‫نبوغ عبد الكريم نعمة‬

‫إيالف كامل عبد السادة‬

‫محمد هاشم‬
 Introduction:
 Acute kidney injury (AKI) , is a clinical syndrome in
which a sudden deterioration in renal function results in
the inability of the kidneys to maintain fluid and
electrolyte homeostasis.
 AKI occurs in 2-3% of children admitted to pediatric
A classification system has been proposed to standardize the definition of AKI in
adults.
criteria of risk, injury, failure, loss, and end-stage renal disease were given the
acronym of RIFLE.A modified RIFLE criteria (pRIFLE) was developed to characterize
the pattern of AKI in critically ill children
 PRERENAL:
 Dehydration
 Hemorrhage
 Sepsis
 Hypoalbuminemia
 Cardiac failure
 INTRINSIC RENAL:
Glomerulonephritis
• Postinfectious/poststreptococcal
• Lupus erythematosus
• Henoch-Schönlein purpura
• Membranoproliferative
• Anti–glomerular basement membrane
 Hemolytic-uremic syndrome
 Acute tubular necrosis
 Cortical necrosis
 Renal vein thrombosis
 Rhabdomyolysis
 Acute interstitial nephritis
 Tumor infiltration
 Tumor lysis syndrome
 POSTRENAL:
 Posterior urethral valves
 Ureteropelvic junction obstruction
 Ureterovesicular junction obstruction
 Ureterocele
 Tumor
 Urolithiasis
 Hemorrhagic cystitis
 Neurogenic bladder
 History: is critical in defining the cause of AKI.

 An infant with a 3 day history of vomiting and diarrhea most likely

has prerenal AKI caused by volume depletion, but hemolytic-
uremic syndrome (HUS) must be a consideration.
 A 6 yr old child with a recent pharyngitis who presents with
periorbital edema, hypertension, and gross hematuria most likely
has intrinsic AKI related to acute postinfectious
glomerulonephritis.
 A critically ill child with a history of protracted hypotension or
with exposure to nephrotoxic medications most likely has ATN.
 A neonate with a history of hydronephrosis on prenatal ultrasound
and a palpable bladder most likely has congenital
urinary tract obstruction, probably related to posterior urethral
valves.
 physical examination: must be careful attention to
volume status.
 Tachycardia, dry mucous membranes, and poor peripheral
perfusion suggest an inadequate circulating volume and the
possibility of prerenal AKI .
 Hypertension, peripheral edema, rales, and a cardiac gallop
suggest volume overload and thepossibility of intrinsic AKI
from glomerulonephritis or ATN.
 The presence of a rash and arthritis might indicate systemic
lupus erythematosus (SLE) or Henoch-Schönlein purpura
nephritis.
 Palpable flank masses may be seen with renal vein
thrombosis, tumors, cystic disease, or urinary tract
obstruction.
 Laboratory abnormalities:
 anemia (the anemia is usuallydilutional or hemolytic, as in SLE, renal vein
thrombosis, HUS).
 leukopenia (SLE, sepsis); thrombocytopenia (SLE, renal vein thrombosis,
sepsis, HUS);
 hyponatremia (dilutional);
 metabolic acidosis;
 elevated serum concentrations of blood urea nitrogen, creatinine, uric
acid, potassium, and phosphate (diminished renal function)and
 hypocalcemia (hyperphosphatemia).
 The serum C3 level may be depressed (postinfectious glomerulonephritis,
SLE, or membranoproliferative glomerulonephritis), and antibodie may be
detected in the serum to streptococcal (poststreptococcal
glomerulonephritis), nuclear (SLE), neutrophil cytoplasmic (granulomatosis
with polyangiitis, microscopic polyarteritis), or glomerular basement
membrane (Goodpasture disease) antigens.
 The presence of hematuria, proteinuria, and red blood cell or granular
urinary casts suggests intrinsic AKI, in particular glomerular disease
and ATN
 The presence of white blood cells and white blood cell casts with low-grade
hematuria and proteinuria suggests tubulointerstitial disease.
 Urinary eosinophils may be present in children with drug-induced
tubulointerstitial nephritis
 Urinary indices may be useful in differentiating prerenal AKI from intrinsic
AKI Patients whose urine shows an elevated specific gravity (>1.020),
elevated urine osmolality (UOsm >500 mOsm/kg), low urine sodium (UNa <
20 mEq/L), and fractional excretion of sodium <1% (<2.5% in neonates)
most likely have prerenal AKI.
Those with a specific gravity of <1.010, low urine osmolality(UOsm < 350
mOsm/kg), high urine sodium (UNa > 40 mEq/L), and fractional excretion
of sodium >2% (>10% in neonates) most likely have intrinsic AKI.
 Chest radiography may reveal cardiomegaly, pulmonary congestion
 (fluid overload), or pleural effusions.
 Renal ultrasonography can reveal hydronephrosis and/or hydroureter,
which suggest urinary tract obstruction, or nephromegaly, consistent with
intrinsic renal disease.
 Renal biopsy can ultimately be required to determine the precise cause
of AKI in patients who do not have clearly defined prerenal or postrenal
AKI.
Medical Management:
 bladder catheter:In infants and children with urinary tract
obstruction, such as in a newborn with suspected posterior
ureteral valves, should be placed immediately to ensure
adequate drainage of the urinary tract. Also be considered in
nonambulatory older children and adolescents to accurately
monitor urine output during AKI.
 Intravenous administration of isotonic saline, 20mL/kg over
30 min, If there is no evidence of volume overload or cardiac
failure. In the absence of blood loss or hypoproteinemia,
colloid containing solutions are not required for volume
expansion. Severe hypovolemia may require additional fluid
boluses. Hypotension caused by sepsis requires vigorous fluid
resuscitation followed by a continuous infusion of
norepinephrine.
 Diuretic therapy:
 Furosemide(2-4 mg/kg) and mannitol (0.5 g/kg) may be
administered as a single IV dose. Bumetanide (0.1 mg/kg)
may be given as an alternative to furosemide.
 If urine output is not improved, then a continuous diuretic
 infusion may be considered. To increase renal cortical
blood flow, many clinicians administer dopamine (2-3
μg/kg/min) in conjunction with diuretic therapy, although
no controlled data support this practice.
 There is little evidence that diuretics or dopamine can
prevent AKI or hasten recovery. Mannitol may be effective
in prevention of pigment (myoglobin, hemoglobin)-
induced renal failure.
 If there is no response to a diuretic challenge, diuretics
should be discontinued and fluid restriction is essential.
 In AKI, rapid development of hyperkalemia (serum potassium level> 6
mEq/L) can lead to cardiac arrhythmia, cardiac arrest, and death.
 The earliest electrocardiographic change seen in patients with developing
hyperkalemia is the appearance of peaked T waves. This may be followed
by widening of the QRS intervals, ST segment depression,ventricular
arrhythmias, and cardiac arrest
 Treatment:
 Procedures to deplete body potassium stores should be initiated when the
serum potassium value rises to >6.0 mEq/L.
 Exogenous sources of potassium (dietary, intravenous fluids, total
parenteral nutrition) should be eliminated.
 Sodium polystyrene sulfonate resin (Kayexalate),1 g/kg, should be given
orally or by retention enema. A single dose of 1 g/kg can be expected to
lower the serum potassium level by about 1 mEq/L. Resin therapy may be
repeated every 2 hr, the frequency being limited primarily by the risk of
sodium overload.
 More severe elevations in serum potassium (>7 mEq/L), especially if
accompanied by electrocardiographic changes, require emergency
measures in addition to Kayexalate.
1. Calcium gluconate 10% solution, 1.0 mL/kg IV, over 3-5 min
2. Sodium bicarbonate, 1-2 mEq/kg IV, over 5-10 min
3. Regular insulin, 0.1 units/kg, with glucose 50% solution, 1 mL/kg, over 1 hr.
4. Persistent hyperkalemia should be managed by dialysis.
 metabolic acidosis:either
 Mild……rarely need treatment
 Severe……(arterial pH < 7.15; serum bicarbonate < 8 mEq/L) or contributes to
significant hyperkalemia,treatment is indicated.
Treatment:
 corrected partially by the intravenous route, generally giving enough bicarbonate to
raise the arterial pH to 7.20 (which approximates a serum bicarbonate level of 12
mEq/L).
 The remainder of the correction may be accomplished by oral administration of
sodium bicarbonate after normalization of the serum calcium and phosphorus
levels.
*Correction of metabolic acidosis with intravenous bicarbonate can precipitate
tetany in patients with renal failure as rapid correction of acidosis reduces the
ionized calcium concentration
 most commonly a dilutional disturbance .
 corrected by fluid restriction rather than sodium chloride administration.
 Administration of hypertonic (3%) saline should be limited to patients with symptomatic
hyponatremia (seizures, lethargy)or those with a serum sodium level <120 mEq/L.
 Acute correction of the serum sodium to 125 mEq/L (mmol/L) should be accomplished using
the following formula:
mEq sodium required
 weight in = 0.6 × kg ×(125− serum sodium in mEq/L).
 Oral or intravenous H2 blockers such as ranitidine are commonly administered to prevent this
complication.
 AKI patients are predisposed to GI bleeding because of uremic
platelet dysfunction, increased stress, and heparin exposure if treated with hemodialysis
or continuous renal replacement therapy..

Hypertension:
 Salt and water restriction is critical, and diuretic administration may be useful Isradipine(
0.05-0.15 mg/kg/dose, maximum dose 5 mg qid) may be administered for relatively rapid
reduction in blood pressure. Longer-acting agents such as calcium channel blockers
(amlodipine, 0.1-0.6 mg/ kg/24 hr qd or divided bid) or β blockers (propranolol, 0.5-8.0 mg/
kg/24 hr divided bid or tid; labetalol, 4-40 mg/kg/24 hr divided bid ortid) may be helpful in
maintaining control of blood pressure.
 Children with severe symptomatic hypertension (hypertensive urgency or emergency)
should be treated with continuous infusions of nicardipine (0.5-5.0 μg/kg/min), sodium
nitroprusside (0.5-10.0 μg/kg/min),labetalol (0.25-3.0 mg/kg/hr), or esmolol (150-300
μg/kg/min) and converted to intermittently dosed antihypertensives when more stable
Hypocalcemia:
 is primarily treated by lowering the serum phosphorus
level. Calcium should not be given intravenously, except
in cases of tetany, to avoid deposition of calcium salts
into tissues.
 a low-phosphorus diet, and phosphate binders should be
orally administered to bind any ingested phosphate and
increase GI phosphate excretion.
 Common agents include sevelamer (Renagel), calcium
carbonate (Tums tablets or Titralac suspension),and
calcium acetate (PhosLo).
 Aluminum-based binders,commonly employed in the past,
should be avoided because of the riskof aluminum
toxicity.
 Neurologic symptoms
 in AKI can include headache, seizures, lethargy,and confusion (encephalopathy).
 Benzodiazepams are the most effective agents in acutely controlling seizures,and subsequent
therapy should be directed toward the precipitating cause.
 Anemia:
 The anemia of AKI is generally mild (hemoglobin 9-10 g/dL) and
primarily results from hemodilution.
 Children with HUS, SLE, active bleeding, or prolonged AKI can require
transfusion of packed red blood cells if their hemoglobin level falls
below7 g/dL.
 In hypervolemic patients, blood transfusion carries the risk of further
volume expansion, which can precipitate hypertension, heart failure,
and pulmonary edema. Slow (4-6 hr) transfusion with packed red blood
cells (10 mL/kg) diminishes the risk of hypervolemia
 The use of fresh, washed red blood cells minimizes the acute risk of
hyperkalemia, and the chronic risk of sensitization if the patient
becomes a future candidate for renal replacement therapy. In the
presence of severe hypervolemia or hyperkalemia, blood transfusions
are most safely administered during dialysis or ultrafiltration.~
 Nutrition is of critical importance in children who develop
AKI.
 In most cases, sodium, potassium, and phosphorus should be
restricted.
 Protein intake should be moderately restricted while
maximizing
caloric intake to minimize the accumulation of nitrogenous
wastes.
In critically ill patients with AKI, parenteral
hyperalimentation with
essential amino acids should be considered.
 Indications for dialysis in AKI include the following:
1. Anuria/oliguria
2. Volume overload with evidence of hypertension and/or
pulmonary edema refractory to diuretic therapy
3. Persistent hyperkalemia
4. Severe metabolic acidosis unresponsive to medical
management
5. Uremia (encephalopathy, pericarditis, neuropathy)
6. Blood urea nitrogen >100-150 mg/dL (or lower if rapidly
rising)
7. Calcium:phosphorus imbalance, with hypocalcemic
tetany that cannot be controlled by other measures
1-inttermittent hem dialysis 
2-peritonial dialysis 
3-counteniouse renal replacement therapy 
 The mortality rate in children with AKI is variable and
depends entirely on the nature of the underlying
disease process rather than on the renal failure itself.
Children with AKI caused by a renal-limited condition such
as postinfectious glomerulonephritis have a very low
mortality rate (<1%); those with AKI related to multiorgan
failure have a very high mortality rate (>90%).
 The prognosis for recovery of renal function depends on
the disorder that precipitated AKI. Recovery of renal
function is likely after AKI resulting from prerenal causes
ATN, acute interstitial nephritis, or tumor lysis syndrome.
Recovery of renal function is unusual when AKI results
from most types of rapidly progressive
glomerulonephritis,
 Chronic kidney disease
Chronic kidney disease (CKD) is determined by the presence of
kidney damage and level of kidney function (GFR)
The stage of the CKD is assigned based on the of level of kidney
function.
The prevalence of CKD in the pediatric population is
approximately 18 per 1 million.
The prognosis for the infant, child, or adolescent with CKD
has improved dramatically since the 1970s because of
improvements in medical management , dialysis
techniques,and kidney transplantationo.
ETIOLOGY
In children, CKD may be the result of congenital,
acquired, inherited,or metabolic renal disease, and the
underlying cause correlates closely with the age of the
patient at the time when CKD is first detected. CKD in
children <5 yr old is most commonly a result of
congenital abnormalities such as renal hypoplasia,
dysplasia, or obstructive uropathy.
Additional causes include congenital nephrotic
syndrome, prune belly syndrome, cortical necrosis, focal
segmental glomerulosclerosis,autosomal recessive
polycystic kidney disease and renal vein thrombosis.
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
other signs of kidney damage described above
STAGE DESCRIPTION GFR (mL/min/1.73 m2)
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 5-29
5 -Kidney failure <15 or on dialysi
PATHOGENESIS
In addition to progressive injury with ongoing structural or metabolic
genetic diseases, renal injury can progress despite removal of the original
insult.
Hyperfiltration injury may be an important final common pathway
of glomerular destruction, independent of the underlying cause of
renal injury. As nephrons are lost, the remaining nephrons undergo
structural and functional hypertrophy characterized by an increase in
glomerular blood flow. The driving force for glomerular filtration is
thereby increased in the surviving nephrons. Although this compensatory
hyperfiltration temporarily preserves total renal function, it can
cause progressive damage to the surviving glomeruli, possibly by a
direct effect of the elevated hydrostatic pressure on the integrity of the
capillary wall and/or the toxic effect of increased protein traffic across
the capillary wall. Over time, as the population of sclerosed nephrons
increases, the surviving nephrons suffer an increased excretory burden,
resulting in a vicious cycle of increasing glomerular blood flow and
hyperfiltration injury.
Proteinuria itself can contribute to renal functional decline.
Proteins that traverse the glomerular capillary wall can exert
a direct toxic effect on tubular cells and recruit monocytes
and macrophages, enhancing the process of glomerular
sclerosis and tubulointerstitial
fibrosis. Uncontrolled hypertension can exacerbate disease
progression by causing arteriolar nephrosclerosis and by
increasing the hyperfiltration
injury.
 Hyperphosphatemia can increase
progression of disease by leading to calcium
phosphate deposition in the renal interstitium
and blood vessels. Hyperlipidemia, a common
condition in CKD patients, can adversely
affect glomerular function through oxidant-
mediated injury.
CLINICAL MANIFESTATIONS
The clinical presentation of CKD is varied and depends on the
underlying renal disease. Children and adolescents with CKD
from chronic glomerulonephritis can present with edema,
hypertension, hematuria,and proteinuria. Infants and children with
congenital disorders such as renal dysplasia and obstructive
uropathy can present in the neonatal period with failure to thrive,
polyuria, dehydration, urinary tract infection,or overt renal
insufficiency. Congenital kidney disease is diagnosed with
prenatal ultrasonography in many infants, allowing early
diagnostic and possible therapeutic intervention. Children with
familial juvenile nephronophthisis can have a very subtle
presentation with nonspecific complaints such as headache,
fatigue, lethargy, anorexia,
vomiting, polydipsia, polyuria, and growth failure over a number of
years.
The physical examination in patients with CKD can reveal
pallor and a sallow appearance. Patients with long-standing
untreated CKD can have short stature and the bony
abnormalities of renal osteodystrophy . Children with CKD
caused by chronic glomerulonephritis (or children with
advanced renal failure from any
cause) can have edema, hypertension, and other signs of
extracellular fluid volume overload.
LABORATORY FINDINGS
Laboratory findings can include elevations in blood urea
nitrogen and serum creatinine and can reveal hyperkalemia,
hyponatremia (if such as renal dysplasia, the urinalysis usually
has a low specific gravityand minimal abnormalities by dipstick or
microscopy.
Inulin clearance is the gold standard to determine GFR, but it is
not
easy to measure. Endogenous creatinine clearance is the most
widely used marker of GFR, but creatinine secretion falsely
elevates the calculated GFR. Several other markers are under
investigation to accurately determine GFR in children, such as
cystatin C and iohexol. In children age 1-16 yr, the degree of
renal dysfunction may be determined by applying a new bedside
formula that estimates GFR between15 and 75 mL/min/1.73 m2:
estimated GFR = 0.43 × height in cm/serum creatinine in mg/dL
TREATMENT
The treatment of CKD is aimed at replacing absent or diminished renal
functions, which progressively deteriorate in parallel with the
progressive loss of GFR, and slowing the progression of renal
dysfunction.
Children with CKD should be treated at a pediatric center capable of
supplying multidisciplinary services, including medical, nursing, social
service, nutritional, and psychological support.
The management of CKD requires close monitoring of a patient’s
clinical and laboratory status. Blood studies to be followed routinely
include serum electrolytes, blood urea nitrogen, creatinine, calcium,
phosphorus, albumin, alkaline phosphatase, and hemoglobin levels.
Periodic measurement of intact parathyroid hormone (PTH) levels and
roentgenographic studies of bone may be of value in detecting early
evidence of renal osteodystrophy. Echocardiography should be
performed periodically to identify left ventricular hypertrophy and
cardiac
dysfunction that can occur as a consequence of the complications
of CKD.
Nutrition
Nutritional management by a dietician experienced in
pediatric renal patients is recommended by the National
Kidney Foundation Kidney Disease Outcomes Quality
Initiative (NKF KDOQI). Counseling based on individualized
assessment should be considered for all children and their
families with CKD stages 2 to 5 and 5D. Patients should
receive 100% of estimated energy requirement for age,
individually adjusted for physical activity level, body mass
index, and response in rate of weight gain or loss. When oral
supplemental nutrition with increased calories or fluid volume
is insufficient, tube feeding should be considered.
Calories should be balanced between carbohydrate,
unsaturated
fat in physiological ranges (per dietary reference intake
[DRI]), and protein. Protein intake recommendation is 100-
140% of the DRI for ideal weight for children with stage 3
CKD, 100-120% of the DRI in stages 4 and 5 CKD, and
100% with allowance for dialysis loss in CKD stage 5D, with
use of commercial supplements as needed. Children with
CKD stages 2-5 should receive 100% of DRI of vitamins and
trace elements; water-soluble vitamin supplements are often
required in CKD stage 5D.
 Definition:
 The term renal osteodystrophy is used to indicate a spectrum of
bone disorders seen in patients with CKD. The most common
condition seen in children is high-turnover bone disease caused by
secondary
hyperparathyroidism
 Pathophysiology:
 Early in the course of CKD, when the GFR declines to approximately
50% of normal, the decrease in functional kidney mass leads to a
decline in renal 1α-hydroxylase activity, with decreased production
of activated vitamin D (1,25-dihydroxycholecalciferol). This
deficiency in activated vitamin D results in decreased intestinal
calcium absorption,hypocalcemia, and increased parathyroid
gland activity. Excessive PTH secretion attempts to correct the
hypocalcemia by increasing bone resorption.
 Later in the course of CKD, when the GFR declines to 20-25% of
normal, compensatory mechanisms that have been operative to
enhance renal phosphate excretion become inadequate, resulting in
hyperphosphatemia, which further promotes hypocalcemia and
increased PTH secretion.
 History and examination: include ;
1. Muscle weakness
2. bone pain,
3. fractures with minor trauma.
4. In growing children, rachitic changes, varus and valgus
deformities of the long bones, and slipped capital
femoral epiphyses may be seen.
 Laboratory studies: can demonstrate a decreased
serum calcium level and increased serum phosphorus,
alkaline phosphatase, and PTH levels.
 Radiographs: the hands, wrists, and knees show
subperiosteal resorption of bone with widening of the
metaphyses.
 The goals of treatment are to prevent bone deformity and
normalize growth velocity using both dietary and
pharmacologic interventions.
 The target phosphorus level for adolescents is between 3.5
and 5.5 mg/dL, and for children 1-12 yr of age it is 4-6 mg/dL.
Children and adolescents should follow a low-phosphorus
diet, and infants should be provided with a low-phosphorus
formula such as Similac .
 It is impossible to fully restrict phosphorus intake, and so
phosphate binders are used to enhance GI phosphate
excretion.
 Although calcium-based binders have historically been the
most commonly used, non–calcium-based binders such as
sevelamer (Renagel) are increasing in use, particularly in older
children and adolescent patients who are prone to
hypercalcemia.
NOTE//// Because aluminum may be absorbed from the GI
tract and can lead to aluminum toxicity, aluminum-based
binders should be avoided.
 The cornerstone of therapy for renal osteodystrophy is
vitaminD administration.
 Vitamin D therapy is indicated in patients with 1,25-
dihydroxy-vitamin D levels below the established goal range
for the child’s particular stage of CKD or in patients with PTH
levels above the established goal range for CKD stage.
 Patients with low 1,25-dihydroxy-vitamin D and elevated PTH
levels should be treated with 0.01-0.05 μg/kg/24 hr of
calcitriol (Rocaltrol, 0.25-μg capsules or 1 μg/mL suspension).
 Newer activated vitamin D analogs such as paricalcitol and
doxercalciferol are increasingly used, especially in patients
who are predisposed to hypercalcemia.
 Phosphate binders and vitamin D should be adjusted to
maintain the PTH level within the designated goal range and
the serum calcium and phosphorus levels within the normal
range for age.
Thank you