ABSTRACT
Background@#Larger middle molecules are important substances associated with cardiovascular complications in end- stage renal disease. Unfortunately, larger middle molecules are not reliably removed by a high-flux dialyzer. A medium cut-off (MCO) membrane could effectively remove larger middle molecules. This study aimed to identify the long -term effect of the MCO membrane for changes of larger middle molecules. @*Methods@#Thirty-four patients were prospectively analyzed for 12 months. The enrolled patients were divided into control and MCO groups. We measured the plasma levels of growth differentiation factor 15, sclerostin, and fibroblast growth factor 23 in larger middle molecules and those of biomarkers including small solutes. Single-pool Kt/V (spKt/V) and reduction ratios also were evaluated. @*Results@#Plasma sclerostin did not increase significantly in patients using the MCO dialyzer (135.3 [–637.7 to 908.3], p = 0.715). And there was a significant difference in change of plasma sclerostin level between the two groups (–1,646.9 [–3,015.2 to –278.7], p = 0.033). Furthermore, a negative association between calcium and sclerostin was not observed in the MCO group (r = –0.142, p = 0.587). Solute clearance of larger middle molecules in the MCO group was significantly higher. Moreover, spKt/V values for patients in the MCO group were significantly increased without albumin loss. Values are presented as mean (95% confidence interval [CI]) or adjusted mean (95% CI). @*Conclusion@#The MCO dialyzer can increase dialytic adequacy and suppress the increase in plasma sclerostin level without significant albumin loss in patients with end-stage renal disease.
ABSTRACT
Background@#Larger middle molecules are important substances associated with cardiovascular complications in end- stage renal disease. Unfortunately, larger middle molecules are not reliably removed by a high-flux dialyzer. A medium cut-off (MCO) membrane could effectively remove larger middle molecules. This study aimed to identify the long -term effect of the MCO membrane for changes of larger middle molecules. @*Methods@#Thirty-four patients were prospectively analyzed for 12 months. The enrolled patients were divided into control and MCO groups. We measured the plasma levels of growth differentiation factor 15, sclerostin, and fibroblast growth factor 23 in larger middle molecules and those of biomarkers including small solutes. Single-pool Kt/V (spKt/V) and reduction ratios also were evaluated. @*Results@#Plasma sclerostin did not increase significantly in patients using the MCO dialyzer (135.3 [–637.7 to 908.3], p = 0.715). And there was a significant difference in change of plasma sclerostin level between the two groups (–1,646.9 [–3,015.2 to –278.7], p = 0.033). Furthermore, a negative association between calcium and sclerostin was not observed in the MCO group (r = –0.142, p = 0.587). Solute clearance of larger middle molecules in the MCO group was significantly higher. Moreover, spKt/V values for patients in the MCO group were significantly increased without albumin loss. Values are presented as mean (95% confidence interval [CI]) or adjusted mean (95% CI). @*Conclusion@#The MCO dialyzer can increase dialytic adequacy and suppress the increase in plasma sclerostin level without significant albumin loss in patients with end-stage renal disease.
ABSTRACT
No abstract available.
Subject(s)
Catheter-Related Infections , Mycobacterium , Peritoneal Dialysis , RhodococcusABSTRACT
No abstract available.
Subject(s)
Acute Kidney Injury , Cholangitis , Granulomatosis with PolyangiitisABSTRACT
No abstract available.
Subject(s)
Hernia, Obturator , Polycystic Kidney, Autosomal DominantABSTRACT
BACKGROUND: Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. METHODS: Pax8–rtTA/tetracycline response element–human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. RESULTS: Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. CONCLUSION: Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.
Subject(s)
Animals , Humans , Mice , Acute Kidney Injury , Albuminuria , Collagen , Fibrosis , Folic Acid , Hyperglycemia , Hypertension , Kidney Diseases , Mice, Transgenic , Renal Insufficiency , Renal Insufficiency, Chronic , Risk Factors , RNA, MessengerABSTRACT
No abstract available.
Subject(s)
Peritoneal Dialysis , Peritoneal Dialysis, Continuous AmbulatoryABSTRACT
No abstract available.
Subject(s)
Glomerulonephritis, IGA , Immunoglobulin A , ImmunoglobulinsABSTRACT
Most rheumatic diseases are chronic inflammatory diseases. Kidney-related symptoms of rheumatic diseases are often present, which increase mortality and morbidity of patients with rheumatic diseases. When patients with rheumatic diseases show signs or symptoms of renal involvement, management for primary rheumatic diseases should be more aggressive. In general, the risk and severity of renal involvement in patients with rheumatic diseases depend on the type of primary rheumatic diseases. Rheumatic disease itself, chronic use of immunosuppressive agents and non-steroidal anti-inflammatory drugs, and comorbidities, such as diabetes, hypertension, and cardiovascular complications, are the main causes of renal involvement in patients with rheumatic diseases. Many studies have reported the predominant features of renal involvement in most rheumatic diseases. We have attempted to summarize the relationships between rheumatic diseases and renal diseases, and clinical or pathophysiological features of renal involvement resulting from primary rheumatic diseases except systemic lupus erythematosus. Review for renal involvement, particularly in relation to early diagnosis and management of renal involvement in rheumatic diseases, is clinically significant because renal involvement in rheumatic diseases generally implies a bad prognosis.
Subject(s)
Humans , Comorbidity , Early Diagnosis , Hypertension , Immunosuppressive Agents , Inflammation , Kidney Diseases , Lupus Erythematosus, Systemic , Mortality , Prognosis , Rheumatic DiseasesABSTRACT
No abstract available.
Subject(s)
Adult , Humans , Alcoholics , Colitis , Liver Cirrhosis, Alcoholic , Nephritis , PurpuraABSTRACT
Posttransplant erythrocytosis (PTE) is a common complication of renal transplantation, which can occur in approximately 10% to 15% of renal transplant patients and usually affects males with relatively good renal function. It is also associated with an increased incidence of thromboembolic events. Clinical manifestations of PTE include malaise, headache, plethora, lethargy, and dizziness. It is correlated with use of cyclosporin, gender, posttransplant renal function, and type of antihypertensive medication. The angiotensin receptor blocker (ARB) or angiotensin-converting enzyme inhibitor is preferred as an initial treatment for PTE because these agents are effective and reasonably safe in the majority of patients with PTE, and can also provide a necessary antihypertensive effect for kidney transplant patients. We report here on a 35-year-old male who had erythrocytosis after renal transplantation. After renal transplantation, his level of hemoglobin was 21 g/dL. We treated this patient with ARB and his symptoms and signs have been completely relieved.
Subject(s)
Adult , Humans , Male , Angiotensin Receptor Antagonists , Angiotensins , Cyclosporine , Dizziness , Headache , Incidence , Kidney Transplantation , Kidney , Lethargy , PolycythemiaABSTRACT
The number of people awaiting organ transplantation continues to exceed the number of organs available for transplantation, especially at a time when kidney transplantation is recognized as the best treatment option for end stage renal disease. There may be many reasons for this disparity of organ supply and demand, including the lack of consent, absence of an experienced coordinator team to help in closing the widening gap between organ supply and demand, and an unstandardized critical care management of potential organ donors. According to the report of the Korean Organ Transplant Registry in March 2014, due to a serious organ shortage in Korea, kidneys of deceased donors with low initial estimated glomerular filtration rate of <45 mL/min/1.73 m2 (21.2%) and expanded criteria donors (18.3%) are frequently used, and the number of wife donors and ABO-incompatible transplants for blood type O recipients is increasing. Because the number of donor organs compared with the demand is very restricted, proper management of deceased donors in the intensive care unit has been recognized as a critical determinant for a successful transplantation. Therefore, for successful transplantation of harvested organs, many medical doctors who play an integral role in the transplantation process should understand the pathophysiology of brain death-related systemic changes and well-designed management guidelines should be used prior to transplantation of deceased donors. This article reports on brain death-related systemic changes and proper management for preservation of function of donor organs.