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PubMed1995

Inert gas single-breath washout after heart-lung transplantation.

We prospectively studied the distribution of ventilation in 22 heart-lung transplant (HLT) recipients. At entry into study, the patients had undergone surgery an average of 6.7 mo earlier, and were followed for a mean period of 16 mo. Vital-capacity (VC) single-breath washouts as well as single-breath washouts using a 1-L inspiration from FRC were performed on a total of 395 occasions. The inhaled gas mixture consisted of 5% He, 5% SF6, and 90% O2, and the expired N2, He, and SF6 concentrations were analyzed. Six patients showed normal standard pulmonary-function tests and indexes of ventilation distribution throughout the study. Five patients gradually developed an irreversible airflow obstruction, presumably due to obliterative bronchiolitis (OB). They showed increases in the slopes of the N2, SF6, and He alveolar plateaus (SN2, SSF6, S(He)), but because S(He) increased more than SSF6, the slope difference (SSF6-S(He)) invariably decreased and became negative in four of five patients. Thirteen patients developed 16 episodes of reversible airflow obstruction as a result of acute infection or rejection of the lung allograft. The alterations in ventilation distribution were qualitatively similar to those seen in patients with OB. We conclude that: (1) ventilation distribution in the lung periphery is normal in HLT recipients with adequate allograft function; (2) the airflow obstruction elicited by OB and acute episodes of lung infection or rejection is accompanied by increases in SN2, SSF6, and S(He) and decreases in SSF6-(He)).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Noninvasive surveillance of allografted kidneys by ultrasonic duplex scanning.

Over a one-year period 1,000 duplex Doppler evaluations were performed in 70 patients submitted to kidney transplantation for end-stage renal failure. Duplex monitoring was performed to evaluate transplant status from hemodynamic patterns of the graft arteries. A duplex scanner with a 3.75 MHz sector transducer was used; pulsed Doppler was utilized to detect blood flow velocities in the main renal, segmental, interlobar and arcuate arteries. Arterial signals were quantified through a pulsatility index (PI). Three cases of acute rejection (AR), 9 cases of chronic rejection (CR), 2 cases of cyclosporine nephrotoxicity (Csa Tox), and 4 cases of acute tubular necrosis (ATN) were recognized and biopsy proved. At each arterial site PI values of normally functioning allografts were lower than 1.5; AR patients showed PI values ranging from 1.7 to 3.1, promptly lowered by immunosuppressive treatment. CR patients had a spectrum of PI from 0.5 to 3.1. Patients with Csa Tox and ATN showed in all the explored sites normal arterial signals and thus normal PI values. PI variations reflect even slight blood flow reductions due to immunologically mediated increases in intrarenal arterial resistances. Duplex sonography of allografted kidneys shows great diagnostic attitudes in the noninvasive characterization of transplant malfunction.

Adult↗

PubMed2004

Matching T-cell receptors identified in renal biopsies and urine at the time of acute rejection in pediatric renal transplant patients.

Urinary monitoring of kidney allograft function has been used for many years. More recently, molecular identification of cytotoxic T-cell products has been used as a diagnostic tool in acute rejection. Monitoring of T-cell infiltrates by analysis of the T-cell receptor (TcR) gene usage has been performed on biopsies with acute and chronic rejection, but not on urine samples. The aim of this study was to identify and compare TRBV gene usage assessing the CDR3 (Complementarity Determining Region 3) length distribution and sequence in urine and biopsies of pediatric renal allograft patients at the time of acute rejection and compare them with peripheral blood. We studied four pediatric renal transplant recipients with acute cellular rejection. We identified restricted and matched TRBV CDR3 spectratypes with overexpressed TRBV families and show identical, clonally expanded TRBV CDR3 sequences in all four patients present in the urine and renal allograft. We demonstrate that urinary monitoring can detect graft-infiltrating lymphocytes in acute rejection and may have a role in the monitoring of renal transplants.

Acute Disease↗

PubMed1992

A prospective randomized trial between Euro-Collins and University of Wisconsin solutions as the initial flush in hepatic allograft procurement.

University of Wisconsin solution is currently recognized as the best solution for long-term organ preservation. It is recommended that UW solution be used as the in situ flush prior to organ explantation. The purpose of our study was to determine if hepatic allograft function was impaired by flushing the graft in situ with Euro-Collins and later flushing the graft ex vivo with UW solution, prior to cold storage. Fifty-six donors were randomly assigned to either an EC (n = 24) or UW (n = 32) in situ flush. The livers flushed with EC in situ were later flushed with 1 L of UW on the back table and stored in UW solution. Livers flushed with UW in vivo were similarly flushed and stored in UW on the back table. Concerning the donor allograft, there was no statistical difference (P greater than 0.05) between groups in sex, race, blood type, arterial anatomy, age, prothrombin time (PT), partial thromboplastin time (PTT), total bilirubin (TBR), direct bilirubin (DBR), aspartate amino transferase (AST), or alanine amino transferase (ALT). In addition, the recipients were compared for differences in sex, race, blood type, preoperative status, number of rejections, recipient age, length of surgery, and ischemia time and patient survival. There was no significant difference between groups (P greater than 0.05). There was no significant difference in patient survival (P = 0.238). Values for TBR, AST, ALT, PT, PTT, and AP were collected immediately preoperatively and postoperatively and on postoperative days 1, 3, 7, 14, and 28. There was no difference between groups in these values (P greater than 0.05). In our study there was no difference between the groups with respect to graft performance. This would justify the use of EC as an in situ flush during solid organ procurement and flushing with UW solution on the back table with an estimated savings of $400 to $1200 per procurement.

Adenosine↗

PubMed2004

Effect of posttransplant anti-HLA antibody on outcome of renal transplantation.

Pretransplant anti-HLA antibody has an impact on renal transplantation (RT) outcome. However, the role of posttransplant anti-HLA antibody in renal allograft outcome remains unclear. We conducted this study to determine whether posttransplant anti-HLA plays an important role in the outcome of renal allografts. Our investigation used a cross sectional design. Class I and II anti-HLA antibodies were obtained in 41 renal transplant patients. Patients had undergone either living-related (n = 15) or cadaveric (n = 26) RT. All patients had been transplanted for >6 months. The correlation of posttransplant class I and class II, anti-HLA antibodies with renal allograft function glomerular filtration rate (GFR) was analyzed. Patients displaying a GFR of >60 mL/min showed positive anti-HLA antibody status for class I (n = 2) and class II (n = 9). In contrast, those whose renal transplants showed a GFR <60 mL/min included three patients positive for HLA class I and 19 patients for HLA class II. Posttransplant class II anti-HLA antibody showed a negative correlation with GFR (r = -0.31, P = .03). Preliminary results indicated that class II posttransplant anti-HLA antibody might be one mechanism of chronic renal allograft rejection and may confirm the important role of HLA matching in renal transplantation outcome.

Adult↗

PubMed1986

Therapy with monoclonal antibody to interleukin 2 receptor spares suppressor T cells and prevents or reverses acute allograft rejection in rats.

The mouse hybridoma ART 18 monoclonal antibody (mAb), which binds to the rat interleukin 2 (IL-2) receptor, was studied for its effect on heterotopic cardiac allograft survival in two histoincompatible inbred rat strain combinations. Treatment with ART 18 mAb for 10 days after transplantation prolonged allograft survival in a dose-dependent fashion up to about 3 weeks (acute rejection normally occurs within 8 days). ART 18 mAb therapy started at 5 days after transplantation the time of major rejection activity) abrogated acute rejection and extended the survival to about 18 days. The dense cellular infiltrate noted histologically in acute rejection had virtually disappeared after ART 18 mAb treatment. Thus, IL-2 receptor-targeted therapy can be successfully used to prevent and/or treat acute rejection. When spleen cells from antibody-treated recipients bearing well-functioning allografts were adoptively transferred to normal untreated rats that received cardiac allografts 24 hr later, the survival of donor-specific, but not third-party, test cardiac allografts was prolonged significantly; this supports the idea that ART 18 mAb induced "sparing" of suppressor T lymphocytes. Combining infusion of ART 18 mAb with exogenous IL-2-rich conditioned medium produced the same effect as if the mAb alone had been administered, suggesting that an excess of IL-2 does not prevent binding of ART 18 mAb to IL-2 receptor-bearing cells in vivo. These results support the important role of the IL-2 receptor-bearing cells in the mechanism of allograft rejection; they may represent an important target for immunosuppression in clinical organ transplantation.

Animals↗

PubMed1993

Intrathymic injection of donor alloantigens induces specific tolerance to cardiac allografts.

The induction of donor-specific tolerance would eliminate the risk of long-term immunosuppression while ensuring allograft function and survival. Male Buffalo (RT1b) rats were exposed to donor alloantigen by an intrathymic, intrasplenic, s.c., or i.v. injection of 25 x 10(6) syngeneic Buffalo (RT1b) or MHC fully mismatched Lewis (RT1l), ACI (RT1a), or UV-B irradiated Lewis (RT1l) splenocytes. The Buffalo recipients were given 1 cc of rabbit antirat antilymphocyte serum (ALS) i.p. at the time of the donor antigen injection, and 21 days later received a heterotopic Lewis or ACI heart transplant. Only intrathymic alloantigen injection induced a donor-specific tolerance which allowed the cardiac allograft to survive indefinitely (mean survival time [MST] > 176.8 days) in > 86% of the recipients without the need for further immunosuppression, whereas groups receiving antigen injections at other sites rejected cardiac allografts in control time (MST approximately 7.0 days). Histologic examination of long-term tolerated Lewis cardiac allografts revealed the presence of healthy cardiac myocytes without mononuclear infiltration. Buffalo rats with a long-term surviving Lewis cardiac allograft did not reject a second Lewis cardiac allograft (MST > 100.0 days), but rejected a heterotopic ACI cardiac allograft in normal time (MST approximately 7.0 days). By limiting dilution analysis (LDA), maturation of donor-specific CTLs (pCTL) from long-term recipient splenocytes was markedly diminished, whereas third party pCTL was not altered, and T helper-precursors were moderately decreased without alteration in the peripheral CD4+ and CD8+ phenotype frequencies. MLC responses of recipients with long-term surviving cardiac allografts to donor-specific and third party stimulation were not significantly different from naive controls. Microchimerism is unlikely because Lewis allograft survival was also prolonged (MST > 96.0 days) in rats receiving UV-B irradiated Lewis splenocytes which cannot proliferate. The absence of increased allograft survival after transfer of long-term recipient splenocytes into naive animals suggests that donor-specific suppressor cells are not present. Additionally, in vitro lymphocyte proliferative responses to mitogenic or allogeneic stimulation in MLC was not diminished by the addition of these long-term recipient splenocytes. This model emphasizes the importance of exposure of T cell precursors to foreign donor alloantigen in the thymic environment for the development of unresponsiveness to a donor-specific vascularized allograft.

Animals↗

PubMed1997

Growth post renal-transplantation in children: lessons from the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS).

Growth retardation following successful transplantation has been noted since the availability of ESRD care for children more than a quarter of a century ago. During the past decade, data collection and analysis of the NAPRTCS data base have detailed the factors which have an impact on growth in renal allograft recipients transplanted in the cyclosporine era. These analyses have led to the following conclusions. 1. Standardized height (z score) worsens in the majority of pediatric recipients following renal transplantation. 2. Catch-up growth (improvement in standardized height) occurs primarily in recipients <6 years of age at transplantation. Therefore, age at transplantation is a significant factor determining the magnitude of post-transplant growth. 3. Reduced allograft function has a profound negative impact on growth following transplantation. 4. Height deficit at the time of transplantation correlates with increment in height following transplantation. The most profoundly growth-retarded recipients exhibit the greatest increase in standardized height. 5. Race has been identified by NAPRTCS as a factor affecting post-transplant growth. Caucasian recipients exhibit a greater improvement in standardized height compared to African-American and Hispanic recipients. 6. Since serial evaluation of NAPRTCS data indicates that catch-up growth is unlikely to occur in 75% of renal allograft recipients, strategies such as the use of growth hormone would be advantageous in the future.

Adolescent↗

PubMed1989

The reuse of OKT3 after previous rejection or induction therapy in cadaveric renal transplantation.

Twenty-three patients were retreated once and two patients were retreated two times with OKT3 after previous rejection or induction therapy in cadaveric renal transplantation. Retreatment was effective when the initial treatment was for rejection therapy or induction therapy protocols. Rejection reversal was 83% in the rejection group and 90% in the induction group. Long-term allograft function was 42% in the rejection group and 78% in the induction group. It is speculated that the immune response is more adequately controlled in the induction group. The antibody responses to retreatment were no antibody production (n = 9), antibody production on retreatment (n = 2), no change in antibody titer (n = 4), and increase in previously identified antibody titer (n = 3). Two patients with high titered antibodies had treatment failures caused by preformed antimouse antibodies. The only changes in antibody specificity occurred in patients with a change in preformed antibody. Retreatment of allograft rejection in patients previously treated with OKT3 has again been demonstrated to be effective. It is suggested that retreatment after OKT3 induction therapy may be the most effective.

Antibodies, Monoclonal↗

PubMed1990

Evidence that HLA class II disparity is required for the induction of renal allograft enhancement by donor-specific blood transfusions in man.

We studied 46 living-related primary renal allograft recipients between June 1980 and Jan 1988 to determine if enhancement of allograft survival by donor specific transfusions requires a major histocompatibility complex mismatch between the blood/kidney donor and the recipient. Recipients were matched for a single HLA haplotype, but differed at various HLA loci on the unshared haplotype. DST (200 ml) was administered either 3 times at two-week intervals pretransplant (n = 17), or once 3-4 weeks pretransplant, together with oral azathioprine (1 mg/kg/day/28 days) (n = 29). Patients were followed for at least 1 year and all clinical rejection episodes were confirmed histologically. Enhanced graft survival by DST was defined as a rejection-free posttransplant course. Incompatibility for class II determinants on the unshared haplotype of donor had a beneficial effect. A significantly greater proportion of recipients had stable, rejection-free, allograft function if incompatible for the DR locus (80% vs. 44%, P = 0.012), for class II public determinants (100% vs. 58%, P = 0.013), or for at least one of the class II gene products (DR, DQ, class II public) (81% vs. 40%, P = 0.006). Graft loss occurred in 7 of 46 (15%); 6 of the 7 recipients were HLA class II-compatible with their blood/kidney donor. Mismatches for HLA class I private or public determinants and other factors known to affect graft outcome did not influence the results. We conclude that enhanced kidney allograft survival by DST may be predicated by factors within the MHC--specifically class II disparity. These observations also suggest that better HLA matching at the class II locus may account for the apparent "disappearance" of the transfusion effect in cadaver renal transplants in the cyclosporine era.

Blood Transfusion↗

PubMed2006

Chronic allograft nephropathy.

With the advent of calcineurin inhibitors, the success of kidney and other solid-organ transplants has improved significantly from the standpoint of reducing the incidence of acute rejection. Over the past 2 decades, both short-term allograft survival and acute rejection rates have dramatically improved with improved diagnostic and therapeutic techniques such as standardized pathology scoring; potent antirejection drugs such as anti-thymocyte globulin, interleukin-2 receptor antibodies, cyclosporine, tacrolimus, sirolimus, and mycophenolate mofetil; and improved infection control such as valganciclovir and antifungal therapy. However, long-term graft loss has remained at nearly constant levels over the same period of time, with the average half-life of a deceased-donor kidney transplant in the United States remaining approximately 1 decade. In addition to death with a functioning allograft and calcineurin toxicity, a chronic fibrotic process-known at various times as chronic rejection, chronic allograft dysfunction, and chronic allograft nephropathy (CAN)-account for the leading causes of transplant failure.

Graft Survival↗

PubMed2004

No association between renin-angiotensin system gene polymorphisms and early and long-term allograft dysfunction in kidney transplant recipients.

BACKGROUND: Genes determining the activity of the renin-angiotensin system (RAS) may be alloantigen-independent factors influencing kidney allograft function. We determined if gene polymorphisms of the RAS are associated with early and long-term post-transplantation graft dysfunction in 405 Caucasian kidney recipients with graft survivals of >2 years. METHODS: We calculated the slopes of serum creatinine(-1)/year and urinary protein excretion/year to follow graft function over time. Subjects were genotyped for the deletion (D) polymorphism of the gene encoding angiotensin I-converting enzyme, the angiotensin II-receptor type1 gene 1166A-C polymorphism and the M235T polymorphism of the angiotensinogen gene. RESULTS: The frequencies of factors predicting graft function were similar in patients with different genotypes. None of the polymorphisms influenced need for dialysis in the first week after transplantation, occurrence of at least one rejection episode, the slope of serum creatinine(-1)/year or the slope of urinary protein excretion/year. Results were independent of blood pressure or the use of angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers or calcineurin inhibitors. The combination of genotypes did not influence the indicators of early and long-term graft dysfunction. CONCLUSIONS: Neither the investigated gene polymorphisms of the RAS in kidney allograft recipients nor their combinations have an impact on early and long-term graft dysfunction.

Adult↗

PubMed2004

Intragraft iNOS induction during human liver allograft rejection depresses cytochrome p450 activity.

Allograft function may become impaired during rejection after human liver transplantation. Cytokines induce nitric oxide (NO) production in hepatocytes, Kupffer cells and infiltrating mononuclear cells. NO inhibits cytoplasmatic cytochrome p450 (CYP) enzyme activity in vitro. It is not known whether this mechanism plays a role in vivo. In order to characterize the role of locally produced cytokines in the pathogenesis of liver dysfunction, we analysed human liver transplant biopsy material for the expression of proinflammatory cytokines as well as for NO synthase and we compared these results to the microsomal liver function in vivo [aminopyrine breath test (ABT)] and in vitro (enzymatic analysis of CYP). Microsomal liver function decreased in vivo during rejection while ABT levels decreased by 40% and increased again by 59% after the acute rejection episode. Similarly, CYP 1A2 and 2E1 activity dropped 42% and 24% in rejecting samples, respectively. Competitive reverse transcriptase polymerase chain reaction (RT-PCR) showed a fivefold upregulation of interferon gamma (IFN-gamma) gene expression. Inducible, but not constitutive NO-synthase gene expression was upregulated fivefold in samples from rejecting patients suggesting a local induction of NO in response to immune events. Our data show a marked impairment of CYP enzyme activity during allograft rejection which is presumably secondary to an increased intragraft production of proinflammatory cytokines and NO.

Aminopyrine↗

PubMed1999

The prognostic importance of severity and type of post-transplant proteinuria.

Proteinuria, developing after renal transplantation may influence allograft and patient outcomes. This study aimed to investigate the effect of proteinuria on patient and allograft survival. Among 514 patients, 56 (11%) patients with good allograft function and proteinuria were evaluated retrospectively. Patients with proteinuria were classified as group P (20 patients with permanent proteinuria, Male/Female: 16/4) and group T (36 patients with temporary proteinuria, M/F: 29/7) according to the type of proteinuria. Also, considering the amount of proteinuria, patients were classified as group M (32 patients with massive proteinuria, M/F: 29/3) and group NM (24 patients with non-massive proteinuria, M/F: 16/8). The mean time interval between transplantation and appearance of proteinuria was 23.7 months (range 0-121 months) and no difference was found between groups. Two- and 5-yr allograft survival rates were found to be 85 and 80% in group M, and 95 and 82% in group NM. respectively (p = 0.24). In terms of type of proteinuria, 2- and 5-yr allograft survival rates were found to be 70 and 58% in group P and 92 and 87% in group T, respectively. The difference between groups P and T was found to be statistically significant (p = 0.02). Most (85%) of the patients with permanent proteinuria also had massive proteinuria. In conclusion, we found a significant relation between type and severity of proteinuria. The type of post-transplant proteinuria had a stronger effect on allograft outcome than the severity of proteinuria.

Adult↗

PubMed1991

Morphometric inflammatory cell analysis of human liver allograft biopsies.

To quantitate the inflammatory cell response within the portal tracts of liver allografts during acute rejection, we retrospectively and in a blinded fashion reviewed 431 biweekly, protocol, core allograft biopsies in 58 consecutive adult recipients. Following the determination of the cross-sectional area of each portal tract, the number of eosinophils, neutrophils, and lymphocytes therein was tabulated. The average number, percentage, and density of each type of portal inflammatory cell were calculated for each biopsy. Each biopsy was prospectively and independently classified as either associated (REJ+) or not associated (REJ-) with acute rejection. Acute rejection consisted of simultaneous allograft dysfunction and qualitative pathologic findings of acute rejection. Biopsies obtained during periods of normal allograft function or during episodes of dysfunction due to other causes were classified as not associated with rejection (REJ-). Ninety biopsies were classified as associated with acute rejection (REJ+) while 241 biopsies were classified as not associated with acute rejection (REJ-). In general, the average portal-tract number, percentage, and density of all inflammatory cells were significantly increased in biopsies associated with acute rejection. In contrast, only the portal-tract eosinophil values were consistently predictive of acute rejection following receiver-operating characteristic curve analysis (sensitivity = 82-86%, specificity = 91-92%). This quantitative method of allograft assessment appears to improve the objectivity of the serial biopsy protocol. By using this method, we found the eosinophil's appearance within the portal tracts to be a dependable indicator of acute rejection.

Adult↗

PubMed2003

Multicentric papillary renal carcinoma in renal allograft.

A renal transplant recipient with 13 years of excellent allograft function was found incidentally to have a malignant mass in his transplanted kidney. After resection, pathological analysis showed 29 separate lesions of renal cell carcinoma. All tumors were confined within the renal capsule. The majority of tumors (21 of 29 tumors) were chromophil basophilic carcinoma with papillary architecture, 5 tumors were clear cell, 2 tumors were mixed cell type, and 1 tumor was chromophil eosinophilic papillary carcinoma. These histological findings are similar to those reported in hereditary papillary renal carcinoma. To our knowledge, this is the first case of multicentric papillary renal carcinoma occurring in the renal allograft. We speculate that the allograft in this case is predisposed to malignant changes because of preexisting genetic mutations, as well as prolonged immunosuppression.

Adenocarcinoma, Clear Cell↗

PubMed1999

Serum cystatin C as a determinant of fasting total homocysteine levels in renal transplant recipients with a normal serum creatinine.

Serum creatinine, a surrogate for both renal function and homocysteine generation, is an important determinant of fasting plasma total homocysteine levels in stable renal transplant recipients. In this study, it is hypothesized that among stable renal transplant recipients with normal creatinine levels (i.e., < or = 1.5 mg/dl), serum cystatin C, a more sensitive indicator of GFR, would better predict fasting total homocysteine levels compared with serum creatinine. Fasting plasma total homocysteine, folate, vitamin B12, and pyridoxal 5'-phosphate levels, along with serum cystatin C, creatinine, and albumin levels, were determined in 28 consecutive renal transplant recipients (mean age 47 +/- 14 yr; 60.7% men) with stable allograft function, whose serum creatinine was < or = 1.5 mg/dl. General linear modeling with analysis of covariance revealed that serum cystatin C was independently predictive (partial R = 0.494; P = 0.023) of fasting total homocysteine levels after adjustment for age, gender, vitamin status, albumin, and creatinine levels. In contrast, creatinine levels were not predictive of fasting total homocysteine levels in this model (P = 0.110) or an identical model that excluded cystatin C (P = 0.131). Serum cystatin C levels may reflect subtle decreases in renal function that independently predict fasting total homocysteine levels among stable renal transplant recipients with a normal serum creatinine.

Adult↗

PubMed1996

Serum albumin and mortality after renal transplantation.

The incidence, causes, and consequences of hypoalbuminemia after renal transplantation are not well defined. We examined clinical correlates of serum albumin measured at 3 months, 6 months, 1 year, and annually thereafter in 706 renal transplant recipients who survived at least 6 months with a functioning allograft. Follow-up was 7.0 +/- 4.2 years. Hypoalbuminemia (< or = 3.5 g/dL) was most common at 3 months (31%, n = 692), least common at 1 year (12%, n = 656), and then became increasingly common among survivors, for example, 14% (n = 466) at 4 years, 20% (n = 204) at 8 years, and 29% (n = 77) at 12 years after transplantation. By multiple linear regression, variables that correlated (P < 0.05) with lower serum albumin at 3, 6, 12, and 24 months included age, diabetes, proteinuria, and cytomegalovirus infection. Other independent correlates on at least one of these occasions included renal function and chronic disease (malignancy, liver disease, and cardiovascular disease). Serum albumin, as a time-averaged and time-dependent covariate, was a strong independent risk factor for death using Cox proportional hazards analysis (relative risk for each g/dL increment, 0.26; 95% confidence interval, 0.16 to 0.44 [1.00 = no risk]). The effects of albumin on mortality were independent of age, diabetes, serum lipids, renal function, chronic liver disease, malignancies, and cardiovascular disease. The effects of albumin on mortality were evident even when the analysis was restricted to patients dying several years after albumin was measured. Thus, hypoalbuminemia is common and serum albumin is a strong independent risk factor for all-cause mortality after renal transplantation.

Actuarial Analysis↗