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.

An Evaluation of the Effect of Using Irrigations at Different Temperatures on Pain, Edema, and Trismus during the Extraction of Bilateral Impacted Mandibular Third Molars: A Randomized Split-Mouth Clinical Trial.

BACKGROUND AND AIM: The surgical extraction of impacted wisdom teeth is a standard practice in dentistry. Unfortunately, inflammatory reactions such as discomfort, edema, and trismus frequently jeopardize patients' well-being after the extraction of third molars. Saline solutions at room temperature (25°C) are routinely used in impacted tooth extraction. Refrigerated saline solutions were used to work with cold solutions, and as the refrigerator temperature was 4°C, this study was designed to have a cold solution temperature of 4°C. This study aimed to assess the influence of saline irrigation at various temperatures (4°C, 25°C) on postoperative edema, pain, and trismus after the extraction of impacted third molars. MATERIALS AND METHODS: Eighteen patients with bilateral symmetrical mandibular impacted third molars were enrolled in this split-mouth, randomized, prospective, double-blind clinical trial. For each patient, one side was irrigated with a saline solution (% 0.9 isotonic sodium chloride) at 4°C (test), and the other side was irrigated with a saline solution at room temperature (25°C) (control). Pain, trismus, and facial edema were noted on the 2nd, 4th, and 7th days. A Mann-Whitney U-test was used to compare pairs, and a Wilcoxon signed-rank test was used to compare groups. RESULTS: The two groups had no considerable differences in terms of pain levels and facial edema (P > 0.05). Regarding trismus, the maximum mouth opening for cold irrigation (4°C) was significantly higher than for room temperature irrigation (25°C) across all postoperative periods (P < 0.05). CONCLUSION: Cold irrigation therapy (4°C) exerts beneficial effects more than room temperature (25°C) irrigation on the trismus after impacted mandibular third molar surgery.

The effect of different positions of unerupted lower third molar teeth on the fragility of mandibular angle: Finite element analysis.

Background: The mandibular bone is the largest and strongest bone in comparison to the other bones in the face skeleton. However, it is the most commonly fractured in facial injuries. The location of the fracture in mandible depends on various factors. The relationship of the impacted lower third molar teeth to mandibular angle fracture has been the subject of many epidemiological studies. It is argued that the risk of fracture in mandibular angle is two to four times more when there are particularly an impacted or partially impacted third molar teeth. However, the effect of the position of the impacted tooth on mandibular angle fracture is not clear yet. Aim: This study seeks to reveal the effect of third molar teeth that are impacted in various positions on the angle fragility. Materials And Methods: This study was performed using three-dimensional finite element stress analysis and static linear analysis methodology. Computed tomography (CT) images obtained previously from a patient were used to construct models of the bone tissue. An ILUMA CBCT device (3M Imtec, OK, USA) was used for tomographic scans. Impacted teeth in various positions were digitally modeled separately. Different direction forces were applied to the mandible, the stress values on the bone surrounding the third molar teeth impacted in different positions were determined. Results: Third molar teeth are impacted in mandibular bone in the following positions: mesioangular, vertical, horizontal, and distoangular positions. The study showed that the force that created the highest stress in the Mandibular angle among the modelled groups is the force by ipsilateral angle. Conclusion: For all kinds of impacted teeth, there was more stress accumulation in the buccal area than in the lingual area when the force is from the symphisis.

Persistent hyperparathyroidism due to mediastinal parathyroid adenoma treated with selective arterial embolization with embosphere: first case in the literature.

Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia in the clinical setting and affects 0.3% of the population. Parathyroidectomy is the only definitive cure. Unfortunately, even in the most experienced hands, persistent primary hyperparathyroidism (P-PHPT) occurs in 4.7% of the patients. Ectopic adenomas are difficult to localize before and during operation and usually end up with P-PHPT. Herein, we presented a case with P-PHPT due to mediastinal parathyroid adenoma that was successfully ablated with selective arterial embolization. A 57-year-old female patient was admitted to our endocrinology clinic with persistent hypercalcemia 4 months after the initial surgery for PHPT that had been performed in another center. The patient did not accept the second operation, and serum calcium and parathyroid hormone (PTH) remained high despite medical treatment with cinacalcet and IV zoledronate. In the 99-m Tc-MIBI scintigraphy with SPECT, a 18 × 12-mm-sized lesion in the mediastinum at the paratracheal region was detected which was confirmed to be a possible parathyroid adenoma with fluorocholine PET and chest computed tomography (CT). The right bronchial artery that was detected to supply the mediastinal mass in CT angiography was selectively catheterized and embolized with embosphere. Right after the procedure, serum PTH and calcium levels were normalized and remained normal in 23 months of follow-up. Selective arterial embolization is a treatment option for ectopically located adenomas which are difficult to resect and in cases with certain comorbidities which constitute a contraindication for surgery.

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.

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.

Amlodipine prevents and reverses the elevation in [Ca2+]i and the impaired phagocytosis of PMNL of diabetic rats.

BACKGROUND: High glucose concentration, through the activation of calcium channels, augments in vitro calcium entry into cells and leads to elevation in the basal levels of [Ca2+]i, the latter causes cell dysfunction. DESIGN OF STUDY: The present study examined whether streptozotocin-induced diabetes mellitus in rats causes a rise in [Ca2+]i of PMNL and impairs their phagocytosis and whether treatment of these rats with the calcium channel blocker, amlodipine, prevents and/or reverses these derangements. Amlodipine was given either from day one of diabetes or after 3 or 12 days of established diabetes. RESULTS: The [Ca2+]i of PMNL was elevated and their phagocytosis was reduced after one day of diabetes. These derangements were present and became more marked with longer duration of diabetes. There was a direct and significant correlation (r = 0.88) between [Ca2+]i of PMNL and blood glucose and an inverse relationship between phagocytosis and blood glucose (r = 0.83) or [Ca2+]i (r = 0.67). Three days of amlodipine therapy were required to completely prevent or reverse the elevation in [Ca2+]i of PMNL. This action of the drug occurred despite the hyperglycaemia. Amlodipine produced marked and significant improvements in phagocytosis but the values remained modestly below normal. Amlodipine given to normal rats did not affect [Ca2+]i or phagocytosis of PMNL. CONCLUSION: The results show that (i) [Ca2+]i of PMNL increases and phagocytosis decreases rapidly after the induction of diabetes; (ii) treatment of diabetic rats with amlodipine normalizes [Ca2+]i of PMNL and markedly improves their phagocytosis, despite hyperglycemia; (iii) high [Ca2+]i is responsible, in major part, for the impaired phagocytosis but other factors are also operative; and (iv) calcium channel blockers could prove useful in the treatment of the metabolic and functional derangements of PMNL in patients with poorly controlled diabetes.

Pathways through which glucose induces a rise in [Ca2+]i of polymorphonuclear leukocytes of rats.

Basal levels of [Ca2+]i are elevated in diabetes mellitus. Such an abnormality is most likely due to both increased calcium influx into cells and decreased efflux of this ion out of the cells. The present study examined the cellular pathways that are responsible for hyperglycemia-induced acute rise in polymorphonuclear leukocytes (PMNL), and explored whether such a rise is due to increased calcium entry into PMNL and/or to calcium release from their intracellular stores. There were dose dependent and time dependent rises in the [Ca2+]i of PMNL exposed to high concentrations of glucose. Similar effects were observed when the PMNL were exposed to high concentrations of choline chloride or mannitol. A substantial part of the rise in [Ca2+]i was inhibited when the media contained verapamil or nifedipine or when the PMNL were placed in calcium free media, and the rise in [Ca2+]i was completely abolished when the PMNL were placed in calcium free media containing ryanodine. GDP beta S or pertussis toxin almost completely prevented the glucose-induced rise in [Ca2+]i of PMNL. Rp-cAMP, H-89 or staurosporine produced significant inhibition of the rise in [Ca2+]i. High concentrations of glucose produced a dose dependent shrinkage of PMNL volume over a period of two hours. The volume of PMNL, however, was normal after 24 hours in vitro incubation studies as well as after 1, 2 and 12 days of streptozotocin-induced hyperglycemia in rats. The results are consistent with the formulation that the osmotic activity (cell shrinkage) of the high glucose concentrations activates G protein(s) which then stimulates the adenylate-cAMP-protein kinase A pathway, phospholipase C system and calcium channels. The stimulation of these cellular pathways permits both calcium influx into the PMNL as well as mobilization of calcium from their intracellular stores. Both of these events contribute to the acute rise in their [Ca2+]i. It is possible that the rise in [Ca2+]i is critical for the stimulation of the events that lead to the generation and accumulation of inorganic osmolytes to restore cell volume to normal.

The frequencies of hepatitis B virus markers and hepatitis C virus antibody in patients with glomerulonephritis.

Hepatitis B virus markers and hepatitis C virus (HCV) antibody were assayed in 72 patients with glomerulonephritis (GN) at the time of biopsy. The patients, 41 males and 31 females, were aged between 16 and 68 years. The frequency of positivity for HbsAg, anti-Hbs, and anti-Hbe, anti-Hbc and anti-HCV antibody was 5.5, 20.8, 2.8, 16.6 and 1.4% respectively. At the same time, HbsAg and anti-HCV positivity were 8.5 and 0.95% in blood donors. We can say that morbidity and prognosis may be affected by hepatitis infection. Infections of hepatitis B and C have to be evaluated in patients with GN, especially in endemic areas. In our study group the frequencies of HbsAg positivity and anti-HCV positivity were not higher in patients with GN than in blood donors.