Renal failure in children can result from pre-renal, renal, or post-renal causes. The kidneys are important for filtering waste and maintaining fluid and electrolyte balance. Acute renal failure is characterized by a rapid decline in urine output and rising BUN and creatinine levels. It can be caused by decreased blood flow, direct kidney damage, or urinary tract obstruction. Prompt diagnosis and treatment are needed to prevent complications and determine if recovery or long-term dialysis will be required.

8. RENAL FAILURERENAL FAILURE
IN CHILDRENIN CHILDREN

9. Importance of kidneyImportance of kidney
MainMain waste excreterwaste excreter
MaintainsMaintains fluid-, electrolyte- and ABBfluid-, electrolyte- and ABB
MakesMakes erythropoietinerythropoietin
MakesMakes thrombopoietinthrombopoietin
Excretes someExcretes some drugsdrugs
BiotransformsBiotransforms
ActivatesActivates VDVD
Nephron:Nephron: glomerulus + tubule: 1 million/Kidneyglomerulus + tubule: 1 million/Kidney
ABB: acid base balanceABB: acid base balance 9

10. Renal Function
10

11. Renal bl. Flow:Renal bl. Flow: 20% of Cardiac OP20% of Cardiac OP
 Renal a.Renal a. afferent arterioleafferent arteriole  glomerulusglomerulus efferent a.efferent a.
 In the cortexIn the cortex
peritubularperitubular
capillariescapillaries
 In theIn the
juxtamedullaryjuxtamedullary
regionregion 
vasa rectavasa recta  renalrenal
veinvein

12. Regulation of RBF.Regulation of RBF. Complex!Complex!
Adults:Adults: auto-regulated withinauto-regulated within MAP 80-160mmHgMAP 80-160mmHg
Auto-regulatedAuto-regulated tto ensure UOPo ensure UOP
– 60%60% byby RAAS and PGs.RAAS and PGs. 40%40% byby adenosine, endothelin, NO,adenosine, endothelin, NO,
dopaminedopamine
– RBFRBF doubles in first 2w of lifedoubles in first 2w of life
 Triples by 1yTriples by 1y
 Adult levels by preschoolAdult levels by preschool
RBF: renal blood f. UOP: urinary output. MAP: mean arterial p. RAASRBF: renal blood f. UOP: urinary output. MAP: mean arterial p. RAAS-renin angiotensin-renin angiotensin
aldosterone sysaldosterone sys

13. Renin-Angiotensin AxisRenin-Angiotensin Axis
HypotensionHypotension ⇒⇒ low afferent a. BPlow afferent a. BP ⇒⇒ low NaCl uptakelow NaCl uptake
⇒⇒ renin fromrenin from JGAJGA ⇒⇒ AG I to AG IIAG I to AG II ⇒⇒ AldosteroneAldosterone ⇒⇒
more Na and water re-absorptionmore Na and water re-absorption ⇒⇒ raises BPraises BP
Increased reninIncreased renin in ARFin ARF
can lower renal damage.can lower renal damage.
Mannitol/loop diureticsMannitol/loop diuretics
can also helpcan also help
RAS- renin angiotensin sys.RAS- renin angiotensin sys.
JGA:JGA: Juxtaglomerular Apparatus.
AG: angiotensin

15. ProstaglandinsProstaglandins
– renalrenal vasodilatorvasodilator, especially in injured kidney, especially in injured kidney
AdenosineAdenosine:: potentpotent renovasoconstrictorrenovasoconstrictor butbut pperipheraleripheral
vasodilatorvasodilator.. MethylxanthinesMethylxanthines are adenosine blockersare adenosine blockers
EndothelinEndothelin:: very potentvery potent vasoconstrictorvasoconstrictor
– in ARF, causes low afferent a. flow and GFRin ARF, causes low afferent a. flow and GFR
– it stimulates ANP release and can increase UOPit stimulates ANP release and can increase UOP
ANP: Atrial natriuretic peptide, a peptide hormoneANP: Atrial natriuretic peptide, a peptide hormone

16. Nitric Oxide (NO)Nitric Oxide (NO)
 Produced by NOS.Produced by NOS. VasodilatorVasodilator. Helps Na re-absorption. Helps Na re-absorption
 Important in the overall homeostasis of RBFImportant in the overall homeostasis of RBF
– NOS blocker: natriuresisNOS blocker: natriuresis
DopamineDopamine
 Reno-vasodilator at low dosesReno-vasodilator at low doses, constrictor at high doses, constrictor at high doses
 Dopamine receptors in the afferent a.Dopamine receptors in the afferent a.
 Also causes natriuresisAlso causes natriuresis
NOS: Nitric oxide synthetaseNOS: Nitric oxide synthetase

17. Tubular FunctionTubular Function
Proximal CT:Proximal CT: Most of reabsorption.Most of reabsorption.
Fluid is isotonic. 70% Na and allFluid is isotonic. 70% Na and all
glucose and amino a. absorbedglucose and amino a. absorbed
Loop of HenleLoop of Henle
– Descending loop:Descending loop: permeable to H2O alonepermeable to H2O alone
– Ascending :Ascending : … to Na alone; critical for u. dilution and… to Na alone; critical for u. dilution and
most often damaged in ARF. It is most sensitive to ischemiamost often damaged in ARF. It is most sensitive to ischemia
– Lasix inhibits Na-K-Cl ATPase and decreases O2 need: less damageLasix inhibits Na-K-Cl ATPase and decreases O2 need: less damage

18. Tubular FunctionTubular Function
Distal CT:Distal CT: Re-absorbs more 12%Re-absorbs more 12%
NaCl. Proximal segment isNaCl. Proximal segment is
impermeable to water; distalimpermeable to water; distal
segment secretes Ksegment secretes K++
, HCO3, HCO3__
Collecting DuctCollecting Duct
Aldosterone increases Na reuptake and K wastingAldosterone increases Na reuptake and K wasting
ADH enhances water reuptakeADH enhances water reuptake

19. GFRGFR
depends on BP within glomerulus; oncotic pressure increasesdepends on BP within glomerulus; oncotic pressure increases
as you progress through itas you progress through it
Podocyte foot processes form filtration slits:Podocyte foot processes form filtration slits:
– allows ultrafiltrate to passallows ultrafiltrate to pass
– limit filtration oflimit filtration of
large particleslarge particles

21. C/of Kidney Diseases in ChildrenC/of Kidney Diseases in Children
 Age <5y:Age <5y: birth defect:birth defect: renalrenal agenesis, -dysplasia, ectopic K,agenesis, -dysplasia, ectopic K,
PUJO, PUV, VUR, etc.;PUJO, PUV, VUR, etc.; hereditary dhereditary d.:.: PKD, Alport syn.PKD, Alport syn.
 5-14y:5-14y: infx.:infx.: APSGN, HUS, IgAN;APSGN, HUS, IgAN; hereditary,hereditary, NS,NS, systemicsystemic
d.:d.: Dm, HTN, VasculitisDm, HTN, Vasculitis
 15-19y:15-19y: glomerulopathy/nephropathyglomerulopathy/nephropathy
Misc.:Misc.: burns, dehydration, bleeding, traumaburns, dehydration, bleeding, trauma
Hb.uria, surgery: hypotension, shockHb.uria, surgery: hypotension, shock
Urine BlockageUrine Blockage

22. ARF (ARF (aka AKF/AKI):aka AKF/AKI): UOP to <300ml/mUOP to <300ml/m‌‌2/2/
dd
Life-threatening ac. fallLife-threatening ac. fall in RF characterized by rise in BUNin RF characterized by rise in BUN
and S. Cr., frequent hyperK, m. acidosis, HTNand S. Cr., frequent hyperK, m. acidosis, HTN
 Oliguria:Oliguria: UOP <1mL/kg/h in infants, <0.5mL in children,
<400mL/d in adults
 Anuria:Anuria: UOP <0.5 ml/kg/h.UOP <0.5 ml/kg/h. <100ml/d in adults
Nonoliguric ARFNonoliguric ARF:: occasional: rising BUN and Cr., oftenoccasional: rising BUN and Cr., often
after severe burns/open heart surgeryafter severe burns/open heart surgery

23. ARF …ARF …
3 forms:3 forms: prerenalprerenal ((commonestcommonest),), renal, postrenalrenal, postrenal
Fate:Fate: significant MM. Partial/complete recovery/ESRD.significant MM. Partial/complete recovery/ESRD.
May develop multi-organ d.May develop multi-organ d.
AAdequate UOP and Px of further damage isdequate UOP and Px of further damage is criticalcritical
Rx:Rx: depends on severity and degree of recovery:depends on severity and degree of recovery:
conservative - dialysis/renal transplantconservative - dialysis/renal transplant
UOP: urinary output. HUS: hemolytic-uremic synUOP: urinary output. HUS: hemolytic-uremic syn

24. Causes of ARFCauses of ARF
Pre-renalPre-renal ((Decreased true/effective IVV): hypovolemia,hypovolemia,
bleed, sepsis, shock, Hb-/myoglobinuria, HUS, HF, salt-bleed, sepsis, shock, Hb-/myoglobinuria, HUS, HF, salt-
losing renal/adrenal d., D insipidus, diuretics; “third-losing renal/adrenal d., D insipidus, diuretics; “third-
spacing” of fluids (NS, sepsis, pancreatitis, capillary leakspacing” of fluids (NS, sepsis, pancreatitis, capillary leak
syn.), hepatorenal syn.syn.), hepatorenal syn.
RenalRenal:: GN, HUS, SCD, RV clot, trauma, ac.GN, HUS, SCD, RV clot, trauma, ac. interstitialinterstitial
nephritis, ATN, PKD, toxins (UA, stings, etc),nephritis, ATN, PKD, toxins (UA, stings, etc), drugs: sp. AB;drugs: sp. AB;
chemo-, contrasts
Post-renal:Post-renal: obstruction:obstruction: calculi, bladder OO, internal or
external ureteral compression
Worldwide:Worldwide: most ARF in children: volume depletion/HUSmost ARF in children: volume depletion/HUS

25. ‘‘Snowstorm’ appearance ofSnowstorm’ appearance of
infantileinfantile polycystic diseasepolycystic disease
MulticysticMulticystic
Dyplastic Kidney.Dyplastic Kidney.
Most severeMost severe
renal dysplasiarenal dysplasia
with large cysts/with large cysts/
ureteral atresiaureteral atresia
UnilateralUnilateral
Sporadic (+/-Sporadic (+/-
VACTERL)VACTERL)
Involutes overInvolutes over
time.time. Remove ifRemove if
doesn’t involutedoesn’t involute

26. NephrotoxinsNephrotoxins
 PCTPCT:: Aminoglycosides, Ampho. B, Cisplatin, contrasts, Ig, MannitolAminoglycosides, Ampho. B, Cisplatin, contrasts, Ig, Mannitol
 DCT:DCT: NSAIDs, ACEIs, Ciclosporin, Li, Endoxan, Ampho …NSAIDs, ACEIs, Ciclosporin, Li, Endoxan, Ampho …
 Tubular Obs.:Tubular Obs.: Sulphas, MTX, Aciclovir, D. glycol, TriamtereneSulphas, MTX, Aciclovir, D. glycol, Triamterene
 Ac int. nephritis:Ac int. nephritis: β-β-lactam, Vancomycin, Rifampicin, Sulphas,lactam, Vancomycin, Rifampicin, Sulphas,
Ciprofloxacin, NSAIDs, H2 blockers, Lasix, Thiazides, PhenytoinCiprofloxacin, NSAIDs, H2 blockers, Lasix, Thiazides, Phenytoin
 Chronic IN:Chronic IN: Li, CiclosporinLi, Ciclosporin
 Acute GN:Acute GN: immune-mediated: Heroin, Pamidronate: FSGS. Gold:immune-mediated: Heroin, Pamidronate: FSGS. Gold:
MGN, PenicillamineMGN, Penicillamine
 D insipidus:D insipidus: Li, Ampho. B: irreversible at HD, Fluoride,Li, Ampho. B: irreversible at HD, Fluoride,
Demeclocycline, FoscarnetDemeclocycline, Foscarnet
 Heavy metals, Aristolochic acids in herbal supplements, Rhubarb:Heavy metals, Aristolochic acids in herbal supplements, Rhubarb:
nephritis in some peoplenephritis in some people

29. Pathophysiology: PrerenalPathophysiology: Prerenal
Sudden fall in RP (hypotension): ischemia: fall in GFRSudden fall in RP (hypotension): ischemia: fall in GFR
 constriction of afferent a.constriction of afferent a.
 uremia; BUN/Cr ratio of >20uremia; BUN/Cr ratio of >20
 IschemiaIschemia  catecholamine, ADH, RAAS: vasoconstrictioncatecholamine, ADH, RAAS: vasoconstriction
 Body re-establishes RP by restoring IVV: afferent a. relax,Body re-establishes RP by restoring IVV: afferent a. relax,
finally, vasodilatory PGs come in to help maintain RP.finally, vasodilatory PGs come in to help maintain RP.
Aspirin or NSAIDs inhibit the vasodilator PGsAspirin or NSAIDs inhibit the vasodilator PGs
RP: renal perfusion. IVV: intravascular volume. PG: prostaglandinRP: renal perfusion. IVV: intravascular volume. PG: prostaglandin

30. Pathophysiology: RenalPathophysiology: Renal (25-40% ARF)(25-40% ARF)
90% have ATN90% have ATN
Primary renal damage is thePrimary renal damage is the most complicated:most complicated: affectsaffects
 FiltrationFiltration
 BFBF
 Salt handling and water processing (tubular damage)Salt handling and water processing (tubular damage)

31. Pathophysiology: post-renalPathophysiology: post-renal
Obstruction:Obstruction: ⇑⇑ in proximal fluid pressure: renal damagein proximal fluid pressure: renal damage
Gross hematuria and colic in stones. Prenatal US: bilateralGross hematuria and colic in stones. Prenatal US: bilateral
HDN, hydroureters in PUV. Palpable flank mass, in PUJOHDN, hydroureters in PUV. Palpable flank mass, in PUJO
UOP and urinary sediment may be variable. In obstructiveUOP and urinary sediment may be variable. In obstructive
uropathy a dilated renal pelvis is frequent on US. Radio- scan:uropathy a dilated renal pelvis is frequent on US. Radio- scan:
isotope collection within the kidney or at any level ofisotope collection within the kidney or at any level of
ureter/UB, with delayed or absent excretionureter/UB, with delayed or absent excretion

33. CF in ARFCF in ARF
Depend on underlying cause
DV, tummy ache, oliguria/anuria, or normal/high UOP
Bleed, pallor, F, rash
H/of recent inf., drugs, heavy metals or toxins, trauma
Edema, SoB
Detectable mass in abdomen
The symptoms of ARF and CRF may resemble other conditions

34. TreatmentTreatment
PICU.PICU. depends on cause and damagedepends on cause and damage
A nephrologist should be involvedA nephrologist should be involved
Goals:Goals: 1. cause. 2. how wastes and water are affecting body1. cause. 2. how wastes and water are affecting body
 Removing cause:Removing cause: drugs and others ingested productsdrugs and others ingested products
 Fluid and electrolyte balance:Fluid and electrolyte balance: correct dehydration. Fluidcorrect dehydration. Fluid
restrictionrestriction:: if overload: diuretic. Replace insensible loss +if overload: diuretic. Replace insensible loss +
loss in outputs - endogenous water. IO chart. Correctloss in outputs - endogenous water. IO chart. Correct
chemical abnormalities: AB balancechemical abnormalities: AB balance
 Increase BF:Increase BF: improve heart function or increase BPimprove heart function or increase BP

35. Treatment …Treatment …
 If no recovery:If no recovery: dialysis. HD x3/w. PD can be done. Mostdialysis. HD x3/w. PD can be done. Most
don't need. In some, residual damage persistsdon't need. In some, residual damage persists
 Caloric management:Caloric management: at least 25% of the daily caloriesat least 25% of the daily calories
 Anemia:Anemia: no BT unless active bleeding, hemodynamicno BT unless active bleeding, hemodynamic
instability, or a hct. <25%instability, or a hct. <25%
Vasoactive Agents:Vasoactive Agents: llow-dose (0.5-3.0 mcg/kg/min) dopamineow-dose (0.5-3.0 mcg/kg/min) dopamine
can improve RP by vasodilation, but it is debated whethercan improve RP by vasodilation, but it is debated whether
this “renal dosing” is beneficialthis “renal dosing” is beneficial

36. FluidsFluids
 If oliguric:If oliguric: rapid bolus of 20mL/kg NS, PCV, or albuminrapid bolus of 20mL/kg NS, PCV, or albumin
(debated). Repeat if low BP or increased HR, low capillary(debated). Repeat if low BP or increased HR, low capillary
refill, or anuria until clinical improvementrefill, or anuria until clinical improvement
 Furosemide/mannitol increase UOP and decrease tubularFurosemide/mannitol increase UOP and decrease tubular
obstruction; also limit O2 consumption in damaged cells.obstruction; also limit O2 consumption in damaged cells.
They alone does not affect RRT. Furosemide inhibits Na-K-They alone does not affect RRT. Furosemide inhibits Na-K-
Cl cotransporter in thick ascending LOHCl cotransporter in thick ascending LOH
 Prior to their use, IVV is restored and fractional excretionPrior to their use, IVV is restored and fractional excretion
of Na determined to identify the type of renal failureof Na determined to identify the type of renal failure

37.  Once IVV is restored, fluid is restricted to 400mL/mOnce IVV is restored, fluid is restricted to 400mL/m22
/d (5%/d (5%
DA) plus UOP and extrarenal losses, if the child has a UOPDA) plus UOP and extrarenal losses, if the child has a UOP
of at least 1 mL/kg/h, has pulmonary edema, has third-of at least 1 mL/kg/h, has pulmonary edema, has third-
spacing of fluids, or meets the criteria for having ARF. Finalspacing of fluids, or meets the criteria for having ARF. Final
fluid adjustments depend on daily wt and close monitoringfluid adjustments depend on daily wt and close monitoring
of IO chartof IO chart
ElectrolytesElectrolytes
 Frequent dyselectrolytemias seen in ARF must be Rx:Frequent dyselectrolytemias seen in ARF must be Rx:
hypoNa, hyperK, m. acidosis, hypoCahypoNa, hyperK, m. acidosis, hypoCa

38. HyponatremiaHyponatremia (<130.0 mEq/L)(<130.0 mEq/L)
usually in hypoNa dehydration. If Na is >120mEq/L), fluidusually in hypoNa dehydration. If Na is >120mEq/L), fluid
restriction or dialysis should be considered, and Na isrestriction or dialysis should be considered, and Na is
corrected to at least 125mEq/L slowly over several hours.corrected to at least 125mEq/L slowly over several hours.
If pt is asymptomatic and Na is <120mEq/L, rapidIf pt is asymptomatic and Na is <120mEq/L, rapid
correction to 125mEq/L should be done because ofcorrection to 125mEq/L should be done because of
increased risk for seizuresincreased risk for seizures
 Rapid vs slow correction is based on duration of hypoNa asRapid vs slow correction is based on duration of hypoNa as
well as cl. appearancewell as cl. appearance
 If symptomatic with seizures, 3% NaCl should be used forIf symptomatic with seizures, 3% NaCl should be used for
rapid correction to 125mEq/Lrapid correction to 125mEq/L
 2 equations can be used for administering 3% NaCl2 equations can be used for administering 3% NaCl

39. HyperkalemiaHyperkalemia
low tubular K secretion, K shift out of cells in acidosis, orlow tubular K secretion, K shift out of cells in acidosis, or
from broken tubular cells. Mild-severe: 5.6-7.6mEq/Lfrom broken tubular cells. Mild-severe: 5.6-7.6mEq/L
 ECG: tall, peaked TECG: tall, peaked T
 It is life-threatening and must be Rx aggressively quicklyIt is life-threatening and must be Rx aggressively quickly
Rx.:Rx.: 10% Ca gl. (10-15mL/kg) to stabilize m. potential;10% Ca gl. (10-15mL/kg) to stabilize m. potential;
bicarb. to shift K intracellularly; insulin (0.1- 0.5 iu/kg) plusbicarb. to shift K intracellularly; insulin (0.1- 0.5 iu/kg) plus
10-25% glucose; resin Na polystyrene sulfonate 1g/kg10-25% glucose; resin Na polystyrene sulfonate 1g/kg
PR/PO to exchange Na for K in colon; takes a few hoursPR/PO to exchange Na for K in colon; takes a few hours
 If not effective: dialysis, especially in anuria. AllIf not effective: dialysis, especially in anuria. All
electrolytes should be monitored (rebound)electrolytes should be monitored (rebound)
 Severe acidosis (bicarb. <10 mEq/L): by IV bicarb.Severe acidosis (bicarb. <10 mEq/L): by IV bicarb.

41. HypocalcemiaHypocalcemia
hyperphosphatemia, low GI uptake, bone resistance to PTHhyperphosphatemia, low GI uptake, bone resistance to PTH
 Rx with IV Ca gluconate in tetany or arrhythmiasRx with IV Ca gluconate in tetany or arrhythmias
 Oral CaCO3 also is effectiveOral CaCO3 also is effective
 Care should be taken when giving these products in theCare should be taken when giving these products in the
presence of hyperphosphatemiapresence of hyperphosphatemia
 Oral phosphate binders (CaCO3 and Ca acetate, non-CaOral phosphate binders (CaCO3 and Ca acetate, non-Ca
PO4 binders can be administered to decrease PO4PO4 binders can be administered to decrease PO4
 VD can be provided to prevent 2y hyperPTH that can occurVD can be provided to prevent 2y hyperPTH that can occur
in patients whose ARF is prolongedin patients whose ARF is prolonged

43. HypertensionHypertension
usually is due to fluid overload (Furosemide/dialysis) orusually is due to fluid overload (Furosemide/dialysis) or
changes in BV tone (anti-HTN drugs). IV anti-HTN are usedchanges in BV tone (anti-HTN drugs). IV anti-HTN are used
if pt. cannot take orally (intubation) or if severe HTNif pt. cannot take orally (intubation) or if severe HTN
(systolic/diastolic BP at 99C). Na nitroprusside is effective,(systolic/diastolic BP at 99C). Na nitroprusside is effective,
but it requires monitoring of thiocyanate (byproduct) conc.but it requires monitoring of thiocyanate (byproduct) conc.
as kidney excretes it. IV labetalol, nicardipine, enalaprilat,as kidney excretes it. IV labetalol, nicardipine, enalaprilat,
diazoxide are used for HTN. If HTN is not severe, short-diazoxide are used for HTN. If HTN is not severe, short-
acting nifedipine can be usedacting nifedipine can be used

44. NutritionNutrition
 Proper nutrition is a major issue in ARF (catabolic state).Proper nutrition is a major issue in ARF (catabolic state).
Mn is common. Infants can be given a formula low in PO4.Mn is common. Infants can be given a formula low in PO4.
Older children can be fed formulas that provide proteinsOlder children can be fed formulas that provide proteins
of high biologic value. IV alimentation SOS. Provide >70%of high biologic value. IV alimentation SOS. Provide >70%
of calories as CHO (as dextrose 25%) and <20% as lipids,of calories as CHO (as dextrose 25%) and <20% as lipids,
proteins 0.5-2g/kg/dproteins 0.5-2g/kg/d
MedicationsMedications
 If the pt already is taking drugs excreted by kidney,If the pt already is taking drugs excreted by kidney,
dosages/intervals should be adjusted to account for thedosages/intervals should be adjusted to account for the
degree of renal impairmentdegree of renal impairment

45. Indications for dialysisIndications for dialysis
 S ureaS urea >150mg/dl>150mg/dl
 S cr.S cr. >10mg/dl>10mg/dl
 K >6.5mEq/l with ECG changes unrelieved by drugsK >6.5mEq/l with ECG changes unrelieved by drugs
 S HCO3S HCO3 <10mEq/l unrelieved by bicarbonate<10mEq/l unrelieved by bicarbonate
 CHF & fluid overloadCHF & fluid overload
Peritoneal vs hemodialysisPeritoneal vs hemodialysis

46. COMPLICATIONSCOMPLICATIONS
 Metabolic acidosis: NaCHO3 used when totalMetabolic acidosis: NaCHO3 used when total
serum bicorbonate is <10mmol/L.serum bicorbonate is <10mmol/L.
 Metabolic alkalosis can developMetabolic alkalosis can develop
 SeizuresSeizures
 InfectionInfection
 PericarditisPericarditis
 AnemiaAnemia

47. Prognosis of ARF.Prognosis of ARF. 3 phases: o3 phases: oliguric, diuretic,liguric, diuretic,
recoveryrecovery
The overall survival rate is 70%The overall survival rate is 70%
 Recovery may take ds-wks, needs frequent assessmentRecovery may take ds-wks, needs frequent assessment
 If ARF continues for several weeks, transition to chr. careIf ARF continues for several weeks, transition to chr. care
may be necessarymay be necessary
 Prognosis depends on several factorsPrognosis depends on several factors
– need for dialysis, delay in presentationneed for dialysis, delay in presentation
– underlying diseaseunderlying disease
 Younger age and multisystem failure do worse. So, earlyYounger age and multisystem failure do worse. So, early
detection and Rx improve outcomedetection and Rx improve outcome

48. ARF: PreventionARF: Prevention
Maintenance of blood flow, hydrationMaintenance of blood flow, hydration
Avoid toxins: Aminoglycosides, ampho. B, NSAIDsAvoid toxins: Aminoglycosides, ampho. B, NSAIDs
Furosemide early in ARFFurosemide early in ARF
Mannitol: may work byMannitol: may work by
 Increasing BF through tubules, preventing obstructionIncreasing BF through tubules, preventing obstruction
 Osmotic action, decreasing endothelial swellingOsmotic action, decreasing endothelial swelling
 Decreased bl. viscosity with increased renal perfusionDecreased bl. viscosity with increased renal perfusion
 Free radical scavengingFree radical scavenging

49. ARF: Prevention …ARF: Prevention …
 Renal dose dopamineRenal dose dopamine
 ThyroxineThyroxine
– More rapid improvement of renal function in animalsMore rapid improvement of renal function in animals
– More ATP or cell m. stabilizationMore ATP or cell m. stabilization
 ANP: iANP: improve R functionmprove R function
 Theophyline: aTheophyline: adenosine antagonistdenosine antagonist

50. Prevention in Specific CasesPrevention in Specific Cases
Hb.uria/MyoglobinuriaHb.uria/Myoglobinuria
 Acid hematin: tubular obstructionAcid hematin: tubular obstruction
 Inhibits BF by PGE inhibition or more reninInhibits BF by PGE inhibition or more renin
– Rx:Rx: aggressive hydration, alkalinization of urine,aggressive hydration, alkalinization of urine,
Mannitol/Furosemide, early hemofiltrationMannitol/Furosemide, early hemofiltration
Uric a. nephropathyUric a. nephropathy
– A thing of the past thanks to RasburicaseA thing of the past thanks to Rasburicase
– Rx:Rx: aggressive hydration, alkalinization of the urine,aggressive hydration, alkalinization of the urine,
Xanthine oxidase inhibitorsXanthine oxidase inhibitors

51. Chronic KidneyChronic Kidney
Disease in ChildrenDisease in Children
ObjectivesObjectives
 Define CKDDefine CKD
 G&D in CKDG&D in CKD
 Immunization for RTImmunization for RT
 Risks & benefits of RTRisks & benefits of RT
 Advantages and dis- of living donor vs deceased donor RTAdvantages and dis- of living donor vs deceased donor RT

52. Definition of CKDDefinition of CKD
Structural/functional abnormalities of kidneys forStructural/functional abnormalities of kidneys for >>3mo3mo
1.1. Kidney damage, with/-out fall in GFR, as defined byKidney damage, with/-out fall in GFR, as defined by
 pathologic abnormalitiespathologic abnormalities
 markers of kidney damage: (blood, urine, imaging)markers of kidney damage: (blood, urine, imaging)
2. Or GFR <60 ml/min/1.73m2. Or GFR <60 ml/min/1.73m22
, with/-out kidney damage, with/-out kidney damage
ESRD:ESRD: GFR <15 ml/min/1.73 mGFR <15 ml/min/1.73 m22
or on dialysisor on dialysis

53. CKD:CKD: 5 stages for children >2yoa5 stages for children >2yoa
 Stage 1:Stage 1: renal damage with GFR (>90 mL/min/1.73 mrenal damage with GFR (>90 mL/min/1.73 m22
))
 S. 2:S. 2: GFR (60-89 mL/min per 1.73 mGFR (60-89 mL/min per 1.73 m22
))
 S. 3: …S. 3: … 30 to 59 mL/min …30 to 59 mL/min …
 S. 4: …S. 4: … 15 to 29 mL/min …15 to 29 mL/min …
 S. 5: …S. 5: … <15 mL/min …<15 mL/min … (ESRS)(ESRS)
Children with CKD present with problems of growth,Children with CKD present with problems of growth,
nutrition, electrolytes, bones, anemia, HTNnutrition, electrolytes, bones, anemia, HTN

54. DiagnosisDiagnosis IncidenceIncidence
Obstructive uropathyObstructive uropathy 22%22%
Aplasia/hypoplasia/dysplasiaAplasia/hypoplasia/dysplasia 18%18%
GlomerulonephritisGlomerulonephritis ∼∼10%10%
Focal glomerulosclerosisFocal glomerulosclerosis ∼∼9%9%
Reflux nephropathyReflux nephropathy 8%8%
Common C/of CKD in ChildrenCommon C/of CKD in Children

56. CF in CKDCF in CKD
 ANV, malaise, irritability, bone pain, stunted growth, HAANV, malaise, irritability, bone pain, stunted growth, HA
 Polyuria, incontinence or no urine outputPolyuria, incontinence or no urine output
 Repeated UTIRepeated UTI
 Pallor, edemaPallor, edema
 Bad breathBad breath
 Hearing deficitHearing deficit
 Abdominal massAbdominal mass
 Poor muscle tone, change in alertnessPoor muscle tone, change in alertness
SS of ac. and chr. RF may resemble other medical conditionsSS of ac. and chr. RF may resemble other medical conditions

57. Presentation in CKDPresentation in CKD
 C/of pediatric CKD are quite different: majority of adultC/of pediatric CKD are quite different: majority of adult
CKD are glomerularopathy and typically present withCKD are glomerularopathy and typically present with
edema, hematuria, proteinuria, HTNedema, hematuria, proteinuria, HTN
 Pediatric CKD, is often related to interstitial renal d.Pediatric CKD, is often related to interstitial renal d.
Most children do not have HTN and edema, rather polydipsiaMost children do not have HTN and edema, rather polydipsia
and polyuria (“drink like a fish and pee like a racehorse”):and polyuria (“drink like a fish and pee like a racehorse”):
often, they are worked up for DMoften, they are worked up for DM

61. Pathogenesis of CKDPathogenesis of CKD
Once CKD: response of failing K is similar:Once CKD: response of failing K is similar:
 InitialInitial adaptive hyperfiltration:adaptive hyperfiltration: often with normal S. Cr.often with normal S. Cr.
Initially beneficial, it causes long-term damage to glomeruliInitially beneficial, it causes long-term damage to glomeruli
(proteinuria, progressive RF)(proteinuria, progressive RF)
 Damage from 2y factors:Damage from 2y factors: anemia, ROD, systemic/glomer.anemia, ROD, systemic/glomer.
HTN, glom. Hypertrophy, m. acidosis, hyperlipidemia,HTN, glom. Hypertrophy, m. acidosis, hyperlipidemia,
tubulointerstitial d., systemic inflam., altered prostanoidtubulointerstitial d., systemic inflam., altered prostanoid
metabolismmetabolism
 Adaptive tubular functionsAdaptive tubular functions permit Na, K, Ca, PO4 and totalpermit Na, K, Ca, PO4 and total
water to remain normalwater to remain normal
This common events in CKD is the basis for the common Rx,This common events in CKD is the basis for the common Rx,
irrespective of etiologyirrespective of etiology

62. Complications of CKDComplications of CKD
 Renal osteodystrophyRenal osteodystrophy
 Growth failureGrowth failure
 AnemiaAnemia
 Electrolyte imbalances, m.Electrolyte imbalances, m. acidosisacidosis
 HTN in later stagesHTN in later stages
 Weakened immunityWeakened immunity
 Periodontal problemsPeriodontal problems
Most commonly CKD in children deteriorates rapidly duringMost commonly CKD in children deteriorates rapidly during
rapid growth (5-15y)rapid growth (5-15y)

64. Renal OsteodystrophyRenal Osteodystrophy
 Ca, PO4, MgCa, PO4, Mg balance are maintained by kidneybalance are maintained by kidney
 CKD:CKD: hypoCa, hyperPO4, lowhypoCa, hyperPO4, low 11,25-DHD,25-DHD33. PTH is degraded. PTH is degraded
by kidneyby kidney
 Low 1,25-DHD3: gut absorption of Ca falls: hypoCa: PTHLow 1,25-DHD3: gut absorption of Ca falls: hypoCa: PTH
increases: abnormal bone mineralization with osteitisincreases: abnormal bone mineralization with osteitis
fibrosa cysticafibrosa cystica
 Dx: levels of Ca, PO4, PTH, calcitriol. Bone biopsy
 Bone pathology must be Rx aggressivelyBone pathology must be Rx aggressively

66. What are intraosseous accumulation of giant cells and osteoclasts inWhat are intraosseous accumulation of giant cells and osteoclasts in
hyperPTH called? Brown Tumor (brown due to hge)hyperPTH called? Brown Tumor (brown due to hge)

67. VD supplementsVD supplements
 Age, ability to swallow, HD or PD. Paricalcitol andAge, ability to swallow, HD or PD. Paricalcitol and
doxercalciferol (also oral form) usually IV in HDdoxercalciferol (also oral form) usually IV in HD
 VD is started once a child has stage 3 CKD. Monitor by S.VD is started once a child has stage 3 CKD. Monitor by S.
PO4 and PTH (upper normal)PO4 and PTH (upper normal)
 HyperPO4 is Rx with phosphate binders and low-PO4 diets.HyperPO4 is Rx with phosphate binders and low-PO4 diets.
Commonly CaCO3 and Ca acetate are used. Aluminum-Commonly CaCO3 and Ca acetate are used. Aluminum-
containing binders are avoided (toxicity more in RF)containing binders are avoided (toxicity more in RF)

68. AnalogAnalog Starting DoseStarting Dose
1,25-DH vitamin D1,25-DH vitamin D33(calcitriol)(calcitriol) 0.01-0.05 mcg/kg/d PO(<3yoa)0.01-0.05 mcg/kg/d PO(<3yoa)
0.25-0.75 mcg/d (>3y)0.25-0.75 mcg/d (>3y)
Titrated to maintain normal PTHTitrated to maintain normal PTH
1-hydroxycholecalciferol1-hydroxycholecalciferol
(alfacalcidol)(alfacalcidol)
0.25-0.5mcg/d PO. Titrated to0.25-0.5mcg/d PO. Titrated to
maintain normal PTHmaintain normal PTH
Vitamin DVitamin D22 (dihydrotachysterol)(dihydrotachysterol)
Vitamin DVitamin D22 (doxercalciferol)(doxercalciferol) Oral and IV dosing available forOral and IV dosing available for
adolescents and adultsadolescents and adults
Synthetic VD analog (paricalcitol)Synthetic VD analog (paricalcitol) 0.04-0.1mcg/kg IV x3/w (>5yoa)0.04-0.1mcg/kg IV x3/w (>5yoa)
Vitamin D AnalogsVitamin D Analogs

70. Deformity in Renal OsteodystrophyDeformity in Renal Osteodystrophy

72. HyperkalemiaHyperkalemia in CKDin CKD
K is reabsorbed in PCT and loop of H. Excretion of 90% intakeK is reabsorbed in PCT and loop of H. Excretion of 90% intake
occurs in DCT. Aldosterone also enhances K secretion byoccurs in DCT. Aldosterone also enhances K secretion by
Na-K exchange in kidneys and colonNa-K exchange in kidneys and colon
 But, hyperK from dietary K can overwhelm compensationBut, hyperK from dietary K can overwhelm compensation
or by drug action (spironolactone, amiloride, or ACEI)or by drug action (spironolactone, amiloride, or ACEI)
 Hypokalemia also can occur in children who have CKD butHypokalemia also can occur in children who have CKD but
tends to develop in tubular defects like Fanconi syn.tends to develop in tubular defects like Fanconi syn.

73. ProductProduct DoseDose
Potential AdversePotential Adverse
EffectsEffects
Sodium bicarbonateSodium bicarbonate ([0.6×bw.kg]×[BCO3desir([0.6×bw.kg]×[BCO3desir
ed− observed])÷2ed− observed])÷2
May causeMay cause
hypocalcemiahypocalcemia
0.5-1mEq/kg IV over 1h0.5-1mEq/kg IV over 1h
Ca gluconate (10%)Ca gluconate (10%) 0.5-1mL/kgIV over 15 min0.5-1mL/kgIV over 15 min ArrhythmiaArrhythmia
Glucose and insulinGlucose and insulin Glucose 0.5g/kg withGlucose 0.5g/kg with
insulin 0.1 units/kg IVinsulin 0.1 units/kg IV
over 30 minover 30 min
HypoglycemiaHypoglycemia
Sodium polystyreneSodium polystyrene
sulfonatesulfonate
1g/kg/dose PR/PO1g/kg/dose PR/PO May causeMay cause
constipation/diarrheaconstipation/diarrhea
Beta agonistsBeta agonists 5-10 mg aerosolized5-10 mg aerosolized Tachycardia, HTNTachycardia, HTN
Treatment of HyperkalemiaTreatment of Hyperkalemia

74. AnemiaAnemia
low erythropoietin, B9, Fe. Maintain Hb 11-12g/dLlow erythropoietin, B9, Fe. Maintain Hb 11-12g/dL
Rx anemia ensures cognitive and heart functions, exerciseRx anemia ensures cognitive and heart functions, exercise
tolerance, decreased mortalitytolerance, decreased mortality
Before EPO use, BT was given (infx., sensitization toBefore EPO use, BT was given (infx., sensitization to
lymphocyte Ag: more RT rejection)lymphocyte Ag: more RT rejection)
Anorexia: poor Fe iron stores by foods. Oral Fe is given 2-3Anorexia: poor Fe iron stores by foods. Oral Fe is given 2-3
mg/kg/d (elemental). Fe is taken on an empty stomach andmg/kg/d (elemental). Fe is taken on an empty stomach and
not with PO4 bindersnot with PO4 binders

75.  Parenteral Fe:Parenteral Fe: blood loss or intolerance to oral Fe. It can beblood loss or intolerance to oral Fe. It can be
given easily to HD pts. Can also be used for PD ptsgiven easily to HD pts. Can also be used for PD pts
 ErythropoietinErythropoietin can be given s.c. or IV x1, 2, or 3/w. Initiallycan be given s.c. or IV x1, 2, or 3/w. Initially
30-300 units/kg/w. Maintain: 60- 600 units/kg/w based on30-300 units/kg/w. Maintain: 60- 600 units/kg/w based on
monthly Hbmonthly Hb
 A new EPO: darbepoetin alfa, with longer t½, once/2w-A new EPO: darbepoetin alfa, with longer t½, once/2w-
once/mo, is being investigated for use in childrenonce/mo, is being investigated for use in children

77. Metabolic acidosisMetabolic acidosis
 Growth failureGrowth failure::
- increased proteolysis- increased proteolysis
- inhibition of GH pulsatile excretion- inhibition of GH pulsatile excretion
Maintain serumMaintain serum bicarbonatebicarbonate atat 22mEq/l22mEq/l

79. Nutritional deficiencies in CRFNutritional deficiencies in CRF
 Protein: 10% of total energyProtein: 10% of total energy
 With vigorous supplements close to 100% of RDA, wt. gainWith vigorous supplements close to 100% of RDA, wt. gain
without linear growth or OFC was seenwithout linear growth or OFC was seen
 Glucose intolerance in uremia is due to insulin resistanceGlucose intolerance in uremia is due to insulin resistance
 Nitrogen retention results in ANV and uremic stomatitisNitrogen retention results in ANV and uremic stomatitis
RDA: recommended dietary allowanceRDA: recommended dietary allowance

80. Diet and CRFDiet and CRF
 Dietary protein is a potent modulator of GFRDietary protein is a potent modulator of GFR
 Limiting it may slow CKDLimiting it may slow CKD
 Children: no <0.6-0.8 g/kg/d (up to 40g/d)Children: no <0.6-0.8 g/kg/d (up to 40g/d)
 Fall in GFR results in anFall in GFR results in an ↑↑ in transcapillary pressurein transcapillary pressure
 Hyperfiltration causes glomerulosclerosisHyperfiltration causes glomerulosclerosis
 Children with CRF maintain nutrition status when givenChildren with CRF maintain nutrition status when given
very low protein diet supplemented with ketoacidsvery low protein diet supplemented with ketoacids

82. Other Complications in CKDOther Complications in CKD
Impaired immunityImpaired immunity
Neurological complication &uremicNeurological complication &uremic
encephalopathyencephalopathy
Duodenal ulcersDuodenal ulcers
Pericardial effusion & pericarditisPericardial effusion & pericarditis
Pulmonary edemaPulmonary edema
Sexual dysfunctionSexual dysfunction
PruritusPruritus

83. DiagnosisDiagnosis
Hx for dehydration, oliguria, anuria, sepsis, shock, toxins,Hx for dehydration, oliguria, anuria, sepsis, shock, toxins,
NSAIDs, DM, HTN, Collagen VD, traumaNSAIDs, DM, HTN, Collagen VD, trauma
Lab.:Lab.: hematuria or proteinuria, casts (GN), creatinine, BUN,hematuria or proteinuria, casts (GN), creatinine, BUN,
HB and C, complements. ImagingHB and C, complements. Imaging
Low C3: lupus or MPGN/APSGNLow C3: lupus or MPGN/APSGN
For GN, a biopsy may be needed in gross hematuria andFor GN, a biopsy may be needed in gross hematuria and
proteinuria, rapidly rising BUN and creatinineproteinuria, rapidly rising BUN and creatinine
In intrinsic renal d.: a low urine osmolality (<350.0 mOsm)In intrinsic renal d.: a low urine osmolality (<350.0 mOsm)
and a high urinary fractional excretion of Na (>2% in olderand a high urinary fractional excretion of Na (>2% in older
child and >2.5 to 3% in the newborn)child and >2.5 to 3% in the newborn)

84. Renal scansRenal scans can be helpful: extent of K. function. Tc-99-can be helpful: extent of K. function. Tc-99-
diethylenetriaminepenta-acetic a. (diethylenetriaminepenta-acetic a. (99m99m
Tc-DTPA) or Tc-99-Tc-DTPA) or Tc-99-
mercaptotriglyclglycine (mercaptotriglyclglycine (99m99m
Tc-MAG-3) scans can delineateTc-MAG-3) scans can delineate
areas of poor function and areas of parenchymal damageareas of poor function and areas of parenchymal damage
by a delay in accumulation of radioisotope and an absenceby a delay in accumulation of radioisotope and an absence
of isotopic excretionof isotopic excretion
BiopsyBiopsy is the next step in determining the c/of intrinsicis the next step in determining the c/of intrinsic
renal d.: rapidly increasing creatinine, Dx of ac vs chr GN,renal d.: rapidly increasing creatinine, Dx of ac vs chr GN,
MPGN, Lupus, hematuria or proteinuriaMPGN, Lupus, hematuria or proteinuria
 It may show an active lesion and immunosuppressant, likeIt may show an active lesion and immunosuppressant, like
steroids, may reverse d. process and enhance recoverysteroids, may reverse d. process and enhance recovery

85. ImmunizationsImmunizations
 CKD pt. is to be kept medically stable to prepare for RTCKD pt. is to be kept medically stable to prepare for RT
 Immunogenicity may be impaired (dialysis, uremia, NS). HBImmunogenicity may be impaired (dialysis, uremia, NS). HB
Ab can be removed by D (frequent measurement)Ab can be removed by D (frequent measurement)
 Live vax. are not given after RTLive vax. are not given after RT
 30% of children do not complete immunizations <RT30% of children do not complete immunizations <RT
 Flu vax./y, PCV if not given <2yoaFlu vax./y, PCV if not given <2yoa
 Response to vax. varies. Occasionally, boosters are neededResponse to vax. varies. Occasionally, boosters are needed
with routine measuring Ab.with routine measuring Ab.
 Meningococcal vax. for adolescents with CKDMeningococcal vax. for adolescents with CKD
RT: renal transplantation. MM: morbidity and mortality. HB: hRT: renal transplantation. MM: morbidity and mortality. HB: hepatitis Bepatitis B

86.  Waiting time for a RT can affect vax. schedule adverselyWaiting time for a RT can affect vax. schedule adversely
 Pts. may need accelerated imm. schedule before RT. 1Pts. may need accelerated imm. schedule before RT. 1stst
MMR-varicella vax. at 9 mo of age before RT in 2-3 moMMR-varicella vax. at 9 mo of age before RT in 2-3 mo
 HB booster if needed. HB vax. is a challenge in CKDHB booster if needed. HB vax. is a challenge in CKD
 CICI to vax. are few. Vax. schedule can be delayed if pt. isto vax. are few. Vax. schedule can be delayed if pt. is
acutely severely illacutely severely ill
 Live vax. should not be given if pt. recently was given IVIGLive vax. should not be given if pt. recently was given IVIG
 Successful completion of pre-RT immunization in CKDSuccessful completion of pre-RT immunization in CKD
requires frequent communication among team membersrequires frequent communication among team members

87. Renal Replacement TherapyRenal Replacement Therapy
 When medical Rx is unsuccessful, dialysis is Rx of choiceWhen medical Rx is unsuccessful, dialysis is Rx of choice
 Indications: CCFIndications: CCF, anemia, hyperK, severe acidosis,, anemia, hyperK, severe acidosis,
pericarditispericarditis
 For the acute presentation that requires D, continuousFor the acute presentation that requires D, continuous
venovenous (CVVH) or continuous arteriovenousvenovenous (CVVH) or continuous arteriovenous
hemofiltration (CAVH), acute HD, or acute PD arehemofiltration (CAVH), acute HD, or acute PD are
appropriate forms for childrenappropriate forms for children
 CVVH or CAVH allows fluid removal in face of very low BP.CVVH or CAVH allows fluid removal in face of very low BP.
Also, neither CVVH nor CAVH interferes with providingAlso, neither CVVH nor CAVH interferes with providing
adequate nutrition, enterally or parentally, for pt in ICUadequate nutrition, enterally or parentally, for pt in ICU

88. Renal Transplantation:Renal Transplantation: For ESRDFor ESRD
Kidney can be obtained from a living related, - unrelated, orKidney can be obtained from a living related, - unrelated, or
deceased donordeceased donor
 1y survival with living donor is 92%, 5y is 85%. For dead1y survival with living donor is 92%, 5y is 85%. For dead
donor it is 84%, and 77%donor it is 84%, and 77%
 In children;In children; many get preemptive RT without ever havingmany get preemptive RT without ever having
D due to family preference and that it does betterD due to family preference and that it does better
 Infants <6mo oa/wt <6kgInfants <6mo oa/wt <6kg get RT rarely due to higher graftget RT rarely due to higher graft
failure due to inf, technical problems, immunosuppression.failure due to inf, technical problems, immunosuppression.
 Mostly recipients are >1yoa, wt 10kgMostly recipients are >1yoa, wt 10kg

89. Renal Transplantation …Renal Transplantation …
CI to RT are few:CI to RT are few: one relative CI is HIV nephropathy as itone relative CI is HIV nephropathy as it
needs more immunosuppression in an immunodeficient.needs more immunosuppression in an immunodeficient.
Other relativeOther relative CIs:CIs: preexisting Ca, devastating neurologic d,preexisting Ca, devastating neurologic d,
potential recurrence of primary d., like oxalosispotential recurrence of primary d., like oxalosis
 Despite theseDespite these,, RT may be offered, depending on familyRT may be offered, depending on family
desire and medical stabilitydesire and medical stability
 Drugs for Px graft rejection: calcineurin inhibitorsDrugs for Px graft rejection: calcineurin inhibitors
cyclosporine and tacrolimus, mycophenolate mofetil, orcyclosporine and tacrolimus, mycophenolate mofetil, or
steroidssteroids

90. Renal Transplantation …Renal Transplantation …
 Complications:Complications: immediate: rejection and inf. Pts areimmediate: rejection and inf. Pts are
followed closely by RT team in conjunction with pediatricfollowed closely by RT team in conjunction with pediatric
nephrologist. The immediate post-RT period is an imp timenephrologist. The immediate post-RT period is an imp time
for general pediatrician to follow pt. If F, blood and urinefor general pediatrician to follow pt. If F, blood and urine
CS, CBC, blood chemistries are done; a BSAB given whileCS, CBC, blood chemistries are done; a BSAB given while
contacting RT/nephrology teamcontacting RT/nephrology team
 Other long-term complications:Other long-term complications:
– noncompliance with drugs, which may lead to chrnoncompliance with drugs, which may lead to chr
rejection or graft lossrejection or graft loss
– Growth: should be re-evaluated for GHGrowth: should be re-evaluated for GH

91. RecommendationsRecommendations
C/of and presentation of CKD in children is differentC/of and presentation of CKD in children is different
 Must be managed by pediatric nephrologistMust be managed by pediatric nephrologist
 Complications of CKD can be managed with drugs and dietComplications of CKD can be managed with drugs and diet
 Adequate and appropriate nutrition is critical in CKDAdequate and appropriate nutrition is critical in CKD
 Rx of ROD, anemia, acidosisRx of ROD, anemia, acidosis
 K, PO4, protein restrictionK, PO4, protein restriction
 Recombinant human GHRecombinant human GH
 Rx of HTNRx of HTN

92. Points to PonderPoints to Ponder
 Obstructive uropathy and reflux nephropathy are majorObstructive uropathy and reflux nephropathy are major
c/of CRF in children in Bangladeshc/of CRF in children in Bangladesh
 Majority are late in presentation; malnourished, stuntedMajority are late in presentation; malnourished, stunted
 Only a few can afford RRTOnly a few can afford RRT
 CKD affects multiple systems: endocrine, hematologic,CKD affects multiple systems: endocrine, hematologic,
immune, CV systemsimmune, CV systems
 Children with CKD requireChildren with CKD require
– close, coordinated attention by PC pediatrician,close, coordinated attention by PC pediatrician,
pediatric nephrologist, andpediatric nephrologist, and
– other subspecialists to ensure G&D to attain successfulother subspecialists to ensure G&D to attain successful
adulthood to the best of their potentialadulthood to the best of their potential
PC: primary carePC: primary care

93. MCQMCQ
Dm is the commonest c/of CKD in adultsDm is the commonest c/of CKD in adults
Obstructive uropathy is the commonest c/of CRF inObstructive uropathy is the commonest c/of CRF in
childrenchildren
APSGN is the commonest c/of hematuriaAPSGN is the commonest c/of hematuria
Renal OD is caused only by raised PTHRenal OD is caused only by raised PTH
Prerenal causes are the commonest c/of ARFPrerenal causes are the commonest c/of ARF