Roodnat Joke I, de Mik-van Egmond Anneke M E, Visser Wesley J, Berger Stefan P, van der Meijden Wilbert A G, Knauf Felix, van Agteren Madelon, Betjes Michiel G H, Hoorn Ewout J
Division of Nephrology and Transplantation, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.
Department of Dietetics, Erasmus Medical Center, Rotterdam, The Netherlands.
Transplant Direct. 2017 Nov 8;3(12):e331. doi: 10.1097/TXD.0000000000000748. eCollection 2017 Dec.
Enteric hyperoxaluria due to malabsorption may cause chronic oxalate nephropathy and lead to end-stage renal disease. Kidney transplantation is challenging given the risk of recurrent calcium-oxalate deposition and nephrolithiasis.
We established a protocol to reduce plasma oxalic acid levels peritransplantation based on reduced intake and increased removal of oxalate. The outcomes of 10 kidney transplantation patients using this protocol are reported.
Five patients received a living donor kidney and had immediate graft function. Five received a deceased donor kidney and had immediate (n = 1) or delayed graft function (n = 4). In patients with delayed graft function, the protocol was prolonged after transplantation. In 3 patients, our protocol was reinstituted because of late complications affecting graft function. One patient with high-output stoma and relatively low oxalate levels had lost her first kidney transplant because of recurrent oxalate depositions but now receives intravenous fluid at home on a routine basis 3 times per week to prevent dehydration. Patients are currently between 3 and 32 months after transplantation and all have a stable estimated glomerular filtration rate (mean, 51 ± 21 mL/min per 1.73 m). In 4 of 8 patients who underwent for cause biopsies after transplantation oxalate depositions were found.
This is the first systematic description of kidney transplantation in a cohort of patients with enteric hyperoxaluria. Common complications after kidney transplantation impact long-term transplant function in these patients. With our protocol, kidney transplantation outcomes were favorable in this population with unfavorable transplantation prospects and even previous unsuccessful transplants.
因吸收不良导致的肠道高草酸尿症可引起慢性草酸肾病并导致终末期肾病。鉴于复发性草酸钙沉积和肾结石的风险，肾移植具有挑战性。
我们制定了一项方案，通过减少草酸盐摄入和增加草酸盐清除来降低移植围手术期的血浆草酸水平。报告了10例使用该方案的肾移植患者的结果。
5例患者接受活体供肾移植，移植肾立即发挥功能。5例接受尸体供肾移植，其中1例移植肾立即发挥功能，4例移植肾延迟发挥功能。对于移植肾延迟发挥功能的患者，移植后延长了该方案的实施时间。3例患者因影响移植肾功能的晚期并发症而重新实施我们的方案。1例高输出量造口且草酸盐水平相对较低的患者，其首次肾移植因复发性草酸钙沉积而失败，但现在在家中每周常规接受3次静脉输液以预防脱水。患者目前处于移植后3至32个月之间，所有患者的估计肾小球滤过率均稳定（平均为51±21 mL/min/1.73 m²）。在8例移植后因病因进行活检的患者中，4例发现有草酸钙沉积。
这是对一组肠道高草酸尿症患者肾移植的首次系统描述。肾移植后的常见并发症影响这些患者的长期移植肾功能。采用我们的方案，对于移植前景不佳甚至既往移植失败的这部分患者，肾移植结果良好。
