Schwille Paul O, Wipplinger J
Mineral Metabolism and Endocrine Research Laboratory, Department of Surgery, University of Erlangen-Nurnberg, Germany.
Eur J Med Res. 2008 Jul 28;13(7):332-42.
In IRCU the possible role of urinary pH (U-pH) as risk factor of calcium (Ca) stones is poorly understood.
To evaluate in IRCU the response to an oral acid load, focussing on post- and pre-load U-pH, other urinary, renal and extra-renal factors, and linkage with Ca stones. -
237 male patients, either Ca stone-free (SF) or -bearing (SB), but without overt signs of systemic metabolic acidosis underwent a standardized laboratory programme that included, besides collection of urine and blood, the intake of an oxalate-free acid test meal (proton content 120 mM). Established analytical methods were used.
In 79 patients the post-meal load U-pH was < or = 5.30 (in healthy individuals accepted as the upper limit after the same proton load), but >5.30 in 158; in these two subsets the mean fasting pre-load U-pH was 5.84 and 6.37 (p <0.001), the mean U-pH in 24 h urine 5.70 and 6.03 (p <0.001), the mean score of stone formation activity 32 and 42 (p = 0.12), the SF/SB ratio 35/44 and 76/82 (not significant). However, when in pre-load urine undissociated uric acid concentration was low due to the high pH, the SF/SB ratio was 53/66 (p = 0.038), whereas isolated increase of U-pH with SF/SB ratio 54/65 (p = 0.059), urinary supersaturation with Ca phosphate (hydroxyapatite), Ca oxalate, uric acid, and isolated decrease of concentration of total protein, total uric acid and the crystallization inhibitors magnesium and citrate failed to affect significantly the frequency distribution of SF and SB patients. Pre-load U-pH was positively associated with urinary ratio sodium/proton excretion, renal reclaim of sodium and protein, negatively associated with body mass index, fasting insulinemia and uricemia, urinary protein concentration, renal reclaim of phosphate.
In IRCU 1) inappropriately high U-pH combined with increase of proteinuria and alteration of renal-tubular transport are frequent; 2) disturbed interactions of renal proton generation with sodium handling, urinary physico-chemical and systemic metabolic factors may initiate the development of Ca-containing concretions, presumably Ca phosphate, at some yet unknown renal anatomic site.
在内科重症监护病房(IRCU),尿pH值(U-pH)作为钙(Ca)结石风险因素的潜在作用尚不清楚。
在IRCU中评估口服酸负荷后的反应,重点关注负荷后和负荷前的U-pH、其他尿液、肾脏和肾外因素,以及与Ca结石的关联。
237例男性患者,分为无Ca结石(SF)组和有Ca结石(SB)组,但无明显系统性代谢性酸中毒迹象,接受了标准化实验室检查,除收集尿液和血液外,还摄入了无草酸盐的酸测试餐(质子含量120 mM)。采用既定的分析方法。
79例患者餐后负荷U-pH≤5.30(在相同质子负荷后,健康个体的上限值),158例患者>5.30;在这两个亚组中,空腹负荷前U-pH平均值分别为5.84和6.37(p<0.001),24小时尿液中U-pH平均值分别为5.70和6.03(p<0.001),结石形成活性平均评分分别为32和42(p=0.12),SF/SB比值分别为35/44和76/82(无显著性差异)。然而,当负荷前尿液中未离解尿酸浓度因pH值高而较低时,SF/SB比值为53/66(p=0.038),而单纯U-pH升高时SF/SB比值为54/65(p=0.059),磷酸钙(羟基磷灰石)、草酸钙、尿酸的尿过饱和度,以及总蛋白、总尿酸浓度的单纯降低和结晶抑制剂镁和柠檬酸盐均未显著影响SF和SB患者的频率分布。负荷前U-pH与尿钠/质子排泄比值、钠和蛋白质的肾重吸收呈正相关,与体重指数、空腹胰岛素血症和尿酸血症、尿蛋白浓度、磷酸盐的肾重吸收呈负相关。
在IRCU中,1)U-pH异常升高并伴有蛋白尿增加和肾小管转运改变的情况很常见;2)肾质子生成与钠处理、尿液物理化学和全身代谢因素之间的相互作用紊乱,可能在一些未知的肾脏解剖部位引发含钙结石(可能是磷酸钙)的形成。