A 4-year-old boy presented with polyuria, polydipsia for 4 months and failure to thrive for 3 months. He also had irregular fever for 2 months. On examination, he was pale, hypertensive, and growth retarded. Chronic kidney disease can reduce lifespan and quality of life by clogging the kidneys. It is defined as kidney damage or decreased GFR for 3 or more months. Risk factors include VUR, obstructive uropathy, previous nephritis, family history, and low birth weight. Stages range from kidney damage with normal GFR to kidney failure. Management focuses on monitoring, controlling hypertension and nutrition, and slowing progression.

1. Case scenario
• A 4 year old Rahim from Kelambakkam came with complaints
of polyuria, polydipsia for past 4 months, failure to thrive for
past 3 months
• On further query he had irregular fever for 2 months, no H/O of
contact with TB, no loss of appetite
• O/E moderately pale, hypertensive, growth retartded, No
organomegaly
Dr GRK CHRI 1

2. Dr GRK CHRI 2

3. Dr. G.Rajkumar MD
Professor of Paediatrics
CHRI
Chronic Kidney Disease in
Children

4. Outline
• CKD is a chronic progressive disease that can clog normal
lifestyle & reduce lifespan
• Definition
• Etiopathogenesis
• Stages
• Clinical features
• Management
Dr GRK CHRI 4

5. Criteria for definition of chronic kidney
disease (NKF KDOQI Guidelines)
Patient has CKD if either of the following criteria are present:
1. Kidney damage for ≥3 months as defined by structural or
functional abnormalities of the kidney, with or without decreased
GFR, manifested by one or more of the following features:
Abnormalities in composition of blood or urine
Abnormalities in imaging
Abnormalities in biopsy
2. GFR < 60ml/min/1.73m2≥ 3 months with or without signs of
kidney damage described above
Dr GRK CHRI 5

6. 3 exceptions in Paediatrics
1. Criteria duration longer than 3 months does not apply for
infant less than 3 months
2. GFR < 60ml/min/1.73m2 cannot be used for children < 2 years
as this group has developmental immaturity leading to low GFR
Urine protein can be used instead of urine albumin excretion in
children
Dr GRK CHRI 6

7. Risk factors for CKD
• VUR with recurrent UTI
• Obstructive uropathy
• Previous history of nephritis or NS
• Family history of PCKD
• Renal dysplasia or hypoplasia
• LBW
• DM/SHT
• SLE, Vasculitis, HSP
Dr GRK CHRI 7

8. Stages of CKD
Stage Description GFR
1 Kidney damage with normal or
increased GFR
≥ 90
2 Kidney damage with mild decrease in
GFR
60-89
3 Moderate decrease in GFR 30-59
4 Severe decrease in GFR 15-29
5 Kidney failure < 15 or on dialysis
Dr GRK CHRI 8

9. Proteinuria categories applicable to
children
Categ
ory
Protein: creatinine
ratio (g/mmol)
Terms
P1 <0.02 Normal
P2 >0.02 - <0.2 Moderate increase, non-
nephrotic range
P3 ≥0.2 Nephrotic range proteinuria
Dr GRK CHRI 9

10. Epidemiology
• Prevalence of CKD in children is 18/10,00000
• Childhood onset ESRD has significant morbidity and 30 fold
increase risk od dying from cardiovascular & infective causes.
Dr GRK CHRI 10

11. Etiology
• In children < 5 yrs. congenital anomalies of kidney & urinary
tract ( renal hypoplasia/dysplasia or obstructive uropathy),
RVT, Prune belly syndrome and is often diagnosed with
perinatal USG
• In children older than 5 yrs. acquired or inherited causes of
glomerulo-nephritis predominate
Dr GRK CHRI 11

12. Non Glomerular
• Aplastic, dysplastic, hypoplastic kidneys
• Cystinosis
• Medullary kidney disease/ juvenile nephrolithiasis
• Obstructive uropathy ( PUV, cloaca, neurogenic bladder)
• Oxalosis
• AD & AR PCKD
• Pyelonephritis, interstitial nephritis, reflux nephropathy
• Renal infarct syndrome of agenesis of abdominal musculature (Eagle Barrett
syndrome)
• Wilms tumour
Dr GRK CHRI 12

13. Glomerular
• Chronic glomerulonephritis ( including FSGS)
• Congenital nephrotic syndrome (CNS)
• HUS
• HSP
• Idiopathic crescentic glomerulonephritis
• Ig A nephropathy
• MPGN
• Membranous nephropathy
• Sickle cell nephropathy
• SLE, Wegener Granulomatosis
• Hereditary nephritis- Alport Syndrome
Dr GRK CHRI 13

14. Pathogenesis
A. Hyperfiltration Injury: final common pathway of all causes of
renal injury
Nephron loss
Rest of nephron undergo structural & functional hypertrophy
Increased glomerular blood flow
Hyperfiltration preserves renal function for a while
Effect of elevated hydrostatic pressure on vessel wall
Toxicity due to increased protein filtration
Dr GRK CHRI 14

15. Dr GRK CHRI 15

16. • Remaining nephrons suffer from increased excretory burden
leading on to a vicious cycle of increased glomerular blood flow
and hyperfiltration injury
Dr GRK CHRI 16

17. B. Proteinuria
Direct toxic effect of proteins on tubular cells
Recruit monocytes & macrophages-glomerular sclerosis & tubule
interstitial fibrosis
C. Uncontrolled Hypertension-arterial nephrosclerosis & enhances
hyperfiltration injury
D. Hyperphosphatemia- calcium phosphate deposition in renal
interstitium & blood vessels
E. Hyperlipidemia- Oxidant-mediated injury
Regardless of etiology, progression of interstitial fibrosis is the
primary determinant of CKD
Dr GRK CHRI 17

18. Pathophysiology
1. Accumulation of nitrogenous waste-d/t decreased GFR
2. Acidosis- decreased ammonia synthesis, decreased bicarbonate
reabsorption, decreased net acid excretion
3. Sodium wasting- solute diuresis, tubular damage
4. Urinary concentrating defect- solute diuresis, tubular damage
5. Hyperkalemia- Reduced GFR, Metabolic acidosis, Excessive
potassium intake, hyporeninemic hypoaldosteronism
6. Renal osteodystrophy- impaired renal production of 1,25
dihydroxycholecalciferol, hyperphosphatemia, hypocalcemia,
secondary hyperparathyroidism
Dr GRK CHRI 18

19. 7. Growth retardation- inadequate calorie intake, metabolic
acidosis, renal osteodystrophy, anemia, GH resistance
8. Anemia-decreased erythropoietin secretion, Iron, Folic acid
and or Vitamin B12 deficiency, decreased erythrocyte survival
9. Bleeding tendency-defective platelet function
10. Infection- Defective granulocyte function, impaired cellular
immunity, indwelling catheters
11. Decreased academic achievement, attention regulation or
executive functioning- hypertension, LBW
Dr GRK CHRI 19

20. 12. Gastrointestinal symptoms ( feed intolerance, abdominal pain)-
GERD, decreased GI motility
13. Hypertension- volume over load, excessive renin production
14. Hyperlipidemia- decreased lipoprotein lipase activity, abnormal
HDL-C
15. Cardiomyopathy-volume overload, hypertension, anemia
16. Glucose intolerance-tissue insulin resistance
17. Neurological Symptoms- fatigue, poor concentration, headache,
memory loss, seizures, peripheral neuropathy-uremic factors,
Aluminum toxicity, Hypertension
Dr GRK CHRI 20

21. Dr GRK CHRI 21

22. Dr GRK CHRI 22

23. Clinical features of CKD
• Appearance: Pallor secondary to anemia
• Hypertension
• Shortness of breath-volume overload, anemia, cardiomyopathy
• Kidneys- B/L small thinned cortices suggests intrinsic disease
(Glomerulonephritis)
U/L small kidney-renal artery disease
Clubbed cortices & cortices scar-Chronic infection
Enlarged cystic kidneys
Itch & cramps
Cognitive changes
GI Symptoms-Anorexia, vomiting, taste disturbances, uremic odour
Urinary changes- polyuria, proteinuria, poor concentrating ability
Dr GRK CHRI 23

24. • Hematuria- immune injury to glomerular capillary wall
• Proteinuria
Tubular- low grade proteinuria (<2 g), Low MW
Glomerular- selective proteinuria > 3.5 g,
• Peripheral edema- salt retention
Dr GRK CHRI 24

25. ESRD
• Stage in which renal dysfunction has progressed in to a point at
which the homeostasis & survival can no longer be sustained
with native kidney function & medical management
• Mx Renal transplant at stage 4 CKD
• Birth to 5 years-Peritoneal dialysis
• > 12 yrs. Hemodialysis
Dr GRK CHRI 25

26. Laboratory findings
• Elevations in BUN & creatinine
• Hyperkalemia
• Hyponatremia- renal salt wasting & volume overload
• Hypernatremia-water loss
• Acidosis
• Hypocalcemia
• Hyperphosphatemia
• Elevation of uric acid
• Hypoalbuminemia-d/t proteinuria
• CBC-N/N anemia
• Dyslipidemia
• AGN-Hematuria, proteinuria
• Congenital abnormalities- low specific gravity
Dr GRK CHRI 26

27. Measurement of renal functions
• By measuring GFR
• Inulin clearance-gold standard- but no routinely available
• Iohexol or Radio isotopes (99m Tc-DTPA, 51 Cr- EDTA, 125
lothalamate)
• Estimating GFR by endogenous markers (creatinine and or
cystatin c)- assess the severity
• GFR(ml/min/1.73m2)= k x0.43 x height(cm)/serum creatinine
(mg/dl)
• k= 0.33 LBW < 1 yr, 0.45 term AGA, 0.55 children & adolescent
female, 0.70 adolescent male
Dr GRK CHRI 27

28. Management of CKD
• CKD treatment is supportive
• Replacing absent/ diminished renal function
• Slowing progression of renal dysfunction
Dr GRK CHRI 28

29. • Close monitoring of blood studies, urine studies(spot PCR,
24hrs urinary protein)
• Ambulatory blood pressure monitoring over 24 hrs
• Masked hypertension-Normal office blood pressure but
abnormal ABPM
• Its seen up to 35% of Paediatric predialysis patients
• 4 fold increased risk of LVH
Dr GRK CHRI 29

30. 1. Nutritional management
• Patient should receive 100% of estimated energy requirement
for age, adjusted to physical activity & BMI, response to weight
gain/loss
• Dietary protein restriction not suggested considering growth
restriction (2.5 g/kg/d)
• MCT fat
• High biological value protein( fish, fowl, meat, egg)
• CKD stages 2-5 should receive 100% of daily requirement of
vitamins& trace elements (Fe & Zn only if deficient)
• Water soluble vitamins
Dr GRK CHRI 30

31. Growth
• Short stature is a long term squeal
• GH resistance( GH IGF )
• Abnormality of IGF binding Protein
• Recombinant human GH (0.05 mg/kg/24 hr)
• Continue until 50th percentile MPH or achieves full adult height
or undergoes renal transplantation
Dr GRK CHRI 31

32. 2. Fluid & Electrolyte management
• Most patients maintain normal sodium & water balance
• Polyuric urinary sodium loss: give high volume, high caloric
density feeding with sodium supplements
• High BP, edema or heart failure: require sodium restriction &
diuretic therapy
• Fluid restriction is rarely unnecessary until ESRD
• Hyperkalemia: restriction of dietary K+intake oral alkalysing
agent kayexalate
• DOC in severe hyperkalemia- Calcium gluconate
Dr GRK CHRI 32

33. 3. Acidosis
• Sodium bicarbonate tablet (650 mg= 8 mEq base)
• Bacitra ( 1 mEq sodium citrate/ml)
• Maintain serum Bicarbonate > 22 mEq/L
Dr GRK CHRI 33

34. 4. Renal osteodystrophy
• Spectrum of bone disease in CKD
• High turnover bone disease
• Secondary hyperparathyroidism
• Osteitis fibrosa cystica
Dr GRK CHRI 34

35. Pathophysiology
• When GFR declines to 50%of normal
• Decline in 1 α hydroxylase
• Decreased production of activated Vitamin D
• intestinal absorption of calcium
• Hypocalcemia
• Secondary hyperparathyroidism
• Increase bone resorption when GFR decline to 25% of normal
• Hyperphosphatemia
Dr GRK CHRI 35

36. Clinical manifestations
• Muscle weakness
• Bone pain
• Fractures with trivial trauma
• Rickitic changes
• Ca Ph alkaline phosphatase PTH normal
• Subperiosteal resorption of bone with widening of metaphysis
Dr GRK CHRI 36

37. Treatment of renal osteodystrophy
• Low phosphorus diet
• Phosphate binders
• Calcium carbonate & calcium acetate
• Sevelamer(Renagel)- calcium binder
• Avoid aluminum based binder
• Vitamin D therapy
• Maintain calcium/ phosphorus product <55
Dr GRK CHRI 37

38. 5. Anemia
• Keep Hb between 12-13g/dl
• Erythropoietin if Hb< 10g/dl-Dose 50-150 mg/kg SC 1-3
times/week
• Darbopoeitin alfa (long acting) Dose 0.45 µg/kg/week
Dr GRK CHRI 38

39. 6. Hypertension
• Salt restriction
• Diuretic therapy
• Hydrochlorothizide-2 mg/kg/d
• Furosemide 1-2 mg/kg/dose
• ACE inhibitors-Angiotensin II blockers for proteinuric renal
failure ( enalapril, lisinopril, losartan)
Dr GRK CHRI 39

40. 7. Immunisation
• As per schedule
• Avoid live vaccine if on immunosuppressants
• Give live vaccine before transplant
• Yearly influenza vaccine
Dr GRK CHRI 40

41. 8. Adjustment in drug dosage
• Drugs excreted by kidney may need dose adjustment to
maximize effectiveness & reduce toxicity
Dr GRK CHRI 41

42. Strategy to slow progression
• Optimal control of hypertension
• Maintain calcium/ phosphorus product <55
• Prompt treatment of infection & dehydration
• Correction of anemia
• Correction of hyperlipidemia
• Prevent obesity
• Avoid NSAIDS
• Dietary protein restriction helpful but not recommended in
children
Dr GRK CHRI 42

43. Long term follow up
• Serum electrolytes
• BUN
• Creatinine
• Calcium
• Phosphorus
• Albumin
• Alkaline phosphatase
• Hb & Hct
• PTH
• Echo
Dr GRK CHRI 43

44. Summary
• CKD is irreversible loss of renal function
• Glomerulonephritis, congenital Renal & urological anomalies, reflux
nephropathy account for major chunk of CKD in children.
• Hypertension & proteinuria are major causes of disease progression
• Presenting complaints include anemia, growth retardation,
hypertension, bone disease, acidosis, encephalopathy, malnutrition
• Adequate management of early stages halt progression
• Psychological & emotional support to patients & parents
• Renal replacement therapy initiated when GFR < 15 ml/min/ 1.73m2
Dr GRK CHRI 44