Dr.Rithwik Sunil, Dr Sathyajith G Nair, Dr C Jayakumar
Two old male status post fulguration 3 times for PUV presented with wet cough, Vomiting and low grade fever of 3 days with dysentery and was receiving Ofloxacin after food from outside eatery
Other system symptoms were negative
Relevant lab result was elevated serum creatinine(4mg/dl) and urea levels(139mg/dl)
PAST HISTORY :
Birth history: 2nd child of Non consanguenous parentage was admitted in the new born itself for UTI and since then he is on prophylactic Nitrofurantoin
Developmental history was normal and Immunized as per Abu Dhabi schedule.
Mother has history of hypothyroidism, history of 3 miscarriages
No history of renal disorder in family
CLINICAL EXAMINATION :
At admission, the child was febrile, tired lookingVitals- Pulse- 114/min, RR-32/min, SpO2-100%in room air,BP:95/68mmhg, CRT<2sec, Pallor +No icterus, cyanosis, clubbing, lymphadenopathy, edemaHead to foot examination: No dysmorphism, no ear anomalies noted, flexed deformity of of interphalangeal joint of right thumb.Auxology: Wt-11kg (b/w 0 & -2SD), Ht-87cm (b/w 0 & -2SD), HC-48cm (b/w 0 &-1SD)
Systemic examination:PA: Soft, no tenderness or organomegaly. Bowel sounds sluggish.RS: AEBE, No added soundsCNS: No focal neurological deficits. No signs of meningeal irritationCVS: S1 S2 heard normally, No murmurs.
Differentials considered:
Dehydration causing Pre renal AKI
PUV with VUR
ATN (secondary to drug intake)
Congenital anomaly of kidney and urinary tract (CAKUT)
Labs done:
Tc: 8 K/uL, N:68%, L:21%, Hb – 11.5, Plt – 200 CRP:57.09mg/l
RFT showed Urea – 139.5 and Serum Creat -4.
LFT showed mild transminitis with no hyperbilirubinemia.
• PT/INR , APTT were normal.
ABG showed pH:7.346, pC02: 29.2, Lac:0.7, HCo3:156
•Na was 126 and he was further worked up with S. Osmolality, Urine Osmolality and urine Na which showed Serum. Osm -291.0mOsm/kg, Urine Na: 39.2 mmol/l Urine Osm- 195.0mOsm/kg.
USG Abdomen done showed Thick trabeculated bladder wall with echogenic contents. Ectopic ,pelvic, right kidney. Echogenic kidneys with bilateral hydroureteronephrosis.
History of cystoscopy and ablation was revealed at this time so also At repeat cystoscopy with ablation was done at one year of age.
Course
Child was started on treatment as per AKI protocol. Fluids were initiated and output was regularly monitored. Child started showing improving RFT and urea levels.
Diuretics were not started and child was able to maintain positive balance
GFR improved from 9 ml/min/1.73m2 to 56 ml/min/1.73m2 in 10 days
C.difficile assay done in view of the bloody stool was negative Repeat MCU done revealed a grade 3 VUR
PUV(Posterior Urethral Valve)
Posterior urethral valves are the most common cause of urinary tract obstruction and chronic kidney disease resulting from obstructive uropathy in the pediatric population.
The valves are actually obstructing membranous folds situated within the posterior urethral lumen attached to the verumontanum. These folds are found exclusively in male patients.
Vesicoureteral reflux (VUR) is characterized the abnormal backward flow of urine from the urinary bladder into the upper urinary tract during voiding.
This condition of retrograde urine flow is often caused a short intramural ureter and is associated with recurrent urinary tract infections, renal cortical scarring, and renal failure in severe cases, including end-stage kidney disease. Voiding cystourethrogram is the preferred diagnostic tool for diagnosing VUR in children
After the procedure, an antibiotic regimen is customized based on the patient’s clinical presentation, kidney anatomy, and treatment response.
Surgical interventions are contemplated for recurrent or unresolved VUR.
Most common causes of Post Renal AKI
Posterior urethral valves and urethral stricture ;
Bilateral pelviureteric junction obstruction ;
Ureteral obstruction (stenosis, stone, and ureterocele) ;
Neurogenic bladder
Take home message;
Always assess the fluid status in a child presenting with AKI. Most cases would resolve on proper fluid management alone.