The document discusses chronic kidney disease (CKD). It defines CKD as kidney damage or decreased glomerular filtration rate (GFR) lasting at least 3 months. CKD is staged based on GFR levels and can progress to kidney failure requiring dialysis or transplant. The causes, risk factors, complications, diagnostic evaluation and management of CKD are described with a focus on pediatric patients.

1. CHRONIC KIDNEY DISEASE
By
Hussain Bangi
Al-Ameen Medical College
Bijapur
1

2. OUTLINE
• Introduction
• Definition
• Stages of CKD
• Epidemiology
• Etiology
• Risk Factors for CKD
• Renal Response to Nephron Loss
• Progression of Renal Damage
• Systemic Features
• Diagnostic Evaluation
• Management
• End Stage Renal Disease
• Summary
2

3. INTRODUCTION
• Chronic kidney disease is characterized by an irreversible deterioration of renal
function that gradually progresses to end-stage renal disease (ESRD) and
eventually requires renal replacement therapy.
3

4. DEFINITION
A patient has CKD if either of the following criteria are present:
1. Kidney damage ≥ 3months, as defined by structural or functional abnormalities
of the kidney, with or without decreased GFR, manifested by 1 or more of the
following features:
• Abnormalities in the composition of blood or urine
• Abnormalities in imaging tests
• Abnormalities on kidney biopsy
2. GFR < 60ml/min/1.73m2 for ≥ three months, with or without the other signs of
kidney damage described above
4

5. STAGES OF CKD
STAGE DESCRIPTION GFR (ml/min/1.73m2)
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
5D Kidney Failure, dialysis dependent <15, on dialysis
5

6. EPIDEMIOLOGY
• Globally, the prevalence of CKD among children, < 16 year old, is 1.5 – 3.0 per
1,000,000 child population.
• Incidence & prevalence of CKD
– Increases with age
– More common in African Americans
– More common in adults than children
– Among children, more common in children older than 6 years
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7. ETIOLOGY
Glomerulonephritis
• Idiopathic
• Associated with multisystem diseases: SLE, polyarteritis nodosa
• Henoch - Schonlein purpura, microscopic polyarteritis
Familial Nephropathy
• Alport syndrome, congenital nephrotic syndrome
Congenital Anomalies
• Bilateral renal dysplasia, hypoplasia, polycystic kidney disease
• Reflux nephropathy
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8. ETIOLOGY (contd.)
Obstructive Uropathy
• Pelviureteric or ureterovesical junction obstruction
• Posterior urethral valve, calculi
Amylodiosis
Hemolytic Uremic Syndrome
Miscellaneous
• Bilateral wilms tumor
• Renal cortical necrosis
8

9. ETIOLOGY (contd.)
Paediatric Patients,
Reflux/Obstruction/Dys
plasia, 0.37, 38%
Paediatric Patients,
Glomerulonephritis/FS
GS, 0.27, 27%
Paediatric Patients,
Cystic Disease, 0.05,
5%
Paediatric Patients,
HUS, 0.03, 3%
Paediatric Patients,
Other, 0.27, 27%
Adult Patien
Diabetes, 0.43
Adult Patients,
Hypertension, 0.27,
27%
Adult Patients,
Glomerulonephritis,
0.08, 8%
Adult Patients, Cystic
Disease, 0.02, 2%
Adult Patients,
Other, 0.2, 20%
Adult Patients
9
Pediatric Patients

10. RISK FACTORS FOR CKD
• VUR associated with recurrent urinary tract infections & renal scarring
• Obstructive uropathy
• Prior history of acute nephritis or nephrotic syndrome
• Renal failure in perinatal period
• Family H/O polycystic kidneys or genetic renal conditions
• Renal dysplasia or hypoplasia
• Low birth weight infants
• Prior history of HSP
• Diabetes, hypertension
• SLE, vasculitis
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11. Renal Response to
Nephron Loss
Functional Changes
• Adaptive
Hyperfilteration
• Maintenance of
tubuloglomerular
balance
Structural Changes
• Hypertrophy of
Cellular & Matrix
constituents of the
glomerulus
• Increase in size &
volume of tubules
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12. RENAL RESPONSE TO NEPHRON LOSS (contd.)
12

13. PROGRESSION OF RENAL DAMAGE –
RISK FACTORS
NON – MODIFIABLE RISK FACTORS
• Foetal Programming : low birth weight
• Angiotensin converting enzyme (ACE) gene
13

14. PROGRESSION OF RENAL DAMAGE –
RISK FACTORS (contd.)
MODIFIABLE RISK FACTORS
• HYPERTENSION
• PROTEINURIA
• Obesity
• Dyslipidemia
• Mineral homeostatsis
• Hyperuricemia
• Anemia
Important & Independent Risk Factors
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15. PROGRESSION OF RENAL DAMAGE (contd.)
Pathophysiologic consequences of
hypertension and proteinuria in
chronic kidney disease
15

16. SYSTEMIC FEATURES
GROWTH RETARDATION
Factors contributing:
– Poor Nutrition
– Metabolic Acidosis
– Bone Disease
– Anaemia
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17. SYSTEMIC FEATURES (contd.)
MALNUTRITION
Factors contributing
• Anorexia
• Nausea and Vomiting
• Abnormal sense of taste
• Imposition of a variety of appropriate or inappropriate dietary restrictions
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18. SYSTEMIC FEATURES (contd.)
Factors contributing:
• Lack of erythropoietin production
• Iron Deficiency
• Chronic Inflammation
• Bone Marrow Suppression
• Increased red cell turnover
• Malnutrition
• Aluminium Toxicity
ANAEMIA
develops once the renal function < 50%
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19. SYSTEMIC FEATURES – ANAEMIA (contd.)
Clinical effects of Anaemia:
• Fatigue
• Loss of appetite
• Depression
• Decreased quality of life
• Sleep disturbances
• Decreased exercise tolerance
• Impaired Cognitive function
• Left Ventricular Hypertrophy
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20. SYSTEMIC FEATURES (contd.)
NEUROLOGICAL ABNORMALITIES
• Infants and young children with moderate CKD are at risk for encephalopathy
• Features
– Hypotonia
– Delayed motor development
– Seizures
– Truncal ataxia and other signs of cerebellar dysfunction
– Uremic neuropathy
– Severe proximal muscle weakness
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21. SYSTEMIC FEATURES (contd.)
BONE AND MINERAL DISORDER [RENAL OSTEODYSTROPHY]
• Systemic disorder of bone & mineral metabolism manifested by either
one or a combination of the following:
– abnormlities of Ca++, phosphorous, PTH or vitamin D
– abnormalities in bone histology, linear growth or strength
– vascular or other soft tissue calcification
• As early as in CKD stage 2 vit D ↓ & serum PTH ↑
• Seen in 30% of patients with ESRD
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22. CHRONIC KIDNEY DISEASE –
MINERAL & BONE DISORDER (CKD - MBD)
Clinical Spectrum of CKD -MBD
• Secondary Hyperparathyroidism - Osteitis fibrosa cystica, Bone resorption,
fractures & deformities
• Alterations in growth plate cartilage – failure of linear growth
• Vit D3 deficiency – rickets/osteomalacia
• Adynamic bone lesions
• Hypotonia & delayed motor development
• Genu valgum, Scoliosis, compression fractures of vertebrae, thoracic deformities
and pathologic fractures of long bones
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23. SYSTEMIC FEATURES (contd.)
METABOLIC ACIDOSIS & DYSELECTROLYTEMIA
HYPERKALEMIA
HYPERTENSION
MISCELLANEOUS
• Anorexia
• Lack of energy
• Increased sleep
• Poor school performance
• Platelet dysfunction
• Gastric Ulceration
• Severe Itching
• Pericarditis
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24. DIAGNOSTIC EVALUATION
DETAILED HISTORY
• Age at onset/ duration
• Polyuria/ polydipsia/ enuresis/hematuria
• Fever/ rash / arthralgia/ arthritis/odema
• Recurrent UTI
• Antenatal detection of any renal anomalies
• Spinal abnormalities
• Uraemic symptoms (fatigue/anorexia/vomiting)
• History of renal disease in the family [Alport syndrome/ Nephronophthisis/
congenital nephrotic syndrome]
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25. CLINICAL EXAMINATION
• vitals [blood pressure]
• assessment for the presence & severity of peripheral odema
• evaluation of growth, pubertal development & nutritional status
• features of anaemia & bone disease
• pericardial rub/ diminished heart sounds
• psychological & intellectual functions
DIAGNOSTIC EVALUATION (contd.)
25

26. LABOROTARY INVESTIGATIONS
• Complete blood counts
• ↓ Hb
• ↑ Total counts
• ↓ Platelet counts
• Renal function test
• ↑s. creatinine/B.urea
• Blood urea nitrogen
• Serum electrolytes
• ↑Na / ↑K+
• Serum calcium, phosphate, ALP & proteins
• Serum cholesterol
• PTH
• Iron studies
DIAGNOSTIC EVALUATION (contd.)
26

27. Urine Analysis
• Look for red blood cells (RBCs), white blood cells (WBCs)
• Most children with chronic kidney disease have broad hyaline casts
• Proteinuria
Glomerular Filteration Rate (GFR)
Estimation of GFR - Schwartz formula
GFR = k X height[cm] / serum creatinine [mg/dl]
k = 0.4 for preterm infants),
k = 0.45 for full-term infants
k = 0.55 for those aged 2-12 yrs and adolescent girls
k = 0.7 years in adolescent boys
DIAGNOSTIC EVALUATION –
LABORATORY INVESTIGATIONS (contd.)
27

28. Age Mean GFR ± SD (ml/min/1.73m2)
1 week term males & females 41 ± 15
2-8 weeks term males and females 66 ± 25
>8 weeks term males and females 96 ± 22
2 – 12 years males and females 133 ± 27
13-21 years males 140 ± 30
13-21 years females 126 ± 22
DIAGNOSTIC EVALUATION –
LABORATORY INVESTIGATIONS – GFR (contd.)
Normal GFR in Neonates, Children and Adolescents
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29. Cystatin C
• Low molecular weight protein [13.36 kD]
• Freely filtered by the glomerulus & metabolized after tubular reabsorption
DIAGNOSTIC EVALUATION –
LABORATORY INVESTIGATIONS (contd.)
Reference Intervals
Preterm Infants 1.34 – 2.57
Fullterm Infants 1.36 – 2.23
>8 days – 1year 0.75 – 1.87
1 – 3 years 0.68 – 1.90
3 – 16 years 0.51 – 1.31
Reference Intervals for Cystatin C
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30. DIAGNOSTIC EVALUATION(contd.)
IMAGING STUDIES
1. Ultrasonography:
• To assess renal size, anomalies & obstruction
• To grade glomerulonephropathy
2. Radionuclide Studies
• 99m-Technetium dimercaptonsuccinic acid (DMSA) – to look for renal scars
• Voiding cystourethrography – to assess the dynamics of the urinary bladder
3. Skeletal survey
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31. DIAGNOSTIC EVALUATION - ULTRASONOGRAPHY (contd.)
31

32. MANAGEMENT
• Adequate management of early stages of CKD retards the decline in renal
function
• Treatment is aimed at maintaining the well being and quality of life
RETARDING THE PROGRESSION OF CKD
1. Control of hypertension
2. Reduction in proteinuria
3. Other strategies
– Management of anaemia
– Prevention and management of dyslipidemia
– Prevention of acidosis
– Non hypercalcemic doses of vitamin D analogs
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33. MANAGEMENT (contd.)
NUTRITION
Dietary Management
Goals –
a) Reduce nitrogen intake
b) Maintain nitrogen balance
c) Cover essential amino acid requirement
d) Supply enough calories
• Energy: Intake equivalent to the RDA of healthy children of the same age
• Infant : 100 – 120 kCal/kg/day
• Children : 80 – 100 kCal/kg/day
• 55 – 60% from carbohydrates
• 30% from fats
• 10% from proteins
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34. MANAGEMENT – NUTRITION – DIETARY MANAGEMENT (contd.)
• Protein:
High protein – aggravates acidosis, hyperkalemia & hyperphosphataemia
Low protein – reduce BUN, improve renal function and reduce GI & neurological symptoms
50% Protein Intake from high biological value proteins(meat, poultry, fish, eggs, milk, cheese,
yoghurt)
Type of CKD 0-1 yr 1-5 yrs 5-10 yrs
Mild (GFR: 20 – 40) 1.8 1.4 1
Moderate (GFR: 5 – 20) 1.4 1 0.8
Severe (GFR: <5) 1 0.8 0.6
Protein Allowance in CKD according to GFR (g/kg)*
Children on dialysis+
Haemo Dialysis → + 0.4g/kg/day Peritoneal Dialysis → +0.8g/kg/day
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35. MANAGEMENT – NUTRITION – DIETARY MANAGEMENT (contd.)
• Fats:
• Saturated fats - < 10% of total calories
• Diets high in PUFA (corn oil, medium chain triglyceride oil & complex carbohydrates)
• Vitamins:
• Recommended dietary intake – 100% of RDA
B1,B2 and folic acid – 1mg each
Pyridoxine & Pantothenic acid – 10mg each
Vitamin C – 50mg
Vitamin B12 – 5mg
Biotin – 300mg
• Vitamin A > 2 x RDA – hypercalcemia, anaemia and hyperlipidemia
• Excessive Vitamin C – oxalate deposition in kidney
• GFR <40 ml/min/1.73m2 – folic acid supplemented to prevent hyperhomocysteinemia
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36. MANAGEMENT – NUTRITION – DIETARY MANAGEMENT (contd.)
• Fluids:
• Fluids should be given without producing water retention
• In case of water retention – give diuretic and restrict sodium
• Thirst or insensible loss + last day’s output
• Next Step Consider dialysis - if water retention and weight gain increase despite diuretic
• Sodium:
• Restrict salt intake to 300-600 mg/day in infants & 1-2g/day in older children
• Potassium:
• Restrict potassium intake
• Hyperkalemia – calcium gluconate, sodium bicarbonate, insulin & glucose, nebulized,
albutrol and Potassium exchange resin (1g/kg/day)
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37. GROWTH
• Resolve nutritional deficiencies
• Improve acid base balance
• Correction of salt depletion, ca++ & vitamin D deficiency
• If growth retardation persists despite these measures recombinant human growth
hormone (rhGH) therapy to be started.
MANAGEMENT (contd.)
37

38. MANAGEMENT (contd.)
ANAEMIA
Key Elements –
• Erythropoietin Stimulating Agents – ESA
• Recombinant Human Erythropoietin – rHuEPO (Epogen, Procrit, Eprex)
• Darbepoetin - ᾱ (Aranesp)
S/C: 100 units/kg/week in two doses
I/V: 150 units/kg/week in three doses
• Iron supplementation
• Oral
• Intravenous
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39. 2. Darbepoetin - ᾱ
• Starting dose
ESA naïve pt’s: 0.5µg/kg/wk
pt’s converting from rHuEPO: 0.42µg/kg/wk
for every 100u/kg/wk of rHuEPO
• Complication:
• Injection site pain
• Pruritus
MANAGEMENT – ANAEMIA
Erythropoietin Stimulating Agents (ESA) (contd.)
39

40. Iron Supplementation
1. Oral Iron
• 3 – 5 mg/kg/day of elemental iron(max 150 – 300 mg/day)
• Adequate therapy in children not on haemodialysis
• Given 1 - 2 hrs before food
• Absorption affected by phosphate binders, H2 receptor antagonists & PPIs
MANAGEMENT – ANAEMIA (contd.)
40

41. 2. Intravenous Iron
• Preparations:
a) Iron Dextran(INFeD)
b) Iron Gluconate(Ferrlecit)
c) Iron Sucrose(Venofer)
• Acute Dosing – Given when TSAT < 20% or ferritin<100ng/ml
Recommended Dose: 1.5mg/kg/dose with a max. of 125mg/dose
• Chronic Dosing – Started at 1mg/kg/week - one dose a week
• Complications:
• Iron dextran: acute anaphylactic reactions
• Iron gluconate: loin pain, hypotension, emesis, paraesthesias
• Iron sucrose: rash, flushing, hypotension
MANAGEMENT – ANAEMIA
Iron Supplementation (contd.)
41

42. MANAGEMENT (contd.)
CKD - MBD
• Control of levels of blood phosphate – most important factor in prevention & treatment of
secondary hyperparathyroidism
• Daily intake of phosphorous: 800 -1000mg
• Dairy products, chocolate, chicken, nuts, dried beans, aerated drinks to be avoided
Treatment Modalities
1. Phosphate binders:
• Calcium salts [calcium carbonate & calcium acetate]
• Sevelamer hydrochloride
2. Vitamin D & its analogues
3. Calcimimetic agents
4. Surgical intervention
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43. HYPERTENSION
• Target level < 90th percentile of bp for age , gender & height
• Salt restriction & diuretics
• Antihypertensive drugs:
1. Thiazides [hydrochlorothiazide 2mg/kg/24r] : GFR upto 30ml/min/1.73m2
2. Loop diuretics [furosemide 1-2mg/kg/dose] : GFR < 30
3. Calcium channel blockers [amlodipine]
4. Beta blockers [atenolol/metoprolol]
5. Centrally acting agents [clonidine]
MANAGEMENT (contd.)
43

44. MANAGEMENT (contd.)
IMMUNIZATION
• All standard immunizations according to the schedule
• Withhold live vaccines when on immunosuppressive medication
• Administer live vaccines before transplantation
• These children should be offered Pneumococcal, Varicella and Rotavirus vaccines.
• Yearly influenza vaccine
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45. END- STAGE RENAL DISEASE
• State in which renal dysfunction has progressed to a point at which homeostasis &
survival can no longer be sustained with native kidney function & medical
management
• Ultimate goal : successful kidney transplantation
• Initiation of renal replacement therapy : stage 4 CKD
• Birth to 5 years: peritoneal dialysis
> 12 yr of age : hemodialysis
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46. SUMMARY
• CKD is irreversible loss of renal function
• Glomerulonephritis, congenital renal & urological anomalies & reflux nephropathy
account for majority of paediatric CKD
• Hypertension & Proteinuria are the most important factors for progression of CKD
• Presenting features include anaemia, growth retardation, malnutrition,
hypertension, bone disease, acidosis or encephalopathy
• Adequate management of early stages retards decline in renal function
• Psychological and emotional support to parents
• Renal replacement therapy initiated when GFR < 15ml/min/1.73m2
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47. THANK YOU
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