The possibility of SARS-CoV-2 transmission in a haemodialysis unit - report from a large in-hospital centre.

Data on the possibility of transmission of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) during the provision of chronic haemodialysis, which often entails many person-to-person contacts, are lacking. We report a follow-up of the in-centre contacts of three positive chronic haemodialysis patients. Under strict preventive measures, only one patient out of 21 patient-contacts and 29 personnel-contacts tested positive within 2 weeks after the last contact. This patient, case #3, most likely became infected during unprotected, organised group transportation to the dialysis centre.

High mortality in the first year after kidney graft failure.

BACKGROUND: The aim of our cohort study was to assess survival of the patients after kidney graft failure. METHODS: Patients starting dialysis after graft failure between January 1, 2004 and December 31, 2010 were identified from the Slovenian Renal Replacement Therapy (RRT) Registry and followed to December 31, 2011. The control group consisted of 351 incident dialysis patients, who were kidney transplant candidates. Survival data were not censored for retransplantations. RESULTS: After a median of 7.4 (interquartile range [IQR]) 0.4-13.0) years with a functioning graft and a median of 15.5 (IQR 7.8-20.7) years on RRT 82 patients started dialysis. Their mean (± standard deviation [SD]) age was 50.4 ± 12.7 years vs 49.2 ± 13.9 years for the incidental transplantation candidates (P = .49). There were sixty-one percent men (vs 64%; P = .67), and all subjects were on hemodialysis treatments. By Dec 31, 2011, 19 (23%) patients had undergone retransplantation and 27 (33%) died after a median of 1.6 (IQR 0.2-5.4) months on dialysis. The causes of death were infection (n = 15), cardio-disease-vascular (n = 6), malignancy (n = 4), or cerebrovascular (n = 2). Deceased patients were significantly older: 60.0 ± 7.9 vs 45.7 ± 12.0 years (P < .001) and more often men: (78% vs 53% P = .05). The unadjusted overall 1- and 3-year survivals rates after graft failure of 70% and 68% were significantly lower than those in the control candidate group of (98% and 93%, respectively (log-rank; P < .001). This difference remained significant upon multivariate analysis (hazard ratio [HR], 12.0; P < .001). The subgroup of 53 patients who started dialysis after chronic graft failure showed unadjusted 1- and 3-year survival rates of 82% and 80%, respectively which were still worse than the control group (P = .001), a difference that remained significant upon multivariate analysis (HR, 1.75; P < .001). CONCLUSION: After kidney graft failure patients experienced increased mortality in the first year after restarting dialysis. However, subjects who survived the first year showed good survival thereafter.

Increase in proteinuria after acute kidney graft rejection is associated with decreased graft function and survival.

BACKGROUND: There are limited data on the relationship between acute kidney graft rejection, proteinuria, and outcome. We hypothesized that an increase in proteinuria after an acute rejection episode is associated with decreased graft function and survival. METHODS: We tested our hypothesis in a national historic cohort study of 506 recipients of deceased donor kidney transplantations between January 2000 and December 2010. The selection criterion was a biopsy-confirmed first acute rejection episode. Proteinuria was measured using urine protein/creatinine ratios (UPCR) at baseline (lowest serum creatinine before biopsy), time of biopsy, and 3 months thereafter. We examined the effects on outcomes of a change in UPCR (ΔUPCR = UPCR at 3 months after biopsy - baseline UPCR). RESULTS: In the observed period, 86 patients experienced a biopsy-confirmed acute rejection episode. Three patients with primary graft nonfunction were excluded. Among the remaining 83 patients the median time to acute rejection was 6 (interquartile range, 2-39) months, and median follow-up was 60 (interquartile range, 35-124) months. Receiver operator characteristic analysis demonstrated that ΔUPCR cutoff value of 20 mg/mmol showed the best discriminatory ability to predict graft loss or patient death (sensitivity, 84%; specificity, 73%). There were 41 patients with ΔUPCR ≥20 mg/mmol, whereas 42 patients had ΔUPCR <20 mg/mmol. Patients with ΔUPCR ≥20 mg/mmol had worse graft function at 3 months after the biopsy with mean (±SD) estimated glomerular-filtration rate (eGFR) of 35 ± 19 versus 47 ± 14 mL/min/1.73 m(2) (P = .002), as well as a higher rate of composite graft loss and patient death (37% vs 10%; P = .004). Cox regression analyses revealed ΔUPCR ≥20 mg/mmol, delayed graft function, and antibody-mediated rejection to be significant factors associated with the composite outcome (hazard ratios, 4.3, 2.5, and 3.4, respectively; P < .05). CONCLUSION: Increased proteinuria after an acute kidney graft rejection episode was associated with decreased graft function and survival, serving as a surrogate marker for poor outcomes.

Plasma exchange and intravenous immunoglobulin in the treatment of antibody-mediated rejection after kidney transplantation: a single-center historic cohort study.

BACKGROUND: Antibody-mediated rejection (AMR) of a kidney graft has been increasingly recognized as an important cause of graft failure. Our historic cohort study sought to analyze its treatment and outcomes at our center. METHODS: All patients with AMR between 2005 and 2011 were treated with plasma exchange (PE), intravenous low-dose cytomegalovirus (CMV) hyperimmune globulin, and adjustment of basal immunosuppression. We analyzed data regarding baseline characteristics, rejection treatment with focus on PE, complications, and 1-year outcomes. RESULTS: Twenty-three AMRs occurred in 23 patients (10 male, 13 female) of mean age 41 ± 16 years, all recipients of deceased-donor kidneys with a median of 3 HLA mismatches. The subjects had a median peak panel-reactive antibodies (PRA) of 7% (interquartile range [IQR] 1%-10%). Basal serum creatinine was 174 ± 84 µmol/L estimated glomerular filtration rate (eGFR) (eGFR 42 ± 22 mL/min/1.73 m(2)), while 3 patients were dialysis- dependent. Median period between transplantation and rejection was 38 months (IQR 1.5-88.5). Concomitant T-cell-mediated rejection was treated in 78% of cases. Median number of PE procedures per patient was 10 (range, 5-17). Treatment was estimated to be successful in 83%. Donor-specific antibodies documented in 12 patients (52%) disappeared or showed reduced titers in 7/10 patients with repeated measurements. An infection was present during treatment in 7 (30%) patients. Among 237 PE, there was 1 (0.4%) mild allergic reaction to fresh frozen plasma and significant metabolic alkalosis occurred after 7 (3%) procedures. One year after rejection the mean serum creatinine level was 144 ± 52 µmol/L and Kaplan-Meier estimated graft and patient survival rates were 62% and 95%, respectively. CONCLUSIONS: Intensive treatment with PE, intravenous immunoglobulin, and adjustment of basal immunosuppression were safe and effective to reverse AMR with improved graft function in the majority of patients. However, AMR was associated with markedly decreased 1-year graft survival and the optimal treatment remains uncertain.

Functional status of hemodialysis arteriovenous fistula in kidney transplant recipients as a predictor of allograft function and survival.

There is no accepted policy for preserving or ligating arteriovenous fistula (AVF) after successful kidney transplantation. The aim of this study was to compare kidney graft function and survival between patients with a functional AVF at 1 year after-transplantation with those having a nonfunctional AVF. This historical cohort study included 311 kidney transplant recipients between January 2000 and December 2008 with a functional AVF at the time of transplantation. Patients were divided into 2 groups according to functional status of AVF at 1 year after transplantation. Graft function was assessed at 1 year by serum creatinine and estimated glomerular filtration rate (eGFR) using the 4-variable Modification of Diet in Renal Disease formula. Kaplan-Meier and Cox proportional hazards analyses were used to assess the relationship between the functional status of the AVF and graft survival. The 311 recipients had a mean age of 47 ± 11 years (range, 14 to 70) with 188 (60.5%) males. Patients with functional AVF at 1 year (n = 239) showed higher serum creatinine and lower eGFR values than those with nonfunctional AVF (n = 72): namely 110 ± 38 µmol/L and 69 ± 21 mL/min/1.73 m(2) versus 99 ± 30 µmol/L and 74 ± 19 mL/min/1.73 m(2), respectively (P < .05). Persistence of a functional AVF at 1 year after transplantation was associated with a greater incidence of eGFR <60 mL/min/1.73 m(2) compared with nonfunctional AVF: 36.8% versus 23.6% (odds ratio, 1.885; 95% confidence interval [CI], 1.031-3.450; P = .038). The 5-year allograft survival rates were 60% among patients with a functional AVF versus 75% among those with a nonfunctional AVF (P = .045). The adjusted analyses revealed the persistence of a functional AVF to be associated with an increased risk for future allograft loss (hazard ratio, 1.336; 95% CI, 1.018-1.755; P = .037). In conclusion, the persistence of a functional AVF was associated with a lower eGFR at 1 year after-transplantation and an increased risk for future allograft loss.

Early kidney graft size and Doppler parameters are associated with kidney graft function 1 year after transplantation.

BACKGROUND: The aim of this study was to assess the association of various ultrasonography (US) and Doppler parameters of kidney graft as measured at 1 month posttransplant with 1-year graft function. MATERIALS AND METHODS: The study cohort included 125 adult recipients of deceased donor kidney transplantations between January 2006 and February 2009. All patients underwent an US-Doppler examination performed by a trained nephrologist at 1 month posttransplant using an Acuson-Siemens Sequoia 512. Graft length and intrarenal Doppler indices were measured at the midsegmental artery level. Relative graft size was calculated by dividing graft length with body mass index. Graft function was assessed at 1 year by estimated glomerular filtration rate (eGFR) using the 4-variable Modification of Diet in Real Disease study equation. Linear and logistic regression analyses were used to assess the relationship between US-Doppler parameters and eGFR. RESULTS: Univariate linear regression showed a significant correlation between eGFR at 1 year and graft length at 1 month (P = .009), relative graft length <0.50 cm per kg/m(2) (P = .004), resistance index >0.75 (P = .031), and end-diastolic velocity <9 cm/sec (P = .006). Logistic regression analyses showed that eGFR <60 mL/min/1.73 m(2) at 1 year was significantly associated with graft length <12 cm at 1 month (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.16-4.92; P = .017), relative graft length <0.5 cm per kg/m(2) (OR, 2.54; 95% CI, 1.20-5.35; P = .014), resistance index >0.75 (OR, 2.86; 95% CI, 1.30-6.29; P = .009), and end-diastolic velocity <9 cm/sec (OR, 2.37; 95% CI, 1.01-5.56; P = .047). CONCLUSION: In this retrospective analysis, kidney transplant recipients with greater graft length at 1 month, specifically when standardized to body size, showed better graft function at 1 year posttransplantation. Higher intrarenal diastolic blood flow and lower resistance index at 1 month were also predictive of better graft function at 1 year.

Pretransplant soluble CD30 serum concentration does not affect kidney graft outcomes 3 years after transplantation.

INTRODUCTION: An elevated serum concentration of soluble the form of CD30 (sCD30), an activation marker of mainly T(H)2-type cytokines producing T lymphocytes, has been reported as a predictive factor for acute cellular rejection episodes and poor graft outcomes in kidney transplantation. This historic cohort study investigated the association of a pretransplant sCD30 serum concentrations with kidney graft function and graft survival 3 years posttransplantation in adult recipients of deceased donor kidney grafts, treated with monoclonal anti-CD25 antibodies as an induction treatment combined with a cyclosporine (CsA)-based maintenance triple therapy. MATERIALS AND METHODS: The pretransplant sera of 296 recipients were tested for sCD30 content using a microsphere flow-cytometry assay. The estimated glomerular filtration rate (eGFR) was determined by the 4-variable Modification of Diet in Renal Disease equation. The incidences of graft loss were calculated with the use of Kaplan-Meier survival analysis and compared using the log-rank test. RESULTS: According to the distribution of the pretransplant sCD30 levels concentration ≥2700 pg/mL was defined as high (n = 146) and concentration <2700 pg/mL as low (n = 150). Three years posttransplantation, the eGFR was not significantly different in the recipients in high and low sCD30 groups (65 ± 24 vs 67 ± 21 mL/min/1.73 m(2); P = .43); there was no association between the eGFR 3 years after transplantation and the pretransplant sCD30 levels (r(2) = 0.002; P = .49). Graft survival 3 years after transplantation was also not different in the recipients in high and low sCD30 groups (P = .52). CONCLUSION: In our adult deceased-donor kidney graft recipients, the pretransplant sCD30 serum concentration was not a predictive factor of immunologic risk associated with the kidney graft function 3 years posttransplantation; neither did it affect graft survival 3 years after transplantation. The immunosuppression with anti-CD25 antibodies as an induction treatment combined with the CsA-based maintenance triple therapy could possibly be decisive for our findings.

Subclinical left ventricular echocardiographic abnormalities 1 year after kidney transplantation are associated with graft function and future cardiovascular events.

Cardiovascular events (CVE) are the leading cause of mortality in kidney transplant recipients. Increased left ventricular mass (LVM) is a risk factor for CVE. This study investigated the associations of LVM with impaired kidney graft function expressed as lower glomerular filtration rate (GFR) at 1 year after transplantation and future CVE beyond 1 year. The prospective study cohort included 68 nondiabetic recipients of a kidney transplant between January 2004 and December 2005 who underwent a transthoracic echocardiographic investigation at 1 year after transplantation. LVM and left ventricular hypertrophy (LVH) were assessed using 2-dimensional M-mode echocardiography. GFR was estimated (eGFR) by the 4-variable Modification of Diet in Renal Disease formula. Cox proportional hazards analysis was used to estimate cardiac CVE (angina pectoris, acute myocardial infarct, coronary angioplasty or bypass surgery, or sudden cardiac death) hazard ratios (HRs) for patients with LVH versus control subjects with no LVH at 1 year after transplantation. All patients had normal systolic function (ejection fraction >50%) with no symptoms or signs of heart failure. LVH was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m(2) compared with 40 patients with eGFR ≥60 mL/min/1.73 m(2) (248 ± 61 g and 86% vs 210 ± 46 g and 50%, respectively; P < .01). After a median follow-up of 4.5 years, there were 18 (26.5%) cardiac CVE. The incidence of CVE was higher in patients with LVH than in patients with no LVH at 1 year after transplantation (36.4% vs 8.3%; P = .020). In adjusted analyses, LVH was associated with an increased risk for future CVE (HR, 4.69; 95% confidence interval, 1.02-21.5; P = .037). In kidney transplant recipients, a lower eGFR at 1 year after transplantation was associated with greater LVM and higher incidence of LVH. Presence of LVH was associated with an increased risk for future CVE.

Treatment of hyperparathyroidism with cinacalcet in kidney transplant recipients.

BACKGROUND: After successful kidney transplantation, hyperparathyroidism can persist in 10%-50% of patients and can harmfully affect bone metabolism. Calcimimetic cinacalcet is a new treatment option in the management of persistent hyperparathyroidism in these patients. METHODS: This prospective, clinical study of 11 patients included those who had a serum intact parathyroid hormone (iPTH) concentration >65 ng/L, a serum creatinine concentration was <200 µmol/L, stable kidney graft function, and were >1 year since transplantation. Patients were not treated with drugs other than calcitriol that could influence bone metabolism. During the 6-month observation period, in which the stability of measured parameters was determined, and in the 12-month treatment period (cinacalcet 30 mg/d), we followed serum concentrations of calcium, phosphate, iPTH, creatinine, vitamin 25OH D(3), bone-specific alkaline phosphatase (ALP), osteocalcin, collagen degradation fragments (CTX), urinary calcium excretion, and bone mineral density (BMD). RESULTS: During the treatment period, the serum calcium concentration decreased significantly (from 2.50 ± 0.12 to 2.32 ± 0.12 mmol/L; P < .01). Serum iPTH concentration decreased significantly (from 247 [range, 199-362] at time 0 to 198 [range, 165-233] ng/L after 1 month of treatment; P < .05), but increased slightly thereafter. After 6 months of treatment, the serum concentration of ALP and CTX increased significantly, but decreased thereafter. There were no significant changes in the other parameters assessed. Renal function remained stable during the treatment period. The BMD of the lumbar spine, hip, and forearm did not change during the 12 months of treatment. CONCLUSION: Cinacalcet was effective in treating posttransplant hyperparathyroidism, resulting in decreased calcemia and transient decreased iPTH. ALP and CTX transiently increased during therapy, but other markers of bone metabolism remained unchanged. Twelve months of cinacalcet treatment did not result in a change in BMD. Cinacalcet seems to be a safe drug with no negative effect on renal function.

Changes in serum procalcitonin, interleukin 6, interleukin 8 and C-reactive protein in neonates after surgery.

INTRODUCTION: Aim of this study was to determine the kinetics of procalcitonin (PCT), interleukin-6 (IL-6), interleukin-8 (IL-8) and C-reactive protein (CRP) serum concentrations after different types of neonatal surgery. MATERIAL AND METHODS: We conducted a prospective, observational study in a level III multidisciplinary neonatal intensive care unit. We enrolled twenty-five (n=25) neonates undergoing major surgery (for gastroschisis, atresia of the small intestine, congenital diaphragmatic hernia, esophageal atresia, coarctation of the aorta, neurosurgical procedures). Serum PCT, IL-6, IL-8 and CRP were measured before surgery, immediately after surgery (POD 0) and on the first and second day after surgery (POD 1, 2). RESULTS: Median preoperative serum concentrations were: PCT 1.3 microg/l, IL-6 985 fmol/l, IL-8 51 pg/ml, CRP 6 mg/l. PCT increased insignificantly after surgery with a peak median concentration on POD 1 (2.0 microg/l), but concentrations varied considerably between patients in the same category of surgery. IL-6 significantly increased on POD 0 (median 2 262 fmol/l), with a peak median concentration on POD 1 (3 410 fmol/l), and decreased thereafter. IL-8 increased significantly after surgery with a peak median concentration on POD 0 (125 pg/ml) and decreased thereafter. IL-8 response was very consistent after all types of surgery. CRP only began to increase on POD 1 (median 20 mg/l) with a peak median concentration on POD 2 (21 mg/l). CONCLUSIONS: The physiological increase in PCT after birth and the impact of underlying disease make the interpretation of postoperative values in the immediate postnatal period difficult. IL-6 is a very sensitive marker of neonatal surgical injury with considerable variation between different types of surgery. IL-8 response after neonatal surgery is similar after all types of surgery, very rapid and transient with relatively low concentrations. CRP response to surgery is slow with persistence of elevated levels throughout the study period. IL-8 could potentially be a useful marker for monitoring infection in the immediate postoperative period in neonates.

Does pretransplant soluble CD30 serum concentration affect deceased-donor kidney graft function 3 years after transplantation?

Elevated serum concentrations of soluble CD30 molecule (sCD30) have been related to acute cellular rejection and poor graft outcomes in kidney transplantation. This historical cohort study investigated the association of pretransplant sCD30 serum concentrations with kidney graft function expressed as estimated glomerular filtration rate (GFR) at 3 years after transplantation. Pretransplant sera from 176 adult deceased-donor kidney graft recipients were tested for sCD30 content using a commercially available automated enzyme-linked immunosorbent assay. The immunosuppression consisted of induction therapy with monoclonal anti-CD25 antibodies and a maintenance regimen of cyclosporine (CsA)-based therapy. GFR was estimated (eGFR) by the four-variable Modification of Diet in Renal Disease (MDRD) Study equation. According to the distribution of pretransplant sCD30 levels (median 66.7 U/mL; interquartile range, 46.6 to 98.6 U/mL), a concentration of 66 U/mL or higher was defined as high (n = 89) and below 66 U/mL as low (n = 87). Three years after transplantation, eGFR was not significantly different among recipients in high versus low sCD30 groups (69 +/- 23 mL/min/1.73m2 vs 66 +/- 21 mL/min/1.73m2; P = .327) and there was no correlation between eGFR and pretransplant sCD30 levels (r2 = 0.001; P = .73). Upon multivariate regression analysis, donor age, recipient body mass index at transplantation, and acute rejection episodes were independent variables affecting eGFR at 3 years after transplantation. This study showed that pretransplant sCD30 serum concentrations were not associated with deceased-donor kidney graft function at 3 years after transplantation. The immunosuppression with anti-CD25 antibodies and a triple CsA-based maintenance regimen could possibly be decisive for our findings.

Left ventricular mass is associated with ventricular repolarization heterogeneity one year after renal transplantation.

Ventricular repolarization heterogeneity (VRH) is associated with the risk of arrhythmia and cardiac death. This study investigated the association between VRH and left ventricular mass (LVM) in renal transplant recipients 1 year after transplantation. Echocardiography and 5-min 12-lead electrocardiogram were recorded and GFR was estimated (eGFR) in 68 nondiabetic patients. Beat-to-beat QT interval variability algorithm was used to calculate SDNN-QT and rMSSD-QT indices of VRH. To quantify QT interval variability relative to heart rate fluctuations, QTRR index was calculated. Left ventricular hypertrophy (LVH) was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m(2) compared with 40 patients with eGFR > or =60 mL/min/1.73 m(2) (248 +/- 61 g and 86% vs. 210 +/- 46 g and 50%, respectively; p < 0.01). A direct correlation was found between LVM and SDNN-QT (R = 0.47, R(2)= 0.23; p < 0.001), rMSSD-QT (R = 0.27; R(2)= 0.10; p = 0.034), and QTRR (R = 0.55; R(2)= 0.31; p < 0.001) indices. In conclusion, greater LVM is associated with increased VRH in renal transplant recipients, providing a link with the high risk of arrhythmia and cardiac death, specifically in patients with decreased graft function.

Basiliximab versus daclizumab combined with triple immunosuppression in deceased donor renal graft recipients.

In this prospective, randomized, open-label, single-center study, we compared the efficacy and safety of two anti-interleukin-2 receptor monoclonal antibodies among adult recipients of at least 1 HLA-mismatched deceased donor renal grafts. Eligible patients were randomized to induction with either basiliximab or daclizumab. Both groups received cyclosporine microemulsion (CsA Neoral), mycophenolate mofetil, and methylprednisolone. An intent-to-treat analysis of 1-year data assessed the incidence of acute rejection episodes, the renal graft function, the safety, and the patient and graft survivals. Among 127 patients, six (10.0%) and seven (11.5%) patients experienced biopsy-confirmed acute rejection at 12 months, in the basiliximab and the daclizumab groups, respectively. Two renal grafts were lost in the basiliximab and six in the daclizumab cohort, one of them due to rejection. One basiliximab and two daclizumab patients died. Hospital treatment was required for 25 and 33 infections in basiliximab and daclizumab groups, respectively. One basal cell carcinoma of skin was detected. One hypersensitivity reaction was observed with daclizumab. At 12 months, serum creatinine was 101+/-28 micromol/L with basiliximab and 109+/-41 micromol/L with daclizumab. Patient survival was 98.4% with basiliximab and 96.7% with daclizumab, and graft survival was 96.8% versus 90.8%, respectively. No significant differences were observed between the groups. Basiliximab or daclizumab combined with triple therapy was an efficient and safe immunosuppression strategy, demonstrated with low incidence of acute rejection episodes, an acceptable adverse event profile, excellent graft function, and high survival rates in adult recipients within the first year after deceased donor renal transplantation.

Effective immunoprophylaxis with basiliximab plus triple therapy in renal transplantation: five-year single-center experience.

We studied prospectively the efficacy and safety of basiliximab combined with triple immunosuppression in adult recipients of > or = 1 HLA-mismatched deceased donor renal grafts. All studied patients received equal immunosuppressive drugs: 20 mg infusion of basiliximab on day 0 and on day 4, cyclosporine microemulsion (Neoral), mycophenolate mofetil, and methylprednisolone. An analysis of 1-year data assessed the incidence of acute rejection episodes, safety of this therapy, renal graft function, and patient and graft survivals. One hundred seventy-two patients were studied. The HLA-antigen mismatches were 2.9 +/- 0.9 (mean +/- SD), and the cold ischemia time was 22.0 +/- 7.5 hours. Fifty-three (31.5%) patients experienced delayed graft function. At 12 months, 5 (3.0%) patients experienced acute rejection. Six renal grafts were lost, but not from rejection. Two patients died. Sixty-six infections required treatment in the hospital. One carcinoma of cervix (in situ) and two basal cell carcinomas of skin were detected. Hypersensitivity reactions and cytokine-release syndrome were not observed. At 12 months, serum creatinine was significantly higher (119 +/- 46 micromol/L; P < .001) in patients with delayed graft function than in patients with immediate graft function (99 +/- 26 micromol/L). Patient and graft survivals were 98.8% and 97.1%, respectively. Basiliximab combined with this triple therapy was an efficient and safe immunosuppression strategy, demonstrated with very low incidence of acute rejections, an acceptable adverse event profile, excellent graft function, and high short-term survival rates in adult recipients of deceased donor renal transplant.

De novo diabetic nephropathy on renal allografts.

BACKGROUND: Posttransplant diabetes mellitus (PTDM) is a well-recognized clinical problem following renal transplantation. Long-term risks of PTDM are similar to those of diabetes mellitus in general population. The aim of our study was to identify de novo diabetic nephropathy (DN) in our group of patients with PTDM. METHODS: Thirty-four patients with PTDM were reviewed retrospectively. Light microscopy, immunofluorescence, and electron microscopy techniques were performed in 10 of 21 patients with graft biopsy. RESULTS: Five patients (four women, one man), aged 47.4 years (range, 29 to 58), four of whom received cadaveric grafts, were found to have de novo DN. Their serum creatinine was 211.4 micromol/L (range, 140 to 294). Three patients were slightly proteinuric (0.3 to 0.5 g/L). PTDM was diagnosed 2.4 months after transplantation (range, 1 to 6). Histologic diagnosis of de novo DN was made, on average, 52.6 months after transplantation (range, 8 to 115), and 50.2 months (range, 2 to 114) after PTDM. De novo DN presented as diffuse diabetic glomerulosclerosis in four patients and nodular diabetic sclerosis in one patient, and combined with transplant glomerulopathy in all five patients. The mean graft survival time for this group of patients was equivalent with a control group. Although the difference in slopes of serum creatinine between the studied groups was clinically relevant, it was not statistically significant. CONCLUSION: In view of our findings, when histologic de novo DN was found in 5 out of 10 patients, one could conclude that de novo DN could be a frequent complication of PTDM.