Normal lower urinary tract (LUT) function is crucial to preserve the graft kidney following transplantation. LUT dysfunction can cause high pressure vesico-ureteric reflux (VUR), increasing the risk of recurrent urinary tract infections (rUTIs) leading to impaired renal function and premature loss of the graft kidney. 

The number of patients waiting for renal transplantation is increasing due to the prevalence of diabetes, high blood pressure and the ageing population, resulting in more patients being anuric or oliguric at the time of transplantation. Anuria and oliguria are defined as a urine output of less than 100ml and 400ml/day respectively. Chronic anuria/oliguria can result in LUT dysfunction directly due to detrusor atrophy or mask LUT symptoms.

The aim of this study is to assess the prevalence of LUT dysfunction identified during video urodynamics (VUDS) in patients who were either anuric/oliguric awaiting renal transplant or who were anuric at the time of transplant.

We retrospectively reviewed the VUDS data of 35 patients.

18 patients who were anuric/oliguric at the time of VUDS were referred due to previous failed transplants (n=8), previous voiding LUTS (n=7), long term anuria (n=2) or reflux on micturating cystourethrogram (n=1).

17 patients who were anuric before of their latest transplant were referred because rUTIS (n=7), declining graft function (n=4) and LUTS (n=6).

All urodynamic studies were conducted in accordance with the ICS Good Urodynamics Practice Document. Fluoroscopic imaging evaluated the presence of vesico-ureteric reflux (VUR) and bladder outlet obstruction (BOO) in the presence of VUR (where PDet may be dampened) as illustrated in figure 1.

35 patients with a median age of 45 years (20-66), 24 males. Table 1 details the presence of detrusor overactivity (DO), reduced bladder compliance (RBC, <40ml/cmH2O), BOO and VUR as well as the likely primary pathology.

26/35 patients had VUR during VUDS assessment. 18 patients had BOO, 7 with primary LOCRBC (in the absence of BOO), 4 idiopathic DO, 4 with idiopathic VUR and 2 with detrusor underactivity and elevated PVRs (in the absence of VUR).  

A total of 28 transplants had failed in 16 patients in our cohort. 8/17 patients who were anuric at their latest transplant had previous renal transplants, totaling 20. 8/18 who were anuric/oliguric at the time of the VCMG (all with one failed transplant).

All 35 patients had LUT dysfunction identified during VUDS assessment. 

VUR was present in 26/35 patients who were anuric/oliguric at the time of VUDS or renal transplantation. VUDS is efficient in understanding the root cause of VUR, allowing for appropriate treatments to be prescribed. 

7 patients had primary  RBC (in the absence of BOO), with a median anuric duration of 3 years (range 2-18), suggesting chronic reduced bladder volumes can result in RBC and potentially affect long term renal grant function if left untreated. 

6/7 patients who had rUTIs post-transplantation had VUR. In the patient without VUR and rUTIs RBC was demonstrated. 4/6 patients had LUT pathology which resulted or worsened the VUR (BOO, LOC or DO), which with intervention would allow for improvement in the VUR and prolong graft function.

Patients who were anuric/oliguric at time of VCMG (n=18) are a selected cohort with 7/18 having previous voiding LUTS. However, 8/18 had previous failed transplants, of which 6/8 had BOO, which likely contributed to the decline of graft function.

LUT dysfunction is prevalent in patients with anuria/olguria. Our results indicate patients with limited urine output, which potentially masks LUTS and/or directly causes LUT dysfunction (reduced bladder capacity and compliance) should be evaluated with VUDS pre-renal transplantation, especially if they have had previously failed transplants, history of voiding LUTS or long-term decreased urine output.