Acute renal failure
(Acute kidney injury)
Asist. prof. Magdalena Stârcea
IVth Pediatric Clinic
Definition:
AKI (acute kidney injury) is defined as a precipitous
and significant (>50%) decrease in glomerular
filtration rate (GFR) over a period of hours to days,
causing abnormal regulation of fluid, electrolytes,
acid–base balance, blood pressure, and removal of
waste products.
(Has replaced the old term –Acute Renal Failure)
Prior to 2004 more than 30 definitions of AKI. We
use now the RIFFLE criteria to define AKI.

Oliguria is defined as a urine output that is less than 1
mL/kg/h in infants, less than 0.5 mL/kg/h in children, and
less than 400 mL/dailly in adults.

It is one of the clinical hallmarks of renal failure. At onset,
oliguria is frequently acute, often the earliest sign of impaired
renal function, and poses a diagnostic and management
challenge to the clinician.

In most clinical situations, acute oliguria is reversible, and
does not result in renal failure. However, identification and
timely treatment of reversible causes is crucial, since the
therapeutic window may be small.

Important and common co-morbid condition in PICU
(pediatric intensive care unit).
Paediatric Incidence of AKI
 10% incidence of AKI in patients admitted to PICU
(Schneider J, et al: Crit Care Med 2010; 38:933–939)

-
AKI increases mortality from 10% to 57.1% in patients
with multi-organ failure,
marrow or solid organ transplantation,
extracorporeal membrane oxygenation, or
acute respiratory distress syndrome
(Askenazi DJ, et al:. Pediatr Crit Care Med 2011; 12:1–6)
Long Term Outcomes
At 3 to 5-yr follow-up, because 40% to 50% of paediatric
patients who had AKI will show signs of chronic renal
insufficiency, indicating that sublethal injury permanently
alters the kidneys.
(Askenazi DJ, et al: Kidney Int 2006; 69:184–189)


In 2004, the Acute Dialysis Quality Initiative group (ADQI) proposes the RIFLE
classification of AKI.
In 2007 - Acute Kidney Injury Network (AKIN) classification come out, based on
the RIFLE system.
Schwartz equation:
GFR (ml/min/1.73m2)= [H(cm)xk]/creatinine
k = 0.35 for preterm, < 2500g, < 4 weeks old
k = 0.45 for infants 1 to 52 weeks old
k = 0.55 for children 1 to 13 years old
k = 0.55 for adolescent females >13years old
k = 0.70 for adolescent males >13years old
Serum creatinine:
 Differs with age, sex, dietary intake, muscle mass, etc.
 Doesn’t reflect dynamic changes, only increases when
there is substantial loss of renal function.
 10 –40% of creatinine is cleared by tubular secretion in
the urine – therefore has the potential to hide a
considerable decline in GFR.
For this reasons is very important to find early markers of AKI.
Newer biomarkers include:
 Neutrophil Gelatinose Associated Lipocalin (NGAL)
Secreted by renal tubular epithelium and excreted in the urine
during normal renal function.
Serum levels rise markedly after epithelial damage following
ischaemic or nephrotoxic injury.
Cystatin C
- Protein secreted by all nucleated cells
- Minimally influenced by weight, sex, race, age, muscle mass.
-May rise earlier than serum creatinine may be a better marker of
acute renal dysfunction.

Kidney Injury Molecule –1 (KIM-1)
Is a protein that is highly upregulated in the proximal tubules
after ischaemic or toxic AKI.


-
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IL-18.
Induced in the proximal renal tubule after AKI.
Seems to be useful in differentiation of acute tubular necrosis
from other types of renal disease.
Is not elevated in chronic kidney disease, UTI and pre-renal
failure
Classification
I. Clinical criteria and depending on diuresis
- AKI with oliguria - daily decrease of urinary output
and clinical signs of renal dysfunction
- AKI without oliguria – increase of serum urea and
creatinine levels despite normal or even increased
urinary volume
II. Pathophysiological criteria
A. Prerenal failure: renal function disturbance due to a decrease
of renal perfusion. Correcting the cause - renal function
recovery
Causes:
1. Decrease the total volume of liquid
- gastrointestinal disorders
- diabetes insipidus
- burns
2. Decreased intravascular volume and effective circulatory
volume
- bleeding
- passing the " third space" fluids after shock, trauma, surgery
- nephrotic syndrome
- shock
- heart failure
- renal vasoconstriction :PG synthetase inhibitors, CyA, high
doses of dopamine / adrenaline in case of shock
B. Intrinsec AKI:
Causes
1. Causes that produce a severe and prolonged ischemia
- shock
- respiratory distress syndrome (newborn and preterm infant!)
- severe heart failure
2. Nephrotoxic causes
- antibiotics, hyperuricemia, cisplatin, contrast agents, heavy metals,
organic solvents (etilenglycols, teraclorura carbon, methanol, toluene)
- rhabdomyolysis, massive hemolysis
3. Vascular / glomerular causes
- renal artery occlusion, renal vein thrombosis
- AGN, rapidly progressive GN
- Microvascular (vasculitis): HUS, malignant hypertension
C. Postrenal causes: produce a disturbance in urinary elimination
1. Functional / structural abnormalities of urinary tract :
- posterior urethra valve, ureteral obstruction, neurogenic Bladder
2. Won abnormalities: blood clot postbiopsie, trauma, retroperitoneal
tumors, stones
Pathophysiology
AKI (acute kidney injury) causes renal arteriolar
vasoconstriction, desquamation of renal tubular cells to form casts,
which causes intraluminal tubular obstruction and increased
glomerular filtration retropresion. Neutrophils adhere to the
endothelium and release proinflamatories mediators.
AKI can be classified in terms of pathophysiology of:
AKI with oliguria
AKI without oliguria, (has a more favorable prognosis)
The difference between oliguric and non – oliguric AKI consists in
renal aggression intensity. Numerous experimental studies in recent
years have shown changes in cellular, molecular and metabolic
accompanying loss of kidney function.
Prerenal insufficiency
 70% of community-acquired cases of acute renal failure
 60% of hospital-acquired cases
 is a functional response of structurally normal kidneys to
hypoperfusion. The early phase of renal compensation for
reduced perfusion includes autoregulatory maintenance of
glomerular filtration rate, via afferent arteriolar dilatation
(induced by myogenic responses, tubulo-glomerular feedback,
and prostaglandins actions), and via efferent arteriolar
constriction (mediated by angiotensin II). The early phase
also includes enhanced tubular reabsorption of salt and water
(stimulated by the renin-angiotensin-aldosterone system and
sympathetic nervous system). Rapid reversibility of oliguria
following timely re-establishment of renal perfusion is an
important characteristic and usual scenario
 prolonged renal hypoperfusion can determinate an undesirable
development from compensation to decompensation.
Excessive stimulation of the sympathetic and reninangiotensin systems can cause profound renal vasoconstriction
and ischemic renal injury.

Intrinsic renal failure is associated with structural renal
damage. This includes acute tubular necrosis (from prolonged
ischemia, drugs, or toxins), primary glomerular diseases, or
vascular lesions. The pathophysiology of ischemic, acute
tubular necrosis is well studied. Ischemia leads to altered
tubule cell metabolism (depletion of ATP, release of reactive
oxygen species) and cell death with resultant cell
desquamation, cast formation, intratubular obstruction,
backleak of tubular fluid, and oliguria. In the majority of
clinical situations, the oliguria is reversible and associated with
repair and regeneration of tubular epithelial cells.
There are four stages of the progression of renal injury in AKI:
Phase I (initiation) = shown by decreased renal perfusion and
ATP depletion
Phase II (extension) = lesions of reperfusion can cause new
lesions. At this stage appear the extension of inflammation and
ischemic effects generating exacerbation of the initial lesions.
Proximal tubules regenerated, but the tubules from renal
medullary suffering necrosis and apoptosis. Lesion severity
installed in this stage will be proportional to the prognosis of
the lesion.
Phase III (hold) = necrosis and apoptosis remains parallel with
inflammation and destruction of the kidney cell.
Phase IV (reverse) = occur simultaneously mechanisms of
regeneration, repair and cell proliferation previously injured.

Postrenal failure is a consequence of mechanical or functional
obstruction to the flow of urine. This form of oliguria and renal
insufficiency usually responds to release of the obstruction.
Mortality/Morbidity:
 Mortality rates in oliguric AKI vary widely according to the
underlying cause and associated medical condition. It ranges
from 5% for patients with community-acquired acute renal
failure to 80% among patients with multi-organ failure in PICU.
 The most common causes of death are sepsis, cardiovascular
and pulmonary dysfunction, and withdrawal of life support.
Race: there is no racial predilection.
Sex: the sexes are equally affected.
Age: oliguria affects all ages.
 It is more common in the neonatal and older age groups because
of co-morbid conditions, and it is more common in early
childhood due to the high incidence of illnesses leading to
dehydration.
Clinical
History:
 Careful evaluation of the patient's history and physical
examination often reveals the cause. This is especially important
in prerenal and postrenal processes, since early diagnosis and
treatment frequently results in complete recovery.

Fluid losses
• Recent history of diarrhea or vomiting should be sought
since this is the most common cause in children.
• Less commonly, fluid loss may result from traumatic
hemorrhage, burns, or following polyuric states such as
diabetes insipidus and diabetes mellitus.
• Loss of intravascular fluid volume into the interstitial space
accompanies surgery, shock syndromes, and nephrotic
syndrome. Children with fluid losses may complain of thirst,
dizziness, palpitations, and fatigue, and there may be a
history of weight loss.

Drugs
• A detailed history of recent medications should be obtained. In
the presence of mild prerenal insufficiency, administration of
medications that impair renal autoregulation can precipitate
oliguric ARF.
• Cyclosporine, tacrolimus, and contrast agents are direct, afferent
arteriolar constrictors that interfere with the myogenic response.
• NSAIDs inhibit the renal synthesis of vasodilatory
prostaglandins. They are an important cause when administered
to febrile children with intercurrent dehydration.
• Drugs that induce direct tubular necrosis include
aminoglycosides, amphotericin B, cyclosporine, tacrolimus,
antineoplastic agents (methotrexate, cisplatin), and contrast
agents.
• Acyclovir and sulfonamides can precipitate within the tubular
lumen and result in obstruction.
• In addition, a large number of medications, especially penicillins,
cephalosporins, sulfonamides, ciprofloxacin, NSAIDs and
diuretics, can cause interstitial nephritis.
• History of ingesting undercooked meat may suggest hemolyticuremic syndrome.


Endogenous tubular toxins
• Myoglobin (following crush injuries, myositis, and
prolonged grand mal seizures)
• Hemoglobin (hemolysis)
• Uric acid (tumor lysis syndrome)
Symptoms of glomerular disease
• Many children have a history of gross hematuria and
edema. An antecedent streptococcal infection may suggest
a post-infectious glomerulonephritis, and a history of
bloody diarrhea often precedes the hemolytic-uremic
syndrome.
• Children with fever, joint complaints, and skin rashes who
present with oliguria, should be suspected to have systemic
lupus erythematosus or allergic interstitial nephritis.
• A history of recurrent sinusitis or lower respiratory tract
infections may suggest Wegener granulomatosis, and
hemoptysis may suggest Goodpasture disease.

Symptoms of urinary tract obstruction
• Complete absence of urine output
• Alternating periods of polyuria and oligo-anuria
• Poor urinary stream or dribbling

Symptoms of chronic renal failure
• Although oliguria is usually acute at initial presentation, it
may also be a presenting symptom of chronic renal failure.
• Children may have additional symptoms suggestive of
previous renal disease such as frequent urinary tract
infections, hematuria, proteinuria, hypertension, edema,
fatigue, pallor, anorexia, and bone pain.
Physical:
 Signs of intravascular volume depletion
- Tachycardia
- Orthostatic hypotension
- Decreased skin turgor
- Dry mucous membranes

Signs of AKI
• Children may present with edema, anemia, and signs of
congestive heart failure such as hepatomegaly, gallop
rhythm, and pulmonary edema.
• Hypertension is common, especially in acute
glomerulonephritis, and may be secondary to volume
overload and alterations in vascular tone.
• Although many children with hypertension are
asymptomatic, it is common to encounter patients with
signs of congestive heart failure, visual disturbances, or
encephalopathy.

Signs specific to the underlying renal disease
• A butterfly rash on the face and joint swelling are highly
suggestive of systemic lupus erythematosus.
• Henoch-Schönlein disease presents with a characteristic
purpuric rash over the buttocks and extensor surface of the
lower extremity.
• Acute interstitial nephritis may be accompanied by fever,
arthralgias, and fleeting maculopapular or urticarial rashes.
• A variety of skin rashes may be detected in vasculitides.
• Oliguria with palpable kidneys during infancy suggests
renal vein thrombosis, polycystic kidneys, multicystic
dysplasia, or hydronephrosis. In older children, enlarged
kidneys should also raise the suspicion of tumors. A
transplanted kidney that is tender to palpation is indicative
of rejection.

Signs of postrenal failure
• Poor urinary stream, urinary dribbling, and a palpably
enlarged urinary bladder are indicative of obstruction.
Diagnosis may be strengthened by re-establishment of
urine output after gentle passage of a catheter.
• The external genitalia may reveal meatal stenosis or
urethral trauma. Patients with indwelling urinary catheters
that develop oliguria should undergo flushing of the
catheter to rule out blockage.
Lab studies

Urinalysis
• freshly voided urine sample is a rapid and inexpensive way
of distinguishing prerenal from intrinsic renal failure.
• In prerenal failure, a few hyaline and fine granular casts
may be seen with little protein, heme, or red cells. Hemepositive urine in the absence of erythrocytes suggests
hemolysis or rhabdomyolysis.
• In intrinsic renal failure, hematuria and proteinuria are
prominent. Broad, brown granular casts are typically found
in ischemic or toxic acute tubular necrosis, and red cell
casts are characteristically seen in acute
glomerulonephritis. The urine in acute interstitial nephritis
shows white cells, especially eosinophils and white cell
casts.

Urinary indexes
• Simultaneous measurement of urinary and serum sodium,
creatinine, and osmolality can help differentiate between
prerenal azotemia, in which the reabsorptive capacity of
tubular cells and concentrating ability of the kidney are
preserved, or even enhanced and intrinsic renal failure, in
which these functions are impaired due to structural
damage.
• In prerenal failure, urine specific gravity is high (greater
than 1020), the ratio of urinary to plasma creatinine is high
(greater than 40), ratio of urinary to plasma osmolality is
high (greater than 1.5), and the urinary-sodium
concentration is low (less than 20 mEq/L).
• The opposite findings are encountered in intrinsic renal
failure, which are urine to plasma creatinine ratio less than
20, urine-to-plasma osmolality less than 1.1, and urinesodium concentration greater than 40 mEq/L.
• The fractional excretion of sodium (FeNa) is the percentage
of filtered sodium that is excreted.
%FeNa = [(U/P)Na]/[(U/P)Cr] x 100
• The %FeNa is typically less than 1% in prerenal azotemia
and greater than 2% in intrinsic renal failure.
Introduced by the KDIGO in 2012, specific
criteria exist for the diagnosis of AKI.
Classic laboratory findings in AKI
Type
UOsm
UNa
FeNa
BUN/Cr
Prerenal
>500
<10
<1%
>20
Intrinsic
<350
>20
>2%
<15
Postrenal
<350
>40
>4%
>15
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

BUN and serum creatinine
• In prerenal failure, there is a marked elevation of BUN and a
BUN/Cr ratio greater than 20. This reflects increased proximal
tubular reabsorption of urea. The hallmark of established AKI
is a daily increase in serum creatinine (0.5-1.5 mg/dL/d) and
in BUN (10-20 mg/dL/d).
Serum sodium
• Hyponatremia is a common finding that is usually dilutional,
secondary to fluid retention and administration of hypotonic
fluids.
• Less common causes of hyponatremia include sodium depletion
(hyponatremic dehydration) and hyperglycemia (serum sodium
concentration decreases by 1.6 mEq/L for every 100 mg/dL
increase in serum glucose above 100 mg/dL).
Acid-base balance
• The impaired renal excretion and decreased tubular reabsorption
and regeneration of bicarbonate results in metabolic acidosis with
a high anion gap.
• Severe acidosis can develop in children who are hypercatabolic
(shock, sepsis) or who have inadequate respiratory compensation.

Serum potassium
• Hyperkalemia is an important complication because of
reduced glomerular filtration, reduced tubular secretion,
metabolic acidosis (each 0.1 unit reduction in arterial pH
raises serum potassium by 0.3 mEq/L), and associated
catabolic state.
• Hyperkalemia is most pronounced in patients with
excessive endogenous-potassium production including
rhabdomyolysis, hemolysis, and tumor lysis syndrome.
• Hyperkalemia represents a life-threatening emergency that
must be treated promptly and aggressively, primarily due to
its depolarizing effect on cardiac conduction pathways.
• Symptoms may include malaise, nausea, and muscle
weakness.

Serum phosphate and calcium
• Hyperphosphatemia and hypocalcemia frequently
complicate oliguric AKI. The phosphate excess is
secondary to reduced renal excretion and can result in
hypocalcemia and calcium phosphate deposition in various
tissues.
• Hypocalcemia results from hyperphosphatemia-impaired
gastrointestinal calcium absorption due to inadequate active
vitamin D production by the kidney, skeletal resistance to
the calcemic action of parathyroid hormone, and coexistent
hypoalbuminemia.
• Acidosis increases the fraction of total calcium in the
ionized form; thus, overzealous bicarbonate therapy in can
decrease ionized calcium.
• Severe hypocalcemia results in tetany, seizures, and cardiac
arrhythmias

Complete blood count (CBC)
• Anemia is a result of dilution and decreased erythropoiesis.
Microangiopathic hemolytic anemia with schistocytes and
thrombocytopenia are indicative of hemolytic-uremic
syndrome.
• Patients with oliguria that is secondary to systemic lupus
erythematosus may display neutropenia and
thrombocytopenia.
• Eosinophilia is consistent with allergic interstitial nephritis.
• Prolonged ARF can result in functional platelet disorders.

Coagulation studies: disseminated intravascular coagulation
associated with sepsis.
Creatine kinase, myoglobinuria: markedly elevated creatine
kinase and myoglobinuria suggest rhabdomyolysis.


Serologies
• Decreased complement levels (C3, C4) are characteristic of
acute post-streptococcal glomerulonephritis but can also be
seen in lupus nephritis and membranoproliferative
glomerulonephritis. A suspected diagnosis of acute poststreptococcal glomerulonephritis can be confirmed by
detection of elevated anti-streptococcal titers. The presence
of antinuclear antibodies is suggestive of lupus nephritis,
and antineutrophil cytoplasmic antibodies indicate
vasculitis.
• Virology: hepatitis B and C; HIV

The news markers of AKI include cystatin C, neutrophil
gelatinase-associated lipocalin (NGAL), kidney injury
molecule-1 (KIM-1) and interleukin-18 (IL-18). None have yet
been recommended for routine use.
Imaging Studies:
 Renal ultrasound very important
• Exceptions may include children with unmistakable
prerenal failure from dehydration who promptly respond to
fluid resuscitation, or those with mild renal insufficiency
secondary to a nephrotoxin who respond to discontinuing
the medication.
• Ultrasound provides important information regarding
kidney size and echogenicity, renal blood flow, collecting
system, and bladder wall.
• Children with acute intrinsic renal failure display
echogenic kidneys that may be enlarged. With prolonged
renal failure, renal cortical necrosis may result in decreased
kidney size. Bilateral, small scarred kidneys are indicative
of chronic renal disease.
• Congenital disorders, such as polycystic kidney disease and
multicystic dysplasia, are easily detected. Stones and
tumors that can cause obstruction may also be detected.
• A Doppler study is critical in the evaluation of vascular
obstruction.
Other imaging studies
• A voiding cystourethrogram is indicated with suspected
bladder outlet obstruction.
• A radionuclide renal scan may be useful in the assessment
of transplant rejection and obstruction.
• A chest radiograph may be indicated if pulmonary edema
is suspected.
• An echocardiogram may be useful in the presence of
congestive heart failure.
ECG
• The earliest sign is appearance of tall peaked T waves.
• Subsequent findings include the following:
 Prolongation of the PR interval
 Flattening of P waves
 Widening of QRS complexes
 ST segment changes
 Ventricular tachycardia
 Terminal ventricular fibrillation


Renal biopsy
• AKI without obvious cause (no toxic or sepsis, or
hypertension)
• Important hematuria and / or proteinuria
• Extrarenal signs directing to systemic disease or vasculitis
(articular manifestations, respiratory or skin)
• Suspected interstitial nephritis immunoallergic, especially
when the suspected drug should be continued
• progressive installation of AKI
• Oliguria or anuria persisting for 2 or 3 weeks
SIGNS OF GRAVITY IN AKI
1. Level of uremic poisoning
- urea> 50 mmol / l, creatinine > 1000 umol / l, confusion, drowsiness
2 Overload hydrosodée:
> 10% of basal weight, pulmonary edema, pleural or pericardial
efusions
3 Water intoxication
- hyponatremia <120 mmol / l, confusion, coma
4 Superinfection (pneumonia, catheter or urinary catheter)
5 Gastrointestinal bleeding, stress ulcer, hematoma at puncture
6 Severe metabolic acidosis
bicarbonatémie <10 mmol / l, pH <7.20
7 Hyperkalemia
potassium> 6 mmol / l, ECG signs
8. Hyperphosphatemia and hypocalcemia
P> 3 mmol / l (risk of precipitation intratubular)
Calcium <1.8 mmol / l (convulsion, tetany)
TREATMENT
Medical Care:
 Prevention
• In clinical situations where renal hypoperfusion or toxic injury is
anticipated, therapy with fluids, mannitol, diuretics, and renaldose dopamine are used to prevent, or reverse, renal injury.
These maneuvers are able of converting the oliguric state to a
nonoliguric AKI, which is more easily managed.
• Vigorous fluid administration has been successfully employed to
prevent AKI following cardiac surgery, cadaveric renal
transplantation, hemoglobinuria, myoglobinuria,
hyperuricosuria, radiocontrast infusion, and therapy with
amphotericin B or cisplatinum.
• A trial of intravenous mannitol or furosemide should be
attempted in a patient with oliguria for less than 48 hours who
has not responded to adequate hydration. The benefit of renaldose dopamine therapy is controversial.
• Once oliguria is established, mannitol may precipitate congestive
heart failure, the risk of ototoxicity from furosemide, and
adverse hemodynamic changes from dopamine are significant.

Fluid management
• The major goal of fluid management is to restore and
maintain normal intravascular volume. This is accomplished
by determination of input and output, body weights, vital signs,
skin turgor, capillary refill, peripheral edema, cardio-pulmonary
examination, serum sodium, and FeNa.
• Children with intravascular volume depletion require prompt and
vigorous fluid resuscitation. Initial therapy includes normal
saline or lactated Ringer's at 20 mL/kg over 30 minutes, which
can be repeated twice if necessary.
• Potassium administration is contraindicated until urine flow
is established. This therapy should result in increased urine
output within 4-6 hours. If oliguria persists (confirmed by
bladder catheterization), central venous monitoring may be
required to guide further management.
• Oliguria with volume overload requires fluid restriction and
intravenous furosemide. Failure to respond to furosemide
suggests the presence of acute tubular necrosis rather than renal
hypoperfusion, and fluid removal by dialysis or hemofiltration
may be required, especially if signs of pulmonary edema are
evident.

Hyperkalemia

K < 6.0 mmol / l - stop the K sparing therapy, food restriction (restriction
dried fruit, bananas, citrus fruits, beans, dried peas, green vegetables,
potatoes)
K - 6.0 - 6.5 mmol / l :
- hydration
- Slow bolus Ca gluconate 10% , 0.5 ml / kg, ECG monitoring
- PIV SG 10-30 % 1ml/kg ( rapid insulin 1U/5g glucose)
- Sorbitol 70 % + Kayexalate the 1g/kgc/po , 2ml/kg
- Where AR < 18 mmol / l - 8.4 % Na bicarbonate , 2mEq/kg/day in 4 parts
- K repeated after 6 hours
K > 6.5 mmol / l :
- Continuous ECG monitoring
- Salbutamol nebuliser
- Emergency hemodialysis



Other electrolytes and acid-base balance
• The primary treatment of hyponatremia is free water
restriction; however, serum sodium less than 120 mEq/L, or
accompanied by central nervous system dysfunction, may
require 3% sodium chloride infusion.
• Management of hyperphosphatemia includes dietary
restriction and oral phosphate binders (calcium carbonate
or calcium acetate).
• Hypocalcemia usually responds to the oral calcium salts
used for control of hyperphosphatemia but may require
10% calcium gluconate infusion if severe.
• Mild metabolic acidosis is treated with oral sodium
bicarbonate or sodium citrate. Severe acidosis (pH less than
7.2), especially in the presence of hyperkalemia, requires
intravenous bicarbonate therapy. It should be recognized
that bicarbonate therapy requires adequate ventilation (to
excrete carbon dioxide produced) to be effective and that it
may precipitate hypocalcemia and hypernatremia.
Hypertension
Antihypertensive therapy :
 hipertensive encephalopathy :
- Diazoxide iv bolus 5mg/kg/dosis
- Na nitroprusside : 0.5 - 8μg/kg/min , iv
- Furosemide: 1 - 2mg/kg , iv slow
 severe hypertension without encephalopathy :
- Minoxidil 0,1 - 0,2 mg / k g / day , max 5mg/24 hours
- Ca channel blockers : from 0.25 to 0.5 mg / kg / dose , max 12mg/kg/zi
Warning: angiotensin converting enzyme inhibitors may
further reduce glomerular filtration and beta-blockers may
exacerbate hyperkalemia !
 acute pulmonary edema: hemodyalisis
 mild hypertension usually responds to salt restriction and
diuretics.
 moderate asymptomatic hypertension is most commonly
treated with oral or sublingual calcium channel blockers or with
intravenous hydralazine.


Dialysis
• The general goal of dialysis is to remove
endogenous and exogenous toxins, and to maintain
fluid, electrolyte, and acid-base balance until renal
function returns.
• The indications for acute dialysis are not absolute,
and the decision to use this modality depends on
the rapidity of onset, duration, and severity of the
abnormality to be corrected.
• The choice between hemodialysis and peritoneal
dialysis depends on the overall clinical condition,
availability of technique, etiology of the renal
failure, institutional preferences, and specific
indications or contraindications.
Common indications of dialysis include:
• fluid overload that is unresponsive to diuretics,
• symptomatic acid-base/electrolyte imbalances (especially
hyperkalemia) that are unresponsive to medications
• refractory hypertension
• symptomatic uremia (central nervous system symptoms,
pericarditis, pleuritis).
• If adequate nutrition cannot be achieved because of fluid
restriction, early institution of ultrafiltration or dialysis
should be considered.
Surgical Care: patients with oliguria secondary to obstruction
frequently require urologic care. The site of obstruction
determines the therapy.
Diet:
 Children with oliguric ARF are frequently in a highly catabolic
state; therefore, aggressive nutritional support is important.
Adequate calories should be given to account for maintenance
requirements, and supplements should be provided to combat
excessive catabolism.
 Protein of high biologic value should be administered in amounts
that are sufficient to maintain neutral nitrogen balance, reflected by
steady BUN levels.
 Oral feeding is the preferred route. Infants should be placed on a
low-phosphorus formula, and older children fed a low-phosphorus,
low-potassium diet.
 Additional calories may be supplied by fortifying foods with
polycose and medium-chain triglycerides.
 Children who are nauseas or anorexia may benefit from enteral
feedings. If enteral feedings are not possible, central intravenous
hyperalimentation may be used to deliver concentrated dextrose
(25%) and lipids (20%).
Activity: children are usually hospitalized; therefore, activity is
restricted.
Complications:
 Infections develop in 30-70% of patients and include the
respiratory system, urinary tract, and catheters infections.
Impaired defenses, due to uremia and inappropriate use of
antibiotics, may contribute to the high rate of infectious
complications.
 Cardiovascular complications are a result of fluid and sodium
retention. They include hypertension, congestive heart failure,
and pulmonary edema.
 Hyperkalemia results in ECG abnormalities and arrhythmias.
 Other complications include the following:
• Gastrointestinal (anorexia, nausea, vomiting, and ileus,
bleeding)
• Hematologic (anemia and platelet dysfunction)
• Neurologic (confusion, asterixis, somnolence, and seizures)
• Other electrolyte/acid-base disorders (metabolic acidosis,
hyponatremia, hypocalcemia, and hyperphosphatemia)
Prognosis:
 Despite significant advances in supportive care and renal
replacement therapy, high mortality rates in the setting of
multiorgan failure have not improved in the past few decades.
 It must be emphasized that patients die with renal failure;
however, they do not die not because of renal failure. The
patient succumbs rather than to involvement of other systems
during the period of renal insufficiency.
 On the other hand, prognosis from prerenal causes, or from
acute tubular necrosis in the absence of significant co-morbid
conditions, is usually quite good if appropriate therapy is
instituted in a timely fashion.
Hemolitic uremic syndrome
This is the most common infant cause of AKI (75%).
Definition and epidemiology:
 HUS is a serious complication of an episode of diarrhea often
bloody, may change in 10% of cases to hemolytic anemia,
thrombocytopenia and acute renal failure, which are the main
characteristics
The mortality rate is now less than 5% in literature.
Histology:
 In the kidney: thromotique microangiopathy lesions of
glomerular capillary wall or cortical necrosis.
Etiologies:
Verotoxin-producing E. coli (VTEC O157 serotipe).
Epidemics in summer.

Mode of transmission
- Contamination is most often food: ingestion of food
consumed raw or undercooked.
- Beef, especially ground
- Raw milk and products made ​from raw milk
- Exceptional consumption of raw vegetables or untreated
water (well water, for example) not contaminated animal
waste.
- Inter-human transmission by fecal-oral transmission within
families or communities is possible failure of hygiene
measures.
- Direct contact with infected animals or their droppings can
also be cause.Il be noted that the infectious dose is very low.
Clinic: typical HUS is D+
- The most common; especially infants.
- Prodromes digestive.
- Evolution favorable.
a. the invasion phase: non-specific:
- Moderate fever;
- Gastrointestinal disorders: diarrhea, sometimes bloody;
- It takes a few hours to a few days.
b. the status phase
- Sudden pallor associated with hemolytic anemia;
- Bleeding disorders with thrombocytopenia;
- AKI with hematuria;
- Frequently HTA;
- Neurological Signs: convulsion.
Paraclinical:
- Severe hemolytic anemia and regenerative.
- Schizocytosis: constantly found (5-10% of cells); early and
ephemeral.
- Thrombocytopenia (<100000plaquettes/mm ³).
- Signs of AKI.
Clinical forms:
A. Atypical HUS:
- Very rare;
- After 3 years;
- No seasonal pattern;
- Without digestive prodrome;
- More severe.
B. Secondary HUS.
C. family HUS.
Treatment:
Symptomatic:
- Renal failure: peritoneal dialysis or hemofiltration.
- Hypertension.
- Anemia: red blood cell transfusion.
Specific: fresh frozen plasma; IV immunoglobulin.
Surveillance - sequelae (hypertension, CKD).
Complications of HUS D+
• Death in the acute phase - 2%
• Convulsions, drowsiness, stupor, coma
• Gastrointestinal disease: ulcerative colitis, ileitis necro haemorrhagic
• Pancreatitis
• Hepatic Impairment
• Heart feailure
HUS D+: bad renal prognosis in case of:
Acute phase:
- Severe neurologic complications
- Severe colitis
- Polymorphonuclear neutrophils > 20 000/mc
- Thrombocytopenia <30000/mmc
- Anuria> 8 days
At distance:
- duration of initial anuria
- Persistent proteinuria after 1 year
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