NSAID induced AKI in pediatrics

1. Case presentation
By: Mohamed Fathelrhman Mohamed

3. History
Name: R A T
Age: 7 yrs.
Sex: female
Origin residence: Alkhoy northern Kordofan
DOA: 2182015

4. History
CO
2 fatigue 14 days
3 vomiting 4 days

5. History
 Condition started 14 days ago with generalized fatigue preventing her from doing
the usual daily activity associated with nausea and loss of appetite.
 There were associated sleep disturbances with the patient being awake most of
the night
 Over the course the patient symptoms became more severe permitting her from
doing even minimal activity
 4 days before admission patient develop vomiting which was once to twice daily
not projectile not bile or blood stain and contain food particle in occasions.

6. History
 No associated fever no diarrhea no abdominal pain
 Systemic review:
 CVS: no palpitation no fainting no cyanosis no SOB.
 CNS: no convulsions no LOC no abnormalities in hearing or
vision no movement or sensation problem.
 MSS: no joint pain no joint deformity nor swelling.
 UT: normal urine amount and color no change in frequency
of urination no burning micturition nor changes in urine
stream.
 Skin: no rash was noticed.

7. History
 Past HX:
 not known case of any chronic illness no hx of long
hospitalization and not on regular follow up plans.
 4 weeks ago my patient has had sore throat with associated
fever and vomiting and was admitted to a nearby health center
for 2 days receiving injectable penicillin and was discharged on
good condition.
 She also has had a complaint of joint pain with the same
episode and did receive analgesia.

8. History
 Family Hx:
 No family hx of Hypertension diabetes or SSA no family hx of
chronic renal disease nor liver disease no family hx of
malignancy.
27 yrs 25 yrs 20 yrs
15 yrs
7 yrs

9. History
 drug Hx:
 Not on regular medication and not Known to be sensitive to
any drug nor penicillin
 Developmental hx:
 Achieved good development currently at 6th grade
elementary school with good performance.

10. History
 Nutrition and vaccination:
 Patient on regular Sudanese diet , fully vaccinated.
 Social hx:
 The family live in there own house her father is a cattle
merchant and her mother is a house wife not under cover of
health insurance .

11. Summary
A year old girl presented with worsening fatigue
for 14 days associated with poor appetite poor
sleep and occasional vomiting ,2 wks. ago
admitted with tonsillitis and treated with iv
antibiotic and analgesics , there is no other past or
family hx of significant, fully vaccinated ,poor
socioeconomic status not under insurance.

12. Examination
Ill pale dehydrated not jaundiced or cyanosed
PR is 100 RR is 25 Temperature is 37,7
 BP is 10065 { normal}
Sunken eyes and dry mucosa
Weight is 20 kg (20th percentile) height is 127 cm(50th percentile)
Hand examination was normal

13. Examination
CVS:
No deformity or visible pulsation nor surgical scars
The apex is in the 5th intercostal space mid clavicular
line no thrill no left parasternal heave.
Normal S1 and S2 no murmur and no added sounds.
RS:
Resonant percussion note
Normal air entry bilaterally front and back normal
breathing sounds and no added sounds .

14. Examination
 CNS:
 Conscious ( GCS=15) oriented intact memory, no cranial
nerve abnormality detected normal power tone and reflexes
in all 4 limbs normal sensation pattern.
 Abdomen:
 Normal looking with everted umbilicus no visible masses
hernia orifices intact
 No mass or tenderness in superficial palpation
 No organomegally in deep palpation
 Normal bowel sounds

17. Investigations
 CBC:
8.3Hb
66MCV
22MCH
11.000( neut= 63%
lymph=35%)
WBCS
456plt

18. Investigations
 RFT:
487Urea
11.9Creatinine
137Serum Na
4.0Serum K
7.2Serum Ca

19. Investigations
 UG: uncountablePus cells
15-20RBCs
NilSugar
NilAcetone
NilBlood
NilNitrate

20. Investigations
 Others :
negativeBFFM
Less than 200ASO titer
negativeCRP

23. AKI
Short progressive course.
No family hx.
No significant past hx .
Apparent dehydration.
CKD
No clear precipitant for AKI.
Apparent anemia.
Low serum calcium.

25. US abdomen:
 Normal liver in texture and size and no apparent CBD stones
normal CBD diameter.
 Both kidneys are enlarged with the left one measuring (11x8)
with normal CM differentiation and multiple large cysts right
kidney measuring (10.6x8) with normal CM differentiation and
multiple large cysts.
 Normal spleen.
 No ascites.
Diagnosis is polycystic kidney disease.

27. Definition of CKD
Structural or functional abnormalities of the
kidneys for >3 months, as manifested by
either:
1. Kidney damage, with or without decreased GFR, as
defined by
• pathologic abnormalities
• markers of kidney damage, including abnormalities in
the composition of the blood or urine or abnormalities in
imaging tests
2. GFR <60 ml/min/1.73 m2, with or without kidney
damage

28. CKD
death
Stages in Progression of Chronic Kidney
Disease and Therapeutic Strategies
Complications
Screening
for CKD
risk factors
CKD risk
reduction;
Screening for
CKD
Diagnosis
& treatment;
Treat
comorbid
conditions;
Slow
progression
Estimate
progression;
Treat
complications;
Prepare for
replacement
Replacement
by dialysis
& transplant
Normal
Increased
risk
Kidney
failure
Damage  GFR

29. Prevalence of CKD and Estimated Number
of Adults with CKD in the US (NHANES 88-94)
Stage Description
GFR
(ml/min/1.73 m2)
Prevalence*
N
(1000s)
%
1
Kidney Damage with
Normal or  GFR
 90 5,900 3.3
2
Kidney Damage with
Mild  GFR
60-89 5,300 3.0
3 Moderate  GFR 30-59 7,600 4.3
4 Severe  GFR 15-29 400 0.2
5 Kidney Failure < 15 or Dialysis 300 0.1
*Stages 1-4 from NHANES III (1988-1994). Population of 177 million with age 20. Stage 5 from USRDS (1998), includes
approximately 230,000 patients treated by dialysis, and assuming 70,000 additional patients not on dialysis. GFR estimated
from serum creatinine using MDRD Study equation based on age, gender, race and calibration for serum creatinine. For
Stage 1 and 2, kidney damage estimated by spot albumin-to-creatinine ratio 17 mg/g in men or 25 mg/g in women in two
measurements.

31. Management
1 renal chart.
2 insensible loss + urine output as IVF
3IV ceftriaxone 1g daily for UTI
4 renal replacement therapy
5 plan for hemodialysis

33. PCKD
Autosomal dominant
 The age of presentation of
renal impairment
 Family hx not present and new
mutation only 7%
Autosomal recessive
 The age of presentation of
renal impairment

34. Follow up
 patient was showing signs of improvement with the vomiting stopped and
activity increases gradually
 RFT was improving after hydration never the less still high:
7531days
289365403487Urea
7.98.710.111.9creatinine

35. Follow up
 At day 11 of admission patient was planned for permanent central line insertion
and to start regular dialysis in the day after.
 Prior to the operation RFT was requested and was showing
40Urea
1.2creatinine
34
1.2

37. Lab error vs. diagnosis
uncertainty
?????????????????????

38. History and history again
 4 weeks ago my patient has had sore throat with associated fever and vomiting and was admitted
to a nearby health center for 2 days receiving injectable penicillin and was discharged on good
condition.
She also has had a complaint of
joint pain with the same episode
and did receive analgesia.

39. History history and history again
analgesia.
Diclofenac sodium inj 75 mg TDS for 3 days.
Ibuprofen tabs 600 mg 6 hourly for 5 days

40. NSAID induced AKI

48. USA Study

50. NSAID kidney syndromes:
1 prerenal AKI.
2 AIN (acute interstitial nephritis).
 3 AIN plus minimal change nephropathy ( nephrotic
syndrome).
 4 salt and water retention.
 5 hyperkalemia.
 6 CKD and papillary necrosis ( analgesic nephropathy).

51. AIN
 Acute interstitial nephritis (AIN) is a renal lesion that causes a
decline in creatinine clearance and is characterized by an
inflammatory infiltrate in the kidney interstitium . It is most
often induced by drug therapy.
 AIN is also caused by autoimmune disorders or other systemic
disease (e.g., systemic lupus erythematosus [SLE], Sjögren's
syndrome, sarcoidosis), a variety of infections remote to the
kidney (e.g., Legionella, leptospirosis, and streptococcal
organisms).

52. Drugs induced AIN ( 90-95%)
The most common drug causes of AIN now include
●Nonsteroidal anti-inflammatory agents (NSAIDs),(60-90%) including selective
cyclooxygenase (COX)-2 inhibitors
●Penicillin's and cephalosporin's ( 20-30%)
●Rifampicin
●Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole
●Diuretics, including loop diuretics such as furosemide and bumetanide, and thiazide-type
diuretics
●Ciprofloxacin and, perhaps to a lesser degree, other quinolones
●Cimetidine (only rare cases have been described with other H-2 blockers such as ranitidine)

53. AIN
Clinical manifestations — With AIN from any cause, patients may present with nonspecific
signs and symptoms of acute renal dysfunction. These may include the acute or subacute
onset of nausea, vomiting, and malaise. However, many patients are asymptomatic .
Patients may be oliguric; in a retrospective study that included 60 cases of AIN (92 percent
of which were drug induced, with the remainder idiopathic), oliguria was present among
51 percent . Gross hematuria occurs in approximately 5 percent of individuals .
Radiographic findings – There are no radiographic findings that are diagnostic for AIN.
Radiographic findings, including marked enlargement of kidneys with multicystic
appearance.

54. Variable course and prognosis with the majority of patient
tend to recover.
Patients with associated connective tissue diseases have the
worst prognosis
Management is stop the drug and manage as AKI

55. History is the key and core of clinical practice always ask as always there is a
hidden thing.
RFT should be a routine for any ill patient especially if non specific presentation
is encountered.
AKI and CKD can be very challenging in differentiating them.
NSAID are hazardous drugs and need to be used in the lowest effective dose.