Single nephron filtration,luminal flow and tubular fluid reabsorption along the proximal convolution and the pars recta of the rat kidney as influenced by luminal pressure changes

Summary Intratubular pressures were measured in free flow and after blockade of tubular flow at different distances from the glomerulum in the kidney of Wistar rats. Free flow pressure wasffp=13.3 ±2.5 Torr and stop flow pressuresfp=41.7±3.8 Torr. With increasing distance of the blockade from the glomerulum the intratubular pressure decreased being 22.4±2.1 Torr, when the tubule was blocked at the end of the pars recta. In a second series single nephron filtration rate (gfr) and late proximal flow rates were measured at different intratubular pressures. Free flowgfr _f was 26.5±5.9 nl/min and . The difference of these flow rates divided by tubular length results in a local reabsorption rate ofC=2.9±0.9 nl/min·mm in the proximal convolution. In the pars recta local reabsorption rate was 1.0±0.3 nl/min·mm. In the proximal convolutionC increased with increasing intratubular pressure: ΔC/Δitp=(2.7±1.2)·10⁻² nl/min·mm·Torr. Filtration was in disequilibrium in these animals under all conditions examined, hydraulic filtration conductance wasK=1.2±0.4 nl/min·Torr. Modified methods have been used for intratubular pressure and for flow rate measurements in order to reduce experimental procedure. It is shown, that fractional reabsorption, calculated on the basis of pressure measurements, is a good approximation to results usually obtained by inulin measurements.     

Functional consequences at the single-nephron level of the lack of adenosine A1 receptors and tubuloglomerular feedback in mice

Mice deficient for adenosine A1 receptors (A1AR) lack tubuloglomerular feedback (TGF). In vivo micropuncture experiments were performed under anesthesia in A1AR-deficient and wild-type littermate mice to study the effects of chronic absence of A1AR on fluid and Na⁺ reabsorption along the nephron, as well as the functional consequences at the single-nephron level of the lack TGF. Evidence is provided for an A1AR-mediated tonic inhibition of Na⁺ reabsorption in a water-impermeable segment of the loop of Henle, possibly the thick ascending limb. In contrast, proximal tubular reabsorption of fluid, Na⁺ and K⁺ was unaffected by the chronic absence of A1AR. Experiments in which artificial tubular fluid was added to free-flowing late-proximal tubules demonstrated an essential role of A1AR/TGF in the stabilization of fluid and Na⁺ delivery to the distal nephron. Further, the occurrence of spontaneous oscillations of hydrostatic pressure in proximal tubule (P _PT) at a frequency of about 32 mHz depended on intact A1AR/TGF. In comparison, the normal, stabilizing reduction in P _PT following the initial rise in P _PT during sustained small increases in proximal tubular flow rate does not require A1AR/TGF; TGF-independent mechanisms appear to compensate in this regard for a lack of TGF under physiological conditions and the lack of TGF is unmasked only when supraphysiological flow rates overwhelm TGF-independent compensation.     

Phosphate reabsorption in juxtamedullary nephron terminal segments

Summary Adult Munich Wistar rats undergoing mild salt diuresis (NaCl 20 g·l^–1, 0.1 ml·min^–1) were injected with tracer doses of³H-Inulin and³²P-sodium phosphate in thin descending and ascending limbs of Henle's loop, collecting ducts accessible at the surface of the papilla and early distal superficial tubules. Kidneys were prepared for simultaneous papillary microinjection and urinary flow collection. Expressed in percent of the amounts injected, unidirectional phosphate reabsorption fluxes were 5±1% and 3±1% for injections into early distal superficial tubules and collecting ducts, respectively. By contrast, the flux was 21.7±3% for injections into either the descending or ascending thin limbs of juxtamedullary nephrons. We conclude from these results that in the rat, a significant amount of phosphate is reabsorbed by the juxtamedullary distal tubules and/or the subsequent arcades connecting the juxtamedullary distal tubules to the collecting ducts.     

Time-dependent heterogeneity of filtration rate in the autoreguiating rat kidney

Experiments were performed to study the regulation of the single-nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephrons, as the left kidney of Sprague Dawley rats was submitted to a reduced arterial pressure of 70 mmHg by means of an aortic clamp. The SNGFR at different cortical levels was measured 0.5, 1, 5, 20 or 45 min after the reduction, in order to ascertain whether the effects of the regulatory mechanisms are modified with time. A Hanssen technique was used, which allows one determination of filtration rates per animal. At a renal arterial pressure (RAP) of 100 mmHg (= control animals) the SNGFR amounted to 20±1.2 and 23± 0.8 nlmin^-1–g^-1 kidney weight in the outer and inner cortical (OC, IC) nephrons. When RAP was further reduced to 70 mmHg, the autoregulation of SNGFR, determined after 0.5 min, was highly efficient for both OC and IC nephrons (19 ± 2.0, 23 ± 2.6). A prolonged reduction in RAP caused a gradual decline in SNGFR. The filtration rate measured after 5 min was 15 ±1.4 for OC and 20 ± 1.8 for IC nephrons. The decline was most pronounced for OC nephrons, which led to a fractional redistribution in favour of IC nephrons. Thus, SNGFR_IC/SNGFR_oc was 1.16± 0.065 when RAP was 100 mmHg and 1.41 ± 0.126 after 5 min with an RAP of 70 mmHg. It is well documented that suprarenal aortic occlusion is a powerful stimulus for the release of renin. This was manifested as an increase in the arterial pressure proximal to the aortic clamp. The fractional redistribution to IC nephrons and the loss of autoregulation, when the renal hypotension was sustained, may be an expression of the intrarenal mechanisms attempting to restore RAP. It is likely that the renin/angiotensin system is involved in these processes.     

The tubulo-glomerular feedback mechanism — a determinant for the autoregulation of the glomerular filtration rate in superficial and juxtamedullary nephrons

Summary The intrinsic myogenic hypothesis and the tubuloglomerular feedback mechanism (TGF) give the presently most cherished explanation to the autoregulation of renal blood flow and glomerular filtration rate. A series of experiments was performed on young, normohydrated rats in order to evaluate the importance of TGF as an autoregulatory factor of the single nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephron populations. Micropuncture techniques were applied to tubular structures of the renal surface and on the papilla for the measurement of hydrostatic pressures and SNGFR. The SNGFR was also measured with a modified Hanssen technique. A TV-technique was used to record the urine free flow rate in the loop of Henle.The net driving forces for glomerular filtration at the afferent end of the glomerular capillaries were estimated to be 19 and 47 mm Hg for superficial and juxtamedullary nephrons respectively, when the urine flow at the macula densa was zero. The SNGFR of the two nephron populations amounted to 29.6 and 84.1 nl·min^–1·g^–1 K.W., as measured with the micropuncture technique. With a modified Hanssen technique the corresponding values were 25.8 and 27.7 nl·min^–1. g^–1 K.W. (kidney weight).The SNGFR was found to be well autoregulated when the urine flow at the macula densa was intact, but not when the urine flow was interrupted.The flow rate in the loop of Henle was in free flow conditions 7.3 nl·min^–1·g^–1 K.W. which shall be compared with 19.2 nl·min^–1·g^–1 K.W. when the urine flow to the macula densa was zero.We conclude that SNGFR is mainly autoregulated by the TGF-mechanism in young, normohydrated rats at lower arterial pressures. In normal conditions TGF is highly activated for juxtamedullary nephrons, but not for the superficial ones. The high urine flow rate in the loop of Henle at reduced flow rates at the macula densa may invalidate the use of loop blockade in studies of water and solute transfer across the loop walls.     

The effect of pressor doses of Angiotensin II on autoregulation and intrarenal distribution of glomerular filtration rate in the rat

This study was designed to investigate the effect of pressor doses of exogenous Angiotensin II (AII) on autoregulation and intrarenal distribution of single nephron glomerular filtration rate (SNGFR) in anesthetized, normotensive rats. SNGFR at all cortical levels of the left kidney was measured with a modified Hanssen technique at three renal arterial pressures (RAP): Spontaneous, 100±1 mmHg and 70±1 mmHg. In control rats, both outer cortical (OC) and inner cortical (IC) nephrons showed complete autoregulation of SNGFR when RAP was redced to 100±1 mmHg. Further reduction to 70±1 mmHg resulted in different responses among the cortical layers, accompanying a decrease in SNGFR.The SNGFR_Ic/SNGFR_oc ratio increased from 1.36±0.053 to 1.52±0.047 and a fractional redistribution of glomerular filtration rate towards IC nephrons was seen. When the kidney was submitted to a RAP of 70±1 mmHg, there was a concomitant increase in central arterial pressure (CAP) from 120±4.3 to 134±3.2 mmHg. A continuous i. v.infusion of All (0.5 μg · min^-1· kg^-1 BW) increased mean arterial pressure from 123±1.4 to 142±3.8 mmHg, an effect corresponding to that on peripheral vascular resistance during reduction of RAP to 70±1 mmHg in control rats. This dose reduced SNGFR at all cortical levels, but did not per se lead to redistribution of SNGFR.A reduction in RAP to 100±1 mmHg during All administration resulted in impaired autoregulation of SNGFR in both OC and IC nephrons. Our results show that exogenous All impairs autoregulation and cannot per se have an effect mimicking the fractional redistribution seen in control rats with a reduction of RAP below the limit for autoregulation. However, in this situation intrarenally formed All may still be of importance for autoregulation and distribution of glomerular filtration rate.     

Micropuncture studies on the filtration rate of single superficial and juxtamedullary glomeruli in the rat kidney

Summary Single nephron filtration rates of superficial and juxtamedullary nephrons were determined in high and low sodium rats. Single nephron GFR was calculated from TF/P inulin and tubular flow rate in superficial nephrons and single juxtamedullary GFR from corresponding data in long loops of Henle. In low sodium rats superficial nephron GFR was 23.5±6.4 (SD)×10^–6 ml/min×g KW, juxtamedullary nephron GFR was 58.2±13.6 and total kidney GFR (C _In) was 0.94±0.16 ml/min×g KW. Using these single nephron values, total kidney GFR and a total number of 30,000 glomeruli per kidney, the number of superficial and juxtamedullary glomeruli was calculated to be 23,267 and 6,733, respectively. During high sodium diet superficial nephron GFR increased to 38.1±11.3 and single juxtamedullary GFR decreased to 16.5±6.6, total kidney GFR increasing to 1.01±0.24. Calculation again revealed the same distribution of the two nephron types. End-proximal TF/P inulin in superficial nephrons was 2.36±0.36 in low sodium and 2.31±0.28 in high sodium rats. Loops of Henle TF/P inulin and intratubular flow rate were inversely related: the highest TF/P inulin values and lowest intratubular flow rates were found in the descending limb. These data quantify the distribution of superficial and juxtamedullary nephrons on a functional basis and suggest a mechanism by which the kidney adjusts sodium excretion by altering the contribution of each nephron type to total kidney GFR.Supported by the Deutsche Forschungsgemeinschaft and the U.S. Department of the Army, through its European Research Office.     

Heterogeniety in regulation of glomerular function

The aim was to study differences in filtration driving forces and glomerular filtration rates between superficial and deep nephrons when urine flow rate was altered at the macula densa region. In young rats stop-flow pressures and single nephron glomerular filtration rates (SNGFR) were measured in the superficial proximal tubules and in the loops of Henle in the papilla. SNGFR was also measured with a modified Hanssen technique. The stop-flow pressures of superficial nephrons amounted to 30.9±0.8 mmHg (mean ± SE) and those of juxtamedullary nephrons to 52.2±1.6 mmHg. In the stop-flow condition the net driving filtration forces were calculated to be about 19 mmHg and 50 mmHg for the superficial and deep glomeruli, respectively. In free flow conditions both net driving forces were calculated to be 19 mmHg. The micropuncture technique gave a SNGFR value for superficial nephrons of 29.6±2.9 and for deep nephrons of 84.1±8.5 nl±min^-1 g^-1 kidney weight (KW). With a modified Hanssen technique the corresponding values were 25.8±3.3 and 27.7±2.9 nl. min^-1.g^-1KW. The tubuloglomerular feedback mechanism is considered to have a powerful regulatory influence on the glomerular filtration rate of deep nephrons.     

Micropuncture study of fluid handling in the cat kidney

Summary Superficial proximal and distal tubules of both kidneys of pentobarbital-anesthetized cats, infused with 2.5% (w/v) polyfructosan in Ringer solution at 0.45 ml/min, were micropunctured. Whole one-kidney GFR averaged 4.1 ml/min. SNGFR averaged 15 nl/min in 51 determinations and was proportional to whole-kidney GFR in individual cats. Absolute fluid reabsorption along the length of the accessible portion of the proximal tubule was 1.6 nl/min·mm. The length of the whole proximal tubule was 6 mm as measured from the glomerulum to the descending thin limb of Henle's loop. The length of the distal tubule was 3.5 mm from the macula densa to the first branching of the collecting duct. Proximal fluid was isoosmolar with plasma whereas fluid entering the distal tubule was markedly hyposmolar. Late distal tubular fluid samples were also isosmolar. The cat appears. to be well suited for micropuncture experiments in terms of freedom from respiratory movements and the presence of surface distal tubules.Supported by the Swiss National Science Foundation, Grant 3.3730.74Preliminary communication: Experientia32, 779 (1976)Performed during tenure as an International Exchange Fellow of the Swiss National Science Foundation, Grant 880.292.74     

The influence of tubulo-glomerular feedback on the autoregullation of filtration rate in superficial and deep glomeruli

Single nephron glomerular filtration rate (SNGFR) of superficial and juxtamedullary nephrons were measured at normal and reduced perfusion pressure in the left kidney of young Sprague Dawley rats. Perfusion pressure was lowered by constricting the aorta proximal to the branching of the left renal artery. The influence of the tubulo-glomerular feedback mechanism on SNGFR was quantitated by measuring SNGFR during intact and interrupted urine flow to the macula densa region. By using a modified Hanssen technique, SNGFR was measured under free-flow conditions. In other experiments, the urine flow to the distal nephron was blocked by a micropuncture technique, which was used for collection of the tubular fluid for measuring the filtration rate. All nephron populations autoregulated SNGFR from 70–80 to 130 mmHg, which was the upper limit of this investigation, when urine flow throughout the nephron was intact. The autoregulation in this pressure range was lost when tubular fluid was prevented from reaching the distal nephron. It was shown that the influence of negative feedback on SNGFR by the macula densa mechanism at normal blood pressure is greater in deep nephrons than in superficial ones.     

A mathematical model of fluid transport in the kidney

A mathematical model of the rat kidney is developed from glomerular and tubular submodels. It is assumed that all nephrons are identical, that the hydraulic pressure in the tubules obeys Hagen-Poiseuille's law, that the rate of fluid reabsorption depends on the flow rate of tubular fluid, and that the tubules are distensible. The independent variables of the model are selected to comply with experimental measurements in the hydropenic rat. The model is used to evaluate the mechanism of glomerulotubular balance: changing the mean ultrafiltration pressure in the glomerular capillaries has a substantial influence on glomerular filtration rate (GFR). A change in the rate of fluid reabsorption in the proximal tubules has a strong influence on GFR notwithstanding that the change in GFR is smaller than that in the rate of fluid reabsorption. The calculated values for the hydraulic pressure profile in the tubular system and the interstitial pressure during ureteral obstruction are in close agreement with experimental measurements. Increasing the arterial haematocrit above normal causes a substantial decrease in GFR, whilst reducing it below normal has only a small effect on GFR.     

Dependence of renal protein reabsorption on glomerular filtration rate and infusion time

Egg-white-lysozyme was infused into rats intravenously to achieve plasma concentrations of lysozyme (P_Ly) in the range of 10–3,500 mg·l^–1. Concentrations of inulin and lysozyme in plasma and urine samples were determined spectrophotometrically. The glomerular filtration rate (GFR) was measured as clearance of inulin. The lysozyme reabsorption rate (T_Ly) was calculated as the difference between the filtered load and excreted amount of lysozyme. T_Ly increased with increasing filtered loads of lysozyme up to 1,000 g·min^–1 whether the increase in load was caused by an increase in P_Ly or GFR. These T_Ly were not dependent upon lysozyme infusion time. At lysozyme loads above saturation of reabsorption (1,000 g·min^–1) T_Ly was dependent on GFR and on the passed time after onset of lysozyme infusion. The results of this study indicated that the transport rate of lysozyme is a function of P_Ly, GFR and duration of lysozyme delivery to tubular cells.     

急性力竭运动模型大鼠鱼腥草素干预后的肾滤过屏障变化

背景：大强度急性力竭运动过程中,机体既要承受由于运动强度的增加内脏血流急骤下降的“运动性缺血”,同时随着运动进行,能源物质耗蝎、代谢产物堆积及氧化应激等因素致使机体出现病理损伤,导致机体运动能力下降,那么,其对肾滤过屏障有何影响?肾组织将如何适应其变化?鱼腥草具有清热解毒、利尿通淋、止血、祛痰止咳、镇痛等多种功能,是否对急性力竭运动引起的肾损伤有保护作用及其机制尚未见有文献报道。 目的：探索急性力竭运动对大鼠肾滤过屏障的影响及鱼腥草素的干预作用。 方法：SD大鼠静养与观察3 d,在速度为10 m/min坡度为0°的跑台上进行适应性跑15 min,筛选出24只能完成跑的大鼠,按体质量分层随机分为正常对照组,力竭运动组和运动给药组,各8只。力竭运动组和运动给药组在坡度为10°的动物跑台上进行的一次性力竭运动;运动给药组在运动前30 min腹腔注射鱼腥草素10 mL/kg;正常对照组大鼠不运动。 结果与结论：与正常对照组比,力竭运动组大鼠血清尿素氮、血清肌酐、尿蛋白含量、丙二醛浓度、肾细胞凋亡率及凋亡指数显著增加,肾组织一氧化氮含量和一氧化氮合酶活性明显下降(P < 0.05或0.01),肾小球滤过上皮细胞、基膜及足细胞的肾滤过屏障损害明显,见大量细胞凋亡,偶见坏死;与力竭运动组比,运动给药组大鼠尿蛋白含量、血清肌酐、丙二醛浓度、肾细胞凋亡率及凋亡指数显著下降,肾组织一氧化氮含量和一氧化氮合酶活性明显增加(P < 0.05),肾组织未见明显病理改变,可见细胞凋亡。提示鱼腥草素可使力竭运动诱导的肾细胞损伤减少,考虑可能与凋亡显著减少;并可使一氧化氮合酶含量增加、丙二醛下降及超氧化物歧化酶明显增高有关,从而对力竭运动诱导大鼠肾组织损伤起保护作用。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

Effect of furosemide on local and zonal glomerular filtration rate in the rat kidney

Furosemide has been reported to produce disproportional changes in blood flow in cortical zones and to inhibit tubuloglomerular feedback (TGF), suggesting that furosemide might alter the intracortical distribution of glomerular filtrate. We have tested this hypothesis by a new method for measuring local and total glomerular filtration rate (GFR) based on proximal tubular accumulation of the basic polypeptide aprotinin (mol wt 6513). Local GFR was calculated in tissue samples dissected from outer cortex (OC), inner cortex (IC) and the corticomedullary border zone (CM) from the plasma clearances of two aprotinin tracers injected i. v. before and after a 3 min i. v. infusion of 25 mg kg^-1 furosemide. The mean of five samples from each region was used to determine zonal GFR. Isotonic saline was infused at a rate corresponding to urine flow. Furosemide reduced whole kidney GFR from 1.17 to 1.00 mL min^-1 and gave a similar reduction of renal artery blood flow. Urine flow increased from 0.6 to 17% of GFR. Haematocrit (? 0.48) and plasma protein concentration (? 55 mg mL^-1) were maintained while the arterial blood pressure tended to decline (118pL5 mmHg to 108pL6 mmHg, P < 0.05). GFR in OC, IC and CM (1.58, 1.18, 0.42 mL min^-1 g^-1) fell to 87, 88 and 88% of control after furosemide infusion respectively. The furosemide/control ratio for each sample showed a coefficient of variation of about 3%. We conclude that furosemide produced a modest GFR reduction that was uniform throughout the renal cortex. The homogenous GFR response suggests a similar TGF constriction tone in preglomerular vessels of deep and superficial nephrons.     

Anatomical and functional heterogeneity of nephrons in the rabbit: Microdissection studies and SNGFR measurements

Summary The single nephron glomerular filtration rate (SNGFR) was determined in superficial (S) and juxtamedullary (JM) nephrons of 10 anesthetized rabbits by the¹⁴C ferrocyanide infusion technique. The length of the proximal tubules and the volume of the glomeruli were also determined for the same nephrons. SNGFR was higher in JM than in S: 28.6±3.4 versus 22.6±3.0 nl/min,P<0.001. In JM nephrons, glomeruli were larger than in S: 1.3±0.1 versus 0.9±0.1 nl,P<0.001, whereas there was no difference between proximal tubule length in either category (S, 8.7±0.3 and JM, 8.9±0.5 mm). In 6 out of 8 animals, SNGFR was significantly correlated to glomerular volume. Lack of correlation was observed between SNGFR and length of proximal tubule in all animals but one. These results show that the rabbit, as well as small rodents and the dog, has a higher SNGFR in juxtamedullary than superficial glomeruli. Although this functional difference is not related to the length of the proximal tubule in each individual animal, the ratio between the mean SNGFR value and the mean length of the proximal tubule in superficial rabbit nephrons is similar to the ratio found in other species.     

Aspects in renal physiology

Summary Renal physiology has been concerned with questions about mechanisms of tubular Na reabsorption, the intrarenal regulation of Na excretion and the tubular handling of non-electrolytes.1. The close coupling between Na reabsorption and H⁺ secretion reflects a dependency of the active transport step on intracellular pH.2. Concerning the intrarenal mechanisms for the adjustment of Na excretion it appears that single nephron filtration rate in the different cortical layers is independently regulated. There is growing evidence that the function of the juxtaglomerular apparatus, in particular its renin-angiotensin system, is involved.3. The postulate of active urea transport in the kidney rests largely on clearance data obtained from experiments performed on cartilagenous fish. These elasmobranchs retain urea in order to increase their plasma osmolarity to that of sea level. The concept of active urea reabsorption in these fish may need revision since a countercurrent system has been found which provides a mechanism by which urea may be passively retained (anatomical support to fascilitate net movement of substances lacking active transport).Summary of the opening address delivered to the 4th Annual Meeting of the American Society of Nephrology, Washington, November 23 and 24, 1970.     

Correlation between fluid reabsorption and proximal tubule ultrastructure during development of the rat kidney

Parallel functional and ultrastructural studies were performed in maturing rats in order to elucidate factors determining the development of proximal tubular fluid reabsorption. Three groups of hydropenic animals, which were 22 to 24, 28 to 32 and 40 to 45 days old, were studied. Nephron function was evaluated at the single nephron level by micropuncture technique. The ultrastructure of the developing proximal tubules was analysed by morphometric techniques following fixation of single nephrons. Kidney weight, proximal convoluted tubule length and diameter increased during postnatal development. SNGFR increased from 2.98 to 8.57 and to 20.5 nl/min in respective group of rats whereas proximal tubular fluid reabsorption Jv (a) increased from 0.15 to 0.22 and 0.34 μm³μm^_2-s ^_1. Parallel to the functional development the relative area of lateral and basal cell membrane increased, resulting in a constant relationship between net fluid reabsorption and the lateral and basal cell membrane area during the fourth postnatal week and then only a slight increase in this relation during the further development. The results suggest that net fluid transport during hydropenia is determined by the amount of available lateral and basal cell membranes where the transporting enzyme for sodium is located.     

半胱氨酸蛋白酶抑制剂C联合肌酐评估慢性肾脏病肾小球滤过率的准确性

目的 验证2008年美国CKD-EPI基于半胱氨酸蛋白酶抑制剂C(cystatinc)开发的肾小球滤过率(GFR)评估方程在中国慢性肾脏病(CKD)患者的适用性.方法 选择2008年12月至2009年4月中山大学附属第二医院68例非透析CKD患者,用体表面积标准化Cockcroft-Ganh方程、简化MDRD方程、改良后简化MDRD方程、肾动态显像以及2008年美同CKD-EPI基于eystatin C开发的3条GFR评估方程计算的GFR(分别为cGFR、aGFR、mGFR、gGFR、CyslGFR、Cys2GFR、Cys3GFR),与双血浆法99mTc-DTPA血浆清除率测定的GFR(即tGFR)进行比较分析.结果 Pearson相关分析显示,7种方法GFR估计值与tGFR明显相关,相关系数从大到小依次为Cys3GFR(0.93)、gGFR(0.91)、mGFR(0.89)、Cys2GFR(0.88)、CyslGFR(0.85)、cGFR(0.85)、aGFR(0.83).在准确性比较中,Cys3GFR较aGFR、CysIGFR准确性高.Bland.Altman分析显示Cys3GFR估计值与tGFR的一致性最好,其一致性限度未超过事先规定的专业界值.线性同归结果显示mGFR偏差最小,精确度最高.结论 cystatin C联合肌酐并包括人口统计学参数的方程(Cys3GFR)应用于中国CKD患者准确性较高,与tGFR相关性和一致性最好.且优于仅包括cystatin C GFR估评方程(CyslGFR)、Cockcrofi-Gauh方程、简化MDRD方程.