Acute kidney Injury

General characteristics

1. Abrupt decline in renal function resulting in a decrease in glomerular filtration rate

(GFR) usually characterized by 1 or all of the following :

a.Increased BUN ( blood urea nitrogen )

b. Increased serum creatinine levels

c. Decreased urine output (although can have nonoliguric AKI with nephrotoxic renal injury
/ neonate )



2. Results in disturbance of normal renal function including impaired nitrogenous

waste excretion, water and electrolyte homeostasis, and acid-base regulation

Pediatric RIFLE criteria definition and classifications of AKI :

reversible

irreversible
Schwartz formula: Estimated creatinine clearance (ml/min/1.73 m2)

eCCl = k × height / SCR

Normal GFR= 100


K constant :

Preterms in first year = 46

Full term In first year = 40

From 1-4 YO = 48 Adolescents = 60

Normal Renal function depends on :

1-Intact nephron perfusion
2-Adequate glomerular ultra-filtration
3-Appropriate tubular function
4-Unimpaired urine out flow
Classification :
Oliguric vs Non-oliguric
-Polyuric: > 4mL/kg/hr

-Oliguria: U.O < 1mL/kg/hr infants, U.O < 0.5ml/kg/hr in children.

-Anuria: U.O < 1mL/kg/day or no U.O.

-Non oliguric ARF:(present late) Commonly with nephrotoxic renal injury, Neonates 


Patho-physiological Mechanism:
- Regardless of cause of AKl , reductions in RBF represent common pathologic pathway for
decreasing GFR

- Causes of pediatric AKI are most commonly classified by their anatomic location as
follows :

1. Prerenal (most common): severe volume depletion leads to decreased renal blood flow
(RBF) hypo perfusion ; nephrons remain structurally intact .

* Hypoperfusion is most commonly caused by hypovolemia, or decreased effective arterial

perfusion due to heart failure, sepsis or cirrhosis .

* Hallmark: normalization of renal function upon therapeutic intervention

 2. Intrinsic: result in structural/functional damage to glomerulus/tubules with release of
renal afferent vasoconstrictors . 

- Due to injury to the renal parenchyma

-Most commonly caused by prolonged hypoperfusion, sepsis, nephrotoxins, or
severe glomerular diseases.

-The damage to the nephrons in ischemic and nephron-toxic AKI is confined to the
tubules while glomeruli are relatively well preserved and vice versa.

3.Postrenal:obstruction of urine 

(a) Initially causes increase in tubular pressure thereby decreasing filtration 

(b) This increase in pressure, causes renal damage, resulting in decreased renal function
- Intra-renal causes of Tubular obstruction (e.g. uric acid precipitation in tumor lysis) must
be considered , or others abnormalities like : urethral valve “in boys”

- Sudden anuria suggest obstruction (bilateral, distal to U.B. or in solitary kidney)



Clinical features:
- Fluid over loud (include edema, reduce urine output, gross hematuria, and/or
hypertension)
- Electrolyte disturbance (↑ K, ↑PO4, ↓Ca, ↓Na)

1. Historical question to establish the underlying diagnosis

a. Has the child had decreased drinking, decreased urine output, vomiting, or
diarrhea? Severe dehydration can cause AKI 


b. Is the child taking medications? Nephrotoxic medications cause AKT

 2. Physical exam findings: pay careful attention to volume status (i.e., do 

they appear fluid depleted or overloaded) and for findings from systemic diseases that
can cause renal dysfunction (e.g., rashes, arthritis, abdominal masses)

Lab Assessment:

1. Urinalysis + Urine c/s:

−  Tea-colored → glomeruli affected!

−  Pink

−  SG + Osmolality

−  Proteinuria

−  Easinophil-uria ( allergy ‘common with interstitial nephritis’ )

−  Hyaline + fine granular casts

−  Renal tubular cells or even casts 




2. Urine electrolytes.

3. CBC.

4. Blood Chemistry + gases:

- FE (X) the fraction of filtered X excreted in urine.

- So FE (X) = U/P (X) / U/P (creat) x 100 


- Notes: diuretic therapy affects FE Na

- Preterm has a higher FE Na 


5. PT, PTT & bleeding time.

2-Radiology and pathology findings

a. Renal ultrasound

b. Renal radioisotope scan: delineates areas of normal or low perfusion 


associated with poor renal function and areas of parenchymal damage by 

showing delay in accumulation of radioisotope

c. CT scan of abdomen and pelvis: may reveal masses or other structural 


abnonnalities that could be contributing to AKI

3- Other findings 

Renal biopsy: treatment and prognosis .

Goals of treatment:

1. Correct pre-existing bio-physiologic abnormalities.

2. Provide anticipatory management to prevent complications.

Management: All patients with ARF should be admitted under close observation

1.Fluid balance:

• Fluid challenge: N.S 20 ml/kg over 30 minutes then frusemide 5-10mg/kg I.V
stat

• Type of fluid depends on serum + urine assessment

• Restriction = insensible losses + urine output

• 2/3 of maintenance fluids will go to urine output, 1/3 for insensible losses
(sweat, breathing)

• Insensible loss calculation depends on surface area = 400 ml/𝒎𝟐/day ( 400 X

surface area )

• Surface area = √𝒘𝒆𝒊𝒈𝒉𝒕 𝑿 𝒉𝒆𝒊𝒈𝒉𝒕 𝟑𝟔𝟎𝟎

 2.Hyperkalemia:

- Factors which exacerbate hyperkalemia: Blood transfusion, Antibiotics with K salts,

Hypercatabolism

- ECG changes depends on Serum K level:

• Peaked T-waves

• decrease R wave amplitude

• Wide QRS

• Absent P-wave

• Asystole

3. Acid base balance

• Unless PH ≤ 7.1, no need for HCO3 therapy (cautious)

• Expand I.V volume + Hypocalcemia

4.Hyperphosphatemia + Hypocalcemia : Phosphate binders (chelating agents)

5.Nutrition:

• The two most important factors which increase catabolism in patients with
ARF: - inadequate calorie intake. - Infection

• Poor nutrition : ill patient, Fluid restriction, Azotemia ( Decrease protein

intake)

6.Dialysis
Duration/prognosis

1. Prognosis for recovery of renal function depends on underlying cause of AKI

2. Recovery is likely if AKI is secondary to prerenal causes, HUS, acute tubular necrosis
(A TN). acute interstitial nephritis, or tumor lysis

3. Recovery is unusual when AKI is due to rapidly progressive GN. bilateral renal vein
thrombosis, or bilateral cortical necrosis

MCQ :

-HIE stage 1 is likely to cause: Renal Failure

-In which of the following organs is erythropoietin primarily produced?

A. Bone marrow.
B. Liver.
C. Kidney

-the BEST for urine culture? suprapubic aspiration

-Most common sign of acute renal failure: edema

-Most common cause of End Stage Renal Disease in children? Congenital anomalies