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Renal Failure in Paediatrics

Ng Inn Shan 051303630 Group E2 Batch 18

Ng Inn Shan

on 3 August 2010

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Transcript of Renal Failure in Paediatrics

RENAL FAILURE in Paediatrics Classifications Intrinsic Postrenal Pre-renal Glomerulonephritis
Hemolytic-uremic syndrome
Acute tubular necrosis
Cortical necrosis
Renal vein thrombosis
Acute interstitial nephritis
Tumor infiltration
Tumor lysis syndrome GLOMERULONEPHRITIS:
Henoch-Schonlein purpura
Anti-glomerular basement membrane Ng Inn Shan
051303630 PRESENTATION BY: Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Hemorrhagic cystitis
Neurogenic bladder Dehydration
Cardiac failure Congenital Inherited Acquired
Metabolic renal disease Renal hypoplasia
Renal dysplasia
Obstructive uropathy
Congenital nephrotic syndrome
Prune-belly syndrome
Cortical necrosis
Polycystics kidney disease
Renal vein thrombosis
Hemolytic Uremic syndrome
Vesicoureteric reflux Familial juvenile nephronophthisis
Alport syndrome
Glomerulonephritis (e.g. lupus nephritis) Cystinosis
Hyperoxaluria Autosomal dominant PCKD Autosomal recessive PCKD Dehydration Most often due to gastroenteritis.
Infants and children are more susceptible to dehydration.
Assessment of degree of dehydration:
Rapid decline in GFR Increase in serum creatinine level Increase in BUN level Oliguria ...can be due to UGIB Sepsis Is the systemic responce to infection
PSAGN Usually presenting after 2-3 weeks after infection
Associated with hematuria, edema and hypertension.
Acute renal insufficiency can occur. Consequently leads to: Oliguria Hypertension Heart failure Encephalopathy Hemolytic Uremic Syndrome (HUS) microangiopathic hemolytic anemia renal cortical injury thrombocytopenia Important cause of acute renal failure
Typically occurs between the ages of 6 months and 4 years.
Usually presenting after diarrhea (prodrome)
Verotoxin is the major aetiology; esp. Shiga-like toxin from E. coli O157:H7 which causes hemorrhagic enterocolitis. Tumor lysis syndrome metabolic emergency often seen in leukemia and lymphoma
can occur during treatment or spontaneously
lysis of large amount of tumour cells hyperkalemia
hyperuricosemia acute uric acid nephropathy
acute renal failure Posterior urethral valve Most common cause of severe obstuctive uropathy in children.
Bladder outlet obstruction that is produced by a membrane within the posterior urethra

prostastic urethra dilates
bladder wall hypertrophy
mild hydronephrosis to severe renal dysplasia also associated oligohydramnios and pulmonary hypoplasia diagnosis done prenatally: bilateral hydronephrosis
distended bladder
oligohydramnios diagnosis at birth: diagnosis at infancy diagnosis later in children distended bladder
weak urinary stream failure to thrive due to septicemia/UTI difficulty in achieving diurnal urinary continence or with UTI diagnosis by MCUG or perineal USG VUR Autosomal recessive PCKD retrograde flow of urine from bladder to the ureter or kidney
incompetence of ureterovesical junction
can be familial or acquired
incomplete voiding backflow pressure recurrent UTI reflux nephropathy renal scarring chronic renal failure diagnosis by MCUG on all children <8y/o with first documented UTI
DMSA identifies renal scarring Alport syndrome Potter facies hereditary nephritis
due to mutation of genes coding for type IV collagen (major component of basement membrane)

Clinical manifestations:
asymptommatic microscopic hematuria (maybe intermittent)
single or recurrent episodes of gross hematuria 1-2days after URTI
proteinuria in males; maybe absent/intermittent in females
progessive proteinuria in 2nd decade of life

Extrarenal manifestations:
hearing deficits (sensorineural deafness)
ocular abnormalities
IgA nephropathy
THANK YOU Citations:

- Nelson Textbook of Pediatrics 18th Edition
- Wikipedia.org
- eMedicine.medscape.com can cause microinfarct...
Presenting with prodromal gastroenteritis.
Weakness, lethargy, irritability and oliguria/anuria.
Pallor, edema, petechiae, hepatosplenomegaly.
Variable hydration status --> dehydrated to overload.
Seizure may occur. Chronic Renal Failure Acute Renal Failure Clinical Presentation Prerenal Renal Postrenal Anemia <8g/dl
Peripheral smear
Thrombocytopenia <60,000/ml
Urine FEME
LDH, BUN, creatinine
Coomb's test negative at birth: oligohydramnios, pulmonary hypoplasia, death
polyuria and polydipsia
hypertension??, chronic heart failure
present later in life in childhood: chronic liver disease, portal hypertension, UGIB

Diagnosis at birth:
Palpable mass of abdomen
Potter facies
Prerenal vs Renal aetiology If elevated specific gravity, elevated ruine osmolality, low urine sodium, FENa <1% most likely it's prerenal ARF

If low specific gravity, elevated urine osmolality, low urine sodium, FENa >2% most likely to have intrinsic ARF Fractional Excretion of Sodium (FENa) = (PCr * UNa ) / (PNa * UCr) % Urolithiasis Calcium oxalate stones Cystine stones Struvite stone ( Mg.NH4.Po4) Uric acid stone Most common cause is due to calcium stone
Hypercalciuria, hyperoxaluria and hypocitruria.
Presentation: gross/microscopic hematuria, renal colic, dysuria, urgency and frequency. May have history of passing small amount of sand-like particle in urine.
90% of renal stones are radiopaque.
Metabolic evaluation is required.
Neuropathic bladder Causes:
Neural tube defects/other spinal abnormalities
CNS tumors
Sacrococcygeal teratoma
Abnormal innervation of bladder or sphincter Consequences:
Urinary incontinence
Hydronephrosis from VUR or detrusor-sphincter dyssynergia
Renal function deterioration Usually happens due to failure of sphincter to relax during a bladder contraction UTI and VUR worsens the condition
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