good ppt for undergraduate medical students

1. 8/12/2022 1

2. ACUTE RENAL FAILURE IN CHILDREN
Dr. Sabona Lemessa (Assistant professor in pediatrics and child health, JUMC)
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3. Outline
Introduction
Definition of ARF
Pathophysiology
Etiology
Clinical manifestation and diagnosis
ARF in Neonate
Complication
Management
Prognosis
Reference
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4. Introduction
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5. ACUTE KIDNEY INJURY
Definition
 Sudden deterioration in renal function
It results in the inability of the kidneys to maintain fluid and electrolyte homeostasis.
Also results in a decline in GFR, retention of urea and other nitrogenous waste products
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6. Cont…
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7. Prevalence
 Occurs in 2-3% of children admitted to pediatric tertiary care centers and in as many as 8% of
infants in NICU.
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8. Pathophysiology of AKI
Three major factors that may account for the development of AKI:
Renal hemodynamics
nephronal factors
metabolic/cellular factors
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9. cont…
Renal hemodynamics
Insult to the renal tubular epithelium results in release of vasoactive compounds
increase cortical vascular resistance causing decreased RBF
Release of vasoconstrictive compounds may then diminish GFR by constricting afferent and
efferent arterioles
thereby causing diminished urine output, or oliguria
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10. Cont…
Nephronal factors:
proximal tubule injury leading to epithelial necrosis and loss of tubular integrity and
impacted cellular debris
Back leak of solute/fluid and tubule obstruction which further lead to diminished GFR and
tubule flow
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11. cont…
Cellular and metabolic mechanisms
Oxygen free radical production contributing to an ischemic insult
Calcium accumulation in tissues which has undergone necrosis contributing to renal cell injury:
 uncouples oxidative phosphorylation
 activation of membrane bound phospholipases
activation of intracellular proteases
inhibition of Na/K-ATPase
Direct effect on intracellular pH.
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12. Cont…
Depletion of tissue adenine nucleotide levels which is a source of energy and concomitant
increase in nucleosides, adenosine and inosine.
These are responsible for renal vasoconstriction following an ischemic insult.
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13. Etiology of ARF
The causes and mechanisms of AKI can be classified based on the anatomic location of the initial
injury:-
Vascular – Blood from the renal arteries is delivered to the glomeruli. Interruption of perfusion to
the kidneys results in prerenal AKI
Glomeruli – Ultrafiltration occurs at the glomeruli forming an ultrafiltrate, which subsequently
flows into the renal tubules
Renal tubule – Reabsorption and secretion of solute and/or water from the ultrafiltrate occurs
within the tubules
Urinary tract – cause postrenal AKI
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14. Cont…
1. Prerenal ARF also called prerenal azotemia
• Due to diminished effective circulating arterial volume → inadequate renal perfusion and a
decreased GFR.
• Evidence of kidney damage is absent
• If the underlying cause of the renal hypoperfusion is reversed promptly renal function
returns to normal.
• If hypoperfusion is sustained, intrinsic renal parenchymal damage can develop
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15. Cont…
2. Intrinsic renal ARF
• renal parenchymal damage, including sustained hypoperfusion and ischemia.
• Many forms of glomerulonephritis can cause ARF
• Ischemic/hypoxic injury and nephrotoxic insults are the most common causes of intrinsic AKI
in the United States
• recovery in 1-2 weeks
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16. Cont…
Three phases of intrinsic renal failure
 Initiation phase- GFR ↓because of decreased glomerular pressure, obstructed flow by casts, necrotic
debris and back leak of filtrate through injured epithelium.
Maintenance phase(1-2wks)
 renal cell injury is established
 GFR remains relatively low for several days
 UOP will be lowest
 uremic complications start to appear
Recovery phase:
 Renal parenchymal cell repair & regeneration
 GFR starts to increase
 retained salt and water will be excreted
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17. cont...
Postrenal ARF
It includes a variety of disorders characterized by obstruction of the urinary tract
Obstruction must be bilateral to result in AKI
Relief of the obstruction usually results in recovery of renal function except in patients with
associated renal dysplasia or prolonged urinary tract obstruction.
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18. Causes of ARF
Prerenal Intrinsic Renal Postrenal
Dehydration
Hemorrhage
Sepsis
Hypoalbuminemia
Cardiac failure
Renal artery stenosis
Glomerulonephritis:
• poststreptococcal
• Lupus erythematosus
• HSP
• Membranoproliferative
• Anti– GBM
Hemolytic-uremic syndrome
Acute tubular necrosis
Cortical necrosis
Renal vein thrombosis
Rhabdomyolysis
Acute interstitial nephritis
Tumor infiltration
Tumor lysis syndrome
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
Tumor
Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder
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19. Clinical manifestation and diagnosis
A carefully taken history is critical in defining the cause of ARF
Thorough physical examination is a must
Careful attention to volume status!
• Tachycardia, dry mucous membranes, and poor peripheral perfusion
• Peripheral edema, rales, and a cardiac gallop
• rash and arthritis might indicate systemic lupus erythematosus(SLE)
• Palpable flank masses – Renal vein thrombosis, Tumor, Urinary tract obstruction
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20. Laboratory and Imaging
Serum creatinine
Urinalysis
CBC
Serologic testing for streptococcal infection
Uric acid
Renal ultrasound
Renal biopsy
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22. Cont…
The sensitivity and specificity of urine sodium of <20 in differentiating prerenal azotemia
from ATN are 90% and 82%, respectively.
Fractional excretion of sodium is :
• urine to plasma (U/P) of sodium divided by U/P of creatinine × 100.
• The sensitivity and specificity of FENa of <1% in differentiating prerenal azotemia from
ATN are 96% and 95%, respectively
Biomarkers of AKI - serum Cr is often a delayed and imprecise test
NGAL, KIM-1, and IL-18 show promise in both their diagnostic and prognostic utility
may allow for early intervention prior to the onset of SCr rise, severe metabolic
derangements and fluid overload
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23. Acute Renal Failure in neonate
sudden impairment in renal function
Lead to an inability of the kidneys to excrete nitrogenous waste
Although the criteria for neonatal ARF have varied among studies, a consensus definition is a
serum creatinine level of more than 1.5 mg/dL
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24. Cont…
Classified as:
Oliguric:- urine flow rate of <1 mL/kg/hr
Nonoliguric:- urine flow rate >1ml/kg/hr.
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25. Cont…
Prevalence
Most reports estimate the incidence of ARF in the hospitalized neonatal population to be 6%
to 8%
although some estimates reach as high as 23%
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26. Causes of ARF in Neonate
Prerenal Renal Postrenal
Dehydration
Hemorrhage
Sepsis
Necrotizing enterocolitis
Congestive heart failure
Drugs: ACEI, indomethacin,
amphotericin, tolazoline
Acute tubular necrosis
Renal dysplasia
Polycystic kidney disease
Renal venous thrombosis
Uric acid nephropathy
Transient acute renal
insufficiency of the newborn
Posterior urethral valves
Bilateral ureteropelvic
junction obstruction
Bilateral ureterovesical
junction obstruction
Neurogenic bladder
Obstructive nephrolithiasis
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27. Clinical presentation
Failure to void for longer than 48 hours may suggest impairment of renal function and should
prompt further investigation
Oliguria, systemic hypertension, cardiac arrhythmia
evidence of fluid overload or dehydration
decreased activity, seizure, vomiting and anorexia
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28. Evaluation
History
A neonate with a history of hydronephrosis seen on prenatal ultrasound studies and a
palpable bladder most likely has congenital urinary tract obstruction, probably related to
posterior urethral valves.
perinatal asphyxia, the pre- or postnatal administration of potentially nephrotoxic drugs
Family history of renal disease.
P/E should focus on
 signs of volume depletion or volume overload
abdomen, genitalia and search for other congenital anomalies
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29. Laboratory finding
In general, each doubling of the serum creatinine level represents an approximately 50%
reduction in GFR
elevated serum creatinine and BUN, hyperkalemia, metabolic acidosis, hypocalcemia,
hyperphosphatemia
 Accurate estimate of GFR can be calculated as:-
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30. Diagnostic Indexes in Acute Renal Failure
TEST PRERENAL ARF INTRINSIC ARF
BUN/Cr ratio (mg/mg) >30 <20
FENa (%) ≤2.5 ≥3.0
Urinary Na (mEq/L) ≤20 ≥50
Urinary Osm (mOsm/kg) ≥350 ≤300
Urinary specific gravity >1.012 <1.014
Ultrasonography Normal May be abnormal
Response to volume challenge UO > 2 mL/kg/h No increase in UO
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31. Management of ARF
Specific treatment of the underlying cause
Fluid management
Electrolyte management
Nutritional support
Adjustment of drug dosing
Renal replacement therapy
Specific pharmacologic therapies
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32. Fluid Management
Hypovolemia:- IV fluid therapy given as a NS bolus (10 to 20 mL/kg over 30 minutes, repeated
twice as needed)
attempt to restore renal function
prevent the progression of prerenal AKI to intrinsic AKI
hypovolemic patients generally void within 2 hr
Failure to do so suggests intrinsic or postrenal AKI
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33. Cont…
Euvoluemia:- Ongoing fluid losses should be balanced
 Insensible fluid [300 to 500 mL/m 2 per day]
 higher in febrile patients and lower for ventilated patients
urine , blood loss and gastrointestinal losses should be replaced
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34. Cont…
Hypervolemia
Child with signs of fluid overload (edema, heart failure and pulmonary edema) requires fluid
removal and/or fluid restriction
omitting the replacement of insensible fluid losses, urine output, and extrarenal losses to
diminish the expanded intravascular volume
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35. Cont…
Diuretic therapy :- Only after the adequacy of the circulating blood volume has been established
 Furosemide (2-4 mg/kg)
Bumetanide (0.1 mg/kg) may be given as an alternative to furosemide
mannitol (0.5 g/kg) may be administered as a single IV dose
If urine output is not improved, then a continuous diuretic infusion (0.1 to 0.3 mg/kg per
hour) may be started
To increase renal cortical blood flow, many clinicians administer dopamine (2-3 μg/kg/min) in
conjunction with diuretic therapy
There is little evidence that diuretics or dopamine can prevent AKI hasten recovery
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36. Electrolyte management
Hyperkalemia:- (K+ > 6 mEq/L)
Lead to cardiac arrhythmia, cardiac arrest, and death
 Exogenous potassium restriction
 Resin therapy :- 1 g/kg orally or by retention enema
- A single dose expected to lower the serum K+ level by about 1 mEq/L
- can be repeated after 2hrs
When it is >7mEq/L, it requires emergency measures
• Calcium gluconate 10% solution, 1.0 mL/kg IV, over 3–5 min
• Sodium bicarbonate, 1–2 mEq/kg IV, over 5–10 min
• Regular insulin, 0.1 U/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
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37. Cont…
Metabolic Acidosis
because of the retention of hydrogen ions, phosphate, and sulfate
but it rarely requires treatment
 treat if acidosis is severe (arterial pH < 7.15; serum bicarbonate < 8 mEq/L) or
If contributes to significant hyperkalemia
the intravenous route, generally by giving enough bicarbonate to raise the arterial pH to 7.20
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38. Cont…
Hyponatremia:
- most commonly a dilutional disturbance that must be corrected by fluid restriction rather
than sodium chloride administration.
- Hypertonic (3%) saline for 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
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39. Cont…
Hypocalcemia
 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
Seizures
 Due to hypertensive encephalopathy, hyponatremia, hypocalcemia, cerebral hemorrhage,
cerebral vasculitis, and uremic state
 Benzodiazepines are the most effective agents in acutely controlling seizures
 subsequent therapy should be directed toward the precipitating cause
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40. Cont…
Hypertension:-
Due to hyperreninemia and expansion of the ECF volume
most common in AKI patients with AGN or HUS
Salt and water restriction is critical
Children with severe symptomatic hypertension (hypertensive urgency or emergency)
- 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
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41. Cont…
Anemia:- usually mild (Hgb 9-10g/dl) and due to hemodilution
Transfuse with packed RBC in children with HUS, SLE, active bleeding or Prolonged AKI and
Hgb <7g/dl
Slow (4-6 hr) transfusion with packed RBC(10 mL/kg) diminishes the risk of hypervolemia
In the presence of severe hypervolemia or hyperkalemia, blood transfusions are most safely
administered during dialysis or ultrafiltration.
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42. Dialysis
Indications
 Anuria/oliguria
Volume overload with evidence of hypertension and/or pulmonary edema refractory
to diuretic therapy
Persistent hyperkalemia
Severe metabolic acidosis unresponsive to medical management
Uremia (encephalopathy, pericarditis, neuropathy)
 BUN >100-150 mg/dL (or lower if rapidly rising)
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43. Prognosis
depends entirely on the nature of the underlying disease process rather than on the renal failure
itself
AKI caused by a renal-limited condition such as postinfectious AGN have a very low mortality rate
(<1%)
Those with AKI related to multiorgan failure have a very high mortality rate (>50%)
Recovery of renal function is likely after AKI resulting from prerenal causes, ATN, acute interstitial
nephritis, or TLS
Complete recovery of renal function is unusual when AKI results from most types of rapidly
progressive glomerulonephritis, bilateral renal vein thrombosis, or bilateral cortical necrosis
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44. Cont…
In neonates
Mortality rates range from 14% to 73%.
In general, those infants with prerenal ARF who receive prompt treatment for renal
hypoperfusion have an excellent prognosis
Infants with postrenal ARF related to congenital urinary tract obstruction have a variable
outcome, which depends on the degree of associated renal dysplasia
long-term sequelae seen in survivors of neonatal ARF include HTN, an impaired capacity for
urinary concentration, renal tubular acidosis (RTA), and impaired renal growth
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45. Reference
Beth A. Vogt Katherine MacRae Dell Ira D. Davis, Fanaroff
Devarajan P. Acute kidney injury: Nat Rev Nephrol . 2017, 21st edition Nelson
KDIGO Guidelines on AKI Professor Alan Cass, Director Menzies School of Health Research
President-Elect ANZ Society of Nephrology
Rajasree Sreedharan . Prasad Devarajan . Scott K. Van Why, 6th edition of pediatric Nephrology
Robert H Squires, Jr, MD, FAAP, Oct 2013
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Thank you