renal failure in children in brief

1. RENAL FAILURE
Dr Kamrun Nahar
Child specialist

2. Acute Kidney Injury (AKI)
 AKI is defined as any insult to kidney and is characterized by
rapid decline in GFR.
Acute kidney injury (AKI), formerly called acute renal failure, is a
clinical syndrome in which a sudden deterioration in renal function
results in the inability of the kidneys to maintain fluid and electrolyte
homeostasis.
 Consequences-
▫ accumulation of nitrogenous wastes in body
▫ Impairment of water, electrolytes and acid-base balance.
AKI embodies a spectrum of renal dysfunction ranging from a
small increase in Serum creatinine to complete anuric renal failure.

3.  Clinical & biochemical features of AKI:
1. Oligouria, anuria
2. Retention of nitrogenous waste products in the body as evident in
elevation of urea, creatinine, blood urea nitrogen (BUN)
3. Dyselectrolytemia e.g. hyperkalemia
4. Acid-base balance e.g. metabolic acidosis
5. Fluid overload, hypertension

4. Pathogenesis:
•Can be classified as prerenal
failure, intrarenal failure, or
postrenal failure.
•Can be reversible.
•Can lead to chronic renal failure.
•Caused by obstruction, poor
circulation, or kidney disease.
•Interruption in flow can lead to
serious failure.

5. Phases of Acute Renal Failure: Oliguric,
Diuretic, Recovery (ODR)
Oliguria (Decreased urine output of
<400 ml/day)
Azotemia (Excess urea levels in blood)
Anuria (Failure to secrete urine).
Increased BUN and creatinine levels
and decreased ratio of BUN to
creatinine
– Normal levels 20:1
– Abnormal levels: 10:1

10. https://www.youtube.com/watch?v=bMp6IxDKK2Q&t=134s

14. Common Causes of Acute Kidney Injury:
PRERENAL:
• Dehydration e.g. diarrhoea, vomiting
• Hemorrhage ● Cardiac failure
• Sepsis ● Hypotension
• Toxins ● Hypoalbuminemia
• Burn
INTRINSIC RENAL:
Glomerulonephritis
• Post-infectious/post-streptococcal
• Lupus erythematous
• Henoch-Schönlein purpura
• Membrano proliferative
• Anti–glomerular basement membrane
Vascular:
• Hemolytic-uremic syndrome
• Renal vein or arterial thrombosis
Tubular:
• Acute tubular necrosis
• Cortical necrosis
• Wasp string, snake venom,drugs
• Rhabdomyolysis
• Tumor infiltration
• Tumor lysis syndrome
Interstitial:
• Acute interstitial nephritis
• Acute pyelonephritis
POSTRENAL:
• Posterior urethral valves
• Uretero pelvic junction obstruction
• Uretero vesicular junction obstruction e.g. blood clot
• Ureterocele Tumor
• Urolithiasis (calculi)
• Neurogenic bladder.

15. Clinical features: (patient’s complaints)
• Scanty urine (Oligouria) or complete cessation of urine (Anuria) – hallmark of AKI
• Other features like – severe vomiting, diarrhoea convulsion
• H/O pre-existing kidney disease e.g. AGN, NS
• Ingestion of nephrotoxic drug, e.g. Diethylglycol in paracetamol
Evaluation of AKI:
• Features of fluid overload:
 Facial puffiness, oedema, HTN
 Features of Heart failure e.g. hepatomegaly, pulmonary edema
• Features of severe dehydration: drowsiness, skin pinch not going back
normally or quickly
• Hemodynamic status: Pulse, BP, CRT
• Toxic features of AKI: unconsciousness, arrhythmia, vomiting, convulsion.
• Per abdomen examination:
 flank- palpable renal mass (RVT), urinary bladder – palpable in PUV
Physical Examination:

16. Investigations: Findings
Blood: Full blood count with PBF • Anemia ( usually dilutional or hemolytic in SLE)
• Leukopenia (SLE, sepsis)
• Thrombocytopenia (SLE, sepsis, HUS)
Blood urea, creatinine, BUN Elevated
S. Electrolytes: Hyperkalemia, Hyponatremia , low HCO3
S. calcium Hypocalcemia,
S. phosphate: Hyperphosphatemia
Arterial blood gas Metabolic acidosis
Urine: Urinary sodium: low (< 20 mEq/L)—prerenal
high(>40 mEq/L)—renal
Urine RME: Hematuria, proteinuria, RBC casts (GN)
WBC &WBC cast (tubulo-interstitial)
Eosinophil (Interstitial nephritis)
Myoglobin (rhabdomyolysis)
Urine CS Concomitant UTI
Imaging: Renal ultrasound scan kidney size, structural anomaly, calculi
Chest x-ray: Pulmonary edema, cardiomegaly
ECG hyperkalemia ( peaked T wave, ST elevation, wide QRS complex)
To find out cause ASO titer, throat swab C/S
C3,C4, ANA, AntiDS- DNA MCUG, Ab to GBM, DTPA, DMSA
Renal biopsy ( unexplained cause)

17. Urinary indices:

18. d
Nelsen, ahmolla –risk 8 hrs, injury 16 hrs, failure 12 hrs
nelsen Ht (cm) X 0.53
GFR (CrCl) = -------------------------
S creatinine (mg/dl)
The original Schwartz formula is:
kX Ht(cm)
CrCl (mL/min per 1.73 m2) = ………………………
S. Creatinine (mg/dl)
here K is
Infant (LBW < 1 year): 0.33
Infant (Term < 1 year): 0.45
Child or Adolescent Girl: 0.55
Adolescent Boy: 0.70
The revised Schwartz formula is:
0.413 X Ht(cm)
GFR (mL/min per 1.73 m2) = …………………………
S. Creatinine( mg/dl)

19. Management AKI
1. Fluid resuscitation –
- If dehydration: Normal saline 20ml/kg X 2 times
- avoid and manage fluid overload
2. Diuretics –when adequate circulatory volume established
Inj Frusemide – 2-4 mg/kg/dose IV max 200 mg
If myoglobin/hemoglobin induce ARF – Inf Mannitol 0.5 g/kg
3. Peritoneal dialysis
4. Maintain associated conditions e.g. dyselectrolytes,
convulsion, anemia
5. Management of Hypertension
6. Treatment of underlying cause – to avoid further renal injury
Nutrition:
• Calorie: high calorie diet,
rich in carb & fat (to reduce
protein catabolism)
•Restrict protein (1g/kg/day),
salt, K containing food and
fluids.
1. Hospitalized the child
2. Counsel parents about illness and its consequences
3. Introduce catheter when suspected obstruction (PUV)
4. Discontinue nephrotoxic drugs
5. Monitor urine output
6. Maintain nutrition

20. Ensuring urine output:
• If no volume overload or CCF, then
• Administer Normal saline 20 ml/kg over 30 mins.
• After volume resuscitation, usually patient void within 2 hours, an
increase in urine output will follow.
• If urine output increases, continue fluid replacement.
- give furosemide 2-4 mg/kg as a single IV dose
• If no response – give continuous diuretic infusion ± inj Dopamine (2-3
g/kg/min) – to improve renal cortical blood flow.
• If a response does not occur within an hour (in u. catheter) of max dose of
frusemide or if the urine output remains low (<0.5 ml/kg/hr)
-Stop further administration of diuretics
-Restrict fluid to insensible losses ([insensible losses (400 ml/m2 /day) +
previous day urine output + ongoing fluid losses].
-Replace any external loss (blood, GIT) meticulously with appropriate fluid.
-Monitor fluid intake, urine and stool output, body wt, S. chemistry level daily
- readjust fluid allocation, if volume overload.

21. Rx of HTN:
Asymptomatic case: Isradipine (0.05-0.15 mg/kg/dose), QID
Nifedipine 0.3-0.5 mg/kg PO
Severe symptomatic (HTN encephalopathy):
Na-nitroprusside (0.5-10µg/kg/min) Or
Labetalol 0.25-3 mg/kg/min in infusion. (under
supervision of pediatric cardiologist)
Others:
- Amlodipine (0.1-0.6 mg/kg/day),BD
- labetalol (4-40 mg/kg/day), BD
Anti hypertensive medicine : Ranjit
Diuretics: Frusemide 2-4 mg/kg max 10mg/kg
Ca Ch blocker: Nifedipine 0.3-0.5 mg/kg PO
Amlodipine 0.1-0.6 0.3-0.5 mg/kg PO BD
Beta blocker: propanolol 0.5-8µg/kg/min
Labetalol: 4-40 g/kg/dose BD

22. Hyperkalemia
• K restriction, 10% Ca gluconate > Sodi bi carb > Regular insulin > Kayexalate
> dialysis
Hyponatremia
• No sodium infusion or intake Fluid restriction is the primary mode of Rx
• If Na <120 mEq/L and or seizures or other symptoms – need to be treated
Hyperphosphatemia
• Give low phosphorus diet
• Phosphorus binding protein – calcium carbonate, calcium oxalate ( will improve hypocalcemia)
Hypocalcaemia
• Inj Calcium glunocate (1-2 ml/kg/dose, 8 hrly) [ should not give until tetany developed]
Metabolic acidosis
• Sodi bi carb - PO or IV (1 ml/kg) Ensure S Ca level >1.8 mmol/L
Anemia
• Blood transfusion if Hb <6 g/dl
Seizures
• Diazepam 0.5 mg/kg k PR most effective
Supportive Mx of AKI

23. Mx of Hyperkalemia in AKI
Do 12-lead ECG and look for hyperkalaemic changes
 If ECG is abnormal or plasma K+ > 7 mmol/l, connect patient to a cardiac monitor
Give the following in sequence:
1. Inj 10% Ca Gluconate 0.5-1.0 ml/kg (1:1 dilution) IV over 5 -10 min (Immediate onset of action)
2. Inj Dextrose 0.5 g/kg (2 ml/kg of 25%) over 15–30 mins IV
3. ± IV short acting Insulin 0.1 unit/kg + 10% DA @ 5 ml/kg over 30 min (onset of action 30 mins).
4. Inj 8.4% sodium bicarbonate 1 ml/kg (1-2 mmol/kg) (1:1 dilution) over 10 - 30 mins IV (Onset 15-30 min)
5. Nebulized 0.5% salbutamol 2.5 - 5 mg (0.5-1 ml+ 3 ml NS) (Onset of action 30 mins)
6. Calcium polystyrene sulphonate 0.25g/kg oral or rectally 4 times/day (Max 10g/dose)
(Ca Resonium/ Kalimate) [Give rectally (NOT orally) in neonates 0.125 – 0.25g/kg 4 times/day]
OR
Na polystyrene sulphonate 1g/kg/day oral or PR 4 times/day (Max15g/dose) [150-250 mg/kg/dose]
(Resonium) for oral mix with 15-30 ml 70% sorbitol for PR 1 gm mix with 10 ml methylcellulose/water
 If serum K level 5.5 - 7 mmol/L without ECG changes, give Ca or Na polystyrene sulphonate; K restriction
If insulin is given after dextrose, monitor RBS / Dextrostix for hypoglycaemia.
Dialysis (haemodialysis or PD) if poor or no response to the above measures.

24. Dialysis:
 Indication of Dialysis in AKI
1. Anuria or oligouria
2. Volume overload with evidence of HTN ± Pulmonary oedema refractory to diuretics
3. Persistent hyperkalemia
4. Severe metabolic acidosis non responsive to medical mx
5. Neurological symptoms e.g. Uraemia (encephalopathy, pericarditis, neuropathy)
6. BUN >100-150 mg/dl
7. Calcium phosphorus imbalance with hypocalcemic tetany (that can not be controlled by other
measures)
8. Inability to provide adequate nutritional intake because of the need for severe fluid restrictions.

26. • CKD is the gradual loss of kidney function over a
period of time.
• It is defined as renal injury/proteinuria and/or GFR
<60 ml/min/1.73m2 for more than 3 months.
• CKD can get worse over time and eventually the
kidneys may stop working altogether, but this is
uncommon. Many people with CKD are able to live
long lives with the condition.

27. Aetiology:

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29. Signs and symptoms
• Patients with CKD stages 1-3 are generally asymptomatic.
• Typically, it is not until stages 4-5 (GFR < 30 mL/min/1.73 m²) that endocrine/metabolic derangements or disturbances in water or
electrolyte balance become clinically manifest.
• In stage 5 CKD:
▫ Signs of metabolic acidosis include the following:
 Protein-energy malnutrition
 Loss of lean body mass
 Muscle weakness
▫ Signs of alterations in the way the kidneys are handling salt and water :
 Peripheral edema
 Pulmonary edema
 Hypertension
▫ Anemia in CKD is associated with the following:
 Fatigue
 Reduced exercise capacity
 Impaired cognitive and immune function
 Reduced quality of life
 Development of cardiovascular disease
 New onset of heart failure or the development of more severe heart failure
 Increased cardiovascular mortality
▫ Other manifestations of uremia in ESRD, many of which are more likely in patients who are being inadequately dialyzed, include the
following:
 Pericarditis: Can be complicated by cardiac tamponade, possibly resulting in death if unrecognized
 Encephalopathy: Can progress to coma and death
 Peripheral neuropathy, usually asymptomatic
 Restless leg syndrome
 Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea
 Skin manifestations: Dry skin, pruritus, ecchymosis
 Fatigue, increased somnolence, failure to thrive
 Malnutrition
 Erectile dysfunction, decreased libido, amenorrhea
 Platelet dysfunction with tendency to bleed

31. Investigations:

32. Management:
• Counseling: about disease nature, progress, treatment options, prognosis.
• Treatment should be done by Pediatric Nephrologist.
• Diet:
 Nutritional balanced diet, protein:Fat:Carbohydrate = 10:30:60
 Calorie: 100%
 Restrict dietary phosphorus intake (milk or milk products), meat,
chicken, nuts, choclates, bean (in advanced stage)
 Restrict salt and K containing food (e.g. citrus fruits, banana, tomato etc)
[in advanced stage]
 Supportive treatment:
1. vitamins: A,C,B (B1,B2,B3,B6,B12, biotin), folic acids, Zinc
2. Dyselectrolytemia: corrected accordingly
3. Hypocalcemia: calcium supplement
4. Hyperphosphatermia: calcium carbonate
5. Acidosis: sodi bi carb
6. Anemia: PRBC with human recombinant Erythropoietin, Iron
supplementation
7. Linear growth: Growth hormone

33. • Renal osteodystrophy: Calcitriol (vit D)
• Hypertension:
- frusemide, Thiazide
- ACE inhibitor (Captropil), Ca channeel blocker, alpha blokcer
• Secondary infection: with non nephrotoxic drugs
 Immunization:
- Advice all standard vaccines
- Meningococcal, pneumococcal conjugate vaccines should be
use.
- Withheld all life vaccines
- Influenza shot every yearly.

35. RRT- Renal Replacement Therapy
Diffusive therapy (hemodialysis) removes small solutes mainly,
whereas convective therapies (hemofiltration and
hemodiafiltration) may also eliminate larger molecules such as
myoglobin or cytokines.
Indications for RRT
includes:
1. Severe metabolic acidosis
2. Hyperkalemia
3. Pericarditis
4. Encephalopathy
5. Intractable volume overload
6. Failure to thrive (FTT) and
malnutrition
7. Peripheral neuropathy
8. Intractable gastrointestinal
symptoms
9. In asymptomatic patients, a
GFR of 5-9 mL/min/1.73
m²,irrespective of cause of CKD
or presence or absence of other
comorbidities.

37. Hemodialysis

39. Thank you…….