Intrarenal manometry in the diagnosis of acute rejection superimposed on acute tubular necrosis in renal transplantation

We used fine-needle intrarenal manometry as a guide for detection of acute rejection superimposed on protracted oliguric acute tubular necrosis occurring in the postoperative course of human renal transplantation. We followed intrarenal pressure (IRP) in 31 patients who received 32 renal transplants, 12 from living related donors and 20 from cadaveric donors. There were 19 rejection episodes and 10 episodes of transient cyclosporin A (CyA) nephrotoxicity. Nine patients had posttransplant acute renal failure. Levels of IRP (mmHg) in acute rejection were (mean +/- SD) 48.6 +/- 11.1, significantly higher (p less than 0.001) than the levels in CyA nephrotoxicity (28.2 +/- 5.21), acute tubular necrosis (24.5 +/- 5.5) and normal functioning grafts (26.4 +/- 6.63). Antirejection treatment was associated with return to normal of IRP after 10 days. Intrarenal manometry was performed routinely ever 2-3 days in patients who had postoperative acute renal failure. Increments in IRP were detected on the 7-10th postoperative day in 7 patients who had 10-25 days of post-transplant oliguria. Renal biopsy findings were compatible with acute rejection, and the patients responded to intravenous bolus of steroids. We suggest that fine-needle intrarenal manometry is a reliable test for the detection of acute rejection in circumstances when traditional parameters of altered renal function cannot be evaluated.     

Combination fine-needle aspiration cytology and intrarenal manometry at the onset of renal dysfunction

Twenty-three consecutive cadaveric renal allograft recipients immunosuppressed with cyclosporin have been monitored three times a week by fine-needle aspiration cytology and intrarenal manometry until discharge from hospital or until 30 days post-transplant. Standard criteria were used to determine the cause of allograft dysfunction. The onset of allograft rejection was marked by an elevation of the total corrected increment score by fine-needle aspiration cytology in 80 per cent of rejection episodes whereas intrarenal pressure was raised in only 46.6 per cent. However, intrarenal pressure was greater than 40 mmHg on a single occasion in 16 measurements performed on allografts showing evidence of cyclosporin nephrotoxicity. By combining fine-needle aspiration cytology and intrarenal manometry the sensitivity of these tests for allograft rejection was increased to 93.3 per cent at the onset of renal dysfunction. Our results demonstrate that fine-needle aspiration cytology is more sensitive than intrarenal manometry as a single investigation. However, the combined test may have an important role in the differentiation of allograft rejection and cyclosporin nephrotoxicity in the early management of renal allograft recipients.     

The use of fine-needle intrarenal manometry in the management of renal transplant patients receiving cyclosporine

The pressure inside a renal transplant can be measured by means of a fine (25-G) needle passed into the kidney, and we have shown previously that a rise in pressure to more than 40 mmHg commonly occurs during rejection episodes. A rise was not observed in patients with cyclosporine nephrotoxicity or acute tubular necrosis, so we have now used this test prospectively as part of our management of 37 patients undergoing renal transplantation. Fine needle intrarenal pressure was recorded weekly during the first three weeks after transplantation, with more frequent measures taken in patients with deteriorating or absent renal function. Treatment was dictated by the result of these tests. Deteriorating function in a kidney registering a normal pressure was diagnosed as cyclosporine nephrotoxicity and the dose of cyclosporine was reduced appropriately. A pressure reading in excess of 40 mmHg was regarded as rejection--and, after obtaining a conventional needle biopsy of the kidney, antirejection treatment was commenced immediately. Nineteen episodes of nephrotoxicity were confirmed and there was only one false-positive result. Twenty-eight of twenty-nine rejection episodes (observed in twenty-three patients) were associated with a significant rise in intrarenal pressure and were treated appropriately. In six patients who were oliguric at the time, as a result of posttransplant acute tubular necrosis, this rise in pressure was the first indication of rejection. A high pressure was recorded on the first day that the creatinine rose in two-thirds of the cases. In the remainder the pressure was seen to rise more slowly, particularly when the rejection was of the chronic vascular type and was occurring two months or more after transplantation. Fine-needle intrarenal manometry accurately identified rejection episodes in newly transplanted patients--and, because the results were unaffected by cyclosporine nephrotoxicity and acute tubular necrosis, the test was of most value in monitoring patients with these conditions.     

An assessment of intrarenal hydrostatic pressure measurements in the diagnosis of acute renal allograft rejection

Postoperative intrarenal pressure measurements may be an aid to the diagnosis of acute renal transplant rejection, especially in patients treated with cyclosporine. Serial measurements of intrarenal pressure were made in 38 recipients using a fine-needle technique. Thirty-two intraoperative and 207 postoperative measurements were made, and 39 clinical rejection episodes (23 confirmed by biopsy) monitored. Intraoperative pressures in grafts with immediate function (37.4 +/- 4.0 mmHg, mean +/- SEM) were not significantly different from those with delayed function (30.9 +/- 4.8 mmHg), whereas postoperative pressures were greater (P less than 0.01) in kidneys with acute tubular necrosis (29.4 +/- 1.9 mmHg) than in functioning grafts (20.4 +/- 0.9 mmHg). Pressures recorded during clinical rejection episodes (44.3 +/- 2.3 mmHg) exceeded (P less than 0.001) those during quiescent periods (23.6 +/- 1.0 mmHg). During rejection episodes, higher pressures (P less than 0.01) were recorded from tender or palpably enlarged grafts (52.5 +/- 3.0 mmHg) than in the absence of these signs (36.3 +/- 3.1 mmHg), and patients whose transplants biopsies showed cellular rejection tended to have greater pressures (50.1 +/- 4.1 mmHg) than those with concomitant vasculopathy (36.4 +/- 3.9 mmHg), but the latter did not reach statistical significance. In 7 cases of cyclosporine toxicity the intrarenal pressure was 17.8 +/- 4.2 mmHg. Using a diagnostic cut off point of 40 mmHg, the investigation failed to recognize 26% of acute rejection episodes--and, in the presence of acute tubular necrosis, it wrongly categorized 21% of nonrejectors. While its predictive capacity was limited, the test may occasionally be helpful in the differentiation of cyclosporine toxicity and rejection in functioning kidneys.     

The role of C-reactive protein in graft dysfunction after renal transplantation

PURPOSE: We investigated whether serial daily measurements of serum C-reactive protein could help differentiate episodes of transplant dysfunction due to rejection, infection, cyclosporin A nephrotoxicity or acute tubular necrosis in renal allograft recipients. MATERIALS AND METHODS: Morning serum was obtained daily from 134 patients during the first 30 days after renal transplantation. All episodes of graft dysfunction were recorded and compared to transplant biopsies. C-reactive protein concentrations were correlated with postoperative graft function and the various causes of graft dysfunction. RESULTS: All patients demonstrated an increase in C-reactive protein in response to surgery and a maximum level was reached on day 2 after transplantation. Mean C-reactive protein concentration was significantly increased for delayed (61.50 microg./ml.) compared to primary (mean 38.01) graft function (p = 0.001, Mann-Whitney U test). There were significant increases in C-reactive protein for bacterial infections other than asymptomatic bacteriuria (33.98 microg./ml), interstitial graft rejection (16.43) and acute tubular necrosis (30.50) compared to uneventful courses. C-reactive protein was unchanged for viral infections or cyclosporin A toxicity. CONCLUSIONS: Serial C-reactive protein measurements help to identify renal transplant dysfunction of different origins. However, rejection, infection and acute tubular necrosis show similar patterns of C-reactive protein increase. Thus, C-reactive protein is unable to discriminate the causes of renal graft dysfunction. Biopsy remains the gold standard for the differential diagnosis of renal allograft dysfunction.     

Fine-needle aspiration and puncture biopsies in the diagnosis of lesions of kidney transplants

270 fine needle aspiration and 41 puncture biopsies were fulfilled after 92 cadaveric renal transplantations to diagnose the status of the grafts. With the clinical and ultrasonographic data, the first method proved to be effective in diagnosing acute graft rejection in 79.9% of cases and in determining the status of graft reversibility or irreversibility, but the fine needle aspiration biopsy failed to differentiate the cellular or vascular types of the rejection. The method was also effective in diagnosing the tubular necrosis, acute cyclosporin nephrotoxicity, infectious transplant complications. The paracentetic biopsy essentially supplements the fine needle one and allows one to diagnose chronic cyclosporin nephrotoxicity and chronic transplant rejection. It appears to be the only method revealing the magnitude of graft rejection during oligoanuria caused by ischemic graft lesion. It was concluded that the results of fine needle aspiration biopsy were the most informative within the first postoperative month because later on it becomes difficult to obtain biopsy specimens adequate to interpret the results correctly.     

Immunohistological analysis of renal allograft biopsies from cyclosporin-treated patients: Induced HLA-class II antigen expression does not exclude a diagnosis of cyclosporin nephrotoxicity

Abstract. Differentiation of cyclosporin nephrotoxicity from renal allograft rejection is often difficult. Induction of tubular HLA-class II antigens and elevated levels of leucocyte infiltration are associated with allograft rejection but their association with cyclosporin nephrotoxicity is unclear. In order to determine these relationships, transplant biopsies ( n =32) from patients considered to have cyclosporin nephrotoxicity, allograft rejection or stable graft function were stained with monoclonal antibodies specific for HLA-class II antigens and infiltrating leucocytes. Leucocyte infiltration was elevated during rejection but not in cyclosporin nephrotoxicity or stable graft function. While HLA-class II antigen expression was induced in 71% of the biopsies obtained during clinical rejection, no increased expression was found in the other 29%. Induced antigens were detected in five of the nine biopsies obtained in the presence of cyclosporin nephrotoxicity 90 days after transplantation. In four of these, induction was attributed to prolongation of increased class II expression following previous rejection episodes. Thus, the presence of induced class II antigens in the renal allograft does not exclude a diagnosis of cyclosporin nephrotoxicity.     

Immunohistological analysis of renal allograft biopsies from cyclosporin-treated patients

Differentiation of cyclosporin nephrotoxicity from renal allograft rejection is often difficult. Induction of tubular HLA-class II antigens and elevated levels of leucocyte infiltration are associated with allograft rejection but their association with cyclosporin nephrotoxicity is unclear. In order to determine these relationships, transplant biopsies (n=32) from patients considered to have cyclosporin nephrotoxicity, allograft rejection or stable graft function were stained with monoclonal antibodies specific for HLA-class II antigens and infiltrating leucocytes. Leucocyte infiltration was elevated during rejection but not in cyclosporin nephrotoxicity or stable graft function. While HLA-class II antigen expression was induced in 71% of the biopsies obtained during clinical rejection, no increased expression was found in the other 29%. Induced antigens were detected in five of the nine biopsies obtained in the presence of cyclosporin nephrotoxicity 90 days after transplantation. In four of these, induction was attributed to prolongation of increased class II expression following previous rejection episodes. Thus, the presence of induced class II antigens in the renal allograft does not exclude a diagnosis of cyclosporin nephrotoxicity.     

Acute rejection episodes after renal transplantation in children under cyclosporin A treatment

Thirty-two pediatric renal transplant patients receiving cyclosporin and 34 receiving azathioprine treatment (historical controls) were investigated for the occurrence of rejection episodes; their clinical symptoms and findings, time of onset, influence of donorship, relation to cyclosporin blood levels and graft function outcome were also studied. In the cyclosporin group, four grafts were lost in the 2nd year, while in the azathioprine group five grafts were lost within the first 5 weeks after transplantation due to acute irreversible rejection. Clinical signs of rejection episodes under cyclosporin were mild and usually presented a silent increase of serum creatinine. First rejection episodes occurred later in patients treated with cyclosporin than in azathioprine-treated patients (50% probability after 7 weeks as opposed to 2 weeks). The percentage of patients receiving cyclosporin who had experienced no rejection episodes was 18,8% as opposed to 11,8% of patients receiving azathioprine. The lowest incidence of rejection episodes was observed in patients with living related grafts receiving cyclosporin treatment, 75% of whom were free of rejection episodes after 2 years. Cyclosporin blood levels below 400 ng/ml were observed in 74% of rejection episodes. Biopsies were often used to differentiate between cyclosporin nephrotoxicity and rejection when the cyclosporin levels were above 400 ng/ml. Both treatment groups exhibited a parallel decline in graft function, which correlated with the number of rejection episodes.     

Flow-cytometric measurement of cellular changes in urine: a simple and rapid method for perioperatively monitoring patients after kidney transplantation.

OBJECTIVE: In renal transplant patients having graft dysfunction, it is usually difficult to obtain the accurate diagnosis, such as acute rejection, acute tubular necrosis, infection, or cyclosporin nephrotoxicity. An accurate diagnosis can provide the proper treatment of these patients, thereby lessening the chance of kidney loss. METHODS: A total of 42 patients were enrolled. By using the flow-cytometric technique, the white cell populations of urine in these patients were analyzed and linked to their clinical course. All patients underwent sonography-guided biopsy of the transplanted kidney with a definitive diagnosis. RESULTS: When 10% lymphocytes and 15% granulocytes in urine were set as the cutoff point of a normal ratio threshold, the flow-cytometric analysis presented the highest sensitivity and the highest negative predictive rate for acute tubular necrosis. However, a lower sensitivity and positive predictive rate was found in acute rejection cases. CONCLUSIONS: Our results suggest that flow-cytometric analysis of the urinary cell population can be used as an adjunct in patient follow-up after kidney transplantation.     

A comparison of duplex Doppler ultrasonography and intrarenal manometry in the diagnosis of acute renal transplant rejection

Renal transplant rejection is frequently difficult to differentiate from other causes of renal dysfunction. This study examined the use of duplex Doppler ultrasound and intrarenal manometry in a consecutive series of 73 patients who underwent renal transplantation. Altogether 327 duplex scans were analyzed and, for each, a resistive index (RI) was calculated. A raised RI predicted rejection in patients with grafts that functioned immediately, but not in those that had delayed function. A rise in intrarenal pressure ( greater than or equal to 40 mmHg) indicated the presence of rejection in both groups. However, neither test had a sensitivity of more than 71% and this was not improved by combining the results of the two tests for each patient. Although both tests have a place in transplantation, renal biopsies may still be required to confirm rejection.     

Limited value of 111-indium platelet scintigraphy in renal transplant patients receiving cyclosporine

Since the differential diagnosis between cyclosporine (CyA) nephrotoxicity and acute graft rejection is still a problem in clinical routine, we studied retrospectively the value of 111-indium (In) platelet scintigraphy in 53 patients immunosuppressed with CyA and prednisolone. Autologous platelets were labeled once per week. After daily gamma camera imaging, the platelet deposition in the graft was expressed as platelet-uptake ratio (PUR). The patients were monitored during the first 4-6 weeks after surgery. PUR values measured during an episode of graft dysfunction were compared to the histological diagnosis. The PUR of well-functioning and stable grafts measured 1.07 +/- 0.11 (mean +/- SD). The 111-In platelet scintigraphy failed to register acute interstitial rejection. The PUR values in episodes of chronic vascular rejection, of acute tubular necrosis due to prolonged ischemia times, of tubular CyA nephrotoxicity and of cytomegalovirus (CMV) infection did not differ from the PUR of well-functioning and stable grafts as well. The PUR was significantly increased to 1.48 +/- 0.26 because of a marked platelet deposition in the graft in episodes of acute vascular rejection. In 4 cases of microvascular CyA nephrotoxicity the same phenomenon of significantly increased PUR (1.33 +/- 0.18), could be encountered, too. Two of these 4 cases resembled the hemolytic uremic syndrome (HUS). The value of PUR measurement for diagnosis of acute vascular rejection and microvascular CyA nephrotoxicity together, was: sensitivity 0.62, specificity 0.95, predictive value of positive result 0.64, predictive value of negative result 0.94.(ABSTRACT TRUNCATED AT 250 WORDS)     

No rise in renal Doppler resistance indices at peak serum levels of cyclosporin A in stable kidney transplant patients.

BACKGROUND: The measurement of intrarenal resistance indices by duplex ultrasound plays an important role in the follow-up care of renal transplant patients. Increasing resistance indices indicate rejection episodes, but may also occur e.g. in parenchymal renal diseases. As calcineurin inhibitors induce vasoconstriction both in vivo and in vitro, we studied whether peak serum levels of cyclosporin A led to an acute rise in renal resistance indices via the induction of intrarenal vasoconstriction. METHODS: The acute impact of peak serum levels of cyclosporin A on intrarenal resistance indices was studied in 36 patients after allogeneic renal transplantation. All patients were transplanted for > 6 months and received an immunosuppressive treatment comprising cyclosporin A. Intrarenal resistance indices were measured by duplex ultrasound immediately before (trough serum level) and 2 h after (peak serum level) the oral intake of cyclosporin A at the individual maintenance dose. RESULTS: Compared with renal resistance indices measured at trough serum levels [resistive index (RI) 0.72 +/- 0.07; pulsatility index (PI) 1.40 +/- 0.27], values remained unchanged at peak serum levels of cyclosporin A (RI 0.72 +/- 0.08; PI 1.43 +/- 0.31). Renal resistance indices correlated with the age of the patients, but not with mean arterial pressure or time since transplantation. CONCLUSIONS: The oral intake of cyclosporin A does not induce an acute rise in intrarenal resistance indices in stable transplanted patients. Thus, timing of duplex ultrasound examinations with regard to the intake of cyclosporin A is not necessary in these patients.     

Cyclosporine in treatment of corticosteroid-resistant episodes of rejection

We used cyclosporine (formerly called cyclosporin A) to treat established episodes of kidney-transplant rejection in six patients in whom the use of corticosteroids either was ineffective or was precluded by preestablished side effects. All patients were followed up by using fine-needle aspiration biopsy and transplant aspiration cytology. In four episodes of rejection with typical blast cell--dominated inflammation, the response to cyclosporine was apparently favorable: the inflammatory cells disappeared within days and the transplant resumed its normal function. One episode of acute rejection was overcome within a week after discontinuing treatment with cyclosporine. In one episode of chronic rejection that was devoid of any distinct blastogenic component, no effect of cyclosporine could be detected. We believe that cyclosporine can be used to treat established episodes of rejection, but what type or types of inflammatory episodes are susceptible to cyclosporine must first be clarified through prerandomized clinical trials.     

The importance of urinary thromboxane B2 excretion in the diagnosis of acute renal rejection

To establish whether or not urinary excretion TxB2 is a useful parameter in the diagnosis of acute renal rejection, 45 renal transplant patients were studied and classified in four groups: Group A. Ten observations of satisfactory clinical outcome (without either acute rejection or tubular necrosis). Urinary TxB2 was initially increased but had settled to normal by the 3rd postoperative day. Two patients had subsequent increases. Group B. Twenty-five episodes of acute rejection on a previously satisfactorily functioning graft. Nineteen had increases in TxB2 values before serum creatinine increased. Group C. Five episodes of tubular necrosis without acute rejection. The evolution was similar to Group A. Group D. Nine acute episodes of rejection on kidneys with tubular necrosis. The urinary output of TxB2 was increased from the beginning. This increase was maintained until the rejection was treated. This group had the highest values of urine TxB2. The principal significance of this parameter lies in its precocity and in its utility for diagnosis of acute rejection in the graft with tubular necrosis, as the persistence of raised values of TxB2 in the urine beyond the 3rd postoperative day is highly suggestive of an acute rejection.     

Is There a Therapeutic Range for Monitoring Plasma Cyclosporin in Renal Allograft Recipients?

Sixty-two consecutive adult cadaveric renal allograft recipientshave been monitored by highperformance liquid chromatographyestimations of trough plasma cyclosporin (CsA) concentrationswithin 30 days of transplantation. The CsA estimations duringgraft rejection (mean $ 1 SD 218.6 $ 126.4 ng/ml) were not significantlydifferent from those obtained during stable renal function (232.3$ 172.8 ng/ml), whereas the estimations during episodes of nephrotoxicity(476.0$ 267.3 ng/ml) were significantly greater (P<0.001).During stable renal function 73.7% of estimations were withinthe therapeutic range of 100–350 ng/mI. However, 37.9%of estimations during nephrotoxicity and 76.7% of estimationsduring rejection episodes were also within this range. The therapeutic window for trough plasma CsA estimations isnot clearly defined. It seems that rejection episodes may occurat apparently adequate CsA concentrations, and although mostnephrotoxic episodes are associated with elevated concentrations,acute nephrotoxicity may occur at apparently therapeutic values.However, in this study, some patients at risk of nephrotoxicitywithin 30 days of transplantation were identified as early as7 days post-transplantation by the simple determination of themean trough CsA concentration for days 1–7.     

Diagnosis of tubular injury in renal transplant patients by a urinary assay for a proximal tubular antigen, the adenosine-deaminase-binding protein

Two murine monoclonal antibodies (URO-4 and URO-4a)--which detect different epitopes of a proximal tubular cell glycoprotein antigen, the adenosine-deaminase-binding protein (ABP)--have been formatted into a sandwich enzyme immunoassay for detection of ABP in the urine. Serial urine samples from 34 renal transplant patients during the first six months posttransplant were analyzed to determine the correlation of this test with clinical rejection and cyclosporin (CsA) nephrotoxicity. In 29/29 acute rejection episodes the ABP level was elevated, beginning 1-7 days prior to treatment of rejection. Eighteen patients were treated for rejection with courses of OKT3 or antithymocyte globulin: 0/6 whose ABP level fell to normal during therapy had rerejection; 10/12 whose ABP level remained elevated had rerejection within 7 days of therapy completion. Of 15 patients treated with CsA, 7 had no rejection or drug toxicity; all 7 had normal ABP levels. The remaining 8 had CsA nephrotoxicity, all in association with elevated ABP levels that rapidly fell to normal with decreased CsA dose. An additional 7 patients with creatinine elevations more than 6 months posttransplant were studied: 5 had chronic vascular changes on biopsy, no response to increased immunosuppression, and normal ABP levels; 2 had a cellular infiltrate on biopsy, response to increased immunosuppression, and elevated ABP levels. We conclude that the urinary ABP assay provides information useful in the management of renal transplant patients with acute and chronic rejection and CsA toxicity.     

Fine-needle Aspiration Cytology Monitoring of Elective Conversion from Cyclosporin to Azathioprine and Prednisolone

The elective conversion of renal allograft recipients from cyclosporin(CsA) to azathioprine and prednisolone has the advantage thatthe long-term risk of CsA nephrotoxicity is reduced, but itmay precipitate a rejection episode. We have monitored thisperiod by fine-needle aspiration cytology (FNAC) in 24 patientsundergoing conversion of immunosuppression 6 months after transplantation. As expected the serum creatinine and alkaline phosphatase weresignificantly reduced and the mean creatinine clearance wassignificantly increased after conversion. FNAC exhibited increasedmononuclear cellular infiltration in 13 of the 24 patients.In nine patients there was a transient infiltration of lymphocytesand monocytes without changes in the normal parameters of renalfunction. In four others ‘blast’ cell infiltrationwas evident in association with rejection episodes. All fourresponded to pulsed doses of methylprednisolone. However, twoother patients had late rejection episodes (2 and 6 months afterconversion) which were steroid resistant and required reintroductionof CsA. No grafts were lost (median follow-up 9 months). This study has shown that although overt rejection occurredin only 16.6% of patients, cellular infiltration was presentin over 50% during conversion of immunosuppression. FNAC failedto identify clearly the patients at risk of rejection duringconversion of therapy.     

The value of pulsed Doppler for the follow-up of the transplanted kidney in the first 3 months of transplantation

This prospective study was conducted in 34 consecutive renal transplant patients. Pulsed doppler was used to evaluate the peripheral resistance (PR) in the transplant vessels. Under normal conditions, the PR of the graft is low, resulting in a continuous diastolic blood flow. The intensity of this blood flow was evaluated by means of a resistance index (RI), Pourcelot's index, calculated as follows: RI = systolic peak - end-diastolic peak/systolic peak This study demonstrated values for RI of 0.71 +/- 0.087 in 14 totally asymptomatic patients. In 10 cases of acute rejection, the RI increased to 0.91 +/- 0.12. The 7 patients with acute tubular necrosis had an RI equal to 1. In patients with cytomegalovirus infection of suffering from cyclosporin overdose, the RI was not modified in relation to asymptomatic subjects. This study demonstrates the existence of a rise in the PR in cases of acute rejection and acute tubular necrosis with a sensitivity of 90% and 100% respectively for these two diagnoses. However, this method cannot be used to distinguish between acute rejection and acute tubular necrosis.     

肾移植患者血小板活化指标测定的临床研究

为探讨移植肾排斥反应与血小板活化指标的关系，应用抗人活化血小板ＧＭＰ－１４０（α－颗粒膜蛋白）特异单克隆抗体Ｓｚ－５１（苏州－５１），检测６８例肾移植患者外周血血小板表面及血浆ＧＭＰ－１４０含量；同时采用放射免疫法测定血浆ＴｘＢ２（血栓烷Ｂ２）含量。术后肾功能正常者ＧＭＰ－１４０及ＴｘＢ２略有升高；发生急慢性排斥反应时两者均显著升高（Ｐ＜０．００１），排斥逆转或移植肾切除后逐渐下降。发生环孢素中毒者其含量无明显变化（Ｐ＞０．０５）。提示移植肾排斥与体内血小板活化有关，活化指标ＧＭＰ－１４０、ＴｘＢ２检测对早期诊断肾移植后排斥反应及环孢素中毒具有一定的临床价值，是监测移植肾排斥反应的一个较灵敏的生物学指标。