyolysis
HUS: Prognosis and Treatment
• Supportive care
9 Fluid and electrolytes: Aggressive nutrition
9 Control Hypertension: Early dialysis
• Avoid antibiotics (Higher HUS risk)
• Anti-thrombotic treatment, Plasmapheresis: no proven benefit
• Diarrheal – 90% survive: 12% ESRD or death
• Worst Prognosis:
9 CNS symptoms
9 WBC: >20,000, ischemic colitis, hypertension
• Transplant does not guarantee no recurrence
• F-U required: some complications manifest 20 years later
3. Tubulointerstitial Nephritis {📖 532}
• Characterized by tubulointerstitial inflammation and damage with
relative sparing of glomeruli and vessels
• Acute and chronic forms; Primary or Systemic/Secondary
3.1 Acute TIN
• Hallmarks: lymphocytic infiltration of tubulointerstitium, tubular
edema, varying degrees of tubular damage
• Eosinophils (drug -induced), granulomas T cell-mediated immune
mechanism, unknown pathology
A-TIN: Clinical Manifestations
• Classic: Fever, Rash, arthralgia + increased serum creatinine
9 Rash: vary from maculopapular to urticarial, often transient
• Non-specific: nausea, vomiting, fatigue, weight loss,
flank pain (2° to stretched renal capsule); 30-40% non-oliguric
• Microscopic hematuria: Significant Hematuria or Proteinuria is
uncommon – except with NSAIDs
• Urinalysis: WBC casts, granular / hyaline casts, no RBC casts
• Eosinophils - not sensitive or specific
A-TIN: Diagnosis
• Clinical and laboratory
• Careful history of timing especially with respect to drug exposure
(usually 1-2 weeks after)
• RUS: not diagnostic but may see echogenic, enlarged kidneys
• Removal of an agent with improvement: highly suggestive
• Severe, rapidly deteriorating – do biopsy – establishes Dx
A-TIN: Treatment and Prognosis
• Supportive, address complications of ARF
9 Hyperkalemia or volume overload
• Corticosteroids
• Best prognosis: rapid improvement without treatment
• Guarded prognosis: prolonged renal insufficiency
3.2 Chronic TIN
• In children, commonly due to underlying congenital renal disease:
obstructive uropathy or vesicoureteral reflux or antimicrobials
• Idiopathic: more common in adults
• Seen in all forms of progressive renal disease
• Severity is most important factor in progression to ESRD
Undefined pathophysiology, maybe immune mediated
JN-MCKD Complex
• Group of inherited cystic renal diseases that share common
histologic phenotype of chronic TIN
• Juvenile Nephrophthisis (JN)
9 Rare; AR (however, in Europe cause 10-2% of ESRD)
9 Polyuria, growth failure, “unexplained” anemia and CRF in late
childhood or adolescence
9 Variants
§ Senior-Loken syndrome (retinitis pigmentosa)
§ Joubert syndrome
§ Oculomotor apraxia type Cogan
• Medullary Cystic Kidney Disease (MCKD)
9 AD; typically presents in adulthood
Tubulointerstitial Nephritis with Uveitis
• Rare autoimmune syndrome
• Chronic TIN + anterior uveitis + bone marrow granulomas
• Usually adolescent females
C-TIN: Pathology
• Grossly: Kidneys – pale and small for age
• Micro: tubular atrophy and “drop out” with interstitial fibrosis and a
patchy lymphocytic interstitial inflammation
• JN: characteristic small cysts in corticomedullary region
• Primary CTIN: glomeruli relatively spared until late disease
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C-TIN: Clinical Manifestations 6. Henoch-Schonlein Purpura Nephritis may manifest after the
• Often non-specific, may have s/sx of chronic renal insufficiency diagnosis of HSP as late as:
• Fatigue, growth failure, polyuria, polydipsia, and enuresis A. 2 weeks C. 8 weeks
• Anemia is common (JN) B. 4 weeks D. 12 weeks
• Significant hypertension: tubular damage = salt wasting 7. A 7-month-old male infant with generalized edema is being worked up
for nephrotic syndrome. Since a 24-hour urine collection is difficult to
C-TIN: Diagnosis do in this age group, you would request for the following instead:
• Signs and Symptoms of renal tubular damage: polyuria, A. Urine dipstick test for albumin C. Urine protein/creatinine ratio
increase creatinine + history suggesting chronic disease (long - B. Urine albumin/calcium ratio D. Urine protein chromatography
standing enuresis or anemia)
8. 5 days PTC, a 6-year-old male had facial edema, distention of the
• RUS: evidence of chronicity, corticomedullary cysts (JN) or
abdomen and edema of lower ext. This was associated with tea-
obstructive uropathy
colored urine, oliguria, headache, and vomiting. On further history, it
9 Vesicocystourethrogram: VUR or bladder abnormality
was noted that he sustained a wound at the left foot that became
• JN: molecular diagnosis
infected 14 days PTC. Urinalysis showed significant hematuria and
• Unclear: do biopsy if not too advanced proteinuria with a low C3 and +ASO titer. Start with:
A. Penicillin C. Digoxin
C-TIN: Treatment and Prognosis B. Prednisone D. Omeprazole
• Fluids and electrolytes; Avoid nephrotoxic agents
• Obstructive uropathy: salt supplement, K+ binding resin 9. What is the latent period on the case on #8?
(Kayexalate → watch out for arrhythmia) A. 7 days C. 11 days
B. 9 days D. 14 days
• Antibiotic prophylaxis
• Variable prognosis, ~ESRD (*JN) 10. For the treatment of Nephrotic syndrome, what is the duration of the
9 Patients with obstructive uropathy or vesicoureteral reflux can 2
initial dose of 60 mg/m /day of prednisone?
have a variable degree of renal damage and thus a variable A. 6 weeks (proposed answer) C. 10 weeks (answer key)
course. ESRD can develop over months to years. Patients with B. 8 weeks D. 12 weeks
JN uniformly progress to ESRD by adolescence. 11. Other than treating UTI in children with appropriate antibiotics, which of
the following is an important part of history which, if present, will need
X. COMPILED SAMPLEX to be addressed?
A. Bladder and bowel dysfunction of the child
Shifting – Identification / Enumeration: B. Dietary and fluid intake
1. Serologic test to assess previous streptococcal infection? C. Past illnesses
9 ASO titer, Neuraminidase test, DNAse test D. Environmental and sanitation conditions
2. Initial imaging procedure for recurrent UTI?
9 KUB ultrasound 12. A 7-year-old male was complaining of dysuria. The patient also had a
3. DOC in IGA Nephropathy? history of a recent cough and colds but no fever. He had gross
9 None; there is no DOC for IGA Nephropathy hematuria a day prior to consult characterized as bright red urine
4. Manifestations of HSP Nephritis except for purpuric rash? with blood clots. PE and vital signs were normal. Initial consideration:
9 Abdominal pain, Arthritis, Glomerulonephritis A. Glomerulonephritis C. Blood disease
5. Complication of Nephrotic Syndrome? B. Hemorrhagic Cystitis D. Intravascular hemolysis
9 Thrombosis, Hypovolemia, Hyperlipidemia, Infection (peritonitis)
13. Hematuria is likely glomerular in nature if:
6. Etiology of PSGN?
A. It is massive
9 Immune complex formation
B. The color of urine is tea-colored
7. Latent period of PSGN?
C. Urinalysis shows significant hematuria and proteinuria
9 10-14 days
D. Urinalysis has a fixed specific gravity suggesting inability of the
8. When can you give live vaccine in Nephrotic syndrome?
kidneys to dilute or concentrate the urine
9 Can be given 4 weeks after cessation of treatment
9. # of RBC to be considered as Significant Hematuria? 14. The best way to document significant protein in the urine is:
9 >5 RBC/hpf on >2 occasions A. Urine dipstick test for albumin
10. Least reliable indicator for UTI? B. 24-hour urine protein/albumin concentration
9 Pyuria (Pus cells / WBC in the urine) C. Urine protein chromatography
D. Urine protein/creatinine ratio
Compiled Major Exam Questions:
1. This renal malformation is associated with Wilms tumor? 15. The most common clinical presentation of UTI in neonates is ★
A. Duplicating renal collecting system A. Urgency C. Fever
B. Neurogenic bladder B. Flank mass D. Sepsis syndrome
C. Vesicoureteral reflex
16. The following is an important renal imaging study that must be done for
D. Solitary renal cyst
patients diagnosed with UTI:
2. Main pathology leading to manifestations of Nephrotic syndrome A. Plain film of the abdomen C. IVP
A. Hypercholesterolemia B. KUB Ultrasound D. CT Scan
B. Massive glomerular protein loss in the urine
17. The average period between the initial streptococcal infection and the
C. Tubular mal-reabsorption of protein
nephritic signs and symptoms is:
D. Elevated levels of renin and aldosterone
A. 1 week C. 3 weeks (answer key)
3. The clinical findings of abdominal pain, arthritis, and purpuric rash B. 2 weeks (proposed answer) D. 4 weeks
on the lower extremities are suggestive of: 18. A 5-month-old male infant was brought for consult because of high-
A. Membranous GN C. Potter’s syndrome
grade fever for 12 hours duration. The child has been irritable since the
B. SLE Nephritis D. Henoch-Schonlein purpura
start of fever. Urinalysis was suggestive of UTI and you performed a
4. Neonates are at risk for RVT if this condition is present. suprapubic tap with results of Klebsiella sp. with a colony count of
A. Nephrotic Syndrome C. Dehydration 10,000 CFU/mL. What will you do?
B. Cyanotic Heart Disease D. Use of contrast media A. Repeat urinalysis and urine culture since colony count is low
B. Re-assure mother that fever would subside eventually since
5. The following is true of post-infectious glomerulonephritis: culture results are normal
A. Antibiotic treatment given early in streptococcal infections modifies C. Start patient on antibiotics against Klebsiella since urine culture is
the clinical course of PIGN. conclusive of UTI
B. Most viral causes have a long latent period. D. Do other lab test to look for other source of infection
C. A complicated course is anticipated for viral PIGN.
D. The prognosis of acute PSGN is guarded. 📌 No proofreading done. Use at your own risk.

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