BACKGROUND: Neointimal hyperplasia and thrombosis are the major factors responsible for vascular access occlusion. Previous studies suggested that the renin-angiotensin system has been implicated in the pathogenesis of neointimal hyperplasia and thrombosis. Recent studies have shown that angiotensin-converting enzyme (ACE) gene polymorphism may have a association with venous thrombosis. We conducted a retrospective case control study to determine the influence of ACE gene polymorphism on the progression of radiocephalic wrist arteriovenous fistulae (RCAVF). Also, we investigated the association between ACE polymorphism and various thrombotic factors in thrombosed and nonthrombosed subjects. METHODS: 56 patients (24 males and 32 females, mean age 49.8, age range 12-81) whose RCAVF had been maintained in good condition after 2 months of vascular access operation were included in this study. Lipoprotein (a), total cholesterol, C-reactive protein (CRP) and homocystein were measured before hemodialysis session in fasting state. Clinical data such as body mass index (BMI), cigarette smoking, hypertension, and diabetes were retrieved from patient's records. The ACE genotype was analyzed by the polymerase chain reaction (PCR). RESULTS: The incidence of diabetes and cigarette smoking were similar in the three genotypes. There were no significant differences in BMI, total cholesterol, lipoprotein (a), CRP and homocystein (p=0.551, 0.429, 0.279, 0.392, 0.124, respectively) among DD, ID and II genotypes. The percentage of the DD, ID and II genotypes were 16%, 43%, 41%, respectively. Compared with the ID and II genotypes, the proportion of the thrombosed AV shunts was larger in DD genotypes. But there was no statistically significant difference between ACE polymorphism and RCAVF thrombosis (x2=1.027, df=2, p=0.598). ACE polymorphism is shown to have no association with body mass index, blood level of total cholesterol, lipoprotein (a), CRP and homocystein. CONCLUSION: These results suggest that ACE polymorphism may have some influences on the vascular access occlusion in maintenance hemodialysis patients and have no relationship with body mass index, total cholesterol, lipoprotein (a), CRP and homocystein.
Arteriovenous Fistula* ; Body Mass Index ; C-Reactive Protein ; Case-Control Studies ; Cholesterol ; Fasting ; Female ; Genotype ; Humans ; Hyperplasia ; Hypertension ; Incidence ; Lipoprotein(a) ; Male ; Polymerase Chain Reaction ; Renal Dialysis* ; Renin-Angiotensin System ; Retrospective Studies ; Smoking ; Thrombosis ; Venous Thrombosis ; Wrist

Hypernatremia is an occasionally encountered electrolyte disorder, which may lead to fatal consequences under improper management. Hypernatremia is a disorder of the homeostatic status regarding body water and sodium contents. This imbalance is the basis for the diagnostic approach to hypernatremia. We summarize the eight diagnostic steps of the traditional approach and introduce new biomarkers: exclude pseudohypernatremia, confirm glucose-corrected sodium concentrations, determine the extracellular volume status, measure urine sodium levels, measure urine volume and osmolality, check ongoing urinary electrolyte free water clearance, determine arginine vasopressin/copeptin levels, and assess other electrolyte disorders. Moreover, we suggest six steps to manage hypernatremia by replacing water deficits, ongoing water losses, and insensible water losses: identify underlying causes, distinguish between acute and chronic hypernatremia, determine the amount and rate of water administration, select the type of replacement solution, adjust the treatment schedule, and consider additional therapy for diabetes insipidus. Physicians may apply some of these steps to all patients with hypernatremia, and can also adapt the regimens for specific causes or situations.

Hyponatremia is primarily a water balance disorder associated with high morbidity and mortality. The pathophysiological mechanisms behind hyponatremia are multifactorial, and diagnosing and treating this disorder remains challenging. In this review, the classification, pathogenesis, and step-by-step management approaches for hyponatremia in patients with liver disease are described based on recent evidence. We summarize the five sequential steps of the traditional diagnostic approach: 1) confirm true hypotonic hyponatremia, 2) assess the severity of hyponatremia symptoms, 3) measure urine osmolality, 4) classify hyponatremia based on the urine sodium concentration and extracellular fluid status, and 5) rule out any coexisting endocrine disorder and renal failure. Distinct treatment strategies for hyponatremia in liver disease should be applied according to the symptoms, duration, and etiology of disease. Symptomatic hyponatremia requires immediate correction with 3% saline. Asymptomatic chronic hyponatremia in liver disease is prevalent and treatment plans should be individualized based on diagnosis. Treatment options for correcting hyponatremia in advanced liver disease may include water restriction; hypokalemia correction; and administration of vasopressin antagonists, albumin, and 3% saline. Safety concerns for patients with liver disease include a higher risk of osmotic demyelination syndrome.

BACKGROUND/AIMS: Predialysis hyponatremia has been recently reported to be associated with mortality in incident hemodialysis patients. However, whether hyponatremia is associated with unfavorable outcomes in elderly patients remains unknown. We hypothesized that nephrology referral inf luences hyponatremia, and aimed to define how nephrology referral affects the association between hyponatremia and mortality in the elderly. METHODS: We retrospectively assessed mortality in 599 incident hemodialysis patients aged ≥ 70 at a tertiary university hospital, between 2000 and 2010. We analyzed 90-day and 1-year all-cause mortality (ACM) in relation to predialysis serum sodium (sNa). We divided the patients into two groups according to predialysis glucose-corrected sNa: hyponatremia (< 135 mmol/L) and normonatremia (135 to 145 mmol/L). RESULTS: Low estimated glomerular filtration rate, high phosphorus, low albumin, nonpreparation of arteriovenous fistula or graft, and late referral were associated with a low sNa in the elderly. Among 599 patients, 106 and 174 patients died at the 90-day and 1-year follow-ups, respectively. Each 10-mmol/L increase in predialysis sNa tended to be associated with lower 90-day and 1-year ACM. When patients were stratified by nephrology referral, hyponatremia was associated with increased mortality in early referral group (90-day ACM: hazard ratio [HR] = 2.335, p = 0.041; 1-year ACM: HR = 1.790, p = 0.024). However, hyponatremia was not associated with mortality in late referral group. CONCLUSIONS: Predialysis hyponatremia at hemodialysis initiation is associated with late referra
Aged* ; Arteriovenous Fistula ; Follow-Up Studies ; Glomerular Filtration Rate ; Humans ; Hyponatremia* ; Mortality* ; Nephrology ; Phosphorus ; Referral and Consultation ; Renal Dialysis* ; Retrospective Studies ; Sodium ; Transplants

BACKGROUND: Few data showed the optimal blood pressure (BP) in noncritically ill patients with acute kidney injury (AKI) relative to mortality or severe AKI. We therefore sought to analyze the data that exist for the ideal target range for BP in noncritically ill patients with AKI. METHODS: We performed a retrospective cohort study involving 1,612 hospitalized patients who were diagnosed with AKI using the Kidney Disease: Improving Global Outcomes definition based on serum creatinine measurements for a period of 1 year. The average systolic BP (SBP) was categorized into 10-mmHg increments (within 48 hours after the development of AKI). The primary outcome was a composite of severe AKI or 90-day mortality. RESULTS: The composite outcome rate in patients was 18.7% (302/1,612). The relationship between BP and the composite outcome followed a U-shaped curve, with an increased event rate observed at both low and high BP values. The average SBP after AKI predicted the composite outcome after adjusting for baseline variables (reference SBP: 120–129 mmHg; < 100 mmHg: hazard ratio [HR] 1.84, P = 0.015; 100–109 mmHg: HR 1.56, P = 0.038; 110–119 mmHg: HR 1.15, P = 0.483; 130–139 mmHg: HR 1.51, P = 0.045; ≥ 140 mmHg: HR 1.73, P = 0.005). CONCLUSION: Among noncritically ill patients with AKI, a U-shaped curve association was observed between the average SBP within 48 hours after AKI and the composite primary outcome of this study, with the lowest event rate for SBP ranging from approximately 110 to 129 mmHg.
Acute Kidney Injury ; Blood Pressure ; Cohort Studies ; Creatinine ; Humans ; Kidney Diseases ; Mortality ; Retrospective Studies

Hypernatremia is a common electrolyte disorder in children and elderly people and has high short-term mortality. However, no high-quality studies have examined the correction rate of hypernatremia and the amount of fluid required for correction. Therefore, in this study, we will compare the efficacy and safety of rapid intermittent bolus (RIB) and slow continuous infusion (SCI) of electrolyte-free solution in hypernatremia treatment. Methods: This is a prospective, investigator-initiated, multicenter, open-label, randomized controlled study with two experimental groups. A total of 166 participants with severe hypernatremia will be enrolled and divided into two randomized groups; both the RIB and SCI groups will be managed with electrolyte-free water. We plan to infuse the same amount of fluid to both groups, for 1 hour in the RIB group and continuously in the SCI group. The primary outcome is a rapid decrease in serum sodium levels within 24 hours. The secondary outcomes will further compare the efficacy and safety of the two treatment protocols. Conclusion: This is the first randomized controlled trial to evaluate the efficacy and safety of RIB correction compared with SCI in adult patients with severe hypernatremia.