大鼠肾小体发育中滤过屏障超微结构的演变

目的:探讨大鼠肾小体发育中滤过屏障超微结构的变化规律。方法:采用光镜、电镜技术,并结合体视学分析方法,对不同发育阶段大鼠滤过屏障超微结构的变化进行形态学观察和体视学测量。结果:在肾小体发育过程中,足细胞和内皮细胞的形状逐渐低平,内皮孔增多,足突及裂孔大量分化增多;足细胞下先出现电子密度较低的基膜,随后内皮细胞下才出现基膜,以后,二者融合形成一层电子密度较高的血管球基膜。结论:在大鼠肾小体的发育过程中,足细胞比内皮细胞先分泌基膜,然后二者融合形成血管球基膜。     

一次力竭性离心运动损伤模型大鼠骨骼肌波形蛋白的表达

背景：由于不同学者采用的实验方法不同,对离心运动后细胞骨架蛋白的变化仍有争议。 目的：构建一次力竭性离心运动损伤大鼠模型,观察不同时刻骨骼肌细胞骨架波形蛋白表达的变化。 方法：雄性48只SD大鼠建立下坡跑运动损伤模型,按运动时间分为安静对照组、运动后即刻组、运动后12 h组、运动后24 h组、运动后48 h组和运动后72 h组,每组8只。各运动组大鼠以速度16 m/min,坡度-16°进行跑台运动,运动100 min后,休息5 min,然后再运动100 min;安静对照组不做运动。应用抗波形蛋白抗体对大鼠骨骼肌波形蛋白进行免疫组化染色,通过观察其目标面积百分比的变化反映在一次力竭性离心运动后不同时刻大鼠骨骼肌细胞骨架波形蛋白的表达水平。 结果与结论：大鼠骨骼肌细胞骨架波形蛋白目标面积百分比结果显示,安静对照组和运动后即刻组两组间差异无显著性意义(P > 0.05);与运动后即刻组相比,运动后12 h组目标面积百分比略有增加,但差异无显著性意义(P > 0.05);与运动后12 h组相比,运动后24 h组目标面积百分比略有增加,但差异无显著性意义     (P > 0.05);与安静对照组和运动后即刻组相比,运动后24 h组目标面积百分比有所增加(P < 0.05);与运动后即刻组和运动后12 h组相比,运动后48 h组目标面积百分比明显增加(P < 0.01);与运动后48 h组相比,运动后72 h组目标面积百分比有所下降(P < 0.05),但没有恢复到安静时水平。提示一次力竭性离心运动后,大鼠骨骼肌波形蛋白出现不同程度的表达,在运动后12 h逐渐增加,运动后48 h达峰值,随后波形蛋白表达开始减少。 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：     

急性缺氧小鼠海马CA1区NOS活力和nNOS蛋白表达的时程变化

目的观察急性缺氧小鼠海马CA1区一氧化氮合酶(NOS)和神经元型一氧化氮合酶(nNOS)阳性神经元的时程变化,探讨NO在脑缺氧中的作用并为抗脑缺氧提供依据.方法复制小鼠急性缺氧模型,采用NADPH-d组织化学和nNOS免疫组织化学方法,研究急性缺氧后不同时程点小鼠海马CA1区NADPH-d和nNOS阳性神经元数量的变化.结果与正常对照组相比较,急性缺氧后0.5h组小鼠海马CA1区NADPH-d和nNOS阳性神经元的数量无明显变化,差异无显著性(P＞0.05),3h、6h和12h组逐渐增多并于12h升高达到最高峰,差异有显著性(P＜0.05),而于24h后开始降低,48h恢复正常.结论急性缺氧后早期海马CA1区NOS和nNOS水平明显增多,NO在缺氧所致早期脑损伤中起重要作用.     

玛咖对力竭运动后老年模型大鼠肾脏线粒体呼吸功能及抗衰老能力的影响

BACKGROUND: Studies have shown that Maca can enhance immune cell function, improve mitochondrial respiratory chain enzymes, and play a role in anti-oxidation and anti-aging. OBJECTIVE: To observe Maca effects on kidney mitochondrial respiratory function and anti-aging capabilities in elderly rats after exhausted exercise.  METHODS: 10-month-old elderly rats were intragastrically administrated Maca powder 5 g/kg, once a day, and did treadmill exercise, 5 days in a week. Rats were randomly divided into control group, Maca group and training group and Maca+training group. At 6 weeks after training, rats in each group did exhausted exercise (35 m/min), and immediately received intraperitoneal injection of 2% sodium pentobarbital. The kidney was obtained, and mitochondria were extracted by differential centrifugation. A spectrophotometer was used to measure mitochondrial respiratory chain activity. RESULTS AND CONCLUSION: (1) Mitochondrial respiratory chain enzyme and antioxidant enzyme activity: mitochondrial respiratory chain enzyme I-III, superoxide dismutase and glutathione peroxidase activities were higher in the Maca+training group than in the control group, Maca group and training group (P < 0.05 or P < 0.01), but malondialdehyde content was lower (P < 0.05 or P < 0.01). (2) Results suggested that the combination of supplement Maca and incremental exercise can improve mitochondrial respiratory function and delay aging in the kidney of aged rats after exhausted exercise. Moreover, supplemented Maca and incremental exercise have a synergistic effect. 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     

长期力竭运动动情周期抑制模型大鼠卵巢组织形态和超微结构的变化

背景：研究运动性月经失调女性性腺和卵巢的功能,以及形态学的改变对于探讨运动性月经失调的发生机制具有重要意义。 目的：通过建立长期力竭运动致动情周期抑制大鼠模型,观察卵巢的组织形态和细胞超微结构的变化。 方法：正常3月龄SD雌性大鼠随机分成对照组和模型组,其中模型组大鼠每日进行一次力竭游泳运动直至其动情周期紊乱,取卵巢组织,苏木精-伊红染色,光镜下观察卵巢组织形态变化,电镜下观察卵巢细胞超微结构的变化。 结果与结论：与对照组相比,模型组大鼠卵巢典型生长卵泡和新鲜黄体明显减少,原始卵泡、闭锁卵泡则相对增加,其颗粒细胞、黄体细胞内细胞器明显减少而含有大量的脂滴。提示长期力竭运动可抑制大鼠卵巢卵泡的发育、成熟、排卵与黄体形成,并使卵巢细胞的超微结构发生抑制性改变。     

铁皮石斛黄酮干预力竭运动模型大鼠肝脏氧化应激及自噬水平的变化

背景:适当的运动能够提高机体的抗氧化能力,抑制和延缓氧化应激的发生,激活机体内细胞自噬.但长时间的耐力训练后至力竭运动大鼠肝脏组织氧化应激及自噬机制十分复杂,铁皮石斛黄酮具有抗氧化、调节免疫和抗炎镇痛等作用,运动前补充铁皮石斛黄酮是否能达到保护肝脏组织的目的目前尚不明确.目的:探究铁皮石斛黄酮对力竭性运动大鼠肝脏组织氧...     

急性缺氧小鼠海马CAl区NOS活力和nNOS蛋白表达的时程变化

目的:观察急性缺氧小鼠海马CAl区一氧化氮合酶(NOS)和神经元型一氧化氮合酶(nNOS) 阳性神经元的时程变化,探讨NO在脑缺氧中的作用并为抗脑缺氧提供依据。方法:复制小鼠急性缺氧模型,采用NADPH-d组织化学和nNOS免疫组织化学方法,研究急性缺氧后不同时程点小鼠海马CAl区NADPH-d 和nNOS阳性神经元数量的变化。结果:与正常对照组相比较,急性缺氧后0.5h组小鼠海马CAl区NADPH-d 和nNOS阳性神经元的数量无明显变化,差异无显著性(P>0.05),3h、6h和12h组逐渐增多并于12h升高达到最高峰,差异有显著性(P<0.05),而于24h后开始降低,48h恢复正常。结论:急性缺氧后早期海马CAl区NOS和nNOS水平明显增多,NO在缺氧所致早期脑损伤中起重要作用。     

力竭运动后大鼠海马NF-κB、BDNF的表达变化

目的:观察力竭运动后大鼠海马NF-κB、BDNF在不同时间点的表达变化,探讨中枢神经系统的损伤及修复机制。方法:雄性SD大鼠70只,随机分为对照组(n=10)和力竭组(n=60)。力竭组进行6周力竭游泳训练后,选择0、4、8、12、16、24 h等不同时间点取脑,采用免疫组织化学和Western Blot技术观察海马内NF-κB、BDNF的表达变化。结果:(1)Western Blot结果显示:与对照组相比,力竭组海马内NF-κB含量在4 h开始升高(P<0.05),8 h达峰值(P<0.05),12～16 h开始回落(P<0.05),24 h恢复到正常水平(P>0.05)。力竭组海马内BDNF含量12 h及16 h组与对照组比较,BDNF的表达明显升高(P<0.05);(2)免疫组织化学结果显示:与对照组相比,力竭训练后0 h组大鼠海马内NF-κB表达以胞浆表达为主,4 h组核内表达逐渐增多(P<0.05),8 h组达高峰(P<0.05),12～24 h组核内表达逐渐减少(P>0.05)。海马内BDNF免疫阳性神经元则在力竭后24 h内持续表达且高于对照组(P<0.05),并于12 h达峰值(P<0.05),其余力竭各组之间差异无显著性(P>0.05)。结论:(1)大鼠力竭游泳运动可以活化海马内NF-κB信号转导系统,后者可能与运动性脑缺血再灌注时的神经细胞凋亡密切相关;(2)力竭运动可能通过诱导海马内BDNF的表达上调,对抗力竭运动性脑损伤,对神经元起到保护作用。     

原花青素干预大负荷运动大鼠腓肠肌相关凋亡蛋白的表达

背景：大负荷运动后给机体带来的损伤与运动后延迟性肌肉酸痛及运动疲劳有相关性。 目的：观察原花青素对大负荷运动后大鼠腓肠肌自由基代谢和细胞凋亡相关蛋白FAS、肿瘤坏死因子表达的影响。 方法：48只成年雌性SD大鼠随机均分为2组。给药组每日灌服10 g/L原花青素水溶液,安慰剂组灌服等量蒸馏水,再将2组大鼠随机分为安静组、运动后即刻及运动后24 h 3个亚组。2周后,除两安静组外其余各组进行一次坡度为-10°、20 m/min大负荷跑台运动。于运动前(安静时)、运动后即刻和运动后24 h断颈处死大鼠。取左后肢腓肠肌进行指标检测。 结果与结论：①运动后即刻两组超氧化物歧化酶活性有下降的趋势,其中给药组活性比安慰剂组下降的幅度小。运动后即刻两组丙二醛含量显著升高,其中安慰剂组升高的幅度高于给药组。运动后各时相给药组超氧化物歧化酶/丙二醛比值降低,幅度要明显小于安慰剂组。②运动后两组腓肠肌细胞FAS蛋白表达显著升高,安慰剂组FAS蛋白表达明显高于给药组。③运动后各时相安慰剂组肿瘤坏死因子表达明显高于给药组。表明原花青素对大鼠一次性大负荷运动后腓肠肌微损伤及凋亡在一定程度上有缓解和抑制作用。     

去卵巢后雌性大鼠下丘脑视前区NOS阳性神经元形态学和突触素表达的变化

目的：为解释围绝经期的精神、神经症状提供实验依据。方法：采用免疫细胞化学方法显示去卵巢雌性大鼠下丘脑视前内侧区(MPA)和视前外侧区(LPA)内NOS阳性神经元,形态学改变以及突触素表达。结果：(1)去卵巢组和对照组大鼠的视前内、外区内可见大量NOS阳性神经元;(2)去卵巢动物的下丘脑内NOS阳性神经元突起长度比对照组的明显变短,分支明显变少;(3)去卵巢组动物下丘脑内突触素表达比对照组的明显减少。结论：大鼠去卵巢后,由于雌激素分泌减少,导致了NOS阳性神经元的突起减少和突触减少,结果NO介导的神经元信号传导失常,这些变化可能是引发围绝经期的精神、神经症状的原因之一。     

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.     

Changes in the glomerular filtration rate after unilateral nephrectomy in rats

Changes in the glomerular filtration rate (GFR) were studied in rats, 4 h to 4 weeks after unilateral nephrectomy (NX). The GFR was determined with a technique using⁵¹Cr-EDTA and a single timed blood sample. The GFR determined in this way corresponded with the GFR calculated by two compartment analysis and with the plasma levels of creatinine and urea.Increases in the GFR, compared with half the GFR of sham operated rats, were observed as early as 4 h after NX. This increase was entirely due to an increase in the GFR per gram of kidney, since no increase in kidney weight was observed at that time. After the initial increase, the GFR remained at that level during the first 48 h after NX. At 48 h a significant increase in kidney weight per 100 g body weight had taken place. The longterm changes in the GFR amounted to an increase of about 80% of that of sham operated rats after 3–4 weeks. After 4 weeks, the increase in the GFR of the remaining kidney was due to an increase in kidney weight of 35% as well as an increase in the GFR per gram of kidney of 20%.These data indicate that the increase in the GFR of the remaining kidney after unilateral NX occurs rapidly and is independent of an increase in kidney weight. Compensatory hypertrophy develops at a later stage and helps to maintain the increased function of the single remaining kidney.Supported by the Sophia Foundation for Medical Research     

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.     

Novel routes of albumin passage across the glomerular filtration barrier

Albuminuria is a hallmark of kidney diseases of various aetiologies and an unambiguous symptom of the compromised integrity of the glomerular filtration barrier. Furthermore, there is increasing evidence that albuminuria per se aggravates the development and progression of chronic kidney disease. This review covers new aspects of the movement of large plasma proteins across the glomerular filtration barrier in health and disease. Specifically, this review focuses on the role of endocytosis and transcytosis of albumin by podocytes, which constitutes a new pathway of plasma proteins across the filtration barrier. Thus, we summarize what is known about the mechanisms of albumin endocytosis by podocytes and address the fate of the endocytosed albumin, which is directed to lysosomal degradation or transcellular movement with subsequent vesicular release into the urinary space. We also address the functional consequences of overt albumin endocytosis by podocytes, such as the formation of pro‐inflammatory cytokines, which might eventually result in a deterioration of podocyte function. Finally, we consider the diagnostic potential of podocyte‐derived albumin‐containing vesicles in the urine as an early marker of a compromised glomerular barrier function. In terms of new technical approaches, the review covers how our knowledge of the movement of albumin across the glomerular filtration barrier has expanded by the use of new intravital imaging techniques.     

Adaptive changes of juxtamedullary glomerular filtration in the remnant kidney

The participation of surviving juxtamedullary nephrons in the adaptive changes of glomerular filtration that occur in response to loss of functioning nephron mass was examined by direct micropuncture of the rat renal papilla. The solitary remnant kidney (RK) in rats with an 85% reduction of renal mass demonstrated strikingly elevated values for single nephron glomerular filtration rate (SNGFR) in both superficial (46.1±3.2 nl/min) and juxtamedullary (73.5±6.1 nl/min) nephrons in comparison to respective values observed in normal hydrophenic rats (superficial SNGFR=15.0±1.9nl/min,P<0.001, and juxtamedullary SNGFR=30.2±3.2 nl/min,P<0.001). In RK rats, the proximal portions of both superficial and juxtamedullary nephrons exhibited a marked increase in absolute fluid reabsorption as well as a markedly enhanced delivery of fluid to more distal portions of the nephron. These observations indicate that similar, not preferential, functional adaptations in glomerular filtration occur concommitantly in both superficial and juxtamedullary nephrons consequent to reduction of renal mass.     

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.     

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.     

Studies on the mechanism of reduction in glomerular filtration rate after benzolamide

In previous studies, we have shown that benzolamide, a carbonic anhydrase inhibitor with diuretic activity confined primarily to the proximal tubule, causes a significant reduction in nephron filtration rate by increasing afferent and efferent arteriolar vascular resistance [30], possibly through an activation of tubuloglomerular feedback mechanism. The present studies were designed to determine if infusion of 1-sar, 8-ala angiotensin II, an angiotensin II receptor antagonist (AIIA) could prevent and reverse the vasoconstriction and resulting reduction in SNGFR with benzolamide. Benzolamide administration to hydropenic rats decreased SNGFR by 5.0±1.3 nl/min and AIIA infusion in these rats completely restored SNGFR to the control, prebenzolamide values. These results occurred when SNGFR was measured in both proximal and distal tubules. In another group of hydropenic rats prior AIIA infusion completely prevented any alteration in SNGFR with benzolamide administration (33.0±2.8 vs. 32.3±1.5 nl/min). Benzolamide administration did increase the late proximal tubular flow rate during AIIA infusion (17.2±1.1 to 23.4±1.1 nl/min,P<0.01), demonstrating that AIIA did not act by preventing the diuretic action of benzolamide in the proximal tubule. AIIA infusion alone did not alter control SNGFR or nephron plasma flow, suggesting that the effect of AIIA was not that of a non-specific vasodilator. These studies suggest that the renal vasoconstriction and reduction in SNGFR which results from benzolamide administration is mediated by the local action of angiotensin II.     

Association of plasma fatty acid-binding protein 3 with estimated glomerular filtration rate in patients with type 2 diabetes mellitus

Background: Fatty acid-binding protein 3 (FABP3) located in renal mesangial and distal tubular cells, and had been shown to be a sensitive marker of renal injury, potentially be a mediator in pathogenesis of chronic kidney disease (CKD). Our previous study revealed that plasma FABP1 and FABP2 were independently associated with CKD, however, little is known about the relationship between plasma FABP3 level and CKD. The aim of this study was therefore to evaluate the plasma levels of FABP3 at different stages of estimated glomerular filtration rate (eGFR) in patients with type 2 diabetes mellitus (T2DM).Methods: A total of 334 subjects with T2DM who enrolled in a disease management program were included in this study and stratified according to eGFR. Plasma FABP3 concentrations were measured by an enzyme-linked immunosorbent assay.Results: FABP3 levels increased in parallel with the eGFR level. Increasing concentrations of FABP3 were independently and significantly associated with eGFR stage G2-G4. Age- and sex-adjusted FABP3 levels were positively associated with uric acid, urinary albumin-to-creatinine ratio, FABP1, FABP2, and fatty liver index, but negatively associated with eGFR and hemoglobin.Conclusion: Our results indicate that circulating FABP3 in patients with T2DM is associated with eGFR, which suggests that increased plasma FABP3 may be involved in the pathogenesis of CKD.