Simultaneous Renal Transplantation and Splenectomy: Double Strike?

Case Report

Austin J Nephrol Hypertens. 2015;2(1): 1032.

Simultaneous Renal Transplantation and Splenectomy: Double Strike?

William EA1,2*, Morsy AA1, Iskander IR1 and Barsoum RS1

1The Cairo Kidney Center, Cairo University, Egypt

2Department of Internal Medicine, National Research Center, Egypt

*Corresponding author: William EA, The Cairo Kidney Center, 3 Hussein El-Memar Street, Cairo, PO Box 91 Bab-El-Louk, Cairo 11513, Egypt

Received: November 28, 2014; Accepted: January 27, 2015; Published: January 29, 2015


We present a 59 year-old female suffering from idiopathic thrombocytopenic purpura and end stage renal disease due to mesangiocapillary (Type III) glomerulonephritis, who received a kidney transplant from a living unrelated male donor. Aiming for a definite and durable management for idiopathic thrombocytopenic purpura and because of calcified pelvic vessels, she had simultaneous splenectomy and left orthotopic renal transplantation after only pulse-steroid induction. Post-transplant immunosuppression comprised tacrolimus, mycophenolic acid and prednisolone. Graft functioned well, apart from transient rise of serum creatinine after few days due to tacrolimus induced thrombotic microangiopathy. The offending drug was withdrawn under cover of 2 doses of basiliximab. The patient achieved normal kidney function thereafter and cyclosporine was introduced instead of tacrolimus. Unfortunately, she experienced a chain of infections caused by different bacterial and fungal infections, starting with superficial wound infection and followed by urinary tract infection and septicemia, which turned out to be superimposed on cytomegaloviral (CMV) activation. Lowering immunosuppressive drug doses, antiviral treatment and culture-based antibiotics failed to control these infections, leading to the patient’s death with a functioning graft, 1 month after transplantation.

Conclusion: despite surgically feasible, simultaneous splenectomy and renal transplantation may carry the risk of over immunosuppression and potentially fatal infection.

Keywords: Idiopathic thrombocytopenic purpura; Renal transplantation; Splenectomy; Cytomegalovirus (CMV); Mesangiocapillary glomerulonephritis


Infection remains the second most common cause of death after cardiovascular causes in kidney transplant recipients. It accounted for 18.8 % of patient’s death in the 2013 USRDS annual data report [1], and 15 % In the ERA-EDTA registry [2]. Nevertheless, certain clinical situations may impose the creation of an environment of over-immunosuppression as in this case.

Case Report

Our patient was a 59 year-old female with long standing hypertension (35 years), Type 2 diabetes (8 years), and multiple autoimmune disorders including hemolytic anemia (12 years), interstitial lung disease (11 years) and thrombocytopenia (1 year). Serological tests for SLE were repeatedly negative. She had a single seizure at 16 years ago with negative Magnetic Resonance Imaging, and deep vein thrombosis of the right lower limb at age 36 years. Impairment of renal function was detected at age 49, with steady progression to end-stage kidney disease (ESKD) in 10 years.

Her chronic kidney disease (CKD) was evaluated when she was 54 years old. She was clinically well, with adequately controlled blood pressure, and no abnormal physical signs apart from a faint hemic cardiac murmur and a palpable spleen 3cm below the costal margin. The ocular fundi showed grade II hypertensive changes, without diabetic manifestations. Midstream urine showed bland sediment with a urinary protein/creatinine ratio 11.5 mg/mg. Serum creatinine was 265 μmol/l, with eGFR (MDRD-4) of 16.3 ml/min/sqm. Serum ANA, anti-DNA, Fractional Extractable Nuclear Antigens and anticardiolipin antibodies were negative. Serum levels of complement C3, C4and CH50 were normal. By ultrasonographic examination, the kidneys were of normal size, yet increased echogenicity. Renal biopsy showed mesangiocapillary (Type III) changes and segmental sclerosis with negative immunofluorescence for IgG, IgM, IgA and complement. She was thus kept on standard conservative management.

She was re-assessed 2 years later, when serum creatinine had reached 309 μmol/l. Her anti-nuclear, anticardiolipin, and anti RNP- 70 antibodies were detected in her serum. Repeat renal biopsy showed the same mesangiocapillary changes, yet with advanced focal and global sclerosis. She received a therapeutic trial with prednisolone and azathioprine, without benefit. She eventually passed to ESKD and started regular hemodialysis.

She was living alone with her daughter and needing her assistance for transportation which interfered with her job. She became depressed and frightened from dialysis and opted to receive a transplant. Preoperative transthoracic echocardiogram showed fair systolic function (ejection fraction 55%) and old rheumatic valve disease in the form of moderate mitral regurgitation and mild mitral stenosis. Neither Rt. nor Lt. Cardiac catheterization were done. Spirometry showed moderate restrictive lung disease, however, chest x-ray and arterial blood gasses were normal. CT angiography showed extensive calcification of the abdominal aorta and iliac arteries. Her platelet count was 62,000/, with absent megakaryocytic budding in the bone marrow.

We designed a plan for proceeding to transplantation in three steps: a) temporarily correcting the platelet count for safe surgery; b) splenectomy for long-term management of her thrombocytopenia; c) simultaneous orthotopic renal transplantation using the splenic artery to avoid the calcified other abdominal vessels, which wouldn’t have been possible in a staged surgery.

She was vaccinated against meningococcus, H.influenza, and pneumococcus 1 month before scheduled surgery.

An attempt to correct the platelet count by prednisolone was partially successful yet un-sustained. So, she was treated with Intravenous Immunoglobulin, in a total dose of 500mg/Kg spread over 4 days, which raised the platelet count over 100,000/ that was sustained throughout the surgery and early post-operative period.

The donor was a healthy live, 25-year old male with matching ABO, cde antigens (A1+), 3/6 mismatching HLA antigens (A3, A30, B18) and a negative lymphocytotoxicity cross match. Both patient and donor sera were negative for HBV, HCV and HIV markers, yet with positive anti-CMV IgG antibodies.

Only steroids were used for induction, given as methyl prednisolone in 3 doses: 250 mg at -12h, 500 mg at 0h and 250 mg at +12h.

Two surgical teams performed the operation on 31st March 2013. While Team A was performing the recipient splenectomy and left nephrectomy, Team B was doing the donor nephrectomy. Both procedures were uneventful.

The recipient’s left renal artery turned out to be of a wider caliber and more accessible for anastomosis; so it was used end-to-end for the graft anastomosis, instead of the planned splenic artery. The graft’s vein was anastomosed to the native left renal vein. The graft’s ureter was sutured to the native left ureter, and a double J catheter was left across the new ureteral anastomosis. The total ischemia time was 45 minutes.

Maintenance immunosuppression comprised Tacrolimus (3 mg) and Mycophenolic acid (360mg) twice daily and prednisolone in daily decremented doses from 100 mg on day +1 to 20 mg on day +7. Ceftazidime was used for chemoprophylaxis in a daily i.v. dose of 1gm.

Diuresis started 6 hours postoperatively and accelerated over the following days, with drop of serum creatinine from 375 μmol/l to 176 μmol/l by day +4. However, it rose to 232 μmol/l on day +5 along with reduction of urine volume. Simultaneously, the tacrolimus trough blood level was 17.4 ng/ml. The dose was reduced to 2mg twice daily, yet serum creatinine continued to rise. By day +7, a graft biopsy was obtained and showed a thrombotic microangiopathy (Figure 1a,1b).

Citation: William EA, Morsy AA, Iskander IR and Barsoum RS. Simultaneous Renal Transplantation and Splenectomy: Double Strike?. Austin J Nephrol Hypertens. 2015;2(1): 1032.

Citation: Bucci J and Hansen KE. Should we treat Secondary Hyperparathyroidism in Patients with Pre-Dialysis Chronic Kidney Disease?. Austin J Nephrol Hypertens. 2015; 2(4): 1046. ISSN : 2381-8964