Is aortic knob width a novel predictor of mortality in hemodialysis patients?

OBJECTIVE: Identifying reliable predictors of mortality in end-stage renal disease patients is crucial for patient outcomes. Aortic knob width is a radiographic parameter used to assess cardiovascular diseases and atherosclerosis. This study investigated the association between aortic knob width and mortality in hemodialysis patients. PATIENTS AND METHODS: The study included data collected between 2007 and 2022 from 103 patients aged between 18 and 85 who had been undergoing hemodialysis treatment for at least one year. Patients were divided into two groups: survivors and deceased. The aortic knob width was measured using a posterior-anterior chest radiograph after midweek hemodialysis. The relationship between aortic knob width and mortality was investigated. RESULTS: Deceased patients had significantly larger aortic knob widths compared with survivors. The deceased group's hemodialysis (HD) duration was shorter, median age was older, Kt/V, hemoglobin, and albumin levels were lower, and the frequency of patients with hypertension, diabetes, and aortic wall calcification was higher. Aortic knob width greater than 37.98 mm was identified as a predictor of mortality in hemodialysis patients. Survival rates for aortic knob width <37.98 mm are 98.1% for 1 year and 64.9% for 15 years. For aortic knob width larger than 37.98 mm, survival rates are 88% for three years, 68% for five years, 45.2% for ten years, and 25% for fifteen years. The most important risk factors for increased aortic knob width were age, male sex, aortic calcification, and hypertension. CONCLUSIONS: Age, male gender, aortic calcification, and hypertension are the primary risk factors for increased aortic knob width in hemodialysis patients. Aortic knob width greater than 37.98 mm, which can be measured simply and rapidly using posterior-anterior chest radiography, may be a predictor of mortality. Graphical Abstract: https://www.europeanreview.org/wp/wp-content/uploads/Graphical-Abstract-10.jpg.

Bone Disease and Serum Fibroblast Growth Factor-23 Levels in Renal Transplant Recipients.

BACKGROUND: Posttransplantation bone disease develops commonly and results in important complications. In this study, we aimed to investigate the relationship between bone diseases and serum fibroblast growth factor-23 (FGF-23) in renal transplant recipients. METHODS: This study was conducted in 106 kidney transplant recipients (KTrs; group G1) and 30 patients with chronic kidney disease (group G2). Patients with fever, heart failure, angina pectoris, acute renal failure, malignant disease, or any gastrointestinal disease were excluded. KTrs were treated with triple immunosuppressive drugs including glucocorticoids. Complete blood count (CBC), blood urea nitrogen (BUN), creatinine, glomerular filtration rate (GFR, Modification of Diet in Renal Disease [MDRD] formula), lipid profile, calcium (Ca), phosphorous (P), parathormone (PTH), 25OHD3, serum levels of tacrolimus/cyclosporine, and intact FGF-23 were measured. Bone mineral density (BMD) was measured with dual energy X-ray absorptiometry. RESULTS: The mean patient age was 40.1 ± 11.1 years and 39.2 ± 11.3 years in G1 and G2, respectively (P > .05). In G1 and G2, 76 and 15 patients were male, respectively. Compared with the G2 patients, G1 patients had lower body mass index (BMI), serum glucose levels, P, Mg, and Ca·P (P < .05 for all). T scores of the lumbar vertebrae/femur were -1.82 ± 0.99/-1.34 ± 0.89 and -1.13 ± 1.34/-0.51 ± 1.18 in G1 and G2 patients, respectively (P < .05 for all). The incidences of osteopenia/osteoporosis in the lumbar spine and femur were 50.9%/27.4% and 57.5%/10.4% in G1 and 16.6%/23.3%, and 40%/3.3% in G2. There were positive correlations between BMD and BMI, the time elapsed after renal transplantation, and GFR. In our study, a statistically significant relationship was found between lipid parameters and BMD, PTH, and 250HD3 levels, as well as use of corticosteroid and calcineurin inhibitors (P < .05 for all). In G1 and G2, BMD of the lumbar spine in patients with serum creatinine >1.5 mg/dL was lower than that in patients with serum creatinine <1.5 mg/dL. CONCLUSION: The association between age and BMD was found only in the femur of KTrs. No relationship was observed between serum FGF-23 levels and BMD values. In both groups, the BMD T score of the lumbar spine was lower compared to the BMD T score of the femur and in patients with serum creatinine >1.5 mg/dL. In long-term follow-up of renal transplantation by as much as 58 months, the incidence of bone disease such as osteoporosis/osteopenia was as high as 67% and was also higher than that of nontransplant patients with similar GFR. In addition to decreased renal function, dyslipidemia, inflammation, and continuing hypophosphatemia were also accompanied by decreased BMD as in cardiovascular disease in KTrs.

Avascular osteonecrosis and accompanying anemia, leucocytosis, and decreased bone mineral density in renal transplant recipients.

BACKGROUND: Avascular osteonecrosis (AVN) is a complication of renal transplantation. In this study, we present 12 cases of AVN associated with renal transplantation. METHODS: Renal transplant recipients (RTRs) with AVN (group I [GI]) were evaluated by using magnetic resonance imaging and blood urea nitrogen, creatinine, glucose, calcium, phosphorus, magnesium, alkaline phosphatase, parathyroid hormone, and urine analysis. We evaluated bone mineral density (BMD) of the femoral neck and lumbar vertebrae. All patients were treated with steroids, cyclosporine, or tacrolimus plus mycophenolate mofetil. Twenty-six RTRs (GII) without AVN were randomly selected as control subjects. RESULTS: The mean ages of GI and GII, were 33.81 ± 6.72 and 34.00 ± 7.65 years respectively (P > .05). The mean interval between transplantation and development of AVN was 12.08 ± 6.48 months. Although levels of blood urea nitrogen, creatinine, calcium, magnesium, and parathyroidhormone, as well as glucocorticoid doses in the first 12 months were similar in GI and GII, there were significant differences in serum alkaline phosphatase, hemoglobin levels, and white blood cell count between GI and GII (P < .05 for each). BMD T score <-1.5 was observed in 8/9 GI and 15/26 patients in GII. All of the patients with AVN except 1, were followed with conservative measures including calcium, magnesium, and vitamin D replacement therapies, bisphosphonate, and reduced or ceased glucocorticoid treatment. Although T scores of the femoral head were similar in GI and GII, the lumbar vertebral T score was significantly lower in GI than in GII (P < .052). CONCLUSION: AVN developed within the first year after transplantation. Decreased lumbar vertebral BMD, which can be an indicator of glucocorticoid effect, accompanied AVN in nearly all patients. Despite the absence of renal dysfunction, increased bone destruction, anemia, and leucocytosis were coincidental or accompanying findings in our patients with AVN.

Bone disease in renal transplantation and pleotropic effects of vitamin D therapy.

Osteoporosis, osteopenia, and osteonecrosis are common in renal transplant recipients. In this study, we evaluated relationship between bone mineral density (BMD) and posttransplant duration; creatinine clearance; serum levels of glucose, calcium, phosphorus, alkaline phosphatase, vitamin D (vitD), parathormone, magnesium, C telopeptide, osteocalcin, lipids, and vit D therapy. Eighty five subjects included in this study had a mean age of 36.25 ± 10.5 years. At least at 6-month intervals we measured femoral neck (FN) and lumbar vertebra (LV) by DEXA and biochemical parameters. VitD was prescribed in 57 patients (vitDG). The mean duration of posttransplantation follow-up was 9.82 ± 2.72 months. T scores (TS) of FN and LV were normal in 29.4% and 21.2%; osteopenia in 56.5% and 49.4%; and osteoporosis in 12.1% and 29.4% of patients, respectively. Upon follow-up, TS improved significantly from -1.58 to -1.46 in FN and from -1.88 to -1.70 in LV (P < .05 for both). In patients receiving vitDG, TS improved significantly from -1.74 to -1.61 on FN and from -2.16 to -1.97 on LV (P < .05 for both). Osteocalcin and vitDG levels decreased in all patients (P < .05 for all). Blood urea nitrogen and serum creatinine increased (P < .05). In VitDG cohort, triglyceride levels decreased (P < .05) with unchanged blood glucose values; but among the other patients, triglycerides were unchanged but glucose levels had increased (P < .05). Bone disease including osteopenia or osteoporosis was observed among 70%. During the follow-up period, BMD increased significantly from baseline at 9.82 ± 2.72 months. VitD therapy caused more prominent improvements in BMD and decreases in serum triglycerides as well as mutigated the increase in blood glucose.

Effects of pentoxifylline on the cytokines that may play a role in rejection and resistive index in renal transplant recipients.

Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. In this study, 22 renal transplant recipients treated with tacrolimus, prednisolone, and mycophenolate mofetil were prescribed PTX (2 x 600 mg/d) for 3 months (GI), and 20 similar patients not receiving PTX were used as controls (GII). Stable subjects whose serum creatinine was lower than 1.8 mg/dL and were more than 6 months posttransplant, were enrolled into this study if the blood pressure was well controlled and there was no diabetes mellitus, infection, or inflammation. At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). Resistive index (RI) decreased in GI but the difference in alterations between baseline and the last visit of GI and GII was marginal. In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. RI also decreased marginally secondary to PTx treatment. PTx was well tolerated and free side effects. PTx did not affect tacrolimus levels or other biochemical and hematological parameters.

Efficacy and safety of vardenafil in renal transplant recipients with erectile dysfunction.

Erectile dysfunction (ED) profoundly affects the quality of life. The prevalence of ED in renal transplant recipients is reported by high as 50% to 60%. We evaluated the efficacy and safety of vardenafil in these patients with ED as well as its effects on graft function and on cylosporine or tacrolimus concentrations. Thirty-nine recipients with ED and serum creatinine values<2 mg/dL were treated with vardenafil. ED was assessed using the self-administered International Index of Erectile Function (IIEF). ED was diagnosed by using penile color-Doppler ultrasonography and intracavernosal injection. Vardenafil efficacy was assessed by readministering the IIEF questionnaire after 4 weeks of therapy. Serum creatinine levels, creatinine clearances, and cyclosporine/tacrolimus concentrations were measured before and after vardenafil therapy. Twenty-one recipients with ED served as placebo controls and 15 without ED as another control group. The IIEF scores improved from 12.80+/-3.5 to 26.46+/-2.4 in vardenafil-treated patients with ED (P<.001). Renal function and cyclosporine/tacrolimus concentrations did not change with vardenafil therapy. Side effects were observed in 7 (18%) patients: headache in three, palpitations in one, flushing in two, and dyspepsia in one. This study demonstrated that ED improved with vardenafil in renal transplant recipients with ED. For 4 weeks vardenafil therapy was free of side effects. Renal function tests did not change. Also, no dose change in immunosuppressive drugs was required during 4 weeks of verdanafil therapy.

Uncommon side effect of MMF in renal transplant recipients.

Mycophenolate mofetil (MMF) is a potent immunosuppressive agent used in renal transplantation. Gastrointestinal and hematological side effects are commonly observed, but hepatotoxicity has not been reported. In this study, we assessed MMF-related hepatotoxicity in renal transplant recipients. A total of 124 renal transplantation recipients (RTRs) were evaluated for elevated liver enzymes associated with MMF, and 79 patients were enrolled to the study. Patients used MMF 2 g/day. The patients who had progressive increase in liver enzymes after renal transplantation and their AST, ALT, GGT, ALP, bilirubin levels, hepatitis, cytomegalovirus (CMV), abdominal ultrasonography, duration of hepatotoxicity, and decreased dosage or withdrawal of MMF were recorded. Also, we evaluated their liver enzymes while the patients were on the waiting list. Of the 79 patients, 11 patients (13.9%) had a progressive increase in liver enzymes. The median (min-max) age of the patients with MMF-hepatotoxicity was 29 (19-54) and 72.7% of them were male. None of the patients had hepatitis B or C, CMV infection, or other possible causes for elevated liver enzymes and their abdominal ultrasonography were normal. High liver enzyme levels regressed after the withdrawal (n=6) or reduce dosage (n=5) of MMF. The median time of the increase in liver enzymes was 28 (4-70) days and after 50% reduction or withdrawal of MMF, returned to normal values in 16 (4-210) days. The median levels of ALT in waiting list (I), before (II), and after (III) reduction dosage or withdrawal of MMF were 22.0 (3-22), 222.0 (51-508), and 33.0 (21-64) U/L, respectively (p I-II=0.004,p I-II=0.013, andp II-III=0.005). There were no differences for ALP, GGT, total bilirubin, and direct bilirubin levels. Also, the correlation between recovery time of ALT and persistence time of ALT elevation before adjustment of MMF was significant (r=0.739, p=0.009). Consequently, after renal transplantation, hepatotoxicity can occur due to a lot of reason including MMF usage. If hepatotoxicity related to MMF is not considered, especially in the early period of renal transplantation, resolution of hepatotoxicity can be required long term.

Long-term comparative results of C0 and C2 monitoring of CyA in renal transplanted patients.

The purpose of this study was to evaluate the effects of CyA monitoring using C0 monitoring (fasting level after 12 h from last dose), and C2 monitoring (2 h after morning dose) on renal functions, lipid levels, CyA levels, and daily dosages of CyA in renal transplanted patients in the posttransplant period from the first month to the 36th month. In our center between 1992-2003, 37 of the 54 renal transplanted patients were treated with CyA, prednisolone, and mycophenolate mofetil or azathioprine. The mean age was 32.36 +/-10.32 and 35.00 +/- 10.23 (p = 0.39) in C0 (M/F: 18/7) and in C2 (9/3), respectively. Cadaveric donor (d), living related d, and living unrelated d were in four patients (p), 17 p and four p in C0, and two p, seven p, and three p in C2, respectively (p = 0.79). Chronic allograft nephropathy (CAN) developed in 13 p (52%) and one p (8.3%) in C0 and in C2, respectively (p =0.013). Creatinine clearance values were 72.31 +/- 23.10 mL/min and 78.73 +/- 22.42 mL/min (p:0.621) at first month, 64.97 +/- 22.58 mL/min and 78.00 +/- 19.90 mL/min (p:0.065) at sixth month, 56.50 +/- 19.62 mL/min and 76.62 +/- 21.06 mL/min (p:0.006) at 12th month, 50.28 +/- 24.79 mL/min and 80.87 +/- 18.24 mL/min (p < 0.001) at 24th month, and 55.15 +/- 19.21 mL/min and 86.65 +/- 14.97 mL/min (p:0.004) at 36th month in C0 and C2, respectively. The mean daily dosages of CyA were 354.35 +/- 122.63 and 266.67 +/- 64.95 mg/d (p:0.031) at first month, 277.17 +/- 77.94 and 250.00 +/- 73.31 mg/d (p:0.228) at sixth month, 247.92 +/- 58.48 and 211.36 +/- 62.61 mg/ d (p:0.09) at 12th month, 232.95 +/- 56.90 and 170.45 +/- 41.56 mg/ d (p:0.003) at 24th month, and 240.63 +/- 52.34 and 153.57 +/- 46.61 mg/d (p:0.002) at 36th month in C0 and C2, respectively. In C2, systolic and diastolic blood pressure, uric acid, total cholesterol (C), LDL-C, and triglyceride levels were lower than those monitored with C0. In C2, HDL-C levels were also higher than those monitored with C0. None of these patients returned to dialysis or died in this period. In conclusion, during the first 36 months with monitoring C2, preservation of renal function, control of blood pressure serum lipids and uric acid were better than those with monitoring C0. In addition, daily dose of CyA was lower in C2 method and, at the same time, this effect of C2 can be accepted as cost effective.

Dipyridamole for renal phosphate leak in successfully renal transplanted hypophosphatemic patients.

AIM AND BACKGROUND: Hyphosphatemia can be seen in renal transplant recipients. Hyperparathyroidism, glucocorticoid treatment, renal denervation and impairment of renal tubular phosphate reabsorption are the most common causes of hyphosphatemia in these patients. It is well-known that dipyridamole enhances renal tubular phosphate reabsorption in some clinical conditions. We did not find any information about the effect of dipyridamole in renal transplant recipients (RTRs) with hypophosphatemia. For this reason, we decided to give dipyridamole 11 RTRs with hypophosphatemia. PATIENTS AND METHODS: Eleven RTRs whose serum phosphate and creatinine levels were below 2.5 mg/dl and 2 mg/dl, respectively, were included in this study. None of the patients received drugs altering phosphate metabolism and they did not change their routine diets. Urinary phosphate excretion and tubular phosphate reabsorption (TPR) were calculated before and 3 weeks after dipyridamole treatment. RESULTS: The mean levels of serum-urine (daily) phosphate and TPR before dipyridamole treatment were 1.94 +/- 0.46 mg/dl, 7,187.5 +/- 1,833.49 mg/day and -2.78 +/- 0.62, respectively. After treatment, the mean levels of serum-urine phosphate and TPR were 2.73 +/- 0.46 mg/dl, 4,845.27 +/- 1,138.99 mg/day and -1.48 +/- 0.80, respectively. Serum and urine phosphate levels and TPR were found to be significantly different before and after dipyridamole therapy (p < 0.05). CONCLUSION: Short-term dipyridamole therapy increased TPR and serum phosphate levels and decreased urinary phosphate excretion. We did not observe negative effect on renal functions in these cases. Although the number of the cases included in this study is small, dipyridamole is an effective choice in management of hypophosphatemic RTRs.

Dyslipidemia and weight gain secondary to lifestyle changes in living renal transplant donors.

We evaluated renal function, lipid profile, body weight, and physical activity of living donors in long-term follow-up after nephrectomy. A total of 121 living donors were compared with 81 healthy subjects with normal renal function and no history of any surgery or disease. Before and after donor nephrectomies, we recorded age, body weight, systolic and diastolic blood pressures, serum creatinine, creatinine clearance, lipids, and serum glucose levels of the donors. Preoperative (baseline) and postoperative (last visit) physical activities of donors and controls were evaluated through the Modified Baecke Questionnaire (occupational activities, sports activities, leisure-time activities). There were no differences between donors and controls for age (P = .772), gender (P = .927), and follow-up period (P = .564). According to baseline levels, blood pressure and serum creatinine were increased and creatinine clearance was decreased (P < .001 for all). The mean increases in body weight (P = .012), LDL (P = .004), and triglyceride (P < .001) were higher in donors than in controls. But the mean decrease in HDL was not different between controls and donors (P = .057). Indices of sports and total activities were lower in donors than in controls on the last visit (P < .001). Indices of occupational and leisure-time activities were similar on the last visit in donors and in controls (P = .126, P = .083). The alterations in total cholesterol and total activity showed significant negative correlations in donors (r = -.581, P < .001). Also, the alterations in total cholesterol and body weight showed a significant correlation (r = .25, P = .02). We followed donors together with serum lipid levels, body weight, and total physical activities as well as blood pressure and renal function tests.

Report of a renal transplanted patient with fibroadenoma occurring in a short time.

The incidence of breast cancer in renal transplant patients is similar to that of general population. But fibroadenomas may be seen as a result of exposure to cyclosporine (CyA). Herein we report the case of a 32-year-old woman who received a renal transplant and had a breast fibroadenoma. She had been prescribed CyA, azathioprine, and steroids for 4 years. At the end of the first year a palpable mass had been detected in her right breast; the pathologic diagnosis was fibroadenoma. At the 4th year after transplantation, immunosuppressive treatment was switched to CyA and mycopholate mofetil (MMF) because of an increased serum creatinine level. Two years later seven breast nodes from both breasts were detected by ultrasonography. Totally excision was performed revealing a histopathologic diagnosis of fibroademata as before. In this case, the combination of CyA and MMF administration seemed to cause an increase in the number of nodules in a short time. The cause of fibroadenomas may be related to drug-induced secretion of proliferative or anti-apoptotic cytokines.

Coexistence of cystic intra-abdominal lymphangiomas and diffuse venous haemangiomas in adult life.

Diffuse haemangioma and intra-abdominal lymphangioma are rare in adults. In this case report, we present a 33-year-old female with coexisting multiple cutaneous and visceral cavernous haemangiomas and two huge intra-abdominal lymphangiomas of 25 and 35 cm in diameter. The organs involved were the liver, pericardium, renal hilus and bladder. She died due to disseminated intravascular coagulation and multiorgan failure, which resembled Kasabach-Merritt syndrome. The coexistence of generalised haemangiomas and intra-abdominal lymphangiomas and the lack of complaints until the age of 33 years makes her an unusual case in the literature. We also emphasise the other clinical conditions that should be considered in the differential diagnosis.