Woo Yeong Park

Comparison of clinical outcomes between ABO-compatible and ABO-incompatible spousal donor kidney transplantation

Background Kidney transplantation (KT) is the treatment of choice for end-stage renal disease patients. The spouse is a major donor in living KT. Clinical outcomes of spousal donor KT are not inferior to those of living related donor KT. In this study, we compared clinical outcomes between ABO-compatible (ABOc) and ABO-incompatible (ABOi) spousal donor KTs. Methods Thirty-two cases of spousal donor KT performed from January 2011 to August 2013 were analyzed retrospectively. Twenty-one ABOc KTs and 11 ABOi KTs were performed. We investigated patient survival, graft survival, acute rejection, graft function, and complications. Results During follow-up, patient and graft survival rates were 100% in both groups. There were no significant differences in the incidence of delayed graft function, acute rejection, and the change in graft function between the 2 groups. Medical and surgical complications were not significantly different between the groups. Conclusion The clinical outcomes of ABOc and ABOi spousal donor KTs were equivalent. In ABOi KT, an emotionally motivated spousal donor KT may be a good alternative to the problem of the absolute shortage of kidney donations.

Allograft Mucormycosis Due to Rhizopus microsporus in a Kidney Transplant Recipient

Mucormycosis is an uncommon infectious complication with fatal outcome after kidney transplantation. We describe a rare form of mucormycosis in allograft kidney. The patient was a 54-year-old man who underwent deceased-donor transplantation. The patient experienced delayed graft function and new-onset diabetes within 1 week after transplantation. Four weeks after transplantation, he was readmitted because of allograft dysfunction without fever or pain. Ultrasonography showed enlarged allograft with normal blood flow. He was received broad antibiotics for 6 days, but allograft function was not recovered. Seven days after admission, allograft biopsy was performed, and in microscopic examination, extensive necrotic areas with disseminated fungal invasion were seen, and it was identified as Rhizopus microsporus by culture and DNA analysis. With allograft nephrectomy, he was treated with amphotericin B. Despite intensive antifungal drugs after graft nephrectomy, the patient died of disseminated fungal infection.

Long-term Clinical Outcomes of First and Second Kidney Transplantation in Patients With Biopsy-Proven IgA Nephropathy

INTRODUCTION The recurrence of IgA nephropathy (IgAN) after kidney transplantation (KT) has an effect on graft survival, but there are few reports about long-term clinical outcomes of KT with recurrent IgAN. This study shows the long-term clinical outcomes of KT in patients with IgAN. METHODS All recipients who had biopsy-proven IgAN were followed from February 1990 to February 2016. We analyzed overall graft and patient survival rates, incidence of recurrent IgAN, factors affecting graft survival, and IgAN recurrence. RESULTS There were 88 patients with first KT. The mean follow-up duration was 82.5 months. Twenty patients went through graft loss and 1 patient died due to sepsis. IgAN recurred in 15 patients, and 11 patients experienced graft failure. Among the patients who had failed graft after first KT, 7 patients underwent retransplantation. The graft survival period, presence of rejection, and proteinuria were the relevant risk factors for recurrence of IgAN. In the first KT patients, presence of rejection and 1-year serum creatinine were the significant risk factors for graft loss. But recurrence of IgAN was not a relevant risk factor. Overall graft survival rates at 5 and 10 years were 93.8% and 73.1% in the first transplantation group and 100% and 100% in the retransplantation group, respectively. CONCLUSION Although IgAN recurrence was a significant risk factor for graft failure, the patient who underwent retransplantation showed favorable results. Retransplantation should be considered in patients who lost their first graft after recurrence of IgAN.

Long-term prognosis of BK virus-associated nephropathy in kidney transplant recipients

Background The long-term prognosis of BK virus-associated nephropathy (BKVAN) in kidney transplant recipients (KTRs) is uncertain. We evaluated the long-term prognosis in KTRs with BKVAN and the clinical significance of BKVAN on post-transplant clinical outcome. Methods We retrospectively analyzed the medical records of 582 patients who underwent kidney transplant (KT) between 2001 and 2014. We divided the patients into a BKVAN group (15 patients) diagnosed by allograft biopsy and a control group (356 patients). Results The incidence of BKVAN was 4.0%, and the mean follow-up duration was 93.1 ± 52.3 months. Median time from KT to BKVAN diagnosis was 5.9 months (interquartile range [IQR], 4.4–8.7). In the BKVAN group, 9 (60.0%) KTRs with combined acute rejection progressed to graft failure, and the median time from BKVAN diagnosis to graft failure was 36.2 months (IQR, 9.7–65.5). Death-censored graft survival rate and patient survival rate in the BKVAN group were significantly lower than those in the control group. BKVAN and rejection were independent risk factors for graft failure. In the subgroup analysis, death-censored graft survival rate of KTRs with BKVAN with acute rejection was significantly worst in comparison with similar patients without BKVAN regardless of acute rejection (P < 0.001). Conclusion The long-term prognosis of BKVAN with acute rejection was very poor because of graft failure caused by inadequate treatment for acute rejection considering BKVAN. Therefore, we should carefully monitor the allograft status of KTRs through regular surveillance tests after treatment for BKVAN with acute rejection.

Long-term Clinical Outcome of Aortic Arch Calcification in Kidney Transplant Recipients

INTRODUCTION Cardiovascular disease is the most common cause of death in kidney transplant recipients (KTRs). Aortic arch calcification (AoAC) is a major risk factor for cardiovascular disease in KTRs. This study aimed to evaluate the long-term outcomes of AoAC in KTRs. METHODS We retrospectively evaluated AoAC in KTRs between 2000 and 2010 using chest radiography. AoAC was semiquantitatively estimated by calculating calcification score. Associations between clinical and biochemical parameters were evaluated. RESULTS A total of 258 patients were enrolled; the mean age was 40.7 years, and 135 (52.3%) were males. Diabetes mellitus was present in 28 (10.9%), and deceased donor kidney transplantation (KT) had been performed in 95 (36.8%). Fifty-three (20.5%) patients had AoAC at the time of KT, with an AoAC score of 0.8 ± 2.0. The proportion of KTRs with AoAC gradually increased to 23.3%, 26.4%, and 28.7% at 1, 3, and 5 years, respectively, after KT. The AoAC score also gradually increased to 1.0 ± 2.3, 1.2 ± 2.8, and 1.6 ± 3.1, respectively, at 1, 3, and 5 years after KT. The 10-year graft survival rate was 83.2% in the AoAC group and 85.1% in the non-AoAC group. The 10-year patient survival rate was 90.6% in the AoAC group and 95.7% in the non-AoAC group. In multivariate analysis, age at KT, deceased-donor KT, and diabetes mellitus were independent predictors for all-cause mortality. CONCLUSIONS AoAC is an independent predictor of poor cardiovascular outcome in KTRs. Age and dialysis duration were independent risk factors for AoAC. Age at KT, deceased-donor KT, and diabetes mellitus were independent predictors for all-cause mortality. Regular follow-up by chest radiography could be a simple and useful method to screen for AoAC and reduce cardiovascular mortality.

MP661ELEVATED PLASMA CYCLOPHILIN A IN HEMODIALYSIS AND PERITONEAL DIALYSIS PATIENTS: A NOVEL LINK TO SYSTEMIC INFLAMMATION AND CARDIOVASCULAR DISEASE

Author(s): Jin, Kyubok; Vaziri, Nosratola D; Kim, Yaerim; Kang, Seong Sik; Park, Woo Yeong; Han, Seungyeup; Park, Sung Bae; Park, Sihyung; Yoon, Jeongsoo

A Pedigree with c.179 Cytosine to Threonine Missense Mutation of SLC12A3 Gene Presenting Gitelman's Syndrome.

A 42-year-old man came to the hospital presenting chest discomfort and general weakness. He had come to the hospital with the same symptoms 3 months ago and 12 years prior. His laboratory test showed hypokalemia, hypomagnesemia and hypocalciuria. The arterial blood gas analysis showed hypochloremic metabolic alkalosis. He had an ultrasonography guided renal biopsy, the result was normal at light microscopy and immunofluorescence microscopy. However, a special stain for Na-Cl cotransporter was weakly expressed compared with the control. The patient and his family underwent genetic sequencing about the SLC12A3 gene. He had a homozygous mutation in the 179th nucleotide of Exon 1 on the SLC12A3 gene (p.Thr60Met) and his parents and sisters were diagnosed as carrier state of Gitelmans syndrome (GS). GS is an inherited tubular disorder which presents mild hypokalemia, hypomagnesemia and hypocalciuria. Since the symptoms and laboratory results are not severe, it can go unnoticed by physicians. Herein we present a family with GS, diagnosed by genetic sequencing.