钙敏感受体活性改变对大鼠泌尿系草酸钙结石形成的影响

目的探讨钙敏感受体（CaSR）活性改变对草酸钙结石形成的影响。方法在实验期间给予乙二醇和氯化铵诱导雄性SD大鼠产生泌尿系草酸钙结石。在造模期间给予不同剂量的CaSR抑制剂（NPS-2390）。实验结束时检测各组大鼠血尿素氮（BUN）、肌酐（Cr）、血磷、血钙、血镁、PTH的含量、24h尿量、尿pH值、尿钙、镁、尿草酸的分泌量,显微镜下观察肾组织切片中草酸钙结晶沉积及病理变化情况及肾脏中CaSR表达情况。从而评价CaSR活性的改变对泌尿系结石形成的影响。结果成石对照组大鼠血BUN、Cr、尿草酸、尿钙较空白组明显升高并且有大量结晶形成,表明建模成功。CaSR抑制剂组较成石对照组甲状旁腺激素（PTH）的分泌增加并且血Ca2＋升高尿钙升高。肾组织病理学检查显示CaSR抑制组的肾脏组织中的草酸钙结晶较成石对照组明显增加,组织病理损伤也较重。结论肾脏中及甲状旁腺中CaSR的表达下降可以导致草酸钙结晶的形成增加。     

α-亚麻酸对草酸钙结石鼠前列腺素E2的影响

目的：探讨前列腺素E2在尿结石形成中的作用以及α-亚麻酸对前列腺素E2的抑制作用。方法：将60只雄性Wistar成年大鼠随机分成空白对照组、成石组、苏子油组、葵花籽油组。所有大鼠适应性喂养1周后，空白对照组随后7周均饮用自来水。成石组前4周饮用自来水，后3周饮用诱石剂水，每日自来水2g／只灌胃1次。苏子油组7周内每日以苏子油2g／只灌胃1次，饮水同成石组。葵花油组7周内每日以葵花油2g／只灌胃1次，饮水同B组。8周后检测大鼠24h尿总钙、尿总镁、尿草酸、肌酐和各组大鼠尿前列腺素E2水平。结果：空白对照组和苏子油组尿总钙明显低于成石组。尿总镁、尿草酸对照组明显低于成石组，苏子油组、葵花籽油组、成石组之间则差异无显著性意义。尿肌酐对照组、苏子油组、葵花油组显著低于成石组。24h尿前腺素E2水平苏子油组、对照组显著低于成石组。葵花籽油组与成石组比较差异无显著性意义。成石组、苏子油组、葵花籽油组前列腺素E2水平与尿总钙含量成正相关性。结论：前列腺素E2可能参与并促进了尿结石的形成，α-亚麻酸可能通过抑制肾前列腺素E2的产生而抑制尿结石形成。     

泽泻提取物对大鼠尿结石形成和间α胰蛋白酶抑制物表达的影响

目的　观察中药泽泻的有效部位提取物对实验性大鼠尿草酸钙结石形成和间α胰蛋白酶抑制物 (IαI)表达的影响。方法　采用乙二醇和氯化铵诱导形成大鼠肾草酸钙结石模型 ,将健康成年雄性Wistar大白鼠随机分成对照组 (A组 )、成石组 (B组 )、泽泻组 (C组 )。用免疫组织化学和计算机图像分析技术检测IαI在肾组织的表达情况 ,并测定血、尿生化和草酸钙晶体在肾组织的分布。结果　泽泻组大鼠肾组织草酸钙晶体分布、血生化等指标均明显低于结石模型组 ;泽泻组大鼠肾组织IαI的灰度值为 2 18.3 2± 7.5 8、肾钙含量 (7.3 2± 1.5 9)mg/g、2 4h尿钙分泌量 (5 .3 4±1.10 ) μmol/2 4h ,模型组大鼠IαI的灰度值为 2 0 3 .40± 14 .69、肾钙含量 (12 .63± 2 .2 9)mg/g、2 4h尿钙分泌量 (8.5 3± 1.73 ) μmol/2 4h ,两组间差异均有显著性 (P <0 .0 5 )。 结论　泽泻的乙酸乙酯浸膏的乙酸乙酯洗脱液提取物可能通过抑制肾组织内草酸钙晶体的形成和减少肾IαI的表达 ,从而能抑制尿结石的形成。     

肾结石大鼠肾组织bikunin mRNA的表达

目的 :研究bikunin在实验性肾草酸钙结石大鼠肾组织的表达及意义。方法 :采用乙二醇和氯化铵诱导大鼠肾草酸钙结石模型形成 ,检测各组大鼠肾功能、肾组织Ca2 + 含量和草酸钙晶体沉积、尿生化指标 ,并用逆转录聚合酶链反应 (RT PCR)检测bikuninmRNA在肾组织的表达情况。结果 :模型组大鼠的血清Cr、BUN、肾Ca2 + 含量、2 4h尿Ca2 + 、草酸 (Ox)分泌量和肾组织bikuninmRNA的表达均明显高于正常组 (P <0 .0 5 )。结论 :高草酸尿和草酸钙结晶的沉积能促使大鼠肾脏通过合成更多的bikunin来抑制大鼠肾组织草酸钙晶体的形成。     

月见草油抑制草酸钙结晶形成的实验研究

目的了解月见草油在草酸钙结石形成中的作用,为临床治疗提供新的方法与思路。方法雄性SD大鼠60只,随机分为4组,各组15只。C组和D组以月见草油（含γ-亚麻酸9.2%）或葵花籽油（含亚油酸70%）10g/kg灌胃4周后,用诱石剂1%乙二醇（EG）加2%氯化氨喂饮,同时继续以月见草油或葵花籽油灌胃4周,8周后检测各组大鼠肾功能、24h血尿生化指标和肾草酸钙结晶情况;仅饲普通饲料（A组,空白组）和普通饲料加1%乙二醇（EG）加2%氯化氨喂饮（B组,成石组）大鼠作为对照。结果月见草油组肾组织水肿较轻,肾内草酸钙结晶数及肾成石率低于成石组（P〈0.05）,尿枸橼酸较成石组高（P〈0.01）,24h尿钙、尿草酸排泄均低于成石组（P〈0.01）,血尿素氮（P〈0.01）、血肌酐（P〈0.05）低于成石组。结论γ-亚麻酸能有效改善肾功能,减少尿钙及草酸的排泄,抑制实验鼠肾草酸钙结晶形成,在尿石症防治方面可能有一定应用价值。     

芭蕉芯和维生素B6对小鼠草酸钙结晶的抑制作用

观察了维生素Ｂ_６和芭蕉芯提取液对实验性高草酸尿症小鼠体内草酸钙结晶形成的抑制作用。结果发现：湿肾组织钙含量各组之间无显著性差异；湿肾组织草酸含量，维生素Ｂ_６治疗组为０．６９８０±０．４０８２μｍｏｌ／ｇ，芭蕉芯提取液治疗组为０．４０３１±０．２１４７μｍｏｌ／ｇ，均分别明显低于成石组（Ｐ＜０．０５及Ｐ＜０．０１）。偏光显微镜观察发现，服用维生素Ｂ_６及芭蕉芯提取液的小鼠肾脏草酸钙结晶形成明显少于成石组。结果表明：维生素Ｂ_６和芭蕉芯提取液都具有抑制实验性高草酸尿症小鼠肾脏草酸钙结晶形成的作用，其中，芭蕉芯提取液的抑制作用明显比维生素Ｂ_６强。     

α-亚麻酸抑制大鼠肾草酸钙结晶形成的实验研究

目的　比较α 亚麻酸和亚油酸预防结石形成的作用。　方法　雄性Wistar成年大鼠 6 0只 ,分 4组 ,每组 15只。C组和D组分别以苏子油 (含α 亚麻酸 6 3% )或葵花籽油 (含亚油酸 70 % ) 2g/d灌胃 4周后 ,用诱石剂 1%乙二醇 (EG)加 1%氯化氨喂饮 ,同时继续以苏子油或葵花籽油灌胃 ,3周后检测各组大鼠肾功能、2 4h血尿生化指标和肾草酸钙结晶情况。仅饮用诱石剂 (B组 ,成石组 )大鼠和正常喂养 (A组 ,空白对照组 )大鼠作对照。　结果　苏子油组肾组织水肿较轻 ,肾内草酸钙结晶数及肾钙含量明显低于成石组 (P <0 .0 1) ,2 4h尿钙排泄、血尿素氮、肌酐浓度显著低于成石组 (P <0 .0 5 ) ,尿肌酐排泄增加 (P <0 .0 5 )。葵花籽油组仅血尿肌酐较成石组明显改善 (P <0 .0 5 ) ,其他指标与成石组差异无显著性意义 (P >0 .0 5 )。　结论　α 亚麻酸能有效改善肾功能 ,减少尿钙排泄 ,抑制实验鼠肾草酸钙结晶形成 ,在尿石症防治方面可能有一定应用价值。     

尿凝血酶原片断1在肾结石模型大鼠肾组织的表达及其意义

目的　研究尿液中尿凝血酶原片段 1(UPTF1)的来源和UPTF1在肾结石模型大鼠肾组织的表达 ,探讨尿结石形成对肾组织UPTF1表达的影响及其在尿结石形成中的意义。方法用乙二醇和 1α 羟基维生素D3 灌胃制作大鼠肾草酸钙结石模型。采用半定量逆转录聚合酶链反应(RT PCR)检测UPTF1mRNA在结石模型大鼠和正常对照大鼠肾组织中的表达及水平变化。结果　偏光显微镜下结石模型大鼠肾乳头和肾皮质内布满草酸钙晶体 ,肾钙含量、2 4h尿草酸和尿钙分泌量分别为 13 8.3 9mg/g、82 .89μmol和97.3 5 μmol;对照组肾钙含量、2 4h尿草酸和尿钙分泌量分别为 1.5 4mg/g、2 4.2 2 μmol和3 .14 μmol,组间差异均有统计学意义(P <0 .0 1)。UPTF1mRNA在所有大鼠肾组织和肝组织中都有表达 ,但在正常大鼠和肾结石大鼠肾组织中的相对表达量分别为 1.73± 0 .2 5、1.86± 0 .19,两组差异无统计学意义意义 (P >0 .0 5 )。结论　尿液中的UPTF1来源于大鼠肾组织的生物合成 ,可能是草酸钙结石形成的生理性抑制因子 ,从而可以借助实验动物模型为研究UPTF1在尿结石形成中的作用提供了依据。     

金钱草及广金钱草对大鼠肾草酸钙结石相关代谢产物作用的研究

目的对比金钱草与广金钱草抑制大鼠肾草酸钙结石的具体机制与作用效果。方法54只SPF级SD雄性大鼠适应性喂养1周至体重180~200 g,使用乙二醇灌胃法建立SD大鼠肾草酸钙结石模型,而后将大鼠按照随机数字表法分为9组处理并进行对照,分别为健康对照组(A组),阳性对照组(建模组,B组),金钱草低、中、高剂量组(C1、C2、C3组,共3组),广金钱草低、中、高剂量组(D1、D2、D3组,共3组),疗效对照组(枸橼酸氢钾钠组,E组),每组各6只。4周后收集标本测定各组大鼠血尿生化指标,并行Von Kossa染色检测肾草酸钙晶体,在偏振光显微镜下观察大鼠肾组织草酸钙结晶沉积情况,利用测算照片中阳性面积百分比与相关血尿生化指标判断两者药效差异。计量资料以均数±标准差(x±s)表示,组间比较采用单因素方差分析,两组间比较采用SNK-q检验;结晶形成情况组间比较采用Kruskal-Wallis检验。结果与阳性对照组相比,高剂量的广金钱草相对金钱草能显著降低肾草酸钙结石大鼠血肌酐水平,应用金钱草后血肌酐水平为(86.70±11.49)μmol/L,应用广金钱草后血肌酐水平为(70.72±9.08)μmol/L,两者差异有统计学意义(P<0.01);高剂量金钱草、广金钱草均能显著升高尿镁水平,降低血尿素水平,两者相比差异无统计学意义(P>0.05);与阳性对照组相比,给予高剂量金钱草(P<0.0001)与高剂量广金钱草(P<0.0001)均能显著抑制大鼠肾草酸钙晶体形成,保护大鼠肾脏,两者作用效果相比差异无统计学意义(P>0.05);给予金钱草与广金钱草均未能观察到显著升高尿pH值与显著降低尿钙、尿草酸、24 h尿量、血钙、血磷、血镁、血尿酸和肾草酸含量的效果。结论广金钱草抑制大鼠肾草酸钙结石发生的功效优于金钱草,对肾功能具有更好的保护作用。     

香豆素对实验性大鼠草酸钙结石形成的影响

应用偏光显微镜和解剖镜观察ＶｉｔａｍｉｎＫ（Ｖｉｔ－Ｋ）拮抗剂香豆素对大鼠草酸钙结石形成影响，观察到香豆素显著地增加大鼠肾内草酸钙结晶数目，肾组织匀浆中草酸含量（１．１４±０．７３ｍｇ／ｇ）也显著高于对照组（０．０３６±０．１５ｍｇ／ｇ，Ｐ＜０．０５）。当停用香豆素后，肾内草酸钙结晶数又可减少。推测香豆素可拮抗Ｖｉｔ－Ｋ使得肾内依赖Ｖｉｔ－Ｋ的羧化作用减弱，肾内草酸钙抑制物Ｎｅｐｈｒｏｃａｌｃｉｎ（Ｎｃ）中谷氨酸转化成γ－羧基谷氨酸（Ｇｌａ）减少，Ｎｃ与钙结合减少，对草酸钙结晶抑制活性降低，易发生草酸钙结石。提示Ｖｉｔ－Ｋ缺乏可促进肾结石形成。     

鱼油抑制实验鼠草酸钙结晶形成

目的 了解鱼油在尿石形成中的作用。方法 ６０只大鼠随机分４组,饮用１％乙二醇（ＥＧ）水,同时喂饲不同剂量的鱼油。４周后检测各组大鼠肾功能、草酸钙结晶、２４小时尿钙和尿草酸。结果 加服鱼油组鼠肾积水、组织水肿减轻,肾组织内草酸钙结晶数及含钙量明显减少,２４小时尿钙排出减少;尿尿素氮、肌酐排出明显增加,而血中尿素氮、肌酐浓度显著低于成石组。结论 鱼油能抑制实验性高草酸尿症大鼠体内草酸钙结晶形成,减少尿     

Study of a rat model for calcium oxalate crystal formation without severe renal damage in selected conditions

BACKGROUND: Although nephrotoxic in high doses, ethylene glycol (EG) has been used with ammonium chloride (NH(4)Cl) or vitamin D(3) to study calcium oxalate stone formation in rat models. In the present study we used EG alone or with NH(4)Cl to study hyperoxaluria, crystaluria, and crystal attachment to renal epithelial cells in rats with minimal renal damage. METHODS: Six-week-old male Sprague-Dawley (SD) rats were given food and special drinking water. In experiment 1 the drinking water contained 1.0% NH(4)Cl plus four different concentrations of EG (0.8%, 0.4%, 0.2%, 0.1%). In experiment 2 the drinking water contained EG alone (0.8%, 0.4%, 0.2%, 0.1%). Urine was collected for 24 h before the rats were sacrificed. In experiment 1 the rats were sacrificed 5-13 days after starting the special water. In experiment 2 the rats were sacrificed 7-21 days after starting the special water. Bladder urine was also obtained. Blood and urine were tested for calcium, phosphorus, and creatinine. In addition, urine was tested for pH, oxalate and N-acetyl-beta-D glucosaminidase (NAG). Kidney sections were stained with hematoxylin-eosin, von Kossa and Pizzolato stain. Crystal morphology was determined using polarizing microscopy, and composition was determined using high-resolution X-ray powder diffraction. RESULTS: Experiment 1: Aggravation of renal function, an increase in urinary oxalate and NAG excretion, and crystals observed in the kidneys all correlated with EG concentration and length of drinking time. In bladder urine, calcium oxalate monohydrate (COM) crystals exceeded calcium oxalate dihydrate (COD) crystals. Experiment 2: Renal function remained unchanged. Oxalate excretion increased and NAG increased slightly. Crystals occurred only in the papillary tip region. Crystals in bladder urine were mostly COD. CONCLUSION: In the current rat model, calcium oxalate crystaluria could be induced without severe renal damage in selected cases. Either and/or both COM and COD might form and interact with kidney epithelium. We propose different experimental conditions to study the various phases of calcium oxalate stone formation in young male SD rats.     

三叶因子1在大鼠草酸钙结石模型肾组织中的表达及其意义

目的 探讨三叶因子1(TFF1)在大鼠草酸钙结石模型肾组织中的表达及其与肾脏草酸钙结石形成机制的关系.方法 分别以1％的乙二醇溶液自由饮用和2％的NH4Cl溶液2 mL/d灌胃2周和4周;用偏光显微镜观察结石结晶形成情况;采用免疫组织化学染色法分别检测成石2周(n=20)、成石4周(n=20)和正常组(n=20)大鼠肾组织TFF1蛋白的表达.结果 TFF1免疫反应阳性物质主要位于肾小球、肾小管,与正常组比较,成石2周肾组织TFF1平均灰度值略下降(P＞0.05),成石4周平均灰度值明显降低(P＜0.05).结论 乙二醇诱导的大鼠草酸钙结石模型肾组织中TFF1低表达,伴随结石结晶数量和密度的增加,TFF1表达降低.TFF1在肾组织中的表达与乙二醇和NH4Cl干预的时限呈负相关;TFF1可能在肾草酸钙结石的形成中起抑制作用.     

Osteopontin knockdown in the kidneys of hyperoxaluric rats leads to reduction in renal calcium oxalate crystal deposition

Osteopontin (OPN) expression is increased in kidneys of rats with ethylene glycol (EG) induced hyperoxaluria and calcium oxalate (CaOx) nephrolithiasis. The aim of this study is to clarify the effect of OPN knockdown by in vivo transfection of OPN siRNA on deposition of CaOx crystals in the kidneys. Hyperoxaluria was induced in 6-week-old male Sprague–Dawley rats by administering 1.5 % EG in drinking water for 2 weeks. Four groups of six rats each were studied: Group A, untreated animals (tap water); Group B, administering 1.5 % EG; Group C, 1.5 % EG with in vivo transfection of OPN siRNA; Group D, 1.5 % EG with in vivo transfection of negative control siRNA. OPN siRNA transfections were performed on day 1 and 8 by renal sub-capsular injection. Rats were killed at day 15 and kidneys were removed. Extent of crystal deposition was determined by measuring renal calcium concentrations and counting renal crystal deposits. OPN siRNA transfection resulted in significant reduction in expression of OPN mRNA as well as protein in group C compared to group B. Reduction in OPN expression was associated with significant decrease in crystal deposition in group C compared to group B. Specific suppression of OPN mRNA expression in kidneys of hyperoxaluric rats leads to a decrease in OPN production and simultaneously inhibits renal crystal deposition.     

Effects of citrate on renal stone formation and osteopontin expression in a rat urolithiasis model

Previous studies have described the inhibitory effects of citrate on calcium oxalate crystallization in place of crystal growth, but the effects of citrate on matrix proteins of stones has not been studied in vivo. To examine the effect of citrate on the matrix, we investigated the effect of citrate on osteopontin (OPN) expression, which we had previously identified as an important stone matrix protein. Control rats were treated with saline while rats of the stone group were treated with ethylene glycol (EG) and vitamin D₃, and the citrate groups (low-dose and high-dose groups) were treated with a citrate reagent compound of sodium citrate and potassium citrate, in addition to EG and vitamin D₃. The rate of renal stone formation was lower in the citrate groups than in the stone group. This was associated with a low expression of OPN mRNA in citrate-treated rats relative to that in the stone group. Citrate was effective in preventing calcium oxalate stone formation and reduced OPN expression in rats. Our results suggest that citrate prevents renal stone formation by acting against not only the crystal aggregation and growth of calcium oxalate but also OPN expression. Received: 7 June 2000 / Accepted: 20 September 2000     

碘海醇对实验性大鼠草酸钙结石形成的影响

目的探讨造影剂碘海醇对大鼠草酸钙结石形成的影响。方法将40只Wister大鼠随机分为成4组：空白对照组（A）、单纯诱石组（B）、单纯碘海醇组（C）、诱石＋碘海醇组（D）。用乙二醇法诱导建立大鼠草酸钙结石模型,C、D组尾静脉注射碘海醇。实验第4周末检测肾组织中丙二醛（MDA）含量及超氧化物歧化酶（SOD）活力,镜下观察肾内草酸钙晶体沉积情况。结果A、B、C、D4组肾脏组织MDA含量（nmol／mg蛋白）分别为2．74±0．48、4．51±1．47、6．92±2．18、8．87±2．31,SOD活力（U／mg蛋白）分别195．21±11．01、170．24±13．59、140．86±25．91、121．54±25．50,各组间差异有统计学意义（P〈0．05）。B、D组结晶等级评分高于A组,D组结晶等级评分高于B组（P〈1．05）。培论碘海醇促进了大鼠肾小管内草酸结晶量的增加,其机制与碘海醇诱导的肾小管上皮氧化应激损伤有关。     

Effects of high-sodium diet on lithogenesis in a rat experimental model of calcium oxalate stones

BackgroundThis study aimed to investigate the effects of a high- and low-sodium diets on lithogenesis in a rat experimental model of calcium oxalate stones.MethodsTwenty male Wistar rats were randomly divided into four groups; group A: 4% NaCl+1% ethylene glycol (EG); group B: 8% NaCl+1% EG; group C: 8% NaCl+normal drinking-water; group D: 1% EG +normal diet. All rats were sacrificed 4 weeks later, and blood samples were collected from the heart. The kidneys were collected for Von Kossa staining to evaluate the formation of calcium-containing crystals. The last 24-h urine samples were also gathered for metabolic analysis.ResultsVon Kossa staining demonstrated that the rats in both group A and group B had significantly more renal calcium crystals than those in group D. However, 24-h urinary volume increased significantly (142.26±20.91 mL) in group B compared with group A (100.52±28.23 mL), group C (107.36±14.24 mL), group D (40.79±8.71 mL) (P=0.004, 0.012, and 0.000 respectively). Level of urine sodium (Na), potassium (K), chlorine (Cl), and calcium (Ca), urea nitrogen were significantly higher in group B compared with group D. The urine phosphorus, oxalate, and creatinine levels; urine specific gravity; and urine PH were similar between group B and group D. The level of serum sodium was higher in group B (151.26±4.06 mmol/L) compared with group D (145.56±1.12 mmol/L) (P=0.002).ConclusionsA high sodium intake might increase the risk of lithogenesis in susceptible individuals (given by EG) or in individuals with water restriction.     

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. I. Renal function and biochemical changes.

BACKGROUND: Both dietary phosphorus restriction and the ingestion of ammonium chloride (NH(4)Cl) given to rats on a high-phosphorus diet have been shown to preserve renal function in the azotaemic rat. Parathyroidectomy also has been reported to preserve renal function and, in addition, to prevent kidney hypertrophy in the remnant kidney model. Our goals were (i) to evaluate in azotaemic rats the effect of dietary phosphorus on renal function in a shorter time frame than previously studied and (ii) to determine whether NH(4)Cl administration (a) enhances the renoprotective effect of dietary phosphorus restriction and (b) improves renal function in the absence of parathyroid hormone (PTH). METHODS: High (H; 1.2%), normal (N; 0.6%) and low (L; <0.05%) phosphorus diets (PD) were given for 30 days to 5/6 nephrectomized rats. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups were HPD + NH(4)Cl, HPD, NPD + NH(4)Cl, NPD, LPD + NH(4)Cl and LPD. The effect of NH(4)Cl administration was also evaluated in 5/6 nephrectomized, parathyroidectomized (PTX) rats on NPD. RESULTS: In each of the three dietary phosphorus groups, creatinine and urea clearances were greater (P<0.01) in rats receiving NH(4)Cl. Neither creatinine nor urea clearance was reduced by high dietary phosphorus. Urine calcium excretion was greatest in the LPD group and was increased (P < or = 0.001) in all three groups by NH(4)Cl ingestion. An inverse correlation was present between plasma calcium and phosphorus in the parathyroid intact (r = -0.79, P<0.001) and PTX groups (r = -0.46, P = 0.02). In PTX rats, NH(4)Cl ingestion increased (P < or = 0.01) creatinine and urea clearances and both an increasing plasma calcium concentration (r = 0.67, P<0.001) and urine calcium excretion (r = 0.73, P<0.001) increased urine phosphorus excretion. CONCLUSIONS: At 30 days of renal failure (i) NH(4)Cl ingestion increased creatinine and urea clearances, irrespective of dietary phosphorus; (ii) high urine calcium excretion, induced by dietary phosphorus restriction and NH(4)Cl ingestion, did not adversely affect renal function; (iii) high dietary phosphorus did not decrease renal function; (iv) the absence of PTH did not preserve renal function or prevent NH(4)Cl from improving renal function; and (v) both an increasing plasma calcium concentration and urine calcium excretion resulted in an increase in urine phosphorus excretion in PTX rats.