Posterior Urethral Valves JIAPS APR-JUNE 2013

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Minu Bajpai, Pradeep K Chaturvedi, Chandra S Bal, Meher C

Sharma, Mani KalaivaniJournal of Indian Association of Pediatric Surgeons

Year : 2013 | Volume : 18 | Issue : 2 |

Page : 74-78


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CRF:in a significant no. of children with PUVs.

16.8% of population of children with ESRD.

RAS activation as a mediator of renal injury &

interstitial fibrosis reported .

Prospective study

Role of RAS blockade by ACE-I after PUV

ablation evaluated & correlated it with tests ofrenal function, micro albuminuria, and PRA


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To study renin angiotensin system (RAS)activity after PUV ablation &

role of early induction of ACE-I on the

outcome of renal function


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Study group: 34 children underwent valveablation b/w 3 -7.5 m.

Serum creatinine and PRA :measured before,between 1 month and 3 months after valveablation & at 1 yearly intervals.

GFR : at 60, 90, 150, and 180 min after 99mTechDTPA injection.

Renal scars evaluated by DMSA scan.


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pts with GFR < 50 mL/min/1.73 m 2

severely scarred kidneys & refluxing units


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Group 1: no e/o VUR & scar formation (n = 13)

Group 2: e/o VUR , no e/o scar formation (n = 6)

Group 3: e/o renal scarring , no e/o VUR ( n = 3)

Group 4: e/o both VUR &scar formation ( n = 12)


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State of RAS activation : by measuring PRA.

ACE inhibitor (Enalapril) : dose - 0.14mg/kg/day

The urinary micro albumin levels :documentedbefore and after RAS blockade

Pre-valve ablation data : serum creatinine

&PRA. Post-valve ablation phase, (early and late) :

S.Creatinine, PRA, VUR, DMSA scan, GFR,urinary micro albuminuria, & blood pressure.


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Post ACE-I therapy data collected after meanduration 18.2 4.0; range 12-28 months

Statistical analysis : using statistical package for

the social sciences (SPSS 11.5 Inc. Chicago,Illinois, USA)

Renal function parameters: compared usingpaired sample t-test.

P values < 0.05 : statistically significant.


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N= 34

Mean age : 3.5 1.9 (range 3-7.5 months)

Duration of follow-up before initiating therapy

with ACE-I was 40.5 4.1 (range 32-47months).

Mean follow-up after initiating therapy with

ACE-I was 18.2 4.0 (range 12-28 months).


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GROUPS % FALL INPRA

% FALL INSERUMCREATININE

Group 1 66.9 23.1

Group 2 67 33.3

Group 3 71.4 25

Group 4 70.7 40

Fall w.r.t pre valveablation value

Sustained fall in PRA &

S. Creatinine in allgroups


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GROUPS

%FALLIN GFR

%RISEIN PRA

%RISE INSERUMCREATININE

Group 1 18.5 4 30

Group 2 24.2 13.3 75

Group 3 13 10 33.3

Group 4 70.7 23.5 8.3

Marginal rise in PRAdue to gradual re-

activation of RAS accompanied by

deterioration in renalfunction parameters


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GROUPS

% RISEIN GFR

% RISEIN PRA

% FALLINSERUMCREATININE

% FALLINMICROALBUMINURIA

Group 1 5.9 19.2 23.1 55

Group 2 5.8 21.6 28.6 55.6

Group 3 4.2 48.4 5.5 64.6

Group 4 5.7 17.7 23.8 55.3

ACE-I -> fall inangiotensin II -> -ve feedback->

marginal rise inPRA

accompanied byimprovement in

renal functionparameters.


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Decline in renal function after valve ablationaccompanied by reactivation of RAS reflectedin a gradual rise in PRA.

Therapy with ACE-I stabilizes & improvesrenal function retarding the pace of renaldamage.


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Progression to CRF even after successful PUVablation multi-factorial

PRA primary player in RAS pathway &

Angiotensin II the final mediator oftubulointerstitial damage.

VUR & renal scars :poor prognosis in PUV.

VUR: high rate of spontaneous resolutionfollowing decompression,may take years


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ACE-inhibitors reduced micro albuminuriaeven in the absence of VUR (55.0%) viz-a-vizwith VUR (55.6%).

In both the group also improvement in GFR &serum creatinine

INFERENCE:

In absence of VUR: ACE-I retard the pace ofongoing renal damage

In presence of VUR: stabilize renal functionwaiting for spontaneous resolution


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Post-valve ablation:gradual re-activation ofRAS apparent in the form of rising PRA &accompanied by deterioration in renal function

parameters. After ACE-I therapy:rise in PRA accompanied

by improvement in renal function parameters.


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Large no of pts with PUVs: renal dysplasia,detected on DMSA scan as photopenic areassimilar to the new renal scars.

Prior to this study, information on PRA notavailable in patients without renal scars.

In the present study, high PRA associated withdecline in renal function & elevated levels ofmicro albuminuria even without renal scars (post-ablation, before ACE-I therapy).


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Early periglomerular fibrosis may repesent'nascent scars' , forerunner of scars visible lateron as photopenic areas on DMSA scan

ACE-I reduced micro albuminuria even inabsence of scars viz-a-viz when scars werepresent by 54.0% and 64.2%, respectively

Also improved GFR and serum creatinine


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Need for initiating ACE-I therapy early,retarding the pace of renal damage andpreventing future scarring, substantial no. of

which progress to renal failure Study highlights urgent need for a randomized

controlled trial for establishing PRA as an earlyprognostic marker


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angiotensin II, as well as metabolites of the PG-TX system, may be important determinants ofpostobstructive renal hemodynamics in rats


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ACE-I (enalapril) ameliorates tubulointerstitialfibrosis following complete unilateral ureteralobstruction in rats.

Increased level of angiotensin II has a majorrole in the development of tubulointerstitialfibrosis following ureteral obstruction.


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Considerable injury is also inflicted to thecontralateral normal kidney while ipsilateralkidney remains obstructed.

Use of RAS blocking drugs found to significantlyimprove renal recovery on contralateral kidney.

Postulated that contralateral renal parenchymalinjury was mediated through activation of RAS.


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Posterior Urethral Valves JIAPS APR-JUNE 2013

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