Does graft mass impact on pediatric kidney transplant outcomes?

Background

The aim of this study is to assess the evolution of renal size and function in pediatric transplant patients according to the graft mass/recipient size ratio.

Methods

Fifty pediatric renal transplant recipients were followed over 2 years. Grafts were weighed, and three different graft mass/m² ratios were determined: (1) low graft mass (58 g/m², range?31–57 g/m²), (2) median (142 g/m², range?59–141 g/m²) and high (267 g/m², range?143–353 g/m²). Patients underwent repeated ultrasound Doppler scans and repeated measurements of estimated glomerular filtration rate (eGFR; 1 week and 1, 6, 12 and 24 months), urinary retinol-binding protein (RBP) and proteinuria (1 week and 6, 12 and 24 months).

Results

The volume of renal tissue increased by 12?±?5.6 cm³ at 24 months (p?=?0.035) in the low graft mass and decreased by ?14?±?7 cm³ (p?=?0.046) in the high graft mass. The eGFR increased when either low (30?±?5 ml/min/1.73 m², p?<?0.001) or median (19?±?4 ml/min/1.73 m², p?<?0.001) graft mass was transplanted but remained stable when high graft mass was transplanted. The resistive index (RI) presented a significant decrease throughout early follow-up in the transplants involving low and median graft mass, whereas a slight rise was observed in those involving high graft mass. A significant difference was apparent 6 months post-transplant. Transplants of low and median graft mass were associated with an initial higher urinary RBP. No significant differences in proteinuria were detected.

Conclusions

Small kidneys undergo increases in volume and function without escalation of either proteinuria or urinary RBP, characterizing an adequate adaptation to the recipient. Children receiving larger kidneys present a reduction in volume, stable GFR and higher RI at 6 months.     

Does knee replacement surgery lead to chronic limb ischemia?

Total knee replacement (TKR) may be associated with chronic limb ischemia (CLI) due to arterial injury intraoperatively. The aim of this study was to determine the incidence of CLI after TKR surgery. Patients who received a unilateral TKR in 2003-2004 were identified from our database. Patients with diabetes mellitus and preexisting peripheral arterial disease were excluded. Patient assessment was by collection of demographic details, completion of the Oxford Knee Score, Short Form-12 Health Survey, and King's College Hospital's Vascular Quality of Life Questionnaire, and measurement of the ankle brachial pressure index (ABPI). Of the 209 eligible patients, 86 (41%) participated (median age, 73 years; 50% male). Five (5.8%) patients had a reduced ABPI compared with population norms of 4.6 to 7%. Patients with reduced ABPI measurements had higher Oxford Knee Scores, but no relationships between other variables were demonstrated. TKR surgery does not appear to increase the risk of CLI.     

Does pretransplant obesity affect the outcome in kidney transplant recipients?

The effect of obesity on renal transplant outcome remains unclear due to conflicting published studies. The purpose of this study was to assess whether obesity affects the outcome in renal transplant patients. METHODS: We retrospectively analyzed 33 obese (BMI >30; mean = 34.1 +/- 3.68; group I) and 35 nonobese (BMI < or = 30; mean = 23.6 +/- 3.18; group II) renal transplants performed at our center between March 1999 to December 2002. These two groups were well matched with respect to age, sex, donor source, hypertension, diabetes, ischemic heart disease, hyperlipidemia, native kidney disease (PCKD, 6 vs 4; diabetic, 5 vs 4; glomerulonephritis, 6 vs 7; FSGS, 2 vs 2 and IgA, 2 vs 7), HLA mismatch and immunosuppressants medications (Neoral, 21 vs 25; tacrolimus, 11 vs 10; Cellcept, 28 vs 31; Prednisone, 33 vs 35; ATG, 7 vs 8; Basiliximab, 14 vs 13 and Rapamycin, 5 vs 2, groups I and II, respectively). Follow-up was from 7 months to 4.4 years. RESULTS: Significant differences were noted in operating time, wound infection, perinephric hematoma, lymphocele, and number of hospital days. There were no significant differences between the two groups in the incidence of wound dehiscence, deep vein thrombosis, pulmonary embolism, atelectasis, urine leak, delayed graft function, acute rejection rate, and the following posttransplant variables: diabetes mellitus, myocardial infarction, hyperlipidemia, hypertension, and incisional hernia. We conclude that obesity significantly increases operating time, wound complications, and hospitalizations.     

Does laparoscopic Nissen fundoplication lead to chronic gastrointestinal dysfunction?

Background Laparoscopic Nissen fundoplication (LNF) efficiently controls the symptoms of gastroesophageal reflux disease (GERD); however, other nonspecific gastrointestinal (GI) symptoms have been reported following LNF. The aim of this study was to evaluate the long-term effects of LNF on nonspecific GI complaints. Methods The basis for this study is the prospective follow-up of 515 patients (mean age 46 ± 13 years) who underwent a LNF between 1992 and 1998. A questionnaire was designed to evaluate GERD symptoms (i.e., heartburn, epigastric pain, regurgitation, dysphagia, and fullness, score 0–60) and nonspecific GI symptoms (i.e., vomiting, diarrhea, constipation, and lack of appetite, score 0–48). Patients were assessed before surgery, at 6 months, 2 years, and 5 years after surgery. Results Laparoscopic Nissen fundoplication was associated with a significant decrease in both GERD and nonspecific GI symptoms score at 6 months and up to 5 years, in the whole group (p < 0.001). 360 patients (69.7%) had preoperative nonspecific GI symptoms and experienced a significant reduction in these symptoms following the surgery and lasting up to 5 years. The other 155 patients (30.3%) had no preoperative GI symptoms (GI symptoms score of 0). In this group, there was a small but statistically significant increase in GI symptoms score (p < 0.001). It was, however, clinically significant (defined as a score >12) in only 9.9% of the patients. Conclusions Laparoscopic Nissen fundoplication provides an efficient treatment of GERD up to 5 years, and in a majority of patients, it is not associated with any significant increase in nonspecific GI complaints. New nonspecific bowel symptoms can develop after LNF in some patients but are unlikely to be clinically significant. Presented to the Society of American Gastrointestinal Endoscopic Surgeons, Hollywood, Florida, April 2005     

Is prolonged cold ischemia a contraindication to using kidneys from acute kidney injury donors?

To determine the impact of prolonged cold ischemia time (CIT) on the outcome of acute kidney injury (AKI) renal grafts, we therefore performed a single‐center retrospective analysis in adult patients receiving kidney transplantation (KT) from AKI donors. Outcomes were stratified according to duration of CIT. A total of 118 patients receiving AKI grafts were enrolled. Based on CIT, patients were stratified as follows: (i) <20 hours, 27 patients; (ii) 20‐30 hours, 52 patients; (iii) 30‐40 hours, 30 patients; (iv) ≥40 hours, nine patients. The overall incidence of delayed graft function DGF was 41.5%. According to increasing CIT category, DGF rates were 30%, 42%, 40%, and 78%, respectively (P = .03). With a mean follow‐up of 48 months, overall patient and graft survival rates were 91% and 81%. Death‐censored graft survival (DCGS) rates were 84% and 88% for patients with and without DGF (P = NS). DCGS rates were 92% in patients with CIT <20 hours compared to 85% with CIT >20 hours (P = NS). In the nine patients with CIT >40 hours, the 4‐year DCGS rate was 100%. We conclude that prolonged CIT in AKI grafts may not adversely influence outcomes and so discard of AKI kidneys because of projected long CIT is not warranted when donors are wisely triaged.     

Does delayed graft function in the first kidney transplant influence graft outcome in a subsequent transplant?

Background

In kidney transplantation, delayed graft function (DGF) portends adverse graft and patient outcomes. It is unclear whether DGF in the first kidney transplant would adversely impact the outcome of a subsequent transplant.

Methods

Utilizing data from the Organ Procurement and Transplant Network, we identified patients ≥ 18 years of age who underwent at least two deceased donor kidney transplantation (DDKT) between 1987 and 2010. Patients were then divided into two groups based on whether or not they developed DGF in the first transplant (1st TXP DGF group and 1st TXP no-DGF group). Unadjusted and adjusted graft survivals (Cox regression) between the groups were compared.

Results

A total of 10,628 patients were identified who received more than one DDKT (3672 patients in the 1st TXP DGF group and 6956 patients in the 1st TXP no-DGF group). A higher incidence of DGF was observed with the second transplant in patients who had DGF in the first transplant (34% vs 26%, P = .001). Unadjusted graft survival for the second transplant was superior in the 1st TXP no-DGF group (P = .002). After correction for confounding variables, DGF in the first transplant did not have significant adverse impact on the graft survival of the second transplant (hazard ratio 1.2 with 95% confidence interval 0.96–1.09, P = .44).

Conclusions

In patients undergoing more than one DDKT, DGF in the first transplant is associated with higher incidence of DGF in the subsequent transplant but did not have independent adverse influence on the outcome of that graft.     

Does subclinical rejection contribute to chronic rejection in renal transplant patients?

Renal allograft biopsies have traditionally been performed in the setting of acute graft dysfunction. However, several groups have performed graft biopsies at times of stable graft function, and more recently, after treatment of rejection episodes. Surprisingly, unequivocal histologic criteria for acute rejection have been demonstrated in a high proportion of these protocol biopsies. The Winnipeg Transplant Group has documented the high prevalence of clinically silent inflammatory infiltrates in early protocol biopsies, and demonstrated their inflammatory and cytotoxic potential by immunohistochemical and molecular biological techniques. Furthermore, in a randomized trial, our group has demonstrated that subclinical rejection, if untreated, is associated with the development of early chronic pathology and late graft dysfunction. In this overview, we will summarize the early data on subclinical allograft inflammation, present the experience of the Winnipeg Transplant Group, and discuss the possible implications of subclinical rejection on the development of chronic rejection.     

Does repeated Ramadan fasting adversely affect kidney function in renal transplant patients?

This is a prospective cohort study in renal transplant patients who fasted or who did not fast for three consecutive Ramadans. The baseline estimated glomerular filtration rate (GFR), mean arterial pressure (MAP), and urinary protein excretion before the first Ramadan were compared to those after the third Ramadan in 35 fasters and 33 nonfasters. The effect of age, time after transplantation, presence of diabetes mellitus (DM), and proteinuria on changes in the GFR were studied. The two groups were comparable in gender, age, donor source, time posttransplantation, presence of DM, hypertension, proteinuria, serum creatinine, and MAP. Among the fasters, there was no change in estimated GFR after fasting for three Ramadans (56.4 mL/min versus 55.4 mL/min, P=0.8) even after adjusting for age, DM, baseline GFR, proteinuria, or time after transplantation. There were no significant differences between the fasters and the nonfasters in the changes in GFR, MAP, and urinary protein excretion between baseline and the third Ramadan.     

Does donor brain death influence acute vascular rejection in the kidney transplant?

BACKGROUND: There is increasing experimental evidence to suggest that donor brain death enhances susceptibility to early inflammatory responses such as acute rejection in the kidney transplant. The aim of the present study was to establish whether the injury induced or aggravated by donor brain death could exert an effect on recipient immunologic tolerance by comparing data from patients receiving a kidney from non-heart-beating donors (NHBD) or from brain-dead donors (BDD). METHODS: We reviewed data corresponding to 372 renal transplants performed from January 1996 to May 2002. The data were stratified according to donor type as 197 (53%) brain-dead and 175 (47%) non-heart-beating donors, and the two groups were compared in terms of acute vascular rejection by Cox's regression analysis. RESULTS: The rate of vascular rejection was 28% in the BDD group and 21.7% in the NHBD (P=0.10). The following predictive variables for acute vascular rejection were established: brain death [RR 1.77 (95% CI 1.06-3.18)], presence of delayed graft function [RR 3.33 (1.99-5.55)], previous transplant [RR 2.35 (1.34-4.13)], recipient age under 60 years [RR 1.86 (0.99-2.28)], female recipient [RR 1.50 (0.99-2.28)], cerebrovascular disease as cause of donor death [RR 1.72 (1.02-2.91)], and triple therapy as immunosuppressive treatment. CONCLUSION: Donor brain death could be a risk factor for the development of vascular rejection in kidney recipients. This process could affect the quality of the graft and host alloresponsiveness. Delayed graft function in transplants from dead brain donors could be a reflection of severe autonomic storm, leading to a higher incidence of vascular rejection in these patients.     

Does neutrophyl to lymphocyte ratio really predict chronic kidney disease progression?

International Urology and Nephrology - Chronic kidney disease (CKD) is an inflammatory process. In addition to increased morbidity and mortality, inflammation also contributes to the progression of...     

Does etiology of end-stage renal disease affect sleep quality in kidney transplant recipients?

BACKGROUND: That hypertension (HTN) as a leading cause of end-stage renal disease (ESRD) is linked to sleep disorders in the general population can be the basis of a hypothesis that HTN may be a contributing factor to the poor quality of sleep in some kidney transplant recipients. This study was designed to investigate the correlation between ESRD secondary to HTN and sleep quality among kidney transplant recipients. METHODS: In this case control study, 201 kidney transplant recipients were divided into group I (ESRD) secondary to HTN, (n=82) and group II (ESRD secondary to other causes, n=119). The groups were matched for medical comorbidities, demographic and clinical data, and symptoms of anxiety and depression. Sleep quality assessed by means of the Pittsburgh Sleep Quality Index (PSQI) was compared between the study groups. RESULTS: The mean (SD) of the total PSQI score was significantly high in group I compared with group II (7.42 +/- 2.36 vs 6.60 +/- 3.07, P=.042). Similar results were observed for the sleep duration scores in the groups (1.22 +/- 1.12 vs 0.86 +/- 1.12, P=.026). In group I, all the other PSQI components were higher than those in group II, difference that were statistically significant. CONCLUSION: Sleep quality and duration was poorer among our kidney transplant recipients with ESRD secondary to HTN compared with the controls. Further studies, however, are required to investigate whether HTN is responsible for the reported poor quality of sleep in some kidney transplant recipients.     

Serum calcitonin and endothelial dysfunction in chronic kidney disease: a novel risk factor?

Background

Endothelial dysfunction (ED) is highly prevalent in patients with CKD. The relationship between ED and calcitonin has not been demonstrated before in CKD patients.

Methods

The study included non-diabetic CKD patients not on dialysis. Demographic data (age, gender, comorbidities, current drug therapy, smoking status, weight, and height) were collected from the individual charts in the hospital’s electronic database. After overnight fasting, laboratory measurements including serum calcitonin levels were performed in all patients. A single observer who was blinded to the results of the study assessed ED by measurement of flow-mediated dilatation (FMD).

Results

In total, 84 CKD patients (41 men, age 45.1 ± 13.3 years) were included. Thirty-seven patients had stage 3 and 47 patients had stage 4 CKD. Patients with calcitonin levels above the median had lower FMD (6.87 ± 0.58 vs. 7.23 ± 0.66, P = 0.008) when compared with patients with calcitonin levels below the median. None of the other demographic, laboratory and clinical parameters was different between the two groups. In multivariate regression analysis, serum calcitonin (P = 0.01), fetuin-A (P < 0.001), high-sensitive C-reactive protein (P < 0.001), and hemoglobin (P = 0.004) were independently associated with FMD.

Conclusion

Our present study demonstrated for the first time that serum calcitonin is independently related with ED. This finding deserves further experimental and clinical exploration, in order to elucidate whether calcitonin is an innocent bystander or has a pathophysiologic relationship with ED in patients with CKD.     

Liver alone or simultaneous liver–kidney transplant? Pretransplant chronic kidney disease and post‐transplant outcome – a retrospective study

The new Organ Procurement and Transplant Network/United Organ Sharing Network (OPTN/UNOS) simultaneous liver–kidney transplant (SLK) policy has been implemented. The aim of this study was to review liver transplant outcomes utilizing the new SLK policy. Liver transplant alone (LTA) and SLK patients between 2009 and 2015 were reviewed. Graft survival and post‐transplant kidney function were investigated among LTA patients meeting the chronic kidney disease (CKD) criteria of the new policy (LTA‐CKD group). To validate our findings, we reviewed and applied our analysis to the OPTN/UNOS registry. A total of 535 patients were eligible from our series. The LTA‐CKD group (n = 27) showed worse 1‐year graft survival, compared with the SLK group (n = 44), but not significant (81% vs. 93%, P = 0.15). The LTA‐CKD group significantly increased a risk of post‐transplant dialysis (odds ratio = 5.59 [95% CI = 1.27–24.7], P = 0.02 [Ref. normal kidney function]). Post‐transplant dialysis was an independent risk factor for graft loss (hazard ratio = 7.25, 95% CI = 3.3–15.91, P < 0.001 [Ref. SLK]). In the validation analysis based on the OPTN/UNOS registry, the hazard of 1‐year‐graft loss in the LTA‐CKD group (n = 751) was 34.8% higher than the SLK group (n = 2856) (hazard ratio = 1.348, 95% CI = 1.157–1.572, P < 0.001). Indicating SLK for patients who meet the CKD criteria may significantly improve transplant outcomes.