Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. Part II--Kidney hypertrophy and calcium deposition.

BACKGROUND: Kidney hypertrophy is stimulated by both partial nephrectomy and NH(4)Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH(4)Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (ii) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition. METHODS: High (HPD, 1.2%), normal (NPD, 0.6%) or low (LPD, <0.05%) phosphorus diets were given to 5/6 nephrectomized rats for 30 days. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups of rats were: (i) HPD + NH(4)Cl; (ii) HPD; (iii) NPD + NH(4)Cl; (iv) NPD; (v) LPD + NH(4)Cl and (vi) LPD. In a separate study, PTX was performed to determine whether PTH affected renal hypertrophy in 5/6 nephrectomized rats given NH(4)Cl. RESULTS: Both with and without NH(4)Cl (+/-NH(4)Cl), kidney weight was greatest (P<0.05) in the HPD groups. In each dietary phosphorus group, kidney weight was greater (P<0.05) in the NH(4)Cl group. In both the +/-NH(4)Cl groups, kidney calcium content was greatest (P<0.05) in the HPD group, but was less (P<0.05) in the NPD and HPD groups given NH(4)Cl. An inverse correlation was present between creatinine clearance and kidney calcium content (r = -0.51, P<0.001). When factored for kidney weight, creatinine clearance was less (P<0.05) in the HPD group in both the +/-NH(4)Cl groups, but was greater in the HPD + NH(4)Cl than in the HPD group. In PTX rats, kidney weight was greater (P<0.05) and kidney calcium deposition was less (P<0.05) in rats given NH(4)Cl. CONCLUSIONS: In azotaemic rats studied for 30 days, NH(4)Cl administration induced kidney hypertrophy. A HPD also induced kidney hypertrophy. The effects on kidney calcium deposition were divergent for which NH(4)Cl administration decreased and a HPD increased calcium deposition. The inverse correlation between kidney calcium content and creatinine clearance suggests that kidney calcium deposition is harmful to renal function. When factored for kidney weight, the lower creatinine clearance in the high phosphorus group suggests that kidney hypertrophy does not completely compensate for the harmful effects of a HPD. This result also suggests that a longer study would probably result in more rapid deterioration in the high phosphorus group. In PTX rats, the absence of PTH did not prevent NH(4)Cl from inducing kidney hypertrophy and reducing kidney calcium deposition. In conclusion, NH(4)Cl and dietary phosphorus each independently affect kidney growth and calcium deposition in the growing rat with renal failure.     

The interaction of PTH and dietary phosphorus and calcium on serum calcitriol levels in the rat with experimental renal failure

BACKGROUND.: Renal failure results in decreased calcitriol production, akey factor in the development of secondary hyperparathyroidism.Phosphorus accumulation and high parathyroid hormone (PTH) levels,both inherent to renal failure, have different effects on calcitriolproduction; moreover, dietary calcium loading may have a separateinhibitory effect on calcitriol production. This study was designedto evaluate the relative effects of PTH and dietary phosphorusand calcium on serum calcitriol levels. METHODS.: Renal failure was surgically induced and rats were divided intonormal, moderate renal failure, and advanced renal failure basedon the serum creatinine. Each group was subdivided and receivedeither a highphosphorusdiet (HPD, 0.6% Ca, 1.2% P) or highcalcium diet (HCaD, 1.2% Ca, 0.6% P) for 14–16 days to determinethe relative effects of dietary calcium andphosphorus loadingon serum calcitriol. In addition the effect of PTH and phosphoruson calcitriol stimulation was determined with a 48-h PTH infusioncombined with either a low (0.16%) or high (1%) phosphorus dietsboth diets had negligible calcium (<0.05%) RESULTS.: With decreasing renal function, PTH increased and was greaterin rats fed the HPD than the HCaD; serum calcitriol decreasedas renal function decreased and was lower in normal rats andrats with moderate renal failure fed a HCaD (P < 0.01). Thecalcitriol response to a PTH infusion decreased as renal functiondecreased (P <0.05) but was greater on a low- (0.16%) thana high- (1%) phosphorus diet (P<0.05) CONCLUSION.: Dietary calcium loading either directly decreases serum calcitriolor acts by modifying the stimulatory effect of PTH; the stimulatoryeffect of PTH on serum calcitriol is modified by dietary phosphorus;in moderate renal failure, serum calcitriol levels depend ona complex interaction between PTH and dietary calcium and phosphorus;and in advanced renal failure, serum calcitriol levels are lowand are difficult to stimulate, presumably because of the lossof renal mass.     

Effect of aluminium on the development of hyperparathyroidism and bone disease in the azotaemic rat

Aluminium toxicity in dialysis patients is associated with arelative parathyroid hormone (PTH) deficiency as well as osteomalacia.In-vitro studies of parathyroid cells have shown that aluminiuminhibits PTH secretion. However, only limited data are availableon how aluminium affects the development of hyperparathyroidismin the azotaemic animal. Four groups of azotaemic rats werestudied; in each group, renal failure was induced by a two-stage5/6 nephrectomy, after which rats were studied for 40 days.In three groups hyperparathyroidism was stimulated by the useof a high phosphorus (1.2%) diet (HPD). The four groups were(1) HPD; (2) HPD+high-dose aluminium (HDAL)—1.5 mg ofaluminium was adminis tered intraperitoneally (IP) 5 days perweek; (3) HPD+low-dose aluminium (LDAL)—0.5 mg of aluminiumwas administered IP 5 days per week; and (4) moderate phosphorus(0.6%) diet (MPD); the MPD group was used to control hyperparathyroidismand thus provide a comparison of PTH levels and azota emic bonedisease. After 40 days, the serum PTH level was higher (P<0.05)in the HPD+HDAL group (37±2pmol/l) than the HPD, HPD+LDAL,and MPD groups (24±3, 28±4, and 6±1 pmol/lrespect ively). The correlation between serum PTH and calcium,serum PTH and phosphorus, and serum calcium and phosphorus wassignificant for the four groups (P<0.02); however, the relationshipbetween serum PTH and calcium, and between serum calcium andphosphorus was altered in the HPD+HDAL group (serum aluminium30.8±2µmol/l). Aluminium administration induceda decrease (P<0.05) in the bone formation rate and the adjustedapposition rate, and an increase (P<0.05) in osteoid volumeand the min eralization lag time. Despite aluminium administration,diet-induced hyperparathyroidism resulted in an increase (P<0.05)in the osteoblast surface. In conclusion, in the azotaemic rat(1) aluminium did not slow the development nor decrease themagnitude of hyper parathyroidism; (2) aluminium appeared toalter the relationship between serum PTH and calcium, and betweenserum calcium and phosphorus; (3) hyperpara thyroidism changedthe expression of aluminium-induced bone disease and may affordthe bone some protection against the toxic effects of aluminium.     

Renal osteopontin protein and mRNA upregulation during acute nephrotoxicity in the rat.

BACKGROUND: The effect of segment-specific proximal tubular injury on spatio-temporal osteopontin (OPN) distribution was determined in two different nephrotoxic rat models to evaluate its conceivability with a possible role for OPN in acute renal failure (ARF). OPN gene expression was further determined in proximal and distal tubular cells to investigate the origin of increased renal OPN. METHODS: Renal OPN protein and mRNA expression were compared in the rat during mercuric-chloride- vs gentamicin-induced ARF using immunohistochemistry and in situ hybridization. RESULTS: Mercuric chloride primarily induced tubular injury and subsequent cell proliferation in proximal straight tubules (PST), whereas gentamicin predominantly injured proximal convoluted tubules (PCT). In both models, the distribution of OPN protein was associated with increased OPN mRNA levels in proximal as well as distal tubular cells. However, upregulation was delayed in the proximal tubular segment suffering most from injury, i.e. PCT in gentamicin ARF vs PST in mercuric-chloride ARF. OPN immunostaining at the apical cell membrane from distal tubules was in contrast to perinuclear vesicular staining in proximal tubular cells. CONCLUSIONS: OPN gene and protein expression is induced in both proximal and distal tubular cells during rat toxic ARF. The distinct subcellular localization in proximal vs distal tubular cells indicates differences in OPN processing and/or handling. The spatio-temporal distribution is consistent with a possible role in renal injury and regeneration.     

How dietary phosphate, renal failure and calcitriol administration affect the serum calcium-phosphate relationship in the rat.

BACKGROUND: The effect of hyperphosphataemia on serum calcium regulation in renal failure has not been well studied in a setting in which hypercalcaemia is not parathyroid hormone (PTH) mediated. In azotemic rats with a normal serum calcium concentration, an increased dietary phosphate burden affects serum calcium regulation because of its effects on skeletal resistance to PTH, calcitriol production, and possibly intestinal calcium absorption. Our goal was to determine how hyperphosphataemia affected the development of hypercalcaemia during calcitriol-induced hypercalcaemia and PTH suppression in azotemic rats with established hyperparathyroidism. METHODS: Rats underwent a two-stage 5/6 nephrectomy or corresponding sham operations. After surgery, rats were given a high phosphate diet (P 1.2%) for 4 weeks to exacerbate hyperparathyroidism and were then changed to a normal diet (P 0.6%) for 2 weeks to normalize serum calcium values in the azotemic rats. At week 7, rats were divided into five groups and sacrificed after receiving three intraperitoneal doses of calcitriol (CTR, 500 pmol/100 g) or vehicle at 24 h intervals. The five groups and dietary phosphate content were: group 1, normal renal function (NRF)+0.6% P+vehicle; group 2, NRF+0.6% P+CTR; group 3, renal failure (RF)+0.6% P+vehicle; group 4, RF+1.2% P+CTR; and group 5, RF+0.6% P+CTR. Both the 0.6% and 1.2% phosphate diets contained 0.6% calcium. RESULTS: Serum creatinine values were increased (P<0.05) in 5/6 nephrectomized rats (groups 3, 4 and 5), as were serum calcium values (P<0.05) in CTR-treated rats (groups 2, 4 and 5) and serum phosphate values (P<0.05) in CTR-treated azotemic rats (groups 4 and 5). Serum PTH values were suppressed (P<0.05) in CTR-treated hypercalcemic rats (groups 2, 4 and 5) and increased (P<0.05) in azotemic rats not given CTR (group 3). In the azotemic groups (groups 3, 4 and 5), an inverse correlation was present between serum calcium and phosphate in each group, despite a wide variation in serum calcium values. The slope of the inverse relationship between serum calcium and phosphate was steeper in CTR-treated azotemic rats on a 1.2% phosphate (group 4) diet than on a 0.6% phosphate (group 5) diet (P=0.02). Thus, for a similar increase in the serum phosphate concentration, serum calcium values decreased more in group 4 than in group 5. The independent effect of dietary phosphate on serum calcium values was also confirmed by analysis of covariance. Finally, the serum calcium concentration was shown to be greater for any given serum phosphate value in CTR-treated rats than in those not on CTR. CONCLUSIONS: In azotemic rats with calcitriol-induced hypercalcaemia, the magnitude of hypercalcaemia is affected by: (i) the serum phosphate concentration; and (ii) differences in dietary phosphate content. Calcitriol administration also acts to shift upwards the relationship between serum calcium and phosphate so that a higher serum calcium concentration can be maintained for any given serum phosphate value.     

The impact of improved phosphorus control: use of sevelamer hydrochloride in patients with chronic renal failure.

Phosphorus control is a primary goal in the care of patients with end-stage renal disease (ESRD). Sevelamer hydrochloride, a novel calcium-free, aluminum-free phosphate binder, allows physicians to control serum phosphorus in patients with ESRD without increasing serum calcium levels or contributing an excess calcium load. Clinical studies have shown that sevelamer provides sustained reduction in markers of soft-tissue and cardiac calcification, specifically serum phosphorus, calciumxphosphorus product, parathyroid hormone and also improves blood lipid profiles. Thus, sevelamer hydrochloride offers the promise of impacting cardiac calcification and thereby reducing patient morbidity and mortality. Long-term studies are underway to evaluate these potential benefits. This paper reviews sevelamer studies to date and addresses ongoing strategies for improving clinical management of phosphorus in ESRD.     

钙通道阻断剂在急性肾衰时抗氧自由基损伤的实验研究

通过测定SD大鼠缺血性急性肾衰时肾组织XOD活力和LPO含量的变化。发现由钙依赖蛋白酶激化的XOD活力明显增高,LPO含量亦明显增高。而给予钙通道阻断剂Verapamil组大鼠肾组织内XOD和LPO均降低,肾组织超微结构损害明显减轻,并能改善肾功能,提高存活率。表明Verapamil在急性肾衰时通过抑制XOD活力,减少氧自由基的生成而达到保护肾脏的作用。     

Dominant factors of the phosphorus regulatory network differ under various dietary phosphate loads in healthy individuals

BackgroundThe purpose of this study was to explore the contribution of each factor of the phosphorus metabolism network following phosphorus diet intervention via Granger causality analysis.MethodsIn this study, a total of six healthy male volunteers were enrolled. All participants sequentially received regular, low-, and high-phosphorus diets. Consumption of each diet lasted for five days, with a 5-day washout period between different diets. Blood and urinary samples were collected on the fifth day of consumption of each diet at 9 time points (00:00, 04:00, 08:00, 10:00, 12:00, 14:00, 16:00, 20:00, 24:00) for measurements of serum levels of phosphate, calcium, PTH, FGF23, BALP, α-Klotho, and 1,25 D and urinary phosphorus excretion. Granger causality and the centrality of the above variables in the phosphorus network were analyzed by pairwise panel Granger causality analysis using the time-series data.ResultsThe mean age of the participants was 28.5 ± 2.1 years. By using Granger causality analysis, we found that the α-Klotho level had the strongest connection with and played a key role in influencing the other variables. In addition, urinary phosphorus excretion was frequently regulated by other variables in the network of phosphorus metabolism following a regular phosphorus diet. After low-phosphorus diet intervention, serum phosphate affected the other factors the most, and the 1,25 D level was the main outcome factor, while urinary phosphorus excretion was the most strongly associated variable in the network of phosphorus metabolism. After high-phosphorus diet intervention, FGF23 and 1,25 D played a more critical role in active regulation and passive regulation in the Granger causality analysis.ConclusionsVariations in dietary phosphorus intake led to changes in the central factors involved in phosphorus metabolism.     

中药对慢性肾衰竭氮质血症及肾血流参数的影响

目的 :探讨中药参麦注射液及复方丹参注射液对慢性肾衰 (CRF)病人血尿素氮、肌酐的治疗作用及其延缓CRF的机制。方法 :1992年～ 1999年本院肾科住院病人 148例 ,BUN11～ 42mmol/L ,Scrl177～ 44 2 μmol/L ,Ccr10～ 2 5ml/min之间。入院后随机分为两组 ,参麦组 (SMI) 76例 ,复方丹参组 (FDI) 72例 ,分别使用参麦注射液或复方丹参注射液 2 0ml,加入 5 %葡萄糖液中静脉滴注 ,每日 1次 ,15d为一疗程。定期复查血象、肝肾功能、彩色多普勒能量图 (CDPI) ,检测肾血流参数、收缩期峰值 (Vmax)、舒张末期流速 (Vmin)、肾血管阻力指数 (RI) ,随访 3年 ,并作相关分析。结果 :治疗后两组病人临床症状均有明显改善 ,BUN、Scr均有降低 ,但参麦组更为明显 ,总有效率 93.4% ;RI与BUN相关系数分别为 0 .78,0 .6 1;Vmin与BUN、Scr的相关系数分别为 - 0 .91、- 0 .75 ;3年后 ,SMI组 86 .4%的病人病情稳定 ,未进入尿毒症期 ;FDI组有 6 2 .4%的病人Scr稳定在 177～ 44 2 μmol/L之间。 结论 :中药SMI、FDI均是治疗CRF有效药物 ,SMI更为明显 ,其改善氮质血症及延缓CRF的进展机制与改善肾动脉血流参数Vmax、Vmin及RI有关。彩色多普勒能量图不仅对肾血流参数的诊断很有价值 ,而且对治疗效果的监测和指导用药也很有意义。     

Effect of dietary phosphate on Na+-dependent phosphate cotransporters function and expression in the rat kidney

Background Three types (typeI, II, andIII) of sodium-dependent phosphate cotransporters have recently been isolated and shown to be expressed in the mammalian kidney. Understanding of the functional roles and regulation of each transporter is still fragmented, however. Methods We analyzed the functional roles of each transporter by using antisense oligonucleotides in theXenopus oocytes expression system, and by localization in the proximal tubules of rat kidney using immunohistochemistry. Results Phosphate uptake in brush border membranes was increased by about 2 times in rats fed a low-phosphate, as compared with a high-phosphate, diet. Expression of typeI, II, andIII transporter mRNAs was observed in renal poly(A)⁺RNA, isolated from the rats fed a low-phosphate diet. Phosphate uptake increased about 2.5-fold inXenopus oocytes injected with the poly(A)⁺RNA, compared with those given RNA from rats fed a high-phosphate diet. Hybrid depletion of the typeII sodium-dependent phosphate transporter (NaPi-2), but not of the typeI (rNaPi-1) or typeIII transporters (PiT-1 and PiT-2), significantly decreased phosphate transport activity in oocytes injected with the poly(A)⁺RNA from each experimental group rat kidney. In rats fed the lowphosphate diet, NaPi-2 immunoreactivity increased markedly in the brush border membranes of renal proximal tubular cells, whereas rNaPi-1 protein was not changed. Conclusion This study suggests that the typeII transporter functions mainly as a sodium-dependent phosphate cotransporter, and is regulated by dietary phosphate in the rat kidney.     

Effect of dietary protein restriction on the progression of renal failure: a prospective randomized trial

One hundred twenty-eight patients with different renal diseasesand chronic renal failure, stratified according to the underlyingdisease, were enrolled in a randomized controlled trial to investigatethe effects on the rate of decline of renal function of twodiets, a controlled protein diet (CPD) of 1 g protein/kg idealbody-weight (i.b.w.)/day, and a low-protein diet (LPD) of 0.6g protein/kg i.b.w./day, given for 27.1±21.8 months.Dietary compliance was assessed by a dietary questionnaire,dietary interviews and measurement of 24-h urinary urea excretion.At the end of 6 months, actual mean protein intake was higherthan expected (1.06±0.25 g/kg i.b.w./day) in CPD patients,and (0.80±0.21 g/kg i.b.w./day) in LPD patients: valueswere similar at 12 and 18 months after the time of enrollment.The end-point, defined as halving of creatinine clearance, wasreached in 40% of patients on CPD, and in 28.6% of those onLPD (P= 0.038 by comparative life-table analysis). Multivariateregression analysis confirmed that CPD was associated with ahigher risk of progression than LPD, and that two additionalparameters (creatinine clearance at the time of randomizationand average proteinuria during the follow-up) were significantindependent risk factors, even more important than protein intake.     

Influence of Vasoactive Substances on Early Toxic Acute Renal Failure in the Dog

The influence of different vasoactive substances on the evolutionof HgCl₂-induced acute renal failure (ARF) was evaluated inthe dog. HgCl₂ alone caused a progressive fall in both glomerularfiltration (GFR) and renal blood flow (RBF) during the first3 h of the mercury administration ( after 3 h:–44% and–39%) and provoked a concomitant stimulation of the renin-angiotensin(RAS) and thromboxane systems. The administration of the thromboxaneinhibitor dazoxiben (2 mg/kg i.v. every 2 h) adequately inhibitedthe activation of the thromboxane system after HgCl₂, but couldnot prevent the fall in GFR and RBF. The continuous intrarenaladministration of the Ca²⁺ entry blocker verapamil (0.005 mg/kgper min) into the left kidney resulted in the prevention ofthe postmercurial fall in GFR and RBF at the perfusion site.This beneficial effect was immediately lost when the verapamiladministration was stopped. Finally, the administration of theconverting enzyme inhibitor captopril (300 µg/kg every2 h) resulted in an effective inhibition of the renin-angiotensinsystem. the prevention of the postmercurial fall in RBF, andthe partial attenuation of the fall in GFR. This beneficialeffect was immediately lost after the intravenous administrationof indomethacin (2 mg/kg). These results indicate that the fall in GFR after HgCl² canbe prevented by vasoactive agents such as captopril and verapamiland point at least in part to a pathophysiological role of therenin-angiotensin system or of an alteration in the equilibriumbetween renin-angiotensin and prostaglandins. The thromboxanesystem is seemingly of no major importance.     

Renal and systemic effects of continued treatment with renin inhibitor remikiren in hypertensive patients with normal and impaired renal function.

BACKGROUND: Remikiren is an orally active renin inhibitor with established antihypertensive efficacy. As a single dose it induces renal vasodilatation, suggesting specific renal actions. Data on the renal effects of continued treatment by renin inhibition are not available, either in subjects with normal, or in subjects with impaired renal function. METHODS: The effect of 8 days of treatment with remikiren 600 mg o.i.d. on blood pressure, renal haemodynamics, and proteinuria was studied in 14 hypertensive patients with normal or impaired renal function.The study was conducted on an ambulatory in-hospital basis and was designed in a single-blind, longitudinal order. RESULTS: Remikiren induced a significant peak fall in mean arterial pressure of 11.2+/-0.8%, with corresponding trough values of -6+/-0.8%. This fall was somewhat more pronounced in the patients with renal function impairment (-13.3 vs -9.6%; P<0.01). Glomerular filtration rate remained stable, whereas effective renal plasma flow increased from 301+/-35 to 330+/-36 ml/min/1.73 m(2) (P<0.05). Filtration fraction and renal vascular resistance fell by 10+/-2% and 15+/-2% respectively (both P<0.01). Remikiren induced a cumulated sodium loss of -82+/-22 mmol and a positive potassium balance of 49+/-9 mmol (both P<0.01). During remikiren, proteinuria fell by 27% (range -18 to -38%; P<0.01) in the patients with overt proteinuria at onset (n=6). In the remainder of the patients albuminuria fell by 20% (range -1 to -61%, P<0.05). No side-effects were observed. CONCLUSIONS: Continued treatment with remikiren induced a sustained fall in blood pressure, renal vasodilatation, negative sodium balance, and a reduction in glomerular protein leakage. These data are consistent with a renoprotective potential of renin inhibition.     

Modification of mesangial cell function by ambient chloride is absent in Dahl salt sensitive rat

Summary: We previously reported that the normally present modification of mesangial cell function by ambient chloride concentration ([Cl]) and insulin was lacking in mesangial cells obtained from spontaneously hypertensive rats (SHR). This aberrant modification of the mesangial cell might be related to the development of hypertension. In this study, we examined if a similar aberrant modification of mesangial cell function by [Cl] and insulin was present in Dahl salt sensitive (DS) rats, which develop hypertension in a NaCl dependent manner. Similar to our previous reports on mesangial cells from normal rats, pre-treatment with low [Cl] apparently attenuated Ca responses induced by angiotensin II and vasopressin in mesangial cells cultured from Dahl salt resistant (DR) rats. In contrast, this attenuation of vasoactive agents-induced Ca signal was absent in the DS rat derived-mesangial cells. Also, the enhancement of prostaglandin E2 production caused by decrease in [Cl] was not observed in the DS rat mesangial cells, while prostaglandin E2 production by DR rat mesangial cell was stimulated when [Cl] was decreased. In contrast, vasopressin-induced Ca signal by insulin was attenuated in both DR and DS rat mesangial cells. Thus, in DS rat mesangial cells, modification of mesangial cell function by [Cl] was absent, but it was different from SHR mesangial cells because insulin was maintained.     

血清钙磷乘积预测老年椎体压缩性骨折风险的意义

目的 研究血清钙磷乘积能否作为预测骨质疏松性椎体压缩性骨折（osteoporotic vertebral compression fracture, OVCF）发病危险性的血清学指标。方法 本研究随机纳入我院2015年8月至2021年4月老年人OVCF患者200名为观察组和同期行因股骨头坏死或骨关节炎行髋、膝关节置换术的患者200名为对照组,收集两组患者的年龄、性别、既往病史(高血压、糖尿病)、入院时初次生化指标主要包括白蛋白、尿素氮、血清肌酐、血清钙、血清磷数值等,并进行统计学分析。结果 观察组白蛋白、血清钙、血清磷、钙磷乘积、校正血钙、校正钙磷乘积均低于对照组,差异有统计学意义（P < 0.05）。经多因素Logistic回归分析显示低数值的血清钙、血清磷、钙磷乘积、校正血钙、校正钙磷乘积均能作为OVCF患者的危险因素。同时,通过绘制ROC曲线得出钙磷乘积、校正钙磷乘积预测骨质疏松性椎体压缩性骨折发病风险的效果良好。其中,钙磷乘积预测效果最佳,对应临界值为29.88,灵敏度0.72,特异性0.62;其次为校正钙磷乘积,对应临界值为30.50,灵敏度0.74,特异性0.62。结论 钙磷乘积及校正钙磷乘积可以作为预测老年人OVCF发病危险性的血清学指标。针对这项危险因素可以早期进行临床干预以进一步降低OVCF的发生风险。     

Renal function and morphometry in the dwarf rat following a reduction in renal mass

BACKGROUND.: The compensatory increase in glomerular filtration rate (GFR)and effective renal plasma flow (ERPF) which follows a reductionin renal mass may be mediated by growth hormone, a renal vasodilator. METHODS.: GFR, ERPF and glomerular morphometry were assessed in the dwarfrat, selectively deficient in GH, and compared its Lewis basestrain. Studies were performed 21-days after sham-operation,unilateral nephrectomy or subtotal nephrectomy in age-matchedanimals. GFR and ERPF were assessed from the renal clearanceof inulin and p-aminohippurate measured under barbiturate anaesthesia. RESULTS.: The dwarf rat had a lower GFR and ERPF than the Lewis rat, inproportion to its lower body weight and lower kidney weight.Kidneys from the dwarf rat had a similar number of glomerulito the Lewis, but smaller glomerular components in proportionto a lower kidney weight. Following unilateral nephrectomy,GFR (dwarf $ 58%, Lewis $ 53%) and ERPF (dwarf $ 58%, Lewis$ 52%) increased to a similar degree in both rat strains. Glomerulardiameter, volume and capillary surface area increased in proportionto kidney growth, although compensatory renal growth (dwarf$ 62%, Lewis $ 78%) was somewhat lower in the dwarf. Following5/6 subtotal nephrectomy, GFR (dwarf $ 143%, Lewis $ 171%) increasedto a similar degree in both rat strains while ERPF (dwarf $108%, Lewis $ 48%) and compensatory renal growth (dwarf $ 115%,Lewis 86%) were greater in the dwarf than the Lewis rat. Subtotalnephrectomy was also associated with an increase in the thicknessof the glomerular basement membrane in both rat strains. CONCLUSIONS.: The results do not support a role for GH in the compensatoryincrease in renal function or hypertrophy which follows a reductionin renal mass, excluding this as a potential mechanism for GH-dependentrenal scarring.     

The Effect of Pre-existing Ischaemic Heart Disease on Renal Dysfunction in Cardiac Transplant Recipients

Renal dysfunction is a recognized complication of cardiac transplantation and can impact on the life expectancy of an already fragile population. A large proportion of these patients require transplantation because of the consequences of ischaemic heart disease (IHD) which, in turn, is often associated with ischaemic nephropathy. We studied the effect of IHD, diagnosed prior to transplantation, on the renal function of recipients who survived more than 6months after surgery. Of the 168 patients transplanted in a single centre over 15 years, 132 were included in the study. Renal dysfunction was defined as a serum creatinine consistently above 200 micromol/L (2.26 mg/dL). Analysis confirmed that IHD was an independent risk factor for developing renal impairment. In transplant recipients with IHD, closer monitoring is warranted to detect and prevent renal dysfunction or to retard its progression.     

肾七方加大黄灌肠汤联合治疗慢性肾衰竭疗效观察

目的:探讨慢性肾衰竭(CRF)的有效治疗措施.方法:将96例CRF患者随机分为两组.治疗组54例,对照组42例.治疗组在一般治疗(优质低蛋白、低磷饮食及对症治疗)基础上配合口服自拟肾七方及中药大黄灌肠汤保留灌肠,14 d为1疗程,连续2个疗程后观察疗效.对照组为一般治疗.两组均加用及静脉滴注黄芪注射液和川芎嗪注射液.观察对比治疗前后临床症状血肌酐(Scr)、尿素氮(BUN)、血红蛋白(Hb)的变化.结果:治疗组总有效率81.48%,显著优于对照组54.76%.结论:肾七方加大黄灌肠联合治疗CRF疗效明显,能保护肾功能,延缓肾衰竭的发展.     

Renal Ischemic Injury Affects Renal Hemodynamics and Excretory Functions in Sprague Dawley Rats: Involvement of Renal Sympathetic Tone

The role of renal sympathetic nerves in the pathogenesis of ischemic acute renal failure (ARF) and the immediate changes in the renal excretory functions following renal ischemia were investigated. Two groups of male Sprague Dawley (SD) rats were anesthetized (pentobarbitone sodium, 60 mg kg^?1 i.p.) and subjected to unilateral renal ischemia by clamping the left renal artery for 30 min followed by reperfusion. In group 1, the renal nerves were electrically stimulated and the responses in the renal blood flow (RBF) and renal vascular resistance (RVR) were recorded, while group 2 was used to study the early changes in the renal functions following renal ischemia. In post-ischemic animals, basal RBF and the renal vasoconstrictor reperfusion to renal nerve stimulation (RNS) were significantly lower (all p < 0.05 vs. control). Mean arterial pressure (MAP), basal RVR, urine flow rate (UFR), absolute and fractional excretions of sodium (U_NaV and FE_Na), and potassium (U_KV and FE_K) were higher in ARF rats (all p < 0.05 vs. control). Post-ischemic animals showed markedly lower glomerular filtration rate (GFR) (p < 0.05 vs. control). No appreciable differences were observed in urinary sodium to potassium ratio (U_Na/U_K) during the early reperfusion phase of renal ischemia (p > 0.05 vs. control). The data suggest an immediate involvement of renal sympathetic nerve action in the pathogenesis of ischemic ARF primarily through altered renal hemodynamics. Diuresis, natriuresis, and kaliuresis due to impaired renal tubular functions are typical responses to renal ischemia and of comparable magnitudes.