Acute kidney injury (AKI) and chronic kidney disease can affect children. AKI is defined as a rapid deterioration of renal function over hours to days. It has various etiologies including pre-renal, renal, and post-renal causes. Management involves treating life-threatening complications, maintaining fluid/electrolyte balance, supportive care, and dialysis. Chronic kidney disease develops over months to years and requires long-term management to delay progression.

1. ACUTE KIDNEY INJURY
&
CHRONIC KIDNEY DISEASE
IN CHILDREN
BY- DR. SAMEEKSHYA PRADHAN
GUIDE- ASSOC. PROF. DR. J .R CHAMPATIRAY

2. ACUTE KIDNEY INJURY

3. DEFINITION
Rapid deterioration of renal function resulting in
retention of nitrogenous wastes and inability of
kidney to regulate fluid and electrolyte homeostasis.
In year 2000 the acute dialysis quality initiative
(ADQI) proposed RIFLE criteria for defining AKI .
Later, Acute Kidney Injury Network (AKIN)
classified AKI based on the RIFLE system.

4. > 3 months

5. INCIDENCE
 The precise incidence of AKI in children is not well
known.
 4-6 % case of AKI seen in general ward and upto
40% in PICU
 AGE with dehydration & shock is a common cause.
 In India, malaria, snake bite are also common causes.
 In PICU, commonly affects children who have
sepsis and multiorgan failure.
 Children undergoing major cardiac surgery and
organ transplantation are also at considerable risk.
 HUS and AGN are important renal causes.
 Post renal causes of AKI are rare.

6. ETIOLOGY
 Pre renal
 Intrinsic or renal
 Post renal
- Both pre and post renal aki are potentially
reversible in early stages but if prolonged can
cause renal parenchymal damage.

7. (A) PRE RENAL
 Also called prerenal azotemia, is characterized
by diminished effective circulating arterial
volume, which leads to inadequate renal
perfusion and a decreased GFR .

8. CAUSES OF PRERENAL AKI
 Acute gastroenteritis
 Hemorrhage
 Shock
 Congestive cardiac failure
 Hepatorenal syndrome (renal vasoconstriction)
 Sepsis (peripheral vasodilaton)
 Profound third space loss (burns, Ac. Pancreatitis,
nephrotic syndrome, massive ascites)
 NSAID’s & ACE inhibitors

9. Renin
Angiotensin II
Aldosterone
Renal Tubular Na
Reabsorption
Vasopressin
Renal Tubular H2O
Reabsorption
Urine Volume
Concentrated Urine
Urine Sodium
Decreased Renal Perfusion
Mechanisms of Sodium and Water
Conservation in Prerenal Azotemia

10. (B) RENAL
CAUSES –
 Obstruction of renal artery or veins -
renal vein thrombosis , renal arterial obstruction,
 Involvement of renal microvasculature –
HUS , HSP, polyarteritis , collagen vascular disease
 Glomerular causes-
AGN ( PSGN ,other infections ), cresentic GN
 Interstitial causes- acute tubulointerstitial nephritis
 Tubular causes (ATN)
Prolongation of pre-renal insult , intravascular hemolysis , sepsis ,
nephrotoxic agents , multiorgan failure , rhabdomyolysis , snakebite ,
other envenomations , falciparum malaria , leptospirosis

11. 1.OBSTRUCTION OF RENAL ARTERIES AND VEINS
 Bilateral renal arterial thrombosis may occur after
umbilical artery catheterization in neonates (rarely
causes aki usually causes intractable hypertension).
 Renal vein thrombosis may be a complication of
infant of diabetic mother especially following
dehydration.
 In older children renal vein thrombosis may occur
with nephrotic syndrome with anasarca and
dehydration.
 Gross hematuria, enlargement of kidney and
azotemia are typical manifestation.

12. 2.INVOLVEMENT OF RENAL MICROVASCULATURE
 HUS is a common cause of AKI in chidren.
 Causes thrombotic microangiopathy
 2 types- D+HUS and D-HUS
 Common causes of D+HUS – EHEC(in developed
countries),Shigella dysentriae type I (in India)
 Following dysentery shigella-toxin enters the circulation
and leads to endothelial injury in microvasculature .
 Localized coagulation and deposition of platelet thrombi
and fibrin occurs in glomeruli causing decrease in GFR.

13. 3.GLOMERULAR DISEASES
 PSGN, Post infectious GN, Cresentric GN, Renal
vasculitis, IgA nephropathy are important causes
in this group.

14. 4.ACUTE INTERSTITIAL NEPHRITIS
 Usually occurs due to hypersensitivity reaction to
some drugs (ampicillin, cephalosporins,
sulfonamides,quinolones, NSAID’s, phenytoin
etc)
 The patient may have fever , arthralgia , rash and
eosinophilia : urine often shows eosinophils
 Renal biopsy should be done if it is strongly
suspected.

15. 5.ACUTE TUBULAR NECROSIS
 Occurs mostly in critically ill infants and children
who have been exposed to nephrotoxic agents
and/or prolonged hypoperfusion/hypoxia.
 Common causes of ATN include renal
hypoperfusion following volume contraction ,
severe renal vasoconstriction , nephrotoxic agents ,
sepsis , shock and hypotension.
 Renal hypoperfusion prerenal aki(reversible)
intermediate stage (slowly reversible) ATN

16. MECHANISM OF ATN

17. (C)POST RENAL
 It includes a variety of disorders characterized by
obstruction of the urinary tract.
 In a patient with 2 functioning kidneys,
obstruction must be bilateral to result in AKI.
 Relief of the obstruction usually results in
recovery of renal function except in patients with
associated renal dysplasia or prolonged urinary
tract obstruction.

18. CAUSES OF POST RENAL AKI
 Posterior urethral valves
 Ureteropelvic junction obstruction
 Ureterovesicular junction obstruction
 Ureterocele
 Tumor
 Urolithiasis
 Hemorrhagic cystitis
 Neurogenic bladder

19. CLINICAL EVALUATION
HISTORY -
 H/o blood loss, diarrhea, vomitting – prerenal aki.
 Past h/o pharyngitis with gross hematuria, edema,
hypertension – acute PSGN.
 Dysentery, petechiae, pallor- HUS.
 Sudden passage of dark red urine, pallor and jaundice with h/o
drug exposure – acute intravascular hemolysis (G6PD def.).
 Rash with arthritis – SLE or HSP.
 H/o prolonged hypotension or exposure to nephrotoxic drugs
– ATN.
 Exposure to certain drugs f/b fever, rash, arthralgia and rising
S.creat – acute TIN
 H/o poor urinary stream with palpable UB or kidney –
obstructive uropathy.
 Abdominal colic,hematuria, dysuria – urinary tract stones.

20. PHYSICAL EXAMINATION -
Obtaining a thorough physical examination is
extremely important . Clues may be found in any
of the following –
 Skin
 Eyes
 Ears
 Respiratory system
 Cardiovascular system
 Abdomen

21. Skin :- Palpable purpura - Systemic vasculitis
Maculopapular rash - Allergic interstitial nephritis
Eye :- Uveitis – interstitial nephritis and necrotizing vasculitis.
Ocular palsy - ethylene glycol poisoning or necrotizing
vasculitis
Ear :- Hearing loss - Alport disease and aminoglycoside
toxicity
Mucosal or cartilaginous ulcerations – Wegener’s
granulomatosis
Respiratory system :- rapid and deep breathing – met.
Acidosis
basal creps - volume overload

22. Cardiovascular examination :
• Pericardial friction rub - Uremic pericarditis
• Increased JVP, Gallop rhythm, pitting edema - CHF
due to volume overload.
Abdomen :
• Renal angle tenderness – nephrolithiasis, papillary
necrosis, renal artery or vein thrombosis.
• Distended bladder – urinary obstruction.
• F/s/o chronic liver disease with ascites with prerenal
aki – hepatorenal syndrome

23. INVESIGATIONS
 Urine R/M
 CBC with CPS
 24 hour urinary protien
 Blood urea and S. creatinine level
 Serum electrolytes
 Throat swab C/S
 ASO titer
 C3 level
 Serum calcium
 Serum phosphate
 Serum uric acid
 ANA
 ABG

24. IMAGING
 Ultrasound of KUB - evaluates renal size, able to
detect masses, obstruction, stones
 Chest x-ray
 DTPA
 DMSA

25. RENAL BIOPSY
Indicated in
 Patient in whom the etiology is not identified.
 Unremitting AKI lasting longer then 2-3 wks or
in assessing the extent of renal damage and
outcome.
 Suspected drug induced AKI in a patient
receiving therapy with a potentially nephrotoxic
drugs.

26. URINARY INDICES
PRE-RENAL INTRINSIC
URINARY SODIUM (mEq/l) < 20 > 40
Urinary osmolality (mOsm/kg) > 500 < 300
Blood urea to creatinine ratio >20:1 < 20:1
Urine to plasma osmolality ratio >1.5 < 0.8 – 1.2
Fractional excretion of sodium < 1 > 1

27. BIOMARKERS FOR EARLY DIAGNOSIS
Biomarkers that indicate renal injury before rise in
S.creatinine values would be helpful in pts. at high
risk of aki like – children undergoing major surgery
or organ transplant, neonates with hypoxia,sepsis or
multi organ failure.
Examples are:
 Neutrophil gelatinase associated lipocalin(NGAL)
 Interleukin -18
 Kidney molecule–1(KIM -1)
 Cystatin -C

28. MANAGEMENT
The basic principles of management include
 Treatment of life-threatening complications
 Maintenance of fluid and electrolyte balance
 Supportive care
 Dialysis & CRRT
 Specific management of underlying disorder

29. A. MANAGEMENT OF LIFE THREATENING
COMPLICATIONS
Such complications are –
 Hyperkalemia
 Fluid overload with heart failure
 Hypertensive emergencies
 Profound acidosis
 Severe anemia

30. 1. Hyperkalemia (>6meq/l):
ECG changes- peaked T waves, widening of QRS interval, ST
depression, arrythmia, arrest.
 Emergency measures(>7meq/l with ECG changes)
 Calcium gluconate 0.5-1 ml/kg over 5 to 10 mins
 Salbutamol(5-10mg)nebulization
 Glucose (50%)0.5-1 gm/kg with 0.1-0.2 unit/kg insulin
 Less urgent(>6meq/l)
 deplete body potassium( stop exogenous sources of
potassium, sodium polystyrene sulfonate resin-kayexalate,
1g/kg orally decreases S.K+ by 1meq/L)

31. 2.Fluid overload :
 fluid restriction
 Insensible water loss(300ml/m²)+UO+extrarenal
fluid loss
 Replace insensible loss by 10%D and UO &
extrarenal loss by N/2D5.
3.Pulmonary Edema
 Oxygen
 Dopamine (5-10) mcg /kg /min infusion in min
fluid
 Frusemide (2-4)mg /kg IV

32. 4.Hypertension
 Symptomatic- Nitroprusside 1-8 mcg/kg/min, Frusemide 2-
4 mg/kg IV
 Asymptomatic- Nifedipine 0.3-0.5 mg/kg PO
5.Severe metabolic acidosis
 pH<7.15, S.bicarbonate<8meq/l
 Sodium bicarbonate – first IV to ↑pH to 7.2 and S.
bicarbonate to 12meq/l, then orally after correction of
S.calcium and phosphorus levels.
 Rapid correction can cause tetany.
6.Severe anemia
 Anemia is generally mild (9-10g/dl)
 If Hb<7g/dl – transfuse PRBCs @10ml/kg slowly over 4-6
hrs.

33. B.MAINTENANCE OF FLUID AND
ELECTROLYTE BALANCE
1.Monitor urine output
2. Volume resuscitation-
• If there is no evidence of fluid overload, then expand
intravascular volume by NS bolus of 20ml/kg over 30min
• Repeat boluses may be given in severe hypovolemia
• Hypovolemic pts should void within 2hr
3.Diuretic challenge-
• After volume resuscitation if no urination occurs a single
IVdose of furosemide(2-4mg/kg) and mannitol(0.5g/kg)
can be given.
• If still no response occurs stop diuretics and start fluid
restriction presuming the pt to be in intrinsic AKI.

34. 4.Hyponatremia(S.Na+<130meq/L)
 Usually cause d/t excessive IV fluids (dilutional
hyponatemia)-t/t is fluid restriction.
 Sodium correction is only given if there is-
»symptomatic hyponatremia
»S.Na+<120meq/L
 Meq of sodium required
=0.6xWt(kg)x{125-S.Na+(meq/L)}
Vol. Of 3% N.S. required is twice of above value
 12 ml/kg of 3% N.S ↑ses S.Na+ by 10 meq/L
 5-10meq/L of S.Na+ should be ↑sed over 30-90mins

35. 5.Hyperphosphatemia,hypermagnesemia, hypocalcemia
• AKI causes phosphate & Mg ions retention.
• Hyperphosphatemia in turn causes hypocalcemia.
• T/t: low phosph. diet,oral phosph. binders(sevelamer, calcium
carbonate)
• Hypocalcemia is usually asymptomatic d/t associated acidosis,
so hypocalcemia should be corrected before correcting acidosis.
• Calcium carbonate/gluconate is given at a dose of 30-50 mg/kg
of elemental calcium.
• There is risk of metastatic deposition of calcium phosphate when
S.Ca2 + x S.PO43ˉ >70.
If fluid is appropriate,then patient should lose 0.5-1% of his wt.
daily and S.Na+ should stay normal.

36. C.SUPPORTIVE CARE
1. NUTRITION
-maximise caloric intake because of ↑sed met. need
-Protein→infant(1.2-2gm/kg),children(0.8-1.2g/kg)
-Energy →min 60kcal/kg
-If on dialysis→protein,fluid & electrolyte
intake should be ↑sed.
-Vit.B-complex & C & micronutrient supplement
2. MANAGE INFECTIONS
-↓sed immunity(azotemia,malnutrition)
-maintain asepsis, maintain oral hygeine
-avoid long term bladder catheterisation

37. 3. DRUGS
-Avoid nephrotoxic drugs(esp. aminoglycosides,
radiocontrast media,NSAID’S,amphotericin-b)
-Dose & dosing interval of other drugs are
modified according to severity of AKI.
-Dopamine in low dose has no role on outcome of
AKI
-Fenoldopam(selective peripheral dopamine rec.
agonist)-may be helpful in preventing AKI
-ANP may be helpful
4. MONITORING
-I/O charting,daily wt. measurement, physical
exam., S.Electrolytes

38. D.DIALYSIS & CRRT
Indication:
Anuria/oliguria
 Uremia(encephalopathy, pericarditis, neuropathy )
 Hyperkalemia: K+ > 6.5 meq/l, K+ 5.5-6.5 meq/l
with ECG changes
 Hyponatremia: Na+ < 120 meq/l if symptomatic
 Fluid overload: resistant to diuretics, CCF,HTN
 Metabolic acidosis: pH< 7.2 despite sodium
bicarbonate therapy.
 Ca:phosphorus imbalance with hypocalcemic tetany
 Hypercatabolic states(marked tissue injury, burns,
sepsis, crush syndrome)

39.  Early dialysis is preferred to prevent complication.
3 types of dialysis-a.intermittent hemodialysis(IHD)
b.peritoneal dialysis(PD) c.CRRT.
a. IHD: prefferd in patients with relatively stable
hemodynamic state.
-Highly efficient, 1 session completes in 3-4 hrs
-Can be done 3-7 times/week
-Complication:hypotension,bleeding,thrombosis,etc
b. P.D: most commonly used in infants & neonates.
-For 1 session→1 cycle of 45-60 min needs to be
repeated for 8-24 hours/day.
-No need for anticoagulation,so ↓sed risk of
bleeding,may cause abdominal pain & peritonitis

40. c. CRRT: Indications-hemodynamic instability,
sepsis, extensive trauma,MODS,tumour lysis
syndrome
-continuos removal of solutes ,fluid & electrolytes
-3 types: CVVH, CAVH, CAVHD
-CVVH:helpful in management of AKI with severe
fluid overload
-CAVHD:most effective type pf CRRT.

41. E.SPECIFIC MANAGEMENT OF UNDERLYING
DISORDER
 Prerenal AKI: administer crystalloids, stop
diuretics, NSAIDs, ACE inhibitors.
 ATN: supportive care, discontinue drugs or toxin,
treat cause of circulatory failure.
 Glomerulonephritis: supportive care, control
hypertension, if its due to shunt infection-
removal of shunt & appropriate antibiotics are
given.

42.  HUS: supportive care, plasma infusion, plasma
exchange
 Vasculitis: immunosuppressive medication, plasma
exchange
 Interstital nephritis: discontinue offending drugs,
consider steroid therapy.
 Renal artery , vein occlusion: anticoagulation,
thrombolysis or surgery.
 Intrarenal obstruction: discontinue offending
drugs, alkaline diuresis for rhabdomyolysis ,
haemoglobinuria or urate crystal.
 Urinary tract obstruction: bladder cathaterization
or nephrostomy, surgical treatment of obstruction.

43. OUTCOME
 Mortality rates from 30-50% have been reported from
developing countries. But the results have markedly
improved at tertiary centers with proper expertise and
modern facilities.
 Outcome depend upon underlying cause.
 Prognosis is favourable in ATN from volume depletion,
intravascular hemolysis, acute interstial nephritis and
drugs or toxin related AKI especially when
complicating factor are absent .
 In cresentic GN, atypical HUS, and AKI associated with
sepsis, multi organ failure the prognosis is less
satisfactory .

44. PREVENTION OF AKI
 Important measures includes prompt rehydration
therapy in acute diarrhea, avoidance or judicious
use of nephrotoxic drugs.
 Maintenance of proper hydration for patients
undergoing diagnostic procedures with radio
contrast media.
 Forced diuresis along with the use of allopurinol
is effective preventing AKI in patient with TLS.

45. CHRONIC KIDNEY DISEASE

46. DEFINITON
 Irreversible loss of renal function that eventually
requires renal replacement therapy
Patient has CKD if either of the following criteria are
present:
1. Kidney damage for ≥3 mo, 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 the blood or urine
• Abnormalities in imaging tests
• Abnormalities on kidney biopsy
2. GFR <60 mL/min/1.73 m2 for ≥3 mo, with or without
the othersigns of kidney damage described above

47. GFR
 Schwartz formula: GFR = k x height(cm)
(ml/min/1.73m²) S.Creatinine(mg/dl)
k= 0.33 for LBW infants
0.45 for term AGA infants
0.55 children & adolescent female
0.70 adolescent male
 New formula by CKD study:
uses k= 0.413,
Can be used for GFR between 15-75 ml/min/1.73m²
In children between 1-16yr.

48. STAGES OF CKD
Stage Description GFR
(ml/min/1.73
m²)
1 Kidney damage with normal or ↑ GFR > 90
2 Kidney damage with mild ↓ GFR 60-89
3 Moderate ↓ in GFR 30-59
4 Severe decrease in GFR 5-29
5 Kidney failure <15 or on
dialysis

49. ETIOLOGY:-
1. UNDER 5 YR
(most commonly congenital abnormalities)
* renal hypoplasia
* renal dysplasia
* obstructive uropathy
* congenital nephrotic syndrome
* prune belly syndrome
* cortical necrosis
* FSGS
* polycystic kidney
* renal vein thrombosis
* hemolytic uremic syndrome

50. 2.AFTER 5 YRS
(acquired and inherited disorders)
* glomerulonephritis
* nephronophthisis
* alport syndrome
3.THROUGHOUT CHILDHOOD YEARS
* cystinosis
* hyperoxaluria
* polycystic kidney disease

51. RISK FACTORS FOR CKD
 H/O AKI
 H/O V.U.R or recurrent U.T.I
 Corrected or uncorrected obstructive uropathy
 H/O A.G.N or N.S
 Family H/O polycystic kidney disease
 Past H/O H.S.P
 k/c/o D.M, HTN,SLE, or vasculitis.

52. PATHOGENESIS
Hyperfiltration Injury
* final common pathway of
glomerular destruction
* hypertrophy of remaining nephrons
* increase glomerular blood flow
* ↑ glomerular filtration in surviving nephrons
* progressive damage to surviving nephrons (due
to elevated hydrostatic pressure/toxic effect of
proteins)
* sclerosis of surviving nephrons
*leads to a vicious cycle of ↑ glomerular filtration
and hyperfiltration injury.

53. Proteinuria:
* exerts a direct toxic effect
* causes infiltration of monocytes / macrophages
* enhancing glomerular sclerosis
Hypertension:
* exacerbate disease progression
* causes arteriolar nephrosclerosis
* and hyperfiltration injury
Hyperphosphatemia :
* calcium phosphate deposition in renal
interstitium and blood vessels.
Hyperlipidemia:
* oxidant mediated injury

54. PATHOPHYSIOLOGY OF CKD
Accumulation of nitrogenous waste products
due to ↓ in GFR
Acidosis
due to ↓ed NH3 synthesis.
Impaired bicarbonate reabsorption
↓ed net acid excretion
Sodium retention
excessive renin production, oliguria
Sodium wasting and urinary concentrating defect
solute diuresis,
tubular damage

55. Hyperkalemia
↓ in GFR
metabolic acidosis
excessive potassium intake
hyporeninemic hypoaldosteronism
Renal osteodystrophy
impaired renal production 1,25-DHCC
hyperphosphatemia
hypocalcemia
secondary hyperparathyroidism
Growth retardation
inadequate caloric intake
renal osteodystrophy, metabolic acidosis
anemia, growth hormone resistance

56. Anemia
↓ed erythropoietin production
iron deficiency, folate deficiency,vit B12
deficiency ,↓ed erythrocyte survival
Bleeding tendency
defective platelet function
Infection
defective granulocyte function,
impaired cellular immunity,
indwelling dialysis catheters
Neurologic symptoms (fatigue, poor
concentration, headache, drowsiness, memory
loss, seizures, peripheral neuropathy)
uremic factors, aluminum toxicity,
hypertension

57. Malnutrition
anorexia,nausea,vomitting(uremic gastritis)
abnormal taste sensation
inappropriate dietary restrictions
protein loss due to dialysis
Gastrointestinal symptoms (feeding intolerance,
abdominal pain)
gastroesophageal reflux
decreased GI motility
Hypertension
volume overload, excessive renin production
Hyperlipidemia
decreased plasma lipoprotein lipase activity
Pericarditis / Cardiomyopathy
uremic factors, hypertension
fluid overload
Glucose intolerance
tissue insulin resistance

58. CLINICAL MANIFESTATION
Features of advanced CKD (stage 3-5)
* lethargy, fatigue,anorexia, vomiting
* growth retardation
* failure of thrive
* anemia
* hypertension
* bone disease
Late features
* itching
* severe acidosis
* hyperkalemia
* LVF, pulmonary edema
* uremic pericarditis
* altered sensorium

59. LABORATORY FINDINGS
* elevated BUN and creatinine
* ↓ GFR
* hyperkalemia
* hyponatremia
* acidosis
* hypocalcemia
* hyperphosphatemia
* elevated uric acid
* hypoproteinemia (if proteinuria)
* normocytic, normochromic anemia
* elevated serum cholesterol and triglyceride
* hematuria & proteinuria(glomerulonephritis)

60. MANAGEMENT OF CKD
AIMS OF TREATMENT
* Retarding the progression of renal dysfunction
*Replacing absent/diminished renal function
ROUTINE MONITORING TO BE DONE OF…
*Blood studies- RFT, S.electrolytes, S.calcium &
phosphorus, S.albumin, alk.phosphatase, Hb%,
*S.Parathormone and bone X-rays- to detect renal
osteodystrophy
*ECHO- To detect LVF & cardiac dysfunction early.

61. STRATEGY TO SLOW THE PROGRESSION
* optimal control of hypertension(<75th percentile)
* reduce proteinuria(goal<300mg/m²/day)
* ACE inhibitors/ ARBs are drugs of choice for both
* maintain serum phosphorus (ca x ph=<55)
* prompt treatment of infections and episodes of
dehydration
* correction of anemia(erythropoetin/darbepoetin-alpha)
* control of hyperlipidemia
* non hypercalcemic doses of vit D analogs
* prevention of obesity
* avoid use of NSAID and nephrotoxic drugs

62. NUTRITION
 Assesment of adequacy of dietary intake(3-day diet record)
 Assesment of nutritional status(wt, wt/age,ht/age, BMI,
HC)-should be done atleast semi-annually.
 If there is malnutrition- 125% of RDA of calories should be
given for catch up growth
 Total calories = 55-60%(carbohydrates),30%(fats),
10%(proteins)
Proteins- low protein diet not recommended
-diet should contain 100%RDA of protein
-of that >50% should be from high biological value proteins
-children on dialysis should take extra 0.4-0.8g/kg/day of
protein
-excessive proein intake should be avoided in children with
metabolic acidosis and hyperphosphatemia

63. Fats- there is ↑sed risk of CVD in CKD.
-Saturated fats should be <10% of total calories
-Diets rich in PUFA,MCT & complex carbs
prefered.
Vitamins-100% RDA of Vit A,B1,B2,B6,B12,D,E,K,
Folic acid,Cu,Zn should be taken.
-Requirements in CKD:B1,B2,F.A→1mg each
pyridoxine,pantoyhenic acid→10mg each
vit C(50mg),vit B12(5mg),Biotin(300mg).
-If GFR<40 then F.A. supplementation is needed in
order to prevent hyperhomocycstinemia.
-Children on PD need vit C,pyridoxine & F.A
supplementation.

64. Restriction of dietary phosphorous:
-In CKD stage 3 to 5 & 5D, 80-100% RDA should
be given.
-foods rich in phosphorous should be
avoided, but taking care not to cause inadequate
protein intake because such foods are also rich
source of protein
Food should be attractive & pleasant.
Unnecessary restriction should be avoided.
Infants needing top feed should receive special
formula with high calorie, low sodium & phosph.
If oral feeding is not adequate, supplemental NGT
feeding can be given.

65. FLUID & ELECTROLYTE
* most patients maintain normal sodium & water balance
*Usual sodium intake is allowed
*2g of salt is allowed daily,no extra salt
*if BP is high- restrict to 0.8-1g/day
*if there is polyuria with urinary sodium loss: give high volume, low
caloric density feeding with sodium supplements
* high BP, edema or heart failure: require sodium restriction & diuretic
therapy
* fluid restriction is rarely necessary untill ESRD
* hyperkalemia: restriction of dietary K+ intake
oral alkalinizing agent
kayexalate
*hypokalemia- due to excessive diuretics- <3meq/l
-supplements rich in potassium given
*potassium intake is restricted if GFR<10 ml/min/1.73m²

66. GROWTH
*Growth impairment occurs when GFR<50%
*Firstly t/t Nutritional deficiencies,acid-base
imbalance,correct salt depletion and calcium and vit D
deficiency
*Short stature is long term sequelae
* growth hormone resistant state
(GH ↑, IGF ↓)
* abnormality of IGF binding protein
*children who remain<-2SD for ht despite adequate
medical support can be given recombinant human
GH (0.05mg/kg/24hrs),SC daily
* continue until the pt reaches50th percentile for MPH
or achieves a final adult height or undergoes
renal transplantation

67. CHRONIC KIDNEY DISEASE-MINERAL BONE DISEASE
The syndrome of clinical,metabolic and imaging deformities
in CKD is termed as CKD-MBD.
The term osteodystrophy should be restricted to description
of histological features on bone biopsy.
Most common condition seen in children is a high turnover
bone disease caused by secondary hyperparathyroidism
The skeletal finding in this condition is Osteitis fibrosa
cystica

68. Pathophysiology of CKD-MBD
* When GFR decline to 50% of normal
* Decline in 1 hydroxylase activity
* Decreased production of activated vit. D
* ↓ intestinal absorption of calcium
* Hypocalcaemia
* Secondary hyperparathyroidism(to correct
hypocalcemia)
* Increased bone resorption
* When GFR declines to 25% of normal
* Hyperphosphatemia – further promotes
hypocalcemia and increased PTH production

69. Clinical manifestations of CKD-MBD
* Muscle weakness, Bone pain
* Fractures with minor trauma
* Rachitic changes, varus or valgus deformity
slipped capital femoral epiphysis.
* s.Ca↓, s. Ph↑, ↑alkaline phosphate, ↑PTH
* Subperiosteal resorption of bone with
widening of metaphysis

70. Treatment of CKD-MBD
* T/t goals-prevent bone deformity and
normalize growth velocity
*Target phosphorus levels-
adolescent(3.5-5.5mg/dl)
children(4-6mg/dl)
*Low phosphorus diet(similac PM 60/40)
* Phosphate binders-
Calcium carbonate & calcium acetate
Sevelamer (Renagel) non calcium binder
Avoid aluminum based binder
* Vitamin D therapy-(Vit D levels
<30ng/ml(insufficiency) <15ng/ml(deficiency)
- oral vit D3- 2lakh -4lakhs unit over 2-3 mnths
- in CKD stg 5 active vit D analogs are used-
paricalcitol,doxercalciferol
* Maintain calcium / phosphorus product (Ca x PO4) at < 55

71. ANEMIA
* Inadequate erythropoeitin production
* Iron deficiency
* Folic acid , Vitamin B12 deficiency
* Decreased erythrocyte survival
* Erythropoeitin if Hb < 10g/dl
dose 50-150 mg/kg/dose S/C 1-3 times/wk
* Keep Hb between 11-12g/dl
* Darbopoeitin alfa (longer acting)
dose 0.45μg/kg/wk

72. HYPERTENSION
* Salt-restriction
* Diuretic therapy
* Hydrochlorothiazide 2 mg/kg/24hrs
* Furosemide 1-2 mg/kg/dose
* ACE inhibitors - angiotensin II blockers
(Enalapril, lisiopril, losartin) for proteinuric
renal disease
* Calcium channel blockers (Amlodipin)
* B-Blockers (propranolol, atenolol)

73. IMMUNIZATIONS
* Immunization according to the schedule
* Avoid live vaccine if on immunosuppressive
drugs
* Give live vaccine(MMR& Varicella vaccine)
before renal transplantation
* Yearly influenza vaccine
* Suboptimal response