1. The kidneys perform several important functions including regulating fluid balance, electrolyte and acid-base homeostasis, and producing hormones like renin and erythropoietin. 2. Acute renal failure in children results in impaired waste excretion, water and electrolyte dysregulation, and loss of acid-base control over hours to days. 3. Causes include prerenal issues like dehydration, decreased blood pressure, or intrinsic renal problems such as glomerulonephritis, tubular injury, or nephrotoxins; evaluation involves lab tests, imaging, and assessing response to fluid resuscitation.

3. Functions of Kidneys
1: Formation of urine (maintain fluid
balance).
2: Maintain Ionic composition of the body
and H+ concentration. (Homeostasis)
3: Endocrinal functions: Production of
Renin and Erythropoietin.
4: Activation of Vitamin D.

4. GLOMERULAR FILTERATION RATE (GFR)
Def.: Amount of glomerular filtrate formed
in all nephrons by both kidneys /min..
 In normal male adult , the average GFR is
125 ml/min, or 180 liters/day.
 Normally 99% of filtrate is reabsorbed in
the renal tubules and the remaining 1%
passes into urine
GFR = (K ×height in cm) /Serum creatinine

6. Acute renal failure in children
Abrupt reduction in kidney function & rapid
decline in GFR over several hours / days.
It results in the disturbance of renal
physiological functions including :
I. Impairment of nitrogenous waste
product excretion(azotemia).
II. Loss of water and electrolyte regulation.
III.Loss of acid-base regulation.

7. Prerenal causes or ARF
Prerenal azotemia results from either:
A- Volume depletion due to:
 Bleeding (surgery, trauma, GIT).
 GIT fluid loss (vomiting, diarrhoea).
 Urinary (diuretics, diabetes insipidus)
 Cutaneous losses (burns).
B-Decreased effective arterial pressure :
Heart failure, shock, or cirrhosis.

8. Intrinsic renal causes of ARF
 Vascular :
 Thrombosis (arterial & venous).
 Hemolytic-uremic syndrome (HUS).
 Malignant hypertension.
 Vasculitis e.g. HSP.
 Glomerular: Acute glomerulonephritis ( AGN).
 Tubular and interstitial disease : (ATN) results
from ischemia due to decreased renal perfusion
or injury from tubular nephrotoxins.
 Nephrotoxic agents: -Aminoglycosides.
-Amphotericin B.
- Contrast agents.
-Heme pigments.

9. All causes of prerenal azotemia
can progress to ATN if renal
perfusion is not restored and/or
nephrotoxic insults are not
withdrawn

10. Post-renal causes of ARF
 Bilateral urinary tract obstruction .
 Urinary tract obstruction, due to
posterior urethral valve.
 chronic obstructive uropathies.

11. CLINICAL PRESENTATION
Tachycardia, dry mucosa, sunken eyes, low BP &
decreased skin turgor suggest hypovolemia.
Dysentery with oliguria (<500 ml/1.73 m2 /day in
children & <1 ml/kg / h in infants) or anuria (absent
urine/<0.5ml/kg/h) is consistent with HUS
H/O pharyngitis or impetigo, a few weeks prior to
the onset of gross hematuria suggests post-
infectious glomerulonephritis (AGN)
Nephrotic syndrome, heart failure & liver failure
may result in oedema and other signs of specific
organ dysfunction.

12. CLINICAL PRESENTATION -Cont..
Hemoptysis suggests pulmonary-renal syndrome.
 Skin findings: malar rash, petechiae, and/or
joint pain , systemic vasculitis, such as SLE or HSP
Anuria or oliguria: in a newborn suggests a major
congenital malformation or genetic disease, like
posterior urethral valve, b/l renal vein thrombosis
or AR kidney disease.
In the hospital, ATN due to hypotension or
nephrotoxic medications (such as
aminoglycosides or amphotericin-B).

13. Symptoms of uremia
 Lethargy
 Anorexia
 Pericarditis
 Neuropathy
 Nausea and vomiting
 Pruritis
 Dyspnea

15. EVALUATION & Dx. OF ARF
Serum creatinine .
Serum BUN/creatinine ratio .
Urinalysis.
Urine Na .
Fractional excretion of Na.
Urine osmolality and urine output.
Renal imaging.
Fluid challange.
Others:
CBC, serum Na, K, P and blood gases.
ECG

16. Value of urinalysis in Dx. of ARF
Normal urine : prerenal disease, urinary tract
obstruction.
Muddy brown/granular & epithelial cell casts: ATN.
Red cell cast: glomerulonephritis.
Pyuria (WBCs), granular, waxy casts & proteinuria:
tubular or interstitial disease or UTI.
Hematuria and pyuria: acute interstitial nephritis,
glomerular disease, vasculitis, obstruction, and
renal infarction.

17. Urine sodium excretion
 Measurement of the urinary Na is
helpful in distinguishing renal from
prerenal ARF due to effective volume
depletion.
above 30 - 40 meq/l. ATN (renal)
below 10 meq/l. pre renal ARF

18. Fractional excretion of Na (FENa)
This is defined by the following equation:
 UNa x PCr
FENa (percent) = —————— x 100
PNa x UCr
 UCr & PCr : urine and plasma creatinine .
 UNa & PNa : urine and plasma sodium .

19. FENa - screening test that differentiates
between prerenal and renal ARF
< 1 % suggests prerenal disease.
 1 -2 may be seen with either disorder.
> 2 % usually indicates ATN (renal cause).

20.  Urine osmolality :
 urine osmolality below 350 m-osmol/kg
suggest renal aetiology.
 urine osmolality above 500 mosmol/kg is
highly suggestive of prerenal cause.
 Urine volume :
 low (oliguria) in prerenal disease due to the
combination of sodium and water loss.
 Patients with ATN may be either oliguric or
nonoliguric .

21. Response to volume repletion
( fluid challenge)
 H/O fluid loss & signs of hypovolemia/oliguria
-give I/V fluid to dif. b/w prerenal ARF & (ATN)
 Fluid infusion is contraindicated in obvious
volume overload or heart failure.
 Normal saline (20 ml/kg) in 20 - 30 min. which
can be repeated if necessary.
 Restoration of adequate urine flow and
improvement in renal function with fluid
resuscitation is consistent with prerenal disease.

22. Additional Lab. Measurements
 CBC : Microangiopathic hemolysis &
thrombocytopenia with ARF confirms HUS
 Anti-neutrophil cytoplasmic antibodies
(ANCA), (ANA), anti-(GBM) antibodies,
ASOT, hypocomplementemia.
 Elevated serum levels of aminoglycosides :
 Eosinophilia : Interstitial nephritis.
 Elevated uric acid :May also induce ARF.

23.  K:Due to oligurea or high K diet like dates,
citrus fruits & increased tissue breakdown.
 P : Once GFR falls below threshold, low P
excretion- resulting hyperphosphatemia.
 Ca: Due to hyperphosphatemia, low GIT
Ca absorption due to low Vit.D3 production .
 Acid-base balance: metabolic acidosis .
Additional Lab. Measurements

24. Renal imaging
 Renal ultrasonography:
 All children with ARF of unclear etiology.
 Follow up of renal size and parenchyma .
 Diagnosing urinary tract obstruction or
occlusion of the major renal vessels.
 Renal biopsy: When noninvasive evaluation
unable to establish correct Dx. & etiology

25. LAB. STUDIES TO D/D PRE-RF& ATN
 Pre-renal Failure
Urine Na excretion:<10
m mol/l (low)
FENa :< 1 %
 Urine osmolality > 500
mosmol/l(serum+100)
U/P creatinine > 40
 U/P urea >8 (high)
Urine sp. g. high >1.020
+ve fluid challenge test
 ATN (renal cause)
 > 40 m mol/l (high)
> 2 %
<350 m osmol/Kg
 < 20
U/P urea <3 (low)
Fixed 1.010-1.020
-ve fluid challenge test

26. Prevention of ARF
Close monitoring of serum levels of
nephrotoxic drugs.
Adequate fluid repletion in hypovolemia.
 Aggressive hydration and alkalinization of
the urine prior to chemotherapy.

27. Management of ARF
Maintenance of electrolyte and fluid balance
Adequate nutritional support.
Avoidance of life-threatening complications
e.g. hyperkalemia, acidosis, hypertension, CCF
Treatment of the underlying cause .

28. Mx. of fluid & electrolyte disturbances
Hyperkalemia
Serum K > 7.0 meq/l is life-threatening & needs
immediate attention and follow up by ECG:
1- I/V calcium , glucose + insulin infusion,
NAHCo3 , beta agonists nebulization to promote
extracellular K movement into the cells.
2-Kayexalate, an anion exchange resin, can
remove excess K
3-Adjust K intake.
4- Renal replacement therapy if medical
management fails to improve hyperkalemia.

29. Acidosis
 Sodium bicarbonate in life-threatening
acidosis or hyperkalemia.
 Serum NaHCo3 levels > 14 meq /l or arterial
pH >7.2 do not require immediate
intervention.

30. Intravascular volume
 Child with ARF may be hypo/ eu/
hypervolemic (including pulmonary
edema and heart failure).
 Appropriate evaluation of volume status
and treatment to maintain euvolemia.
 Insert urinary catheter.
 If no response to diuretics after restoration
of I/V volume (CVP), stop diuretics and
start fluids as insensible water loss plus
urine output only.

31.  Hypertension: result of hypervolemia.
Use antihypertensives.
 Nutrition :
 Adequate calories to promote recovery.
 If sufficient calories cannot be achieved
with oliguria / anuria without causing
hypervolemia, then renal replacement
therapy is recommended.

32. Renal replacement therapy
INDICATIONS:
1) Signs and symptoms of sever uremia .
2) Azotemia (BUN > 80 - 100 mg/dl).
3) Severe fluid overload refractory to medical
therapy .
4) Severe electrolyte abnormalities (eg.
hyperkalemia and acidosis) that are
refractory to supportive medical therapy
5) Nutritional support in oliguria / anuria.
6) Severe uncontrolled hypertension.

33. Renal Replacement Therapy
 Hemodialysis, peritoneal dialysis (PD), and
continuous renal replacement
therapy(CAPD).
 The choice of modality is influenced by
-clinical presentation and
-status of the patient including
. presence of multi-organ failure
. indication for renal replacement
therapy.

35. Prognosis of ARF
The prognosis of ARF depends upon :
 Etiology.
 Age of the patient.
 Clinical Picture.
 Status of the patient.
 Hypotension and need for inotropic
support during renal replacement
therapy are significant poor predictors
for patient survival.