A PowerPoint presentation for medical students about AKI in children

1. ACUTE RENAL FAILURE IN CHILDREN
IBRAHIM SANDOKJI, MD, FAAP
Pediatric Nephrologist, Assistant Professor
Board Certified by the American Board of Pediatrics
Taibah University
isandokji@taibahu.edu.sa
+966 50 632 5770

2. How do you approach this
child?
 While you are in the ER, a 3-year-old boy was brought with history
of vomiting and diarrhea for two days. He did not urinate for the last
day. He appears dry on your examination. He was unable to drink or
eat anything. You ordered IV fluids and obtained labs which show:
Lab Normal
Complete blood
count
Normal
Sodium 140 mmol/L 135–145 mmol/L
Potassium 6 mmol/L 3.5–5.0 mmol/L
Urea 12 mmol/L 1.8–6.4 mmol/L
Creatinine 150 μmol/L 44–88 μmol/L
Hyperkalemia
Uremia
Rise in creatinine (=decrease in GFR

3. ACUTE RENAL FAILURE
ACUTE KIDNEY INJURY (AKI)
 Abrupt loss of kidney function
 That results in
 A decline in glomerular filtration rate (GFR)
 Retention of urea and other nitrogenous waste products
 Dysregulation of extracellular volume and electrolytes
AKI, not ARF, defines renal dysfunction more clearly as a continuum, rather than a discrete change in renal
function

4. Kidney Disease Improving Global Outcomes (KDIGO) Diagnostic
Criteria

6. INTRINSIC RENAL
Vascular
Renal vein or artery
thrombosis
Hemolytic uremic syndrome
Tubular (ATN)
Ischemia, sepsis
Nephrotoxins:
Aminoglycosides, amphotericin,
chemotherapy, radiocontrast
Glomerular
PIGN, RPGN, HSP, SLE
Interstitium
Interstitial nephritis:
Antibiotics, PPIs, NSAIDs,
diuretics

7. Mechanism Etiology
Prerenal causes
Decreased intravascular volume Dehydration, hemorrhage, burns, shock, nephrotic syndrome
Decreased cardiac function Heart failure
Peripheral vasodilatation Sepsis, anaphylaxis, antihypertensive medication
Renal vasoconstriction Sepsis, nonsteroidal anti-inflammatory drugs, ACE inhibitor
Intrinsic causes
Tubular injury
(acute tubular necrosis)
Prolonged ischemia, nephrotoxins, hypotension, sepsis
Renal vascular diseases Hemolytic uremic syndrome, vasculitides, thrombosis
Interstitial diseases Interstitial nephritis, infections
Glomerulonephritides PIGN, RPGN, HSP
Most common cause of AKI

8. ACUTE TUBULAR NECROSIS (ATN)
Muddy Brown Casts
 Common cause of AKI
 Ischemic injury
 Toxic injury
 Endogenous
 Drugs (gentamicin, amphotericin,
cisplatin)
 Toxins (heavy metals, radiocontrast)
 Exogenous
 Heme pigments -> rhabdomyolysis
 Uric acid -> tumor lysis syndrome

9. HISTORY
Fluid loss Glomerular diseases
•Diarrhea, vomiting
•Burns
•Surgery
•Shock
•Streptococcal infection: PIGN
•Bloody diarrhea: HUS
•Joint symptoms, rash, or purpura: HSP
Nephrotoxic agents Obstruction
•NSAIDs
•Aminoglycosides
•Contrast agents
•Complete anuria
•Poor urinary stream

10. Intravascular volume depletion Palpably enlarged kidneys
•Tachycardia
•Delayed capillary refill
•Low blood pressure
•Weak peripheral pulses
•Dry mucous membranes
•Hydronephrosis
•Polycystic/multicystic kidney
disease
•Renal vein thrombosis
Fluid overload Obstruction
•Edema
•Hypertension
•Heart failure
•Pulmonary edema
•Poor urinary stream
•Palpably enlarged bladder
•Therapeutic catheterization
Systemic causes
•Rash: HSP, acute presentation of SLE, interstitial nephritis due to drug reaction
•Joint findings (tenderness or swelling): HSP, acute presentation of SLE
EXAMINATION

11. LABORATORY AND IMAGING EVALUATION
 Electrolytes
 Urinalysis
 Renal ultrasound
 Considered in some patients:
 CBC
 C3, C4
 Testing for streptococcal infection
 Fractional excretion of sodium (FeNa)
 Renal biopsy — rarely indicated in
AKI.
 Done if Suspected
 Acute GN
 Interstitial nephritis
 Lupus nephritis

12. PREVENTION
Fluid management Avoid nephrotoxins

13. MANAGEMENT STRATEGIES
 Treat the underlying cause
 Fluid management
 Hypovolemia –> fluid
 Euvolemia –> balanced intake/output
 Hypervolemia -> fluid removal and/or
restriction
 Management of AKI complications:
 Electrolyte disturbances
 Metabolic acidosis
 Hypertension
 Adequate nutrition
 Drug management
 Avoidance of nephrotoxic agents
 Dosing readjustment of renally
excreted drugs
 ? Dialysis

14. HOME READING

15. White Blood Cell Casts Red Blood Cell Casts
Hyaline Casts Muddy Brown Granular Casts
Waxy Casts
Fatty Casts
In which condition(s) do you see each one of these casts in the urine?

16. Pre-renal AKI vs intrinsic AKI (ATN)
Measurement Prerenal AKI Intrinsic AKI
Urine specific gravity >1.020 <1.010
Urine Na (mEq/L) <20 >40
FENa <1 percent >2 percent

17. Role of Renal Ultrasound in AKI
 Delineate renal size
 Survey the renal parenchyma
 Diagnose urinary tract obstruction
 Diagnose occlusion of the major renal vessels
 Document the presence of one or two kidneys
 Differentiating AKI from CKD
 Typically, the kidneys in AKI are normal in size or enlarged (due to inflammation or edema), with increased
echogenicity, whereas those in CKD are frequently small and shrunken

18. AKI Management Based on KDIGO Guidelines

20. HYPERKALEMIA MANAGEMENT

21. INDICATIONS OF DIALYSIS IN AKI
 Fluid overload unresponsive to diuretics
 Hyperkalemia unresponsive to non-dialytic therapy
 Hypertension unresponsive to pharmacologic therapy
 Uremic encephalopathy
 Pulmonary Edema
 Heart failure

23. You are seeing a child for a routine physical
examination and found elevated creatinine and BUN.
How to know this process is acute or chronic?
Finding Acute kidney injury (AKI) Chronic kidney disease (CKD)
Serum BUN and Cr Progressive rise in BUN and Cr Stable elevated BUN and Cr
Historical clues
Positive history for AKI etiology (eg, recent
streptococcal infection: poststreptococcal
glomerulonephritis)
History of chronic hypertension
Growth Normal growth Impaired growth
Bone status Normal bones
Evidence of renal osteodystrophy: History of fractures,
abnormal tibial torsion
Urine sediment No broad urinary casts Broad waxy urinary casts
Hematocrit Anemia usually mild Anemia usually severe
Renal ultrasound Normal or enlarged kidney size Small shrunken kidneys

24. OUTCOME
AFTER AKI