Search

We report a patient who developed urinary retention due to the presence of necrotic tissues in the bladder 5 months after kidney transplantation. The patient was a 47-year-old female who had been diagnosed with immunoglobulin A nephropathy. She requested to receive a living-donor kidney transplant from her husband, and was referred to our hospital. Given that the patient had anuria preoperatively, her bladder capacity was presumed to have decreased following the transplantation. There were no events regarding vascular anastomosis during the surgery. However, since ureteroneocystostomy was difficult to perform due to the thinning of the bladder wall, the recipient's own ureter was anastomosed to the ureter of the transplanted kidney. Since the patient had difficulty voiding soon after the indwelling urinary catheter was removed, clean intermittent self-catheterization was initiated. Abdominal computed tomography revealed perforation of the bladder and extravesical urinary leakage on postoperative day 15. An indwelling urinary catheter was reinserted as conservative treatment. We removed the indwelling urinary catheter on postoperative day 25. The patient was discharged on postoperative day 30. Five months after transplantation, the patient suddenly developed urinary retention. Cystoscopy revealed some tissue hanging from the anterior wall of the bladder. The tissue was removed, and her voiding function improved. On pathology, the tissue was found to be non-specific necrotic tissue. This finding suggested that the necrotic tissue had caused urinary retention 5 months after transplantation. The symptoms of urinary retention markedly improved after the treatment.

We report a patient who developed urinary retention due to the presence of necrotic tissues in the bladder 5 months after kidney transplantation. The patient was a 47-year-old female who had been diagnosed with immunoglobulin A nephropathy. She requested to receive a living-donor kidney transplant from her husband, and was referred to our hospital. Given that the patient had anuria preoperatively, her bladder capacity was presumed to have decreased following the transplantation. There were no events regarding vascular anastomosis during the surgery. However, since ureteroneocystostomy was difficult to perform due to the thinning of the bladder wall, the recipient's own ureter was anastomosed to the ureter of the transplanted kidney. Since the patient had difficulty voiding soon after the indwelling urinary catheter was removed, clean intermittent self-catheterization was initiated. Abdominal computed tomography revealed perforation of the bladder and extravesical urinary leakage on postoperative day 15. An indwelling urinary catheter was reinserted as conservative treatment. We removed the indwelling urinary catheter on postoperative day 25. The patient was discharged on postoperative day 30. Five months after transplantation, the patient suddenly developed urinary retention. Cystoscopy revealed some tissue hanging from the anterior wall of the bladder. The tissue was removed, and her voiding function improved. On pathology, the tissue was found to be non-specific necrotic tissue. This finding suggested that the necrotic tissue had caused urinary retention 5 months after transplantation. The symptoms of urinary retention markedly improved after the treatment.

Reperfusion of ischemic organs induces a potent inflammatory response initiated by the generation of reactive oxygen species (ROS) that directly damage tissue and promote leukocyte infiltration and activation that also mediate tissue injury. We recently found that radiation-induced tissue injury, which is caused by radiation induced ROS, is attenuated by administration of CBLB502, a pharmacologically optimized derivative of the Toll-like receptor 5 (TLR5) agonist flagellin. Therefore, we tested the ability of CBLB502 to attenuate injury in a murine model of acute ischemic renal failure. CBLB502 given 30 minutes before imposition of bilateral renal pedicle occlusion provided marked protection against the renal dysfunction and inflammation that follows reperfusion of ischemic kidneys, including marked decreases in leukocyte infiltration, proinflammatory cytokine production, and tubular injury. Importantly, CBLB502 given within 30 minutes after ischemic kidney reperfusion reproduced the protective effects of pretreatment with the TLR5 agonist, indicating a window following reperfusion in which CBLB502 administration abrogates acute renal ischemic failure. Bone marrow reconstituted chimeras were used to show that the protective effects of CBLB502 could be delivered by intact MyD88 signaling on renal parenchymal cells. Consistent with this, antibody staining of kidney sections indicated that cells lining the renal vasculature expressed TLR5. Overall, these results indicate the use of TLR5 agonists as mitigators and protectants of acute renal ischemic failure.