Schwarz Anke, Rustien Gunnar, Merkel Saskia, Radermacher Joerg, Haller Hermann
Department of Nephrology, Hannover Medical School, Carl Neuberg Strasse 1, D-30625 Hannover, Germany.
Nephrol Dial Transplant. 2007 Feb;22(2):584-91. doi: 10.1093/ndt/gfl583. Epub 2006 Oct 11.
Persistent secondary hyperparathyroidism after renal transplantation may require parathyroidectomy (PTX). Clinical experience suggests that these patients commonly develop decreased renal function thereafter.
To test this notion, we evaluated 76 transplant patients who underwent pararhyroidectomy between 1997 and 2003.
In half the patients (47%), creatinine clearance decreased >20% (before vs after PTX, 57 +/- 21 vs 38 +/- 17 ml/min, P = 0.001). The patients with decreased creatinine clearance had higher parathyroid hormone (PTH) concentrations before and lower values after PTX compared with those who did not (594 +/- 392 vs 447 +/- 234 pg/ml before PTX, P = 0.03; 35 vs 123 pg/ml thereafter, P = 0.002). They also had lower serum calcium concentrations after PTX (2.0 vs 2.2 mmol/l, P = 0.005) and they required more calcium and vitamin D analogues. These patients also more commonly underwent total PTX with autotransplantation, compared with subtotal (75 vs 50%, P = 0.03). However, in multivariate analysis, only the delta PTH decline (%) after PTX was a significant predictor of deteriorating renal function (P = 0.005) and was correlated with the creatinine clearance decrease (R = 0.369, P = 0.001). Prospectively measured inulin and para-amino-hippuric acid (PAH) clearance decreased significantly after PTX in a subgroup of 19 patients (inulin before vs after PTX 67 vs 55 ml/min/1.73 m(2), P = 0.001; PAH 360 vs 289 ml/min/1.73 m(2), P = 0.001). Transplant biopsies revealed calcification in 70% of biopsied cases.
Since PTH has a known positive regulatory effect on renal perfusion and glomerular filtration rate, we conclude that relative hypoparathyroidism after PTX is the main mechanism contributing to decreased renal function in these patients. There was no difference in 10-year-graft survival between the deteriorating and the non-deteriorating group.
肾移植后持续性继发性甲状旁腺功能亢进可能需要进行甲状旁腺切除术(PTX)。临床经验表明,这些患者此后通常会出现肾功能下降。
为验证这一观点,我们评估了1997年至2003年间接受甲状旁腺切除术的76例移植患者。
半数患者(47%)肌酐清除率下降超过20%(PTX前后分别为57±21和38±17 ml/min,P = 0.001)。与肌酐清除率未下降的患者相比,肌酐清除率下降的患者PTX前甲状旁腺激素(PTH)浓度更高,PTX后更低(PTX前分别为594±392和447±234 pg/ml,P = 0.03;此后分别为35和123 pg/ml,P = 0.002)。PTX后他们的血清钙浓度也更低(分别为2.0和2.2 mmol/l,P = 0.005),且需要更多的钙和维生素D类似物。与次全甲状旁腺切除术相比,这些患者更常接受甲状旁腺全切加自体移植术(分别为75%和50%,P = 0.03)。然而,在多变量分析中,只有PTX后PTH下降百分比(%)是肾功能恶化的显著预测指标(P = 0.005),且与肌酐清除率下降相关(R = 0.369,P = 0.001)。在19例患者的亚组中,PTX后前瞻性测量的菊粉和对氨基马尿酸(PAH)清除率显著下降(PTX前后菊粉分别为67和55 ml/min/1.73 m²,P = 0.001;PAH分别为360和289 ml/min/1.73 m²,P = 0.001)。移植肾活检显示70%的活检病例有钙化。
由于已知PTH对肾灌注和肾小球滤过率有正向调节作用,我们得出结论,PTX后相对甲状旁腺功能减退是这些患者肾功能下降的主要机制。肾功能恶化组和未恶化组的10年移植肾存活率无差异。