Pediatric lecture notes on nephrology

Dipti’s Page 1 of 22
11. Lecture Notes in Pediatric Nephrology1
11.1. Acute Nephritis.
11.2. Acute kidney injury.
11.3. Hematuria.
11.4. Proteinuria.
11.5. Nephrotic Syndrome.
11.5.1. Idiopathic Nephrotic syndrome.
11.5.2. Congenital Nephrotic syndrome.
11.6. Urinary tract infection.
11.7. Chronic kidney disease.
11.8. Peritoneal Dialysis.
11.9. Hemolytic Uremic Syndrome.

11.1. Acute Nephritis.
1. Definition: Disease characterized by sudden onset of:
a) Hematuria.
b) Generalized edema.
c) Hypertension.
d) Oliguria.
e) Acute kidney injury.
2. Etiopathogenesis: Immune complex mediated nephritis: Most common form.
Typically follows infection of throat or skin with certain ‘Nephrogenic strains of
group A Beta hemolytic Streptococci (Pharyngitis or pyoderma)
Common strain-throat serotype 12, skin serotype 12, skin serotype 49.
May occur after infections with other organisms, infective endocarditis, shunt
nephritis.
Acute nephritis may also be seen in small vessel vasculitides (microscopic
polyangiitis, granulomatosis with polyangiitis) pauci-immune
glomerulonephritis, and anti-glomerular basement membrane disease.
Evidence in favor of immune complex disease.
a) Depression of serum complements C3 level.
b) Complement activation is primarily through alternative pathway rather than
classic pathway.
3. Pathology: Morphological features:
1) Kidney appears symmetrically enlarged.
2) By light microscopy.
A. All glomerular are enlarged and pale, relatively bloodless.
B. Glomerular hypercellularity:
a) Diffuse mesangial cell proliferation.
b) Increased mesangial matrix.
c) Crescents and interstitial inflammation may be seen in severe
cases.
3) Immunofluorescent microscopy.
Lumpy dumpy deposits of immunoglobulins and compliment on glomerular
basement membrane and mesangium.
4) Electron microscopy.
Electron dense deposit or humps are seen on epithelial side of GBM.
4. Clinical features:
Age: Rare before 3years of age, common age 5-12 years.
Onset: 1-2 weeks after antecedent streptococcal infection for post streptococcal
nephritis.
Clinical presentation: Six clinical presentation.
1) Asymptomatic: microscopic hematuria.
2) Hematuria: cola cored urine.
3) Anasarca: (Generalized edema)
4) Rapidly progressive glomerulonephritis (RPGN): Acute kidney injury,
oliguria, deranged renal functions.
5) Hypertension presenting as:
a) Hypertensive CHF: Dyspnea, Tachycardia, tachypnoea.

b) Hypertensive encephalopathy: Seizures, Headache.
Nonspecific symptoms: Malaise, Lethargy, abdominal pain, fever.
Resolution: Usually within 6-8 weeks following onset. Urinary abnormalities
especially microscopic hematuria may persist for more than 1 year.
5. Diagnosis:
1) Urine Examination:
a) RBC, RBC casts.
b) Proteinuria: Mild to moderate.
c) Polymorphs can be seen.
2) Blood:
a) Normochromic anemia because of hemodilution and low-grade
hemolysis.
b) C3 level decrease.
3) Throat culture positive for streptococcus suggests carrier stage.
4) Antibody titer to DNA se B antigen (streptozyne test)
5) Biochemical – Elevated blood urea & Sr. creatinine.
6) ECG: Changes of hyperkalemia.
Indication for Biopsy Presence of systemic features: Fever, Rash, Joint pain, heart
diseases.
• Normal levels of C3.
• Mixed nephritic-Nephrotic features.
• Azotemia requiring dialysis (suspected rapidly progressive GN)
Atypical course:
• Persistence of oliguria, hypertension and/or Azotemia beyond 7-10 days.
• Persistence of gross hematuria beyond 3-4 weeks or nephrotic range
proteinuria beyond 2weeks
• Low C3 level beyond 12 weeks.
• Persistent proteinuria beyond 6months persistent microscopic hematuria
beyond 12-18 months.
6. Differential Diagnosis
a) Hematuria:
1) Glomerular disease.
a. IgA Nephropathy.
b. Idiopathic hematuria.
c. Membranous Glomerulopathy.
d. Hemolytic uremic syndrome.
2) Infection (UTI).
a. Bacterial.
b. Tubercular.
c. Viral.
3) Blood.
a. Bleeding disorder.
b. Thrombocytopenia.
c. Renal vein thrombosis.
d. Sickle cell disease.
4) Renal stone.

5) Hypercalciuria.
6) Anatomic Abnormalities.
a. Polycystic kidney.
b. Tumors.
c. Vascular abnormality.
d. Congenital abnormality.
7) Trauma.
8) Exercise.
9) Drug.
b) Edema:
Nephrotic syndrome, Hypoproteinemia, CHF.
7. Complications:
1) Uremia.
2) Hypertensive CHF.
3) Hypertensive encephalopathy.
4) Hyperkalemia.
5) Hyperphosphatemia.
6) Hypokalemia.
7) Acidosis.
8) Seizures.
8. Treatment:
I. General measures:
Diet – Salt restricted, in case of clinical edema, restrict fluid.
II. Daily monitoring of:
 Blood pressure.
 Intake output chart (sply urine output).
 Weight.
 Edema. (Diuretics for management of edema.)
III. Treatment of complications:
a. Renal failure.
b. Hypertension.
c. Acidosis.
d. Hyponatremia.
e. Seizures.
11.2. Acute kidney injury.
1. Treatment of AKI.
There have been various definitions for AKI over the years. The acute dialysis quality
initiative group (ADQI)proposed a definition of AKI for the adults using the RIFILE
criteria. RIFILE is an acronym where each letter means a level of severity of AKI
(R=risk, I=injury, F=failure, E=end stage kidney disease.) This is modified as pediatric
scale or is modified as the pediatric scale or ‘pRIFILE’ scale. The proposed ‘pRIFILE
criteria is based on the decrease in estimated creatinine clearance (eCCI) and the child’s
urine output based on body weight as shown in Table
Classification Estimated creatinine
clearance (Eccl)
Urine output

Risk Decreased by 25% <0.5mL/kg/hr ×8hrs.
Injury Decreased by 50% <0.5mL/kg/hr×16hrs.
Failure Decreased by 75% or Eccl
<35mL/min/1.73m2
<0.5mL/kg/hr×24hrs or
Anuric×12hrs.
Loss Persistent failure >4/52weeks.
End stage renal disease. End stage renal failure (Persistent failure
>3/12months)
Modified Schwartz
formula5
for
Eccl(ml/min/1.73m2
)
Height (cm)×0.413
Serum Creatinine (mg/dL)
Treatment of Acute kidney injury”
I. Assess patient’s volume status
• If hypovolemic rapidly establish euvolemia with 0.9% NS boluses.
• If urine output remains low after euvolemia is established, begin fluid
restriction (insensible loss and urine output)
Impending renal failure – furosemide may be tried but it does not
change the outcome of AKI and may cause toxicity. Mannitol may
be harmful in AKI and low dose dopamine has been shown to be
ineffective in improving kidney function.
II. Renal failure:
a) Fluid restriction.
I.V. fluid quantity: Insensible losses (400mL/m2
/24hy) + Amount of
urine output/day + any additional losses.
Type – Glucose solution – 10to30% without electrolyte, without K+
.
b) Measure to reduce hyperkalemia.
i. Serum K+ >5.5 mEq/L
1) High concentration of IV glucose (10-50%)
2) Resin – Sodium polystyrene sulphonate resin
(Kayexalate)
Dose – 1gm/kg, route orally, rectal enema.
Method – suspended in 70% sorbitol 2ml/kg, repeat
2hrly.
M.O.A. – Resin exchanges Na+ for K+
Sorbitol causes osmotic diarrhea leading to K+
loss.
ii. Serum k+>7mEq/L
1) Calcium gluconate:
a) 10% solution.
b) Dose – 0.5ml/kg.
c) Duration: 10 mins.
d) Route – I.V.
e) Monitor H.R. if fall 20bts/min – stop.
M.O.A. Counteract K+
induced myocardial
irritability.
2) NaHCO3 – 7.5%
a) Dose – 3mEq/kg.
b) Route – I.V.

c) Complication – B.P. increase tetany.
d) M.O.A. – decreases K+
.
3) 50% Glucose + Insulin.
Dose: 1gm/kg glucose with
Insulin 1unit/5gm of glucose.
Route – I.V.
Duration – 1hr.
Precaution – monitor hypoglycemia
M.O.A. – Shifts k+
from extracellular to intracellular.
M.O.A. – (Mechanism of action)
4) ꞵ Adrenergic receptor agonists: Salbutamol Route
aerosol.
5) Dialysis:
i. Indications: - Acidosis, Hyperkalemia, CNS
involvement, increase B.P., fluid overload, CHF.
ii. Types:
1. Hemodialysis.
2. Peritoneal Dialysis.
3. Continuous renal replacement therapy.
2. Acidosis treatment:
a) pH< 7.15 or bicarbonate < 8mEq/L require treatment.
b) Corrected partially by I.V. bicarbonate up to pH 7.2.
c) Side effect: Precipitates tetany (Reduces ionic Ca+2
)
3. Treatment of Hypertension:
A. Fluid and salt restriction
B. Diuretics – Hydrochlorothiazide – 1-2 mg/kg/24hr orally.
Furosemide – 1-6mg/kg/24hr. orally, I.V. 1mg/kg.
C. Antihypertensive Drugs:
i. Propranolol – Vasodilator (1-3mg/kg dose)
ii. Hydralazine – (Vasodilator) – 0.1 – 0.4 mg/kg/dose I.V.
0.25 – 1.0 mg/dose 6-8 hrly orally.
iii. Nifedipine – 0.25 – 0.5 mg/kg/dose.
iv. I.V. diazoxide – 1-3 mg/kg/dose I.V. (max. 150mg)
4. Treatment of Hyponatremia: Fluid restriction.
5. Treatment of Seizures: Treat cause of Seizures:
i. Electrolyte imbalance.
ii. Cerebral edema.
iii. Uremia.
iv. Hypertension.
Treatment: Diazepam 0.3mg/kg/I.V.
Prognosis: The like hood of recovery from AKI depends on the underlying
causes.
AKI may result in full recovery, or incomplete recovery leading to
chronic kidney disease. In severe cases, non-recovery may lead to End stage
disease (ESRD).
Long term follow-up to monitor renal function is recommended.

11.3. Hematuria.
1. Definition: Microscopic hematuria is defined as the presence of at least five RBC per
high power field in freshy voided and centrifuged urine.
2. Causes:
I. Glomerular causes:
1) Isolated renal disease.
a) IgA Nephropathy.
b) Post streptococcal Glomerular Nephritis.
c) Membranous Nephropathy.
d) Membranoproliferative GN.
e) Focal segmental GN.
f) Alport syndrome.
2) Multisystem diseases.
a) SLE Nephritis.
b) Henoch – Schoenlein purpura nephropathy.
c) Polyarthritis nodosa.
d) Good pasture’s syndrome.
e) Sickle cell glomerulopathy.
f) HIV nephropathy.
g) Wegener granulomatosis.
II. Extraglomerular Hematuria:
1) Upper urinary tract:
a) Pyelonephritis.
b) Interstitial nephritis.
c) Acute tubular necrosis.
d) Papillary necrosis.
e) Nephrocalcinosis.
f) Vascular
g) Crystal urea.
h) Hemoglobinopathy.
i) Hydronephrosis.
j) Polycystic kidney disease.
k) Hydronephrosis.
l) Polycystic kidney disease.
m) Tumors – Wilms, Rhabdomyosarcoma, angiomyolipoma.
n) Trauma.
2) Lower urinary tract:
a) Cystitis.
b) Urethritis.
c) Urolithiasis.
d) Trauma.
e) Coagulopathy
f) Heavy exercise.
3. Diagnostic Approach:
I. Glomerulo Hematuria.
Features:

1) Brown color.
2) Significant proteinuria may be present.
3) RBC cast, dysmorphic RBS’s.
Investigations:
a) CBC with differential count.
b) Electrolytes – Na+
, K+
, Ca+2
.
c) BUN/Creatinine.
d) Sr. protein/ albumin.
e) Cholesterol.
f) C3 /C4.
g) ASO/Anti DNASE B
h) Urine protein/Creatinine Ratio.
II. Extra Glomerular Hematuria.
Step I:
Urine culture.
Step II:
a) Urine Ca+2
Creatinine.
b) Ultrasonography.
Step III:
a) Urine analysis.
b) Serum electrolytes.
c) If Crystalluria – Urolithiasis or Nephrocalcinosis, 24-hour urine for Ca+2
,
Creatinine, Uric acid and oxalate.
d) If hydronephrosis:
 Cystogram.
 Renal scan.
 I.V.P.
 Voiding cystourethrogram.
11.4. Proteinuria:
1. Definition: Normal protein secretion in healthy children is 150mg/day or 4mg/m2/hr.
Abnormal protein excretion 4 – 40 mg/m2/hr. Nephrotic Range 40mg/m2/hr.
2. Diagnosis:
Dipstick is reported as:
a) Negative or trace – 10 – 20mg%.
b) 1+ = 30mg%.
c) 2+ = 100mg%
d) 3+ = 300mg%
e) 4+ = 1000 – 2000 mg%
More than 1% is clinically significant.
3. Causes:
1) Transient proteinuria: Fever, Exercise, Dehydration, CHF, Seizures, stress.
2) Postural proteinuria.
3) Glomerular Diseases:
a) Acute Nephritis.

b) Nephrotic syndrome.
c) IgA Nephropathy.
d) Lupus Nephritis.
e) Henoch – Schoenlein purpura Nephritis.
f) Sickle cell Nephropathy.
g) Diabetic Nephropathy.
h) Alport Syndrome.
4) Tubular Diseases:
a) Reflux Nephropathy.
b) Polycystic kidney diseases.
c) Renal dysplasia.
d) Acute tubular necrosis.
e) Galactosemia.
f) Cystinosis.
g) Wilson disease.
h) Heavy metal poisoning.
4. Nephrotic Syndrome.
1. Definition: It is a syndrome characterized by:
1) Heavy proteinuria: >3.5gm/24 hr. in adult and >40gm/m2/hr. in children.
2) Hypoalbuminemia: <2.5 gm%.
3) Edema.
2. Etiology:
1) 90% cases are idiopathic nephrotic syndrome:
Causes
a) Minimal changes disease – 75%.
b) Mesangial proliferation – 5%.
c) Focal segmental glomerulosclerosis – 5to20%
d) Membranous nephropathy 1-2%
e) Membrano-proliferative glomerulonephritis 4-5%.
2) 10% secondary nephrotic syndrome:
a) Systemic diseases: SLE, HSP, Diabetes, Amyloidosis.
b) Leukemia, Lymphoma, Sickle cell disease.
c) Infectious diseases: Hepatitis B, Hepatitis C, HIV, Malaria,
Toxoplasmosis.
d) Drugs: Gold, Penicillamine, Heroin.
3. Pathophysiology:
1) Underlying abnormality in Nephrotic syndrome is increase in
permeability of glomerular capillary wall, which leads to massive
proteinuria and hypoalbuminemia.
2) Causes of increased permeability:
a) In minimal lesion NS T dysfunction leads to alteration of cytokines
which causes loss of negatively charged glycoproteins within the
glomerulo capillary wall.
b) In focal segmental glomerular sclerosis – A plasma factor
produced by lymphocyte may responsible.

3) Mechanism of edema:
a) Urinary protein loss leads to hypoalbuminemia Decrease oncotic
pressure Transudation of fluid in interstitial space.
b) Reduction in intravascular volume and decrease renal perfusion
pressure which:
i. Activate renin angiotensin and aldosterone system increases
tubular reabsorption of Na+.
ii. Also stimulate ADH – increase reabsorption of water.
c) Primary renal avidity for sodium water.
4) Cause of lipid elevation:
a) Hypoalbuminemia stimulates generalized hepatic protein synthesis
including lipoproteins.
b) Lipid catabolism is diminished due to decrease lipoprotein lipase by
increase loss of enzymes in urine.
11.5.3. Idiopathic Nephrotic syndrome.
1) Incidence: - 90% children have idiopathic Nephrotic syndrome.
2) Types: Commen histological types:
A. Minimal changes disease (85%).
B. Mesangial proliferation (5%).
C. Focal segmental glomerulosclerosis (10%).
3) Pathology:
A. Minimal change disease (85%).
a) Glomeruli appear normal.
b) Minimal increase in mesangial cells and matrix.
c) Immunofluorescent microscopy – No abnormality detected.
d) Electron microscopy – Effacement of epithelial cell foot
processes.
B. Mesangial proliferation (5%).
a) Diffuse increase mesangial cells and matrix.
b) Immunofluorescent microscopy reveals trace to 1+ mesangial
IgM and or IgA staining.
c) Electron microscopy:
i. Increase mesangial cells matrix.
ii. Effacement of epithelia cells. Foot process.
C. Focal segmental glomerulosclerosis (10%).
Light microscopy:
a) Mesangial proliferation.
b) Segmental scarring.
Immunofluorescent microscopy: May be normal.
Electron microscopy:
a) Segmental scarring of glomeruli tuft.
b) Obliteration of glomeruli capillary lumen.
Disease progress and ultimately involves all glomeruli.
4) Clinical features: Age 2-6 yrs. (6months to childhood)
i. Sex: - More in males (M:F – 2:1)
ii. Edema (Anasarca):

Initially mild edema around eyes and lower extremities with time it
becomes generalized with development of ascites, pleural effusion and
genital edema.
iii. Anorexia, Irritability, abdominal pain and diarrhea.
iv. Rarely hypertension and hematuria.
5) Diagnosis:
1. Urine exam: Proteinuria exceeds 3.5 gm/24hr in adults, 40mg/m2/he in
children.
2. Random urine protein to creatinine ratio exceeds – 2.
3. Sr. Albumin - <2,5gm%.
4. C3 and C4 normal.
5. Renal biopsy normally not required.
6) Treatment:
1. Diet: Salt restriction when edema present, High protein diet.
2. Drug therapy:
a) Initial episode therapy:
Drug of choice – Prednisolone.
Dose – 60mg/m2
/day given in 2 divided doses.
Or
2mg/kg/day (Max. 80mg)
Duration: 6weeks.
Followed by 40mg /m2
/day or 1.5mg/kg/day on alternate day
for 6weeks.
b) Alternate day medication is given as a single dose in the
mornings. The initial episode is treated with 6weeks daily and
6weeks alternate day steroids as described above.
3. Remission: Urine protein should be negative ore trace for three
consecutive days.
• Relapse: Urinary protein ≥3+ by Dipstick for 3 consecutive
days.
• Frequent relapse: two or more relapses in 6months of initial
response 4 relapses in any 12 months period.
• Steroid dependence: Occurrence of two consecutive relapses
during steroid therapy or within two weeks of its cessation.
• Steroid resistance: Failure to achieve remission after 4weeks
of daily therapy with oral prednisolone at a dose of 2mg
/kg/day.
4. Treatment of relapse: Relapse treated with daily prednisolone
(2mg/kg/day) Until remission i.e. Urine negative for protein for three
consecutive days, followed by alternate day steroids (1.5mg/kg/day)
for 4weeks.
5. Treatment of steroid dependent or frequent relapses.
a) Cyclophosphamide: Along with alternate day prednisolone
therapy.
Dose: 2mg/kg/day.
Duration: 12 weeks.

Side effects: Neutropenia, Hemorrhagic Cystitis, Alopecia,
Sterility, increase risk of future malignancy.
b) Levamisole: 2mg/kg on alternate days for 18-24 months.
Wean steroids to 0.25 to 0.5 mg/kg on alternate day slowly.
Side effects: Common – Leukopenia, Rarely – Liver toxicity,
convulsions and skin rash.
c) Mycophenolate mofetil: Dose 800-1200 mg/m2
in BID dosing
with tapering prednisolone for 12-24 months.
Side effects: Pain, Diarrhea, Leukopenia.
d) Cyclosporine: Dose: 3-5mg/kg/day for 12-24 months; with
weaning dose of steroids.
Side effects: Nephrotoxicity, Hypertension, Hyperkalemia,
hyperlipidemia.
Cosmetic symptoms: Gum hypertrophy, Hirsutism.
7) Complications:
A. Infections: Spontaneous bacterial peritonitis is most common
complication.
Organism: Streptococcus pneumonia. Is common. E. Coli may be
encountered.
B. Thromboembolic Events: Both arterial and venous thrombosis are
seen.
Cause:
a) Increase fibrinogen.
b) Thrombocytosis.
c) Hemoconcentration.
d) Relative immobilization.
e) Decrease fibrinolytic factors.
C. Vitamin D Deficiency Rickets.
D. Prognosis: Majority of patients have Relapses up to 2nd decade of
life but, overall prognosis is good.
11.5.4. Congenital Nephrotic syndrome:
1) Definition: Infants who develop nephrotic syndrome in the first three months
of life.
2) Type: (Finnish type)
a) Autosomal recessive disorder.
b) Caused by mutation in NPHS 2 Gene located on chromosome 19.
This gene encodes protein nephrin.
c) Pathology.
i. Dilation of proximal tubules.
ii. Mesangial hypercellularity.
iii. Glomerular sclerosis.
d) Features:
i. Massive proteinuria.
ii. Large placenta.
iii. Marked edema.
iv. Prematurity.

v. Respiratory Distress.
vi. Separation of cranial sutures.
e) Course – Progressive renal failure with death by the age of 5yrs.
f) Treatment:
i. ACE inhibitor.
ii. Indomethacin.
iii. Unilateral nephrectomy.
iv. Bilateral nephrectomy.
v. Dialysis.
vi. Aggressive nutritional support.
vii. Kidney transplantation.
g) Antenatal Diagnosis:
 Increase amniotic protein α fetoprotein.
 DNA Analysis.
3) Other Causes:
i. Congenital infection:
a) Syphilis, Toxoplasmosis.
b) Rubella, CMV, HIV, Hepatitis B.
ii. Diffuse mesangial sclerosis.
Difference between Acute Nephritis and Acute Nephrotic
syndrome. is as follows:
S.
No.
Acute Nephritis Nephrotic Syndrome
I Definition: Characterized by:
A Hematuria Heavy proteinuria >3.5 gm / day.
B Edema Hypo-albuminemia.
C Hypertension Edema
D Oliguria/Renal failure Hyperlipidemia.
II Etiology
A 90% Post infective, Immune complex
disease.
90% Idiopathic.
III Relapses
A Usually only one attack Relapses common.
IV Pathology
Immune complex deposits on basement
membrane.
Minimal changes, retraction of epithelial foot
processes.
V Clinical features
A Mainly presenting as mild to moderate
edema.
Gross massive edema.
B Hypertension is present. Usually absent.
C Renal failure common. Uncommon.
D Hematuria commonly present No Hematuria.
VI Urine Examination:
A Albumin 1, 2+ proteinuria <2gm% Massive proteinuria (<3.5 gm%) with selective
albuminuria.
B Hematuria (RBC) No RBC
C RBC Cast, granular cast No RBC.
VII Blood Urea

A Raised Usually not raised
VIII Treatment:
A Penicillin/Erythromycin.
Corticosteroid is drug of choice for minimal LNS.B Treatment of Hypertension.
C Treatment of Renal failure.
IX Diet:
Protein restriction High protein diet.
5. Urinary tract infection.
1. Incidence:
Girls – 3-5%
Boy’s 1%
In newborn period it is more commen in males, beyond newborn period more in
females.
2. Predisposing factors:
1) Vesicoureteric reflux, Neurogenic bladder.
2) Obstructive uropathy, Renal calculi.
3) Urinary instrumentation.
4) Female sex, Pregnancy, Sexual activity, malnutrition.
5) Uncircumcised males, Labial adhesions.
6) Children on immunosuppressive therapy.
7) Diabetes.
8) Constipation.
3. Route of infection:
A. During neonatal period:
• Blood stream.
• Urethra.
B. During childhood: Usually from bellow ascending UTI.
4. Etiology:
Mainly caused by Colonic bacteria.
In females – 75 to 90% cases, it is caused by E coli (Escherichia coli) followed by
klebsiella, proteus, and staphylococcusaprophyticus.
Viral – Especially Adenovirus causing cystitis.
5. Pathology:
1) Acute bacterial cystitis:
a. Mucosal congestion, edema, petechiae, hemorrhages.
b. Functional capacity of bladder is decreased.
2) Chronic cystitis: Cystitis cystica.
3) Acute pyelonephritis:
a. Kidney are enlarged.
b. Renal micro abscesses.
4) Chronic pyelonephritis:
a. Renal scar:
Cortical scar with underlying calyceal deformity is diagnostic.
b. Microscopic:
i. Lesions are patchy with Glomerular fibrosis.

ii. Interstitial chronic inflammation and fibrosis.
iii. Atrophy of tubules.
5) Proteus infection can cause stone formation.
6. Clinical features: Three basic forms of UTI.
a. Asymptomatic bacteriuria.
b. Pyelonephritis.
c. Cystitis.
A. Infancy: Fever, weight loss, failure to thrive, nausea, vomiting, acute
diarrhea and Jaundice.
B. Children:
i. PUO.
ii. Urinary frequency.
iii. Painful micturition.
iv. Urinary incontinence.
v. Urinary urgency.
vi. Bed wetting in dry child.
vii. Abdominal pain.
viii. Foul smelling urine.
C. Chronic recurrent cystitis: Day time incontinence.
D. Hemorrhagic cystitis: Hematuria at the end of urination.
E. Acute pyelonephritis:
i. Fever with chills.
ii. Flank pain and tenderness.
iii. Kidney’s enlarge and palpable.
7. Investigations:
I. Urine Examination: Mild stream urine is collected after clearing urethral
meatus with povidone, iodine with rinsing.
a) In females’ labia should be spread manually.
b) In male’s prepuce should be retracted.
c) Urine can also be collected by catheterization or suprapubic aspiration.
d) Urine should be transported immediately to the laboratory to the
laboratory or stored at 4⁰C for 12-14hours.
Result: Uncentrifuged samples of urine suggest infection when:
a. On microscopy: More than 10WBC /Cumm.
b. On Gram’s staining:
c. Positive dipstick test:
d. Centrifuged urine - > 4WBCs/ Cumm Suggest UTI.
II. Urine culture:
a) Colony count ≥105/mL of single organism is Diagnostic of UTI.
b) Colony count ≥ 104
/mL – 105
mL with symptomatic UTI.
III. Computed topography:
IV. Renal cortical 99m Tc DMSA or glucoheptonate scan. It detects cortical
scars.
V. Blood examination: TLC increase, Neutrophilia, increase ESR, C-reactive
proteins. Marked leukocytosis in renal abscess.
VI. Approach to a child with first episode of UTI is shown in table:

Age < 1year 1 – 5Years >5Years.
USG USG & DMSA USG
MCU If abnormal If abnormal
DMSA Scan MCU MCU/DMSA
USG – Ultrasonogram, MCU – Micturating Cystourethrogram, DMSA –
Dimercapto succinic acid.
8. Differential diagnosis:
i. Vulvitis.
ii. Vaginitis.
iii. Eosinic cystitis.
9. Treatment:
1) Send urine culture first.
2) Drug used for cystitis.
a) Trimethoprim – Sulfamethoxazole.
Dose – 8to10mg of trimethoprim for 5-10 days.
b) Nitrofurantoin.
Dose – 5to7 mg/kg/day × 7days not used for febrile UTI.
c) Amoxicillin: Dose 50mg/kg/day. × 7days.
3) Pyelonephritis treatment:
A. Parenteral treatment: Duration depends on depends on severity of illness
and age of patient.
a) Ceftriaxone
Dose 50-75 mg /kg/day.
b) Ampicillin
Dose: 100mg/kg/day.
+
Aminoglycosides (Gentamycin)
Dose: 3-5 mg/kg/day in two divided doses.
B. Oral third generation cephalosporins such as cefixime is also effective
except for pseudomonas.
C. Fluoroquinolones: Ciprofloxacin uses for resistant microorganism especially
for pseudomonas for patient older than 17years.
D. Surgical treatment
 Renal and perirenal abscess.
 Obstructive uropathy.
E. No need for follow up urine culture to document cure.
F. Find out predisposing factors if recurrent UTI then treat.
G. Prophylaxis for recurrent UTI.
a. Sulfamethoxazole + Trimethoprim combination (1/3rd
Dose –
1to2mg/kg/day.)
b. Nitrofurantoin (1to2mg/kg/day)
6. Chronic kidney disease.
1. Definition:
Presence of structural or functional abnormalities of the kidney for ≥ 3months with or
without decreased GFR, manifested by ≥ 1 of the following features:

o Abnormalities in the blood or urine tests.
o Abnormalities in imaging tests.
o Abnormalities on kidney biopsy.
GFR ≤ 60 mL/min/1.73 m2
for ≥ 3months with or without other signs of
kidney damage.
2. Etiology:
1) Causes in younger than 5yrs. Of age.
a. Congenital anomalies – renal hypoplasia, dysplasia.
b. Obstructive uropathies.
2) After 5yrs. Of age.
a. Glomerulonephritis.
b. Inherited disorders – familial juvenile nephrolithiasis, Alport
syndrome.
3) Metabolic disorders.
a. Cystinosis.
b. Hyperoxaluria.
4) Polycystic kidney disease.
3. Pathogenesis:
Progressive renal injury is caused by following mechanisms:
1) Hyperfiltration injury.
2) Persistent proteinuria.
3) Systemic hypertension.
4) Intrarenal hypertension.
5) Renal calcium, phosphorus deposition
6) Hyperlipidemia.
A. Final common pathway is hyperfiltration injury as the populations
of sclerosed nephrons increase, surviving nephrons have increased
excretory burden and ultimately hyperfiltration injury.
B. Proteinuria is other factor causing renal injury by transversing across
glomerular capillary wall and have direct toxic effect causing
glomerular sclerosis.
C. Hyperphosphatemia may increase the progression of disease.
Staging of chronic kidney disease. (Normal GFR – 90 – 120 mL/min/1.73m2
)
a. Stage 1 With normal or high GFR (GFR >90m L / min).
b. Stage 2 Mild CKD (GFR = 60to89 mL/min)
c. Stage 3 A moderate CKD (GFR = 39to59 mL/min).
d. Stage 4 Severe CKD (GFR = 15to29 mL/min).
e. Stage 5 End stage CKD (GFR = 60to89 mL/min)
1) Neonatal period (Congenital disorders)
Presents as failure to thrive, dehydration, UTI, Overt renal insufficiency.
2) Patients with familial juvenile nephropathies:
They present as headache, fatigue, lethargy, anorexia, vomiting, polydipsia,
polyuria, and Growth failure.
3) CRF form of glomerulonephritic origin:

It presents as edema, hypertension, hematuria and proteinuria.
4) Renal osteodystrophy:
Muscle weakness, bone pain, fractures, with minor trauma, rachitic changes.
5) Physical examination:
a. Pallor, Anemia.
b. Sallow appearance of skin.
c. Short stature
d. Renal osteodystrophy.
e. Edema.
f. Hypertension.
5. Lab Diagnosis:
1) BUN increases.
2) Serum creatinine increases.
3) GFR – K × height in cms/serum creatinine (mg%) K = 0,413.
4) Serum K+
increase, Serum Na+2
decrease, Sr. Ca+2
decrease.
5) Acidosis.
6) Hyperphosphatemia.
7) Uric acid increases.
8) Hypoalbuminemia in heavy proteinuria patients.
9) CBC – normochromic, normocytic anemia.
10) Sr. Cholesterol increase, increase triglycerides.
11) Urine examination – Hematuria, Proteinuria, low specific gravity.
6. Treatment: Principles of treatment.
1) Renal replacement therapy dialysis when indicated.
2) Slow progression of disease.
I. Monitoring clinical and laboratory status:
a. Routine testing of HB, Sr. Electrolyte, BUN, Creatinine, Ca++
,
P, Albumin, alkaline phosphate.
b. Periodic assessment of parathyroid hormone. (PTH)
II. Fluid electrolyte management:
a. In renal dysplasia patients require high volume, low calorie
density feedings with sodium supplementation.
b. Patients with edema, hypertension and CHF.
• Sodium restriction.
• Diuretic therapy.
c. K+
Mostly K+
positive balance is maintained but hyperkalemia
may be treated by:
• Restricting K+
intake.
• Oral alkalinizing agent.
• Kayexalate – Resin.
III. Acidosis:
→ Sodium bicarbonate tablet 650mg daily. (1=8mEq bases.)
IV. Nutrition:
a. Restriction of phosphorus, K+
, Na+2
, may be required according
to blood levels.
b. Calorie – Daily requirement as per age.

c. Proteins – 2.5 gm/kg/day. Quality proteins, high biological
values should be given.
Example: - Egg, meat, milk, fish.
d. Vitamin supplementation, water soluble vitamins only.
V. Growth: Recombinant Human growth hormone may be used. Start
with 0.05mg/kg/day S.C. till final height is achieved.
VI. Anemia:
• Erythropoietin:
Dose – 50 – 150mg/kg/dose.
Routes – Subcutaneous.
Erythropoietin should be supplemented with oral and IV iron.
Packed cell transfusion if required may be given.
VII. Renal Osteodystrophy:
o Vitamin D therapy Calcitriol 0.01 – 0.5 mg/kg/day.
o Phosphate binders: Calcium carbonate and calcium acetate.
VIII. Treatment of hypertension: Hypertension with volume overload.
a. Salt restricted diet.
b. Furosemide.
c. ACE inhibitor – Enalapril, Lisinopril.
d. Angiotensin II blockers in diabetic nephropathy – losartan.
e. In resistant cases use following drugs:
a) Calcium channel blockers.
o Nifedipine.
o Amlodipine.
b) Clonidine.
c) ꞵ Blockers – Atenolol.
IX. Immunization: Immunization should be completed.
X. Drug dosage adjustment: Either decrease the dose or increase the
drug interval or both.
XI. Prompt treatment of infection.
XII. Dialysis indications:
a. If GFR < 15ml/min/1.73m2
b. Refractory fluid overload.
c. Electrolyte imbalance.
d. Acidosis.
e. Growth failure.
f. Uremic symptoms.
XIII. Renal transplantation: Indicated in end stage renal disease.
7. Peritoneal Dialysis.
1. Principle:
a) Peritoneal membrane acts as dialyzer.
b) Excess body water is removed by osmotic gradient created by high dextrose
concentration.
c) Metabolic wastes are removed by diffusion from peritoneal capillaries into
dialysate.

2. Methods:
Entry to peritoneal cavity is achieved by surgical inserted tunneled Tenckhoff
catheter.
3. Types:
a) CAPD: Continuous ambulatory peritoneal dialysis.
b) CCPD: Continuous cyclic peritoneal dialysis.
c) IPD: Intermittent peritoneal dialysis.
d) NIPD: Nocturnal Intermittent peritoneal dialysis
4. Advantages:
1) Can be performed at home.
2) Technically easier.
3) Freedom to attend school and after school activities.
4) Less restrictive diet.
5. Disadvantages:
1) Catheter malfunction.
2) Infections.
3) Impaired appetite.
4) Negative body image.
5) More Expensive.
8. Hemolytic Uremic Syndrome
1. Definition:
HUS is characterized by:
a) Microangiopathic hemolytic anemia.
b) Thrombocytopenia.
c) Uremia.
2. Etiology:
a) Acute diarrhea caused by shiga toxin producing Escherichia coli 0157:
H7 precedes the disease.
b) Toxin is absorbed from intestine and initiates endothelial injury.
c) Rarely association with shigella, salmonella, campylobacter, Streptococcus
Pneumonae and Bartonella.
d) Virus: Coxsackie, Echo, Influenza, Varicella, HIV and Epstein bar.
e) It may develop with use of oral contraceptives, mitomycin and cyclosporin.
f) Also reported with SLE, malignant, hypertension, preeclampsia, Post partum
renal failure.
g) Radiation nephritis.
3. Pathology:
Glomeruli:
a) Thickening of capillary wall, narrowing of capillary lumen, widening of
mesangium.
b) Fibrin thrombi are seen in glomerular capillaries.
c) Glomerular sclerosis in severe cases.
Pathogenesis:
i. Primary event
Endothelial cell injury

Localized clotting
1) RBC damaged due to microangiopathy.
2) Intra renal platelet adhesion – Thrombocytopenia.
ii. Decrease thrombomodulin
+
Decrease tissue plasminogen activator.
+
Heparin like molecule
Activate antithrombin III
Prothrombotic state.
iii. Before renal injury following factors are increased:
PAF, tissue plasminogen – activator antigen von Willebrand factor
(vWF) thromboxane A2.
1) Age < 4yrs (usually).
2) Preceding features of GIT infection – fever, vomiting, pain in abdomen,
diarrhea.
3) Pallor, lethargy, irritability.
4) Oliguria, Renal failure.
5) Petechiae.
6) Dehydration, Hepatosplenomegaly.
5. Laboratory findings:
1) HB decrease – 5-9gm%.
2) PBF – Helmet cell, burr cells, Fragmented RBC.
3) Plasma hemoglobin level increased.
4) Plasma haptoglobin decreased.
5) Reticulocyte counts increased.
6) WBC increase 30,000mm3.
7) Platelet decrease – 20,000-1,00,000/mm3.
8) Urine – Microscopic hematuria, proteinuria.
9) PT – normal, PTT – normal.
6. Differential diagnosis:
Bilateral renal vein thrombosis – features.
1) Renal enlargement.
2) Renal Doppler – Ultrasonography revels absence of renal vein flow.
7. Complications:
1) Anemia.
2) Acidosis, Hyperkalemia, Uremia.
3) Heart failure, Hypertension.
4) CNS – infarcts, cortical blindness, coma.
5) GIT – Colitis, Intestinal perforation, intussusception, hepatitis, focal
pancreatic necrosis.

6) CVS – Pericarditis, Arrythmia.
7) Others – Skin, necrosis, parotitis, adrenal dysfunction, rhabdomyolysis.
8. Treatment: (Principle of treatment):
1) Fluid – electrolyte balance.
2) Control of hypertension.
3) Aggressive nutrition.
4) Early dialysis (peritoneal).
5) Avoid antibiotic for acute enteritis caused by E. coli.
6) Plasmapheresis may be beneficial.
7) Fresh frozen plasma may be help.
8) Management of Acute renal failure.
References:
1 Parthasarathy, K Nedunchalian, Gowri Shankar HC, Textbook of Balram chowdhary’s Pediatrics
Lecture notes, PEE PEE Publication, 2nd edition, Pg no. 273 – 289.
2 Bellemo R, Ronco C, Kellium J, Mehta RL, Palevsky P, Acute renal failure – Definition, outcome
measures, animal models, fluid therapy and information technology needs; the second international
concensus conference of the acute dialysisQuality initiative (ADQI) Group. criticare (London,
England). 2004; 8(4): R204 – 12.
3. Akcan – Arikan a, Zapptelli M, Lofftis LL, Washburn KK, Jefferson LS, Goldstin SL, Modified
Rifile criteria in critically ill children with acute kidney injury, kidney int. 2007; Volumme 71: 1028
– 35.
4. Indian society of Pediatric nephrologists. Revised statement on management of UTI. Indian pediatr.
2011; 58: 709 – 717.

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