A 64 year old lady was admitted electively for live related donor renal transplantation. She had progressed to ESRD from a primary diagnosis of chronic membranoproliferative glomerulonephritis and had been on haemodialysis for 5 years.
Her Past Medical History comprised a history of Ischaemic Heart Disease without need for surgical revascularisation and obstructive sleep apnoea. She had been compliant with CPAP prior to surgery and had required a period of more intensive ultrafiltration prior to surgery to ensure appropriate fluid balance.
The surgical note documented that the kidney had 2 arteries, with the lower pole sluggish to perfuse on the table. However, there was urine production prior to wound closure and the patient had a primary fall in creatinine by day 1.
A routine ultrasound of the renal graft on the third post-op day noted sluggish perfusion of the lower pole despite appropriate anticoagulation (see figure below).
At Day 5 the patient developed features of a urinary tract infection with a urine culture positive for E. coli; she was empirically commenced on intravenous piperacillin/tazobactam. Despite an initial response to treatment, she continued to have low grade temperatures with grumbling elevations of white cell count and C-reactive protein. At Day 7 of antibiotics, a repeat ultrasound of the transplanted kidney noted a collection at the lower pole of the transplanted kidney and a decision was made to proceed to exploratory surgery. Purulent fluid was found deep to the graft and communicated with a superficial collection found at opening of the cutaneous tissues.
Drains were placed in the surgical bed and culture yielded a vancomycin resistant enterococcus that required a 14 day course of daptomycin, metronidazole and ciprofloxacin. The patient’s appetite was significantly reduced due the combination of antibiotics but she was discharged 57 days post surgery to attend transplant clinic a few days later.
Unfortunately when she attended clinic, she had developed profuse diarrhoea, failure to thrive and recurrent fever. She was admitted for fluid resuscitation.
Investigations noted the following:
- Hb 10 g/dL
- WCC 3 x 109 cells/L
- Plt 69
- Cre 272 umol/L (203 umol/L on discharge)
- Albumin 25g/L
Despite cytomegalovirus serology being positive prior to surgery (and receiving a CMV positive kidney) her CMV PCR load was quantified at 120 million copies per milliltre. She required 14 days of intravenous ganciclovir for treatment of invasive CMV disease; her PCR load fell below 100,000 copies at Day 14 and switched to oral Valganciclovir for a total 3 months antiviral therapy. She was discharged definitively from transplant ward 84 days following transplant with a serum creatinine of 123 umol/L and normal full blood count. CMV PCR levels became undetectable at Day 28 following antiviral therapy.
- The vascular anatomy of graft has important implications for the transplant ureteric anastomosis to the bladder. If there is more than one renal artery on the donor kidney, the donor ureter blood supply is derived from the lowest polar artey. Although the frequency of ureteric complications such as urnary leak have reduced with modern surgical technique, the risk of ureter leak correlates strongly with the number of donor vessels on the graft (An excellent link regarding ureteral complications post transplant can be found here). Though a ureteric leak was presumed to be the cause of the lower pole collection, the ureter appeared intact on direct visualization.
- The lower pole collection contained vancomycin resistant enterococcus. Risk factors for this patient acquiring VRE included: Having an indwelling invasive device; Use of broad-spectrum antibiotics; Being Immunosuppressed (See Patel and Snydman AJT 2009). Consequences of Resistant Organisms in Solid Organ Transplants include prolonged hospital stay and an increased risk of inpatient mortality.
- The risk for reactivation of cytomegalovirus is highest in donor-positive, recipient-seronegative (D+R–) solid organ transplants at a rate approaching 30%. As a result this subgroup of patients should receive pre-emptive anti-viral prophylaxis with Valganciclovir (Chiche et al. 2001). It has become more recently recognized that CMV virus can reactivate in previously CMV immune patients in the context of critical illness, malnourishment or over-immunosuppression and potentially a poor prognostic marker for patients in critical care settings (Heininger 2011). Treatment comprises intravenous ganciclovir though oral Valganciclovir has equivalent efficacy in mild CMV disease. In the context of the huge viral load, intravenous therapy was instituted from initial identification of CMV disease.