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PubMed1991

Detection of allograft endothelial cells of recipient origin following ABO-compatible, nonidentical cardiac transplantation.

Endothelial cells serve an important role in augmenting immune responses through enhanced expression of MHC class II antigens. Immune-mediated vascular injury associated with rejection requires reendothelialization to restore vascular integrity. The origin of the reparative endothelial cells can be determined when ABO antigens expressed on these cells differ in the donor and recipient. To assess the frequency and significance of reendothelialization by recipient endothelial cells, we stained serial endomyocardial biopsies for ABO antigens in 34 (13%) compatible, nonidentical cardiac allograft recipients of 268 cardiac transplant procedures. In ten (30%) the allograft endothelial cells expressed the characteristics of the recipient (five partial and five complete) within 7.5 +/- 1.0 months (mean +/- SEM) after transplantation. Over 26.3 +/- 2.5 months follow-up no differences could be detected in pretransplant characteristics, allograft survival, survivor rejection morbidity, long-term allograft function, and presence of coronary vasculopathy between those whose endothelial cells expressed recipient blood group antigens and those who did not, which may merely be a reflection of the small sample size. This study indicates that recipient reendothelialization occurs frequently following cardiac transplantation and may result from immune-mediated vascular injury. The effect of recipient reendothelialization on allograft tolerance requires further investigation.

ABO Blood-Group System↗

PubMed2004

Pancreas-after-kidney transplantation: an increasingly attractive alternative to simultaneous pancreas-kidney transplantation.

BACKGROUND: Historically, the clinical acceptability of pancreas-after-kidney (PAK) transplantation has been hampered by relatively high acute rejection rates and lower pancreas graft survival rates when compared with the more commonly performed simultaneous pancreas-kidney (SPK) transplantation. The purpose of this study was to compare PAK transplantation to SPK transplantation in the Thymoglobulin induction era. METHODS: The authors reviewed all bladder-drained PAK (n=47) transplants receiving rabbit antithymocyte globulin induction from June 1998 to June 2002 and compared them with SPK (n=25) transplants during the same time period at their institution. The authors retrospectively studied data on demographics, patient survival, graft (pancreas and kidney) survival, complications, and biopsy-proven rejection episodes. RESULTS: The actuarial 1-year patient survival was 93% for the PAK group versus 100% for the SPK group (P =not significant [NS]). The actuarial 1-year pancreas graft survival was 87% for the PAK group versus 92% for the SPK group (P =NS). Waiting time for PAK was significantly shorter than for SPK (6.3 +/- 5.2 vs. 16.2 + -13.7 months, P <0.05). Clinical acute rejection rates were similar in the two groups (4.3% for PAK vs. 4.0% for SPK). PAK recipients demonstrated a greater decline in renal function after transplantation compared with SPK. A multivariate analysis failed to elucidate the cause. CONCLUSIONS: Newer immunosuppressive regimens allow PAK transplant patients to achieve immunologic outcomes similar to SPK transplant patients. Although the shorter waiting time and the ability to use living-donor kidneys make PAK an increasingly attractive alternative to SPK transplantation, its effect on renal allograft function deserves further attention.

Antilymphocyte Serum↗

PubMed1995

Downregulation of intragraft IFN-gamma expression correlates with increased IgG1 alloantibody response following intrathymic immunomodulation of sensitized rat recipients.

A single intrathymic injection of donor-specific spleen cells (2 x 10(7)) abrogates accelerated (24 hr) rejection of LBNF1 cardiac allografts in presensitized LEW rats and prolongs graft survival to about 11 days. This effect is donor-specific, gamma-irradiation-sensitive, thymus-dependent, and requires no concomitant therapy. We have recently shown that following intrathymic alloantigen administration, there is an earlier and increased systemic production of alloreactive IgM, and subsequently a premature isotype switching to IgG with the predominant IgG1 and IgG2a alloantibody responses. There is also a preferential binding of these IgG subclasses to the endothelium of well-functioning allografts. In this work, we analyzed the early cell activation and related cytokine elaboration patterns at the mRNA and protein levels by competitive template RT-PCR and immunohistochemistry, respectively. We found that prolonged cardiac allograft survival following intrathymic administration of donor spleen cells in presensitized rats was associated with markedly depressed intragraft IFN gamma mRNA and protein expression. Moreover, intrathymic allostimulation has led to a defect in the IL-2 pathway as the expression of IL-2 and IL-2R protein at the graft site was inhibited despite stable IL-2 mRNA levels. The inhibition of cell activation was also demonstrated by reduced MHC class II and the lack of ICAM-1, and TNF-alpha expression by immunohistochemistry. The expression of biologically active IL-12 (p70) by mononuclear and endothelial cells was detected in rejecting grafts between 3 and 12 hr. The well-functioning grafts after intrathymic allostimulation were devoid of IL-12 (p70), which in turn may have contributed to the downregulation of IFN-gamma mRNA and protein. Treatment with r.IFN-gamma, but not with r.IL-2, recreated the rejection response, and the characteristic IgG subclass pattern associated with accelerated graft loss. Hence, intrathymic immunomodulation with alloantigen results in selective inhibition of IFN-gamma-producing cells and a preferential upregulation of IgG1 alloantibodies. These data support the notion of the interlocked immunoregulatory roles of cytokine and alloantibody networks in rat allograft recipients.

Animals↗

PubMed2002

A Monocyte chemoattractant protein-1 (MCP-1) polymorphism and outcome after renal transplantation.

Among the factors modulating transplant rejection and cardiovascular disease, chemokines and their respective receptors deserve special attention. In this respect, increased expression of MCP-1 and the corresponding receptor CCR2 have been demonstrated in renal transplant rejection and coronary artery disease. The impact of the MCP-1-2518G and CCR2-64I genotypes on renal allograft function was investigated in 232 patients who underwent transplantation over an 11-yr period. Genomic DNA was genotyped using PCR with sequence-specific primers followed by restriction fragment length polymorphism analysis. Eighteen (7.8%) patients were homozygous for the MCP-1-2518G mutation. The G/G allele of MCP-1 -2518 behaved as a determinant for long-term allograft survival and resulted in reduction of the mean graft survival, as compared with the heterozygous (A/G) or wild-type (A/A) allele (67 +/- 14 versus 95 +/- 4 mo; Log rank P = 0.0052). The 64I mutation of CCR2 had no effect on kidney graft failure (93 +/- 6 and 91 +/- 5 mo, respectively; P = 0.81). None of the investigated polymorphisms showed a significant shift in gene frequency in acute rejection and rejection-free groups. In conjunction with these findings, peripheral blood mononuclear cells from kidney transplant recipients carrying the G-allele were characterized by a 2.5-fold higher MCP-1 secretion (P < 0.05). In conclusion, recipients of renal transplants homozygous for the -2518 G mutation of the MCP-1 gene are at risk for premature kidney graft failure. This variant of MCP-1 may be a future predictor for long-term kidney graft failure.

Acute Disease↗

PubMed1992

Success of kidney transplantation in oxalosis is unrelated to residual hepatic enzyme activity.

We evaluated hepatic alanine glyoxylate aminotransferase (AGT) activity in percutaneous hepatic biopsy material obtained from four children with long-term renal allograft function following transplantation for primary hyperoxaluria type 1 (PH 1). The study was performed to determine whether these successes had occurred because relatively high residual levels of AGT activity had introduced a selection bias. The children ranged from seven months to eight years at transplant and are currently well 7 to 11 years later, with no oxalate deposition on repeated allograft biopsies and creatinine clearances of 80 to 128 ml/min/1.73 m2. AGT activity ranged from 0 to 13.8%, and in two of three patients with detectable levels the AGT was in mitochondria rather than peroxisomes. These results indicate that long-term renal allograft success can occur in spite of severe AGT deficiency. Thus, the therapeutic choice of kidney alone versus combined kidney-liver transplant cannot currently be made by measuring residual hepatic AGT in PH 1. Kidney transplant alone remains a reasonable initial therapeutic alternative for patients with recent onset of renal insufficiency due to PH 1.

Adolescent↗

PubMed2005

Low serum magnesium is associated with decreased graft survival in patients with chronic cyclosporin nephrotoxicity.

BACKGROUND: Hypomagnesaemia is a common side effect of cyclosporin A (CsA) therapy. Animal studies suggest that magnesium (Mg) supplementation inhibits chronic CsA nephropathy. METHODS: To determine if low Mg levels correlate with true CsA-induced nephrotoxicity in humans, we examined kidney transplant biopsy records at our centre for all transplant biopsies performed between 1990 and 2002. We simultaneously reviewed the medical records to determine whether serum Mg levels were checked at the time of biopsy. Those individuals with histologically proven CsA nephrotoxicity were studied. RESULTS: Serum total Mg levels were available for 320 patients, 60 of whom were diagnosed with chronic CsA-mediated nephropathy. Patients were divided in two groups, a low Mg [n = 29, 1.8 (1.67-1.9) mg/dl or 0.74 (0.68-0.78) mmol/l] and a normal Mg group [n = 31, 2.2 (2.0-2.4) mg/dl or 0.9 (0.82-0.98) mmol/l, P<0.05] based on the median Mg level in the entire cohort (2 mg/dl or 0.82 mmol/l). Both groups were analysed for disease progression and graft loss using the slope of creatinine clearance (CCR) and multivariate analyses. Although the CCR at the time of biopsy was greater in the low Mg group [44.3 (36.3-64.3) ml/min vs 37.8 (25.2-47.3) ml/min, P<0.05), the decline in graft function was faster in this group (-8.9+/-3.5 vs 1+/-2.7 ml/min/year; P = 0.02) compared with the normal Mg cohort. Using Cox proportional hazards analyses, the adjusted graft survival was significantly reduced in the low Mg group 5 years after biopsy. CONCLUSIONS: Our study demonstrates that low serum Mg levels were associated with a faster rate of decline in kidney allograft function and increased rates of graft loss in renal transplant recipients with chronic CsA nephropathy. This suggests that hypomagnesaemia could potentiate CsA-mediated nephropathy.

Adult↗

PubMed2002

Pulmonary vein gas analysis for assessing donor lung function.

BACKGROUND: Radial artery oxygenation (PaO2) is the standard method for assessing potential lung donors. This study was proposed to assess the use of pulmonary vein gases (PvO2) in selection of donor lung for transplantation. METHODS: We studied 170 lungs from 85 consecutive donors. Lungs were classified into group A, PaO2 and PvO2 > 300 mm Hg; group B, PaO2 < 300 mm Hg, and PvO2 > 300 mm Hg; and group C, PvO2 < 300 mm Hg. RESULTS: Lungs retrieved from group A and group B were used for transplantation. Allograft function, assessed by the arterial and alveolar oxygen tension ratio, was similar at 12 hours and at 24 hours after operation (0.69, 0.73, vs 0.70, 0.71, for groups A and B, respectively (p = 0.8, 0.7, respectively). Similar radiologic appearance was seen in both groups (p = 0.2). Median duration of intubation was also similar (p = 0.6). The 30-day mortality rate was 12% versus 11.3% (p = 0.8), and 1-year survival rate was 80% versus 82% (p = 0.8) for recipient received lungs from group A and B donors, respectively. CONCLUSIONS: Selective pulmonary veins analysis gives an accurate assessment of individual gas exchange in comparison with arterial PaO2, identifying more potential donor lungs for transplantation.

Adult↗

PubMed1981

Patient and graft survival in amputated versus nonamputated diabetic primary renal allograft recipients.

Between September 23, 1968 and March 22, 1980, primary renal allografts were performed in 373 uremic patients with insulin-dependent diabetes. After transplantation 65 of the diabetic patients (17%) underwent 151 amputations involving at least a digit or a limb. The lower extremity was involved in 72% of the amputations. Twenty-four patients had only one procedure, while 41 required multiple procedures. Mean interval from transplantation to first amputation was 25.2 +/- 2.4 (SE) months. Patient and graft loss (perioperative risk) in the first 3 months after amputation was 13%. Diabetic renal allograft recipients living long enough to require amputation have more severe manifestations of vascular disease. These amputees display both an 11% lower patient and graft survival after the first year following transplantation, as well as an accelerated rate of graft loss following amputation. Those diabetics requiring an amputation do significantly more poorly than nonamputees of the corresponding demographic category if diabetes onset occurred at age 10 to 20 years, diabetes duration prior to transplant was less than 20 years, age at transplant was less than 30 years, dialysis duration was less than 4 months, and donor type was HLA-nonidentical related. Nevertheless, more than 50% of the diabetics undergoing amputation will be alive with functioning allografts 4 years after amputation. On the other hand, diabetics not requiring amputation do particularly well if they survive 1 year, with more than 80% chance that they will be alive with a functioning graft 4 years after transplantation.

Adult↗

PubMed1991

Recombinant human growth hormone treatment of children following renal transplantation.

Nine growth-retarded renal allograft recipients received either thrice weekly or daily subcutaneous recombinant human growth hormone (rhGH) for 6-30 months. The annualized growth velocity for the initial year of rhGH treatment was significantly greater than that of the preceding year (2.5 +/- 2.1 vs 5.7 +/- 2.7; P less than 0.0001). There was no advancement in bone age greater than the increase in chronological age, no significant increase in the mean fasting serum glucose or insulin levels, nor significant decrease in the calculated creatinine clearance following rhGH treatment. However, two patients experienced rejection episodes following rhGH treatment indicating the potential adverse consequences of the treatment on allograft function. This will require further delineation in prospective controlled studies. The serum insulin-like growth factor-1 levels significantly increased at 6 months (P less than 0.009) and 12 months (P less than 0.002) following rhGH treatment compared with baseline values. These preliminary data indicate that rhGH treatment may be effective in improving the growth velocity of growth-retarded renal allograft recipients.

Adolescent↗

PubMed1994

Postrenal transplant erythrocytosis: further evidence implicating erythropoietin production by the native kidneys.

True erythrocytosis is a relatively common complication of successful renal transplantation. From a group of 17 patients with post-transplant erythrocytosis (PTE), four underwent selective venous catheterization of the native and transplanted kidneys because of arterial hypertension. In three who presented with active PTE at the time the procedure was performed the peripheral blood (PB) concentration of EPO was elevated, and the level of erythropoietin (EPO) in native kidney veins was significantly higher than the PB and allograft EPO levels. Additionally, only one of the three cases had high levels of plasma renin activity (PRA). The fourth patient showed normal levels of EPO and PRA in PB and in venous blood from the native and transplanted kidneys. However, the PTE had subsided 4 months before the performance of the catheterization after he redeveloped terminal renal failure; the loss of a functioning allograft might have blunted the overproduction of EPO by the native kidneys. In conclusion, in patients with PTE, inappropriate EPO production seems to originate from the diseased native kidneys, and there seems to be no correlation between the production of EPO and the PRA.

Adult↗

PubMed1990

Donor antigen-specific immunosuppression in cadaveric and living-related donor kidney allograft recipients.

This is a review of the University of Alabama Hospital's clinical experience with 1-haplotype-mismatched LRD renal transplants, utilizing a stored-blood DST protocol and with cadaveric renal transplants utilizing DBM transfusion. Stored-blood DST does not significantly improve LRD allograft survival either in Aza-, P-, or CsA-treated patients, although there is a trend toward better survival in Aza/DST versus Aza/no-DST recipients (78% vs 84% 12-month allograft function). Importantly, although the early acute phase graft loss was slightly diminished by DST, the late phase loss (slope of curve) was essentially identical to nontransfused patients. Thus, we cannot demonstrate a beneficial effect by the use of DST in achieving improved long-term graft survival in recipients of 1-haplotype-matched recipients. The use of cryopreserved DBM transfusions in cadaveric allograft recipients, however, has resulted in significantly improved survival compared to control patients who received the marrow donor's contralateral kidney and similar immunosuppression without marrow infusion [92% vs 73% (p = 0.01)]. DBM-transfused patients demonstrate diminished donor-specific responsiveness in MLC compared with controls. P withdrawal can be accomplished safely in the majority of marrow recipients; however, this has not been tested in the controls. Donor-nucleated cells persist in the peripheral blood of some DBM-transfused patients for at least 2 years following transplantation. Presently, the significance of persistent chimerism in these patients with respect to donor responsiveness and allograft tolerance is unclear.

Azathioprine↗

PubMed1994

[Acute postoperative renal insufficiency in renal transplantation. Incidence and risk factors].

Delayed renal function (DFG) is known to influence both the short and long-term outcome of transplanted kidneys. Data collected retrospectively on all 129 cadaveric renal transplants performed between January 1991 and January 1993 within a single center were analyzed. 42 (32.55%) cases of acute renal failure (ARF) occurred during the immediate postoperative period and 28 patients required dialysis. When compared with immediate good allograft function, DGF was associated with previous failed transplant (7/15 vs 35/114, p = 0.01), donor age (39.2 +/- 13 vs 30.1 +/- 12 years, p = 0.01), and episodes of collapsus of the donor (11/25 vs 31/104, p < 0.01). The graft function of the recipient was not correlated with the serum creatinine of the donor. There was no apparent relationship between the cold ischemia or the anastomosis time and the occurrence of DGF. One-year patient and graft survival were similar in the two groups (respectively for the group ARF and without ARF: 96.4% and 96.5%; 88.8% and 89%), but patients with DGF had higher serum creatinine values at 12 months post DGF (185.6 +/- 44.8 mumol/l vs 157.5 +/- 30.8 mumol/l, p = 0.06). This study suggests that DGF is related to the characteristics of the donor graft and is more frequently encountered in previously transplanted recipients.

Acute Kidney Injury↗

PubMed2005

Selectin blockade plus therapy with low-dose sirolimus and cyclosporin a prevent brain death-induced renal allograft dysfunction.

Both antigen-dependent and -independent factors influence long-term organ allograft function and survival. Brain death (BD), a significant antigen-independent, donor-related injury upregulates a variety of inflammatory mediators in peripheral organs. One of the earliest responses to such an insult is the expression of selectins by endothelial cells of the transplanted tissues; these in turn trigger a cascade of nonspecific events, that enhance host alloresponses and which may be worsened by toxic effects of long-term immunosuppression. Using a rat model in which donor BD accentuates subsequent renal allograft injury, we have tested the effects of therapy with recombinant P-selectin glycoprotein ligand (rPSGL-Ig) alone, or in combination with sirolimus (SRL) and cyclosporin A. We found that in contrast to the effects of standard doses of SRL or cyclosporine, rPSGL-Ig decreased inflammation in the early posttransplant period such that lower doses of maintenance immunosuppression were sufficient to maintain long-term graft function.

Animals↗

PubMed2005

Differences in suppressor of cytokine signaling-1 (SOCS-1) expressing islet allograft destruction in normal BALB/c and spontaneously-diabetic NOD recipient mice.

BACKGROUND: The ability to block interferon signaling represents an important strategy in designing therapies to prevent beta-cell destruction during islet allograft rejection. METHODS: The SOCS proteins regulate cytokine signaling by blocking activation of JAK/STAT proteins. Using islets isolated from SOCS-1 transgenic mice (SOCS-1-Tg; these mice express SOCS-1 under the control of the human insulin promoter and are on the C57BL6/J background), we investigated whether SOCS proteins can prevent the destruction pancreatic islet cells transplanted beneath the kidney capsule of major histocompatibility complex mismatched normal BALB/c and spontaneously-diabetic NOD mouse recipients. RESULTS: Immunohistochemical staining for insulin confirmed the presence of donor SOCS-1-Tg islets in islet allografts harvested at 22 days posttransplant, whereas grafts of control non-Tg islets were destroyed by 14 days. In contrast, SOCS-1-Tg allogeneic islets were not protected from beta-cell destruction in clinically diabetic NOD mice. The islet allografts functioned for 1 week posttransplant; however, hyperglycemia returned after 2 weeks and the grafts were destroyed. Rejection of SOCS-1-Tg and non-Tg islets in autoimmune diabetic NOD mice was associated with an infiltrate of both CD4+ and CD8+ T cells and a T2-type cytokine response (IL-4) rather than the conventional T1-type cytokine response observed during islet allograft rejection. Self-antigen upregulation in response to IFN-gamma stimulation did not appear to be a factor in rejection of the islet allografts. CONCLUSIONS: These results demonstrate that expression of SOCS-1 in islets delays islet allograft rejection but cannot circumvent destruction of the islets by the recurrence of the tissue-specific autoimmune process of spontaneous diabetes.

Animals↗

PubMed1995

Endogenous ANP in postischemic acute renal allograft failure.

Circulating atrial natriuretic peptide (ANP) levels and glomerular binding sites for ANP were examined in 23 subjects undergoing renal transplantation. Subjects were divided into two groups, group 1 (n = 12) with prompt and group 2 (n = 11) with delayed allograft function. Sixty to 180 min after graft reperfusion, renovascular resistance was threefold higher and glomerular filtration rate (GFR) depressed by 79% in group 2 vs. group 1. Corresponding median plasma ANP (114 vs. 140 pg/ml) and guanosine 3',5'-cyclic monophosphate (cGMP) levels (22 vs. 28 pmol/ml) were similarly elevated in the two groups [P = not significant (NS)]. Autoradiographic analysis of glomeruli in an allograft biopsy revealed the median density of total receptors (24 vs. 28 fmol/mm3), A receptors (15 vs. 19 fmol/mm3), and C receptors (6 vs. 9 fmol/mm3) for ANP to also be similar in group 2 vs. group 1, respectively (P = NS). By postoperative day 3, allograft GFR averaged only 6 +/- 2 in group 2 vs. 59 +/- 4 ml/min in group 1. Median plasma ANP levels doubled in each group to 262 and 251 pg/ml, respectively (P = NS). However, median values for plasma levels (38 vs. 17 pmol/ml) and the fractional clearance of cGMP (1.9 vs. 1.2) were significantly higher in group 2 than group 1. We conclude that, despite an adequate density of glomerular ANP receptors and enhanced cGMP generation, neither renal vasoconstriction nor hypofiltration is alleviated by a progressive elevation of plasma ANP levels in renal transplant recipients with sustained postischemic injury. We infer that constricted afferent arterioles are unresponsive to the vasorelaxant action of endogenous ANP in this form of postischemic, acute renal failure.

Acute Kidney Injury↗

PubMed1996

Comparison of pancreas transplantation with portal venous and enteric exocrine drainage to the standard technique utilizing bladder drainage of exocrine secretions.

Although bladder drainage of pancreatic exocrine secretions has been reported to decrease morbidity and improve pancreas allograft survival, significant complications remain associated with this technique. Furthermore, this technique requires systemic venous drainage of pancreas allografts. Evidence suggests that portal venous drainage of pancreas grafts prevents hyperinsulinemia and improves lipoprotein composition. This report documents our initial experience with portal venous and enteric exocrine drainage of pancreas allografts (portal/enteric technique) and compares it with the standard technique of systemic venous and bladder exocrine drainage (systemic/bladder technique). Patient and allograft survival, as well as allograft function, were comparable for the two procedures. There were no significant technical complications in this pilot series. Enteric exocrine drainage was associated with a significant reduction in the incidence of acidosis and dehydration when compared with bladder drainage (P<0.005). The portal/enteric technique also avoided reoperation for enteric conversion, as was required by 33% of patients in the systemic/bladder group. The incidence and outcome of allograft rejection were similar for the two techniques. These data suggest that combined pancreas/kidney transplantation with portal venous and enteric exocrine drainage is safe and results in outcomes similar to the standard technique, while eliminating many complications of bladder drainage. These findings should encourage additional studies to determine the consequences of portal venous drainage.

Drainage↗

PubMed2003

Prolonged islet allograft survival in diabetic NOD mice by targeting CD45RB and CD154.

Clinical islet transplantation is a successful procedure that can improve the quality of life in recipients with diabetes. A drawback of the procedure is the need for chronic administration of immunosuppressive drugs that, among other side effects, are potentially diabetogenic. Definition of immunosuppressive protocols that utilize nondiabetogenic compounds could further improve islet transplantation outcome. We used the NOD mouse to assess the effect of targeting the T-lymphocyte surface receptors CD45RB and CD154 in preventing loss of allogeneic islet grafts as a result of recurrence of autoimmunity and allorejection. Administration of the two antibodies led to significantly prolonged allograft survival, with a percentage of grafts surviving long-term. The therapeutic efficacy of the treatment was paralleled by a shift in CD45RB isoform expression on T-lymphocytes, increased in vitro responsiveness to interleukin-7, and increased in vitro gamma-interferon production after anti-CD3 antibody stimulation. Furthermore, graft infiltration by CD8+ T-cells was remarkably reduced. Recipient mice bearing functioning allografts were otherwise immunocompetent, as assessed in vivo and in vitro by numerous tests, including intragraft cytokine production, responsiveness to polyclonal stimulation and alloantigens, and analysis of cell subset phenotype. These data show that nondiabetogenic regimens of immunomodulation can lead to prolonged islet allograft survival in the challenging NOD mouse model.

Animals↗

PubMedDate not supplied

Possible immunological effects of psychotropic medication.

Psychoactive drugs provide an essential intervention in the care of organ transplant recipients, yet little is known of their effect on immunological function. Human and animal data on immunological effects of neuroleptic (e.g., haloperidol, phenothiazines) and antidepressant agents (e.g., tricyclic antidepressants, fluoxetine) lead to conflicting hypotheses. Lithium carbonate acts through the phosphoinositide system and has a bipolar effect on neuronal activity. Lithium is known to have immune-enhancing properties and is difficult to administer in the peritransplant period but nonetheless deserves study for possible beneficial effects on allograft function.

Humans↗