Overlooked Factors Causing Renal Damage in Vesicoureteric Reflux!
Authors: Chatterjee Uday Sankar , Basu Ashoke Kumar , Mitra Debasis , Basak Dhananjay 
Published: May 2024

Introduction:
Vesicoureteric reflux (VUR), recurrent urinary tract infection (RUTI), febrile urinary tract infection (FUTI), renal scarring, and renal damage are intimately related. Key factors of renal damage in VUR are suspected to be RUTI and FUTI. Hence, conventional treatments are targeted toward the prevention of RUTI and FUTI. However, literatures have witnessed that control of infection is not sufficient enough. That means we are missing some hidden, enigmatic, or overlooked factors which are essentially responsible for renal damage. We know RUTI occurs from the stasis of urine in system and stasis might occur from obstruction somewhere in system. Moreover, obstruction builds up back pressure in the bladder and ureters, and ultimately in kidneys; that pressure is independently harmful to renal function. Pressure is further harmful if this joins together with infection. We know that RUTI and FUTI along with pressure in the urinary tract are harmful to renal parenchyma. Nevertheless, search for the nexus of obstruction, pressure, stasis, infection, and damage (OPSID) of renal function is not yet focused on in VUR research. In this retrospective study on secondary VUR, we would like to find the overlooked factors or nexus of OPSID associated with VUR causing renal damage.

Patients and Methods:
A total of 170 renal units of 135 patients with VUR resulted from the posterior urethral valve and from repaired bladder exstrophy, from March 2005 to April 2019, had adequate data regarding control/correction of obstruction and urodynamic studies. The mean patient's age was 2.8 years (range 1 day–14 years). The diagnosis of VURs was made with postnatal cystogram in patients of the posterior urethral valve and of repaired continent augmented bladder exstrophy. We do cystogram not micturating cystogram following ultrasonography if showing dilated ureter/s. If we find no residual in ureter/s after 30 min in cystogram, we label it as “rise and fall” VUR (raf_VUR), i.e., without obstruction. On the other hand, if there is post void residual in ureter/s for more than 30 min, we label it as “rise and stasis” VUR (ras_VUR) means combination of VUR with uretero vesical junction obstruction (UVJO). Along with this, all patients were followed up with albumin creatinine ratio, creatinine clearance, USG Renometry, DTPA renal scan, uroflowmetry, and urodynamic study (UDS). Repeat cystoscopy, if necessary, was done following UDS for secondary bladder neck incision (BNI) or for repeat BNI if necessary.

Results:
Mean duration of follow-up was 7.2 years (range 3–14 years). Out of 170 renal units, 132 renal units had VUR without VUJO, i.e., raf_VUR and 38 renal units had ras_VUR. All patients of UVJO were relieved either with anticholinergics or with DJ stenting or by re-implantations. Twenty-nine patients out of 135 had high pressure on UDS, and they needed BNI. We were able to prevent upstaging of chronic kidney disease (USCKD) in all 135 patients.

Conclusions:
Our tangible goal of treatment in VUR is the prevention of USCKD. We differentiated raf_VUR from ras_VUR with cystogram. Patients with ras_VUR and patients with raf_VUR with high bladder pressure were actively treated. This particular subset VUR was treated with prophylactic antibiotic and surgical corrections. We prevented renal damage by eliminating obstruction and stasis which helped to prevent RUTI and FUTI. Possibly, similar management might also help to manage “primary VUR.” Possibly those overlooked factors which are essentially responsible for renal damage are veiled in nexus OPSID of the kidney.