Nitric Oxide Regulates Expression of Sonic Hedgehog and Hypoxia-Inducible Factor-1α in an Experimental Model of Kidney Ischemia-Reperfusion

This study was designed to determine the effect of L-arginine on hypoxia inducible factor alpha (HIF-1 α) and Sonic hedgehog (Shh) levels considered to be involved in the development of ischemia/reperfusion (I/R) injury. Unilaterally nephrectomized Sprague-Dawley rats were subjected to 60 minutes of left renal ischemia followed by 45 minutes of reperfusion. Group 1 were sham-operated animals; group 2, I-R/Untreated animals; and group 3, I-R/L-Arg-treated animals. Serum creatinine, blood urea nitrogen (BUN), and kidney malondialdehyde (MDA) levels were determined as well as examining the kidneys histologically. The treatment of rats with L-Arg produced a significant reduction in the levels of BUN, creatinine, MDA, and histopathological score compared to renal I/R groups. The Shh expression in the tubulus epithelia were intensely increased in the I-R/L-Arg group when compared to that of the Sham-control and the I-R/untreated groups. Additionally, the HIF-1α expression in the tubulus epithelia and the interstitial spaces were intensely increased in the I-R/L-Arg group. These findings suggest that NO reduces the renal dysfunction associated with I/R of the kidney and may act as a trigger to induce Shh and HIF-1 activity.     

Urinary Tissue Inhibitor of Metalloproteinase and Insulin-like Growth Factor–7 as Early Biomarkers of Delayed Graft Function After Kidney Transplantation

Background

Recently, urinary tissue inhibitor of metalloproteinase–2 (TIMP-2) and insulin-like growth factor–7 (IGFBP-7), markers for G1 cell cycle arrest, have been identified and validated in predicting the development of acute kidney injury in critically ill patients. It is unknown, however, whether these two biomarkers could predict the development of delayed graft function (DGF) after kidney transplantation (KT).

Decreased Hypoxia-Inducible Factor-1α in Gastrocnemius Muscle in Rats with Chronic Kidney Disease

Background/Aims: Hypoxia-inducible factor (HIF)-1α is responsible for increased expression of genes engaged in angiogenesis. Our previous study indicated capillary rarefaction and atrophy of glycolytic fibers, mainly in locomotor muscles of uremic animals. Perhaps these changes are secondary to disturbances of HIF-1α in skeletal muscles. Methods: Expression of HIF-1α at mRNA and protein levels, as well as mRNA of vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS), in gastrocnemius muscle (MG) and longissimus thoracic muscle (ML) were measured by RT-PCR and Western blot. Rats were randomized to subtotal nephrectomy (CKD5/6), uninephrectomy (CKD1/2) or sham operation (controls). Results: For CKD5/6 versus controls, mRNA levels for HIF-1α, VEGF-A, VEGFR-1 and VEGFR-2 were significantly reduced only in MG, while eNOS was significantly decreased and iNOS was significantly increased only in ML. Western blot analysis indicated significantly increased HIF-1α protein levels in MG and ML from CKD1/2 animals versus controls, whereas in the CKD5/6 group, the level of HIF-1α protein decreased significantly in MG and increased significantly in ML versus controls and CKD1/2. Conclusion: The reduced expression of HIF-1α mRNA and protein in locomotor muscle from CKD5/6 animals may be involved in the pathogenesis of uremic myopathy. Increased expression of iNOS in the postural muscles may act as a protective factor through HIF-1α stabilization.     

Is Serum Magnesium Level Associated With Serum Lipid Levels in Kidney Transplant Recipients?

BackgroundMagnesium (Mg) is key in diabetes mellitus, hyperlipidemia, and cardiovascular disease.MethodsThis is a retrospective cross-sectional study including 103 kidney transplant recipients. Patients aged under 18 years, patients treated with Mg supplementation, antihyperlipidemic agents, or diuretics, and patients with active infection or malignancy were not enrolled. Patients were divided into 2 groups according to median serum Mg level. The atherogenic index of plasma was calculated by a logarithmic transformation of the number acquired by dividing the molar concentrations of serum triglyceride by high-density lipoprotein value.ResultsThe mean serum Mg level was 1.91 ± 0.28 mg/dL. Six patients (5.8%) had hypomagnesemia (Mg <1.5 mg/dL), and 2 (1.9%) had hypermagnesemia (Mg >2.6 mg/dL). Serum Mg level was negatively correlated with body mass index, estimated glomerular filtration rate (eGFR), and tacrolimus trough level and positively correlated with levels of phosphorus, total cholesterol, and low-density lipoprotein (LDL-C). There was no correlation between serum Mg and triglyceride, high-density lipoprotein, atherogenic index of plasma, and cyclosporin A trough level. Patients with Mg >1.87 mg/dL had lower eGFR, tacrolimus, and cyclosporin A trough level and higher total cholesterol and LDL-C compared to those with Mg ≤1.87 mg/dL. In adjusted ordinal analysis, eGFR (hazard ratio (HR): 0.981, 95% CI 0.964-0.999, P = .036) and total cholesterol (HR: 1.015, 95% CI 1.004-1.027, P = .008) were independently associated with serum Mg. In multivariate linear regression analysis, serum Mg level was independently associated with LDL-C (β = .296, t = 3.079, P = .003) and total cholesterol (β = .295, t = 3.075, P = .003).ConclusionSerum Mg level may have an important impact on dyslipidemia in kidney transplant recipients.     

Perioperative Fluid Management in Kidney Transplantation: Is Volume Overload Still Mandatory for Graft Function?

Kidney transplantation is now recognized as the treatment of choice for patients with chronic renal failure. Despite the extension of indications to patients suffering severe hypertension, ischemic heart disease, and chronic heart failure, the worldwide results are superb. However, perioperative cardiac complications occur in 6% to 10% of transplanted patients. Aggressive intraoperative volume expansion is still recommended to maximize graft functional recovery (up to 30 mL/kg/h, central venous pressure [CVP] > 15 mm Hg), but patients with preexistent cardiac disease or poor myocardial function are exposed to the risk of fluid overload, acute respiratory failure, and prolonged ventilation. Among the last 90 cases performed at our institution, good functional recovery of the graft was present in 94% of the patients within 2 weeks, despite a much more conservative intraoperative hydration policy (crystalloids 2400 +/- 1000 mL, 15 mL/kg/h, CVP 7-9 mm Hg). Graft failure which occurred in 5 patients was significantly correlated only with donor age, while perioperative cardiovascular complications had been present in 9 cases (10%) who were coronary artery disease patients (55%). Age above 50 years was the only significant risk factor. Supranormal volume loading is probably not always warranted in kidney transplantation.     

Is There Any Association Between Triglyceride–Glucose Index and Graft Function in Kidney Transplant Recipients?

BackgroundAlthough previous studies have illustrated the relationship between chronic kidney disease, coronary artery disease, erectile dysfunction, and the triglyceride–glucose index (TyGi), the relationship between this index and postoperative graft function in patients undergoing renal transplantation has yet to be investigated. In the present study, we aimed to reveal the association between the TyGi and renal graft outcomes in patients who underwent renal transplantation.MethodsWe retrospectively collected data on living and cadaveric kidney donor recipients between May 2019 and April 2022. The recipients’ age, sex, body mass index, preoperative fasting glucose and triglyceride levels, TyGi, estimated glomerular filtration rate (eGFR), and serum creatinine measurement data were recorded. The patients were divided into 2 groups according to their GFR values (group 1: GFR <60 mL/min/1.73 m²; group 2: GFR ≥60 mL/min/1.73 m²). Follow-up serum creatinine–eGFR levels and TyGi measurements were compared between the recipients in group 1 and group 2.ResultsThe mean TyGi measurements of the recipients were 8.79 ± 0.64 in group 1 and 8.83 ± 0.72 in group 2. There was no statistically significant difference in terms of the TyGi measurements between the 2 groups (P >. 05). No statistically significant correlation was found between the recipients’ creatinine, eGFR, and TyGi at 1st, 6th, and 12th postoperative months (P > .05).ConclusionsWe believe that the relationship between the TyGi and renal graft function can be more clearly understood in prospective studies that include a higher number of patients and a longer follow-up period.     

Implication of Donor–Recipient Age Gradient in the Prognosis of Graft Outcome After Deceased-Donor Kidney Transplantation

Purpose

Successful kidney transplantation leads to greater survival and improved quality of life for patients with end-stage renal disease. Among the most important influences on graft outcomes is donor age. We evaluated the relationships between the donor–recipient age gradient (DRAG) and the graft outcomes after deceased-donor kidney transplantation (DDKT).

Methods

From February 1995 to March 2011, a consecutive series of 526 adult DDKT recipients were analyzed. DRAG values were divided into two groups (negative versus positive years) and then four groups (≤−21, −20 to −1, 0 to 20, and ≥21 years).

Results

Median age of donors and recipients were 39 (range, 1–75) and 41 (range, 18–74) years, respectively. The degree of DRAG was not associated with episodes of allograft rejection. High or low DRAG had no effect on posttransplant serum creatinine levels or estimated glomerular filtration rates. However, negative levels of DRAG, particularly less than −20 years, were significantly correlated with superior 10-year death-censored graft survival (86.4% and 83.1% vs 72.2% vs 53.9%; overall P = .031), but not increased overall graft or patient survival.

Conclusion

This study demonstrated that DRAG is a prognostic indicator of long-term graft outcomes after DDKT.     

Stable Expression of Hypoxia-Inducible Factor-1α in Human Renal Proximal Tubular Epithelial Cells Promotes Epithelial to Mesenchymal Transition

Background

Late kidney allograft dysfunction is becoming a significant problem and tubular atrophy and interstitial fibrosis are main causes. It was reported that hypoxia could induce epithelial—mesenchymal transition (EMT) in renal tubular epithelial cells (TECs), and hypoxia-inducible factor-1 (HIF-1) is one of the important regulators of cellular adaptive to hypoxia.

Methods

In this study, we used an HIF-1αΔODD–expressing adenovirus, which could stably and functionally express HIF-1α under normoxia conditions, and used a hypoxia/reoxygenation cell model to simulate ischemia/reperfusion (I/R) injury in vitro, to investigate the effect of HIF-1α on EMT-related gene expressions.

Results

Our results demonstrated that HIF-1α could significantly upregulate α-smooth muscle actin expression, and reduced the E-cadherin expression in HK-2 cells during I/R injury. Moreover, miR-21 expression had a positive correlation with HIF-1α in this process.

Conclusion

These results suggest that HIF-1α may promote the EMT development through regulating fibrotic gene expression during I/R injury in human renal TECs, and miR-21 could be among the important regulatory pathways in the process.     

Recovery of Endogenous ��-Cell Function in Nonhuman Primates After Chemical Diabetes Induction and Islet Transplantation

OBJECTIVE—To describe the ability of nonhuman primate endocrine pancreata to reestablish endogenous insulin production after chemical β-cell destruction.RESEARCH DESIGN AND METHODS—Eleven monkeys (Macaca fascicularis) were rendered diabetic with streptozotocin. Eight diabetic monkeys received intraportal porcine islet transplantation.RESULTS—Two monkeys transplanted after 75 days of type 1 diabetes showed recovery of endogenous C-peptide production a few weeks after transplantation, concomitant with graft failure. Histological analysis of the pancreas of these monkeys showed insulin-positive cells, single or in small aggregates, scattered in the pancreas and adjacent to ducts. Interestingly, numerous CK19⁺ cells costained with proinsulin and PDX-1 antibodies. Furthermore, the peculiar double phenotype glucagon-positive/GLUT2⁺ was observed. In these monkeys as well as in all others, the original islets showed no insulin staining.CONCLUSIONS—Our data provide evidence that, in nonhuman primates, the pancreas can reestablish endogenous insulin production after chemical β-cell destruction. This seems to be a nongeneralizable event with only 2 out of 11 monkeys recovering β-cell function. In these two monkeys, younger age and islet graft behavior might have played a role in triggering endogenous β-cell recovery.Until a few years ago, lesions of the endocrine pancreas, as occur in type 1 diabetes, were thought to be permanent and irreversible, since diabetic patients require hormone replacement therapy for life (1). Despite the clinical evolution of the disease, it is still unknown whether the islet β-cells possess, at least in part, the ability to heal from an injury (2).In mouse models, evidence has accrued that adult animals retain the ability to expand their β-cell mass after stimulation with a variety of triggers (3–8). It remains largely uncertain, however, through which molecular and cellular mechanisms the reparative process works (2).In humans, the ability of the postnatal pancreas to expand the β-cell mass after injury is still debated (9,10). Spontaneous recovery of β-cell function has been reported in only few patients previously diagnosed with type 1 diabetes (11).Although nonhuman primates do not develop autoimmune diabetes, a permanent diabetes status can be induced by total pancreatectomy or by chemical destruction of the β-cells with streptozotocin (STZ) (12,13).In this study, a group of 11 monkeys were rendered diabetic by high STZ doses. Eight of them received intraportal pig islet transplantations under an immunosuppressive regimen based on anti-CD154 antibody and mycophenolate mofetil (14).In two recipients where pig islet grafts functioned for a few weeks and eventually failed, we observed increasing endogenous C-peptide production paralleled by metabolic improvement. We reviewed all metabolic data, did extensive histological analysis, and here report evidence of recovery of endogenous insulin production in these two monkeys.     

The Role of Hypoxia-Inducible Factor-1α and -2α in Androgen Insensitive Prostate Cancer Cells

ObjectivesThe aim of this study was to investigate the effects of induction and knocking down of hypoxia-inducible factor (HIF)-1α and/or -2α on tumor biology in androgen insensitive prostate cancer cell lines.Materials and methodsThe induction patterns of HIF-1α and -2α after treatment with ZnSO₄ were evaluated in PC3 and DU145 cells. Both cell lines were transfected with siRNA targeted against HIF-1α and/or -2α, and the expression patterns of these 2 HIF isoforms were examined. We next performed cell counting Kit-8 (CCK-8) assays and matrigel invasion assays. Potential additive effects of HIF blockade to chemotherapy (docetaxel) or target agents (sunitinib and sorafenib) were examined. In addition, gene expression changes were determined in ZnSO₄-treated DU145 cells using Western blotting.ResultsZnSO₄ affected the expression of HIF in a dose-dependent manner. HIF expression was increased within the first 3 hours but then decreased. Cells in which HIF-1α and/or -2α had been knocked down using siRNA showed decreased cell viability. Invasion abilities were increased by ZnSO₄ treatment in both cell lines overexpressing HIF. However, invasion potencies were decreased in response to treatment with HIF siRNAs. Blocking HIF prominently augmented the antitumor effects of target agents. The underlying mechanism could be associated with p21, cMET, IGF-1, and GLUT-1.ConclusionsOur results demonstrate that HIF-1α and -2α are important for cell proliferation and invasion ability in prostate cancer. Together, our results indicate that combinations of target agents with HIF knockdown may represent a promising strategy for the treatment of prostate cancer.     

Non-Invasive Assessment of Graft Fibrosis After Living Donor Liver Transplantation: Is There Still a Role for Liver Biopsy?

Non-invasive methods have evolved as a surrogate for liver biopsy such as indirect markers (aspartate transaminase to platelet ratio index, fibro-α score), transient elastography (TE), and magnetic resonance elastography (MRE).The aim of this study is to prospectively compare the value of MRE, TE, and indirect markers in detecting and staging allograft fibrosis compared to liver biopsies in patients who have undergone living donor liver transplantation for complications related to hepatitis C virus.A total of 31 living donor liver transplantation recipients with hepatitis C virus recurrence underwent a liver biopsy, TE, and MRE within 3 months of a liver biopsy. Fibrosis was assessed according to the biopsy and staged according to Metavir criteria.There was a significant correlation between both MRE and fibro-α scores, as well as histologic classification by liver biopsy (P = .02, .002). The diagnostic accuracy of MRE and fibro-α scores in diagnosing significant fibrosis (F ≥ 3) was measured as the area under the curve (.708 and .833, respectively). Both methods showed good diagnostic performance. TE and aspartate transaminase to platelet ratio index were insignificantly correlated with the degree of fibrosis in liver biopsy (P value of .134, .535). At a cutoff value of 5.5 kPa, MRE predicted graft fibrosis (Metavir stage ≥ 3) with 71.43% sensitivity, 75% specificity, 45.5% positive predictive value, and 90% negative predictive value; at a cutoff value > 1.47, fibro-α scores predicted significant graft fibrosis (Metavir stage ≥ 3) with 85.7% sensitivity and 70.83% specificity, with a positive predictive value of 46.2% and a negative predictive value of 94.4%. These data suggest that non-invasive methods could be considered a reliable tool in assessing significant graft fibrosis post-living donor liver transplantation.     

Long-Term Outcomes of Pancreas After Kidney Transplantation in Small Centers: Is It Justified?

Background

Currently, the long-term advantages of having a pancreas transplantation (PT) are debated, particularly in patients receiving pancreas after kidney (PAK) allografts. The United Network for Organ Sharing (UNOS) requires that a transplant center perform a minimum number of PT per year to remain an active PT center. The long-term outcomes and challenges of PAK in small pancreas transplant centers are not well studied.

Methods

In this retrospective analysis, we report short- and long-term outcomes in a small center performing 2–9 PT annually.

Results

Forty-eight PT (25 simultaneous pancreas and kidney transplantation [SPK], 23 PAK) were performed in our center. Donor and recipient demographics were similar in both groups. All suitable local donors were used for SPK. All organs for PAK transplantation were imported from other UNOS regions. Mean follow-up was 61 ± 46 and 74 ± 46 months for SPK and PAK, respectively. Patient and graft survival rates were similar in SPK and PAK groups and better than the reported national average. Four patients (11%) died (1 due to trauma, 1 brain lymphoma, 1 ruptured aneurysm; and 1 unknown cause). Two patients (4%; 1 SPK, 1 PAK) lost their grafts because of thrombosis on postoperative days 3 and 5 in 2002. No graft thrombosis occurred since 2002. Seven patients (15%) required reoperation (4 for bleeding, 2 anastomotic leaks, 1 small bowel perforation). Two patients (4%) developed post-transplantation lymphoproliferative disease. Five patients (11%) experienced cytomegalovirus antigenemia which responded well to antiviral therapy.

Conclusions

Compared with outcomes for diabetic patients on dialysis, current SPK and PAK short- and long-term results are favorable even in a small PT center. Therefore, unless there is a contraindication, PT should be offered to all type 1 diabetic patients with end-stage renal disease at the time of kidney transplantation or afterward.     

Is Urinary γ-Glutamyl Transpeptidase Superior to Urinary Neutrophil Gelatinase–Associated Lipocalin for Early Prediction of Acute Kidney Injury After Liver Transplantation?

In this prospective study, we comparatively evaluated the accuracy of several biomarkers of acute kidney injury (AKI) on predicting its occurrence after liver transplantation (LT). The parameters evaluated were urinary tubular enzymes (γ-glutamyl transpeptidase [γGT], alkaline phosphatase, and urinary lactate dehydrogenase) and urinary neutrophil gelatinase–associated lipocalin. These parameters were evaluated both as isolated variables and divided by urinary creatinine. Samples were collected by the end of surgery (determination 1) and at 12 to 24 hours after surgery (determination 2). The study endpoint was the development of AKI. The study was performed over a 1-year period, and 61 of 77 patients were enrolled (main exclusion criteria were perioperative death, previous known renal failure, and insufficient data for analysis). Of these 61 patients, AKI was observed in 19 (group 1). The main relevant parameter to predict AKI was the absolute value of urinary γGT at determination 1 (area under the curve, 0.74; specificity, 72.5%; sensitivity, 70.3%; cutoff, 36 U/mL). Urinary neutrophil gelatinase–associated lipocalin was not as accurate; the best predicted value for this parameter was absolute value at D1 with an area under the curve of 0.5 (specificity, 84.2%; sensitivity, 35.7%; cutoff value, 44.6 ng/mL). We concluded that the absolute value of urinary γGT evaluated at the end of LT was the most accurate parameter to predict AKI in our cohort. Urinary enzyme levels must be taken into account in future analysis of this issue.     

Is Early COVID-19 in Kidney Transplant Recipients Concerning Enough to Halt Transplantation? A Multicenter Comparative Analysis from India

BackgroundLimited data exist on the incidence and outcome of early coronavirus disease 2019 (COVID-19) in kidney transplantation recipients (KTR).MethodsA retrospective multicenter research study was conducted across 12 centers in India. We explored the symptomatology, demographic, laboratory findings, and outcome of COVID-19 within 30 days of transplantation. The outcome was compared with the overall KTR and waitlisted patients acquiring COVID-19.ResultsThe incidence of early COVID-19 was 2.6% (n = 22) for the cumulative 838 renal transplants performed since nationwide lockdown in March 2020 until May 2021. Overall, 1049 KTR were diagnosed with COVID-19 and 2% of those had early COVID-19. The median age of the early COVID-19 cohort was 43 (31-46) years. COVID-19 severity ranged from asymptomatic (18.2%), mild (59.1%), moderate (9.1%), and severe (13.6%). Among clinical symptoms, dyspnea and anosmia were frequent, and in laboratory parameters, neutrophil lymphocyte ratio, high-sensitivity C-reactive protein, and D-dimer were higher in patients requiring oxygen. The mortality in early COVID-19 was not higher than overall KTR (4.5% vs 8.5%; P = 1). COVID-19 severity (23.9% vs 15.7%; P = .0001) and mortality (15.5% vs 8.5%; P = .001) among waitlisted patients (n = 1703) were higher compared with overall KTR.ConclusionsWe report higher burden of COVID-19 in waitlisted patients compared with KTR and a favorable outcome in early COVID-19 in KTR. Our report will help the transplant physicians in dealing with the ongoing dilemma of halting or resuming transplantation in the COVID-19 era.     

Analysis of Donor Factors for Non–Heart-Beating Donors With Regard to Cadaveric Kidney Transplantation in the Western Region of Japan

Background

Kidneys from non–heart-beating donors are thought to be marginal, and careful evaluation is required. Mass analyzed data are limited, and each transplant surgeon must evaluate these organs on the basis of their own experience.

Serum Tumor Necrosis Factor-α Is Inversely Associated With the Psoas Muscle Index in Both Male and Female Patients Scheduled for Living Donor Liver Transplantation

BackgroundPatients on a waiting list for liver transplantation frequently show core muscle wasting, referred to as sarcopenia, which results in poor prognosis. To date, there has been a lack of research on the association between inflammation mediators, including cytokines, and loss of core muscle mass in cirrhotic patients scheduled for living donor liver transplantation (LDLT).MethodsCytokines in serum, such as interleukin (IL)-2, IL-6, IL-10, IL-12, IL-17, interferon-γ, and tumor necrosis factor (TNF)-α, were retrospectively investigated in 234 LDLT patients 1 day before surgery. The psoas muscle area was measured using abdominal computed tomography within 1 month before surgery and used to calculate the psoas muscle index (PMI = psoas muscle area/height²). The study population was classified into 2 groups according to the interquartile range of PMI: a non-sarcopenia group (> 25th quartile) and a sarcopenia group (≤ 25th quartile) in each sex.ResultsIn both sexes, IL-10 and TNF-α levels were significantly higher in the sarcopenia group than the non-sarcopenia group. In a univariate analysis, male patients showed that serum IL-10 and TNF-α levels were potentially associated with sarcopenia. Serum TNF-α was independently associated with sarcopenia in a multivariate analysis. In female patients, TNF-α was significantly associated with sarcopenia in both univariate and multivariate analyses. Male patients with a PMI ≤ 25th quartile had significantly higher TNF-α levels than those in other quartile ranges, and female patients with a PMI ≤ 25th quartile had a significantly higher TNF-α level than those with a PMI > 75th quartile.ConclusionsSerum levels of TNF-α are inversely associated with skeletal muscle wasting in both male and female patients scheduled for LDLT.     

Is the Graft Function of Living Donor Renal Transplants Associated With Renal Mass Matching by Computed Tomography Angiographic Volumetry?

Background

Donor renal volume, which can be easily measured by computerized tomographic angiography with 3-dimensional reconstruction, may influence graft outcomes. Low functional renal mass and donor kidney–recipient body size mismatch can lead to progressive renal injury and poor graft function.

Materials and methods

This single–center retrospective analysis of 51 consecutive living donor renal transplantations performed between January 2005 and December 2011 defined transplant renal volume per unit recipient body surface area (BSA; mL/m²). The patients were divided into 2 groups: group I (n = 31, donor–recipient BSA ratio ≤1) and group II (n = 20, BSA ratio >1). We analyzed the clinical characteristics and laboratory data of donors and recipients to ascertain correlations with, renal volumes and graft outcomes.

Results

The renal volumes of living donors correlated with estimated glomerular filtration ratios (eGFR; r = .314, P = .025). Serum creatinine after renal transplantation correlated with transplanted renal volume at 1, 3, and 12 months (r = −.319, P = .048; r = −.407, P = .010; r = −.472, P = .002). Serum eGFR also correlated with transplanted renal volume at 3 and 12 months after renal transplantation (r = .318, P = .049 and r = .388, P = .015). There were no significant differences between groups for acute or chronic rejection, infection or delayed graft function. However, serum creatinine levels were higher (P = .011, P = .022, and P = .007) and serum eGFR significantly lower in group I at 1, 3, 6, and 12 months after renal transplantation (P = .036, P = .042, P = .042, and P = .049, respectively). There was no significant difference in graft survival.

Conclusions

Renal volume of living donors may reflect renal function and have a significant impact on graft outcomes. Renal volume matching should be considered to select donor–recipient pairs for living donor renal transplantation.