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Fractional excretion of sodium in hepatorenal syndrome:Clinical and pathological correlation
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作者 Ali A Alsaad Hani M Wadei 《World Journal of Hepatology》 CAS 2016年第34期1497-1501,共5页
AIMTo determine the accuracy of fractional excretion of sodium (FeNa) in the diagnosis of hepatorenal syndrome (HRS). METHODSEighty-eight liver transplantation candidates with renal dysfunction and/or proteinuria were... AIMTo determine the accuracy of fractional excretion of sodium (FeNa) in the diagnosis of hepatorenal syndrome (HRS). METHODSEighty-eight liver transplantation candidates with renal dysfunction and/or proteinuria were included in the study sample. The baseline characteristics of the patients were obtained. All the 88 patients underwent iothalamate glomerular filtration rate testing, 24-h urine collection for urinary sodium and protein excretions, random urine for sodium and creatinine testing, and percutaneous kidney biopsy. FeNa was calculated using the equation [(urine sodium &times; serum creatinine)/(serum sodium &times; urine creatinine)] &times; 100%. Diuretic use was recorded among the participants. Patients on renal replacement therapy were not included in the original sample. RESULTSSeventy-seven (87%) of the 88 patients had FeNa P = 0.4). FeNa P = 0.47). Calculated positive predictive value and negative predictive value for FeNa P = 0.41). CONCLUSIONFeNa 1%. 展开更多
关键词 fractional excretion of sodium Hepatorenal syndrome Renal dysfunction Liver transplantation Urinary sodium excretion ACCURACY
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Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia 被引量:1
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作者 John K Maesaka Louis J Imbriano Nobuyuki Miyawaki 《World Journal of Nephrology》 2017年第2期59-71,共13页
Hyponatremia, serum sodium 〈 135 mEq/L, is themost common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the... Hyponatremia, serum sodium 〈 135 mEq/L, is themost common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the causes of hyponatremia has hampered the delivery of appropriate therapy. This is especially applicable to differentiating syndrome of inappropriate antidiuresis (SIAD) from cerebral salt wasting (CSW) or more appropriately, renal salt wasting (RSW), because of divergent therapeutic goals, to water-restrict in SIAD and administer salt and water in RSW. Differentiating SIAD from RSW is extremely diffcult because of identical clinical parameters that defne both syndromes and the mindset that CSW occurs rarely. It is thus insuffcient to make the diagnosis of SIAD simply because it meets the defned characteristics. We review the pathophysiology of SIAD and RSW, the evolution of an algorithm that is based on determinations of fractional excretion of urate and distinctive responses to saline infusions to differentiate SIAD from RSW. This algorithm also simplifes the diagnosis of hyponatremic patients due to Addison’s disease, reset osmostat and prerenal states. It is a common perception that we cannot accurately assess the volume status of a patient by clinical criteria. Our algorithm eliminates the need to determine the volume status with the realization that too many factors affect plasma renin, aldosterone, atrial/brain natriuretic peptide or urine sodium concentration to be useful. Reports and increasing recognition of RSW occurring in patients without evidence of cerebral disease should thus elicit the need to consider RSW in a broader group of patients and to question any diagnosis of SIAD. Based on the accumulation of supporting data, we make the clinically important proposal to change CSW to RSW, to eliminate reset osmostat as type C SIAD and stress the need for a new defnition of SIAD. 展开更多
关键词 HYPONATREMIA Cerebral-renal salt wasting fractional excretion of urate
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Vascular response to vasodilator treatment in microalbuminuric diabetic kidney disease
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作者 Narisa Futrakul Prasit Futrakul 《World Journal of Nephrology》 2013年第4期125-128,共4页
Under common practice, the conventional diagnostic marker such as microalbuminuria determination does not recognized early stage of diabetic kidney disease (normoalbuminuria, chronic kidney disease stage 1, 2); due ... Under common practice, the conventional diagnostic marker such as microalbuminuria determination does not recognized early stage of diabetic kidney disease (normoalbuminuria, chronic kidney disease stage 1, 2); due to the insensitiveness of the available marker. Treat-ment at later stage (microalbuminuria) simply slows the renal disease progression, but is rather diffcult to restore the renal perfusion. Intrarenal hemodynamic study in these patients revealed an impaired renal per-fusion and abnormally elevated renal arteriolar resis-tances. Treatment with vasodilators such as angiotensin converting enzyme inhibitor and angiotensin receptor blocker fails to correct the renal ischemia. Recent study on vascular homeostasis revealed a defective mecha-nism associated with an impaired nitric oxide production which would explain the therapeutic resistance to va-sodilator treatment in microalbuminuric diabetic kidney disease. This study implies that the appropriate thera-peutic strategy should be implemented at earlier stage before the appearance of microalbuminuria. 展开更多
关键词 MICROALBUMINURIA Diabetic kidney disease Renal hemodynamics fractional excretion of magne-sium Renal function
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Association of serum uric acid with different levels of glucose and related factors 被引量:29
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作者 YUAN Hui-juan YANG Xu-guang +2 位作者 SHI Xiao-yang TIAN Rui ZHAO Zhi-gang 《Chinese Medical Journal》 SCIE CAS CSCD 2011年第10期1443-1448,共6页
Background Previous studies have demonstrated that serum uric acid (UA) is an independent predictor of incident type 2 diabetes mellitus (T2DM) in general populations. This study aimed to investigate specific char... Background Previous studies have demonstrated that serum uric acid (UA) is an independent predictor of incident type 2 diabetes mellitus (T2DM) in general populations. This study aimed to investigate specific characteristics of UA and its relationship between UA and blood glucose and other risk factors in the Chinese population.Methods A total of 946 subjects were included in this study. UA, glucose, insulin, fractional excretion of UA (FEua),creatinine clearance rate (Ccr), hemoglobin A1c (HbA1c), fructosamine (FA), blood pressure and lipids were studied and also reexamined after the patients underwent two weeks of combined therapeutics.Results UA levels were the highest in subjects with impaired glucose regulation (IGR), followed by subjects with normoglycemia (NGT) and finally by subjects with T2DM. The level of the 2-hour postprandial insulin and the area under the curve for insulin (AUCins) showed a similar tendency. The UA levels initially increased with increasing fasting blood glucose (FBG) and postprandial blood glucose (PPBG) levels, up to 7 mmol/L and 10 mmol/L, respectively, and thereafter decreased at higher FBG and PPBG levels. Compared with subjects in the lower serum UA quartile, subjects in the upper quartile of serum UA levels had higher weights, triglyceride levels, and creatinine levels as well as lower Ccr and FEua levels. Compared with women's group, UA levels were higher, and FEua levels were lower in men's group. Sex,body mass index (BMI), mean arterial blood pressure (MAP), serum triglycerides (TG), FA and Ccr were independent correlation factors of UA. UA decreased and FEua increased after the patients underwent a combined treatment.Conclusions UA increased initially and then decreased as glucose levels increased from NGT to IGR and T2DM.Compared with NGT and T2DM, IGR subjects had higher SUA levels, which related to its high levels of insulin. Under T2DM, male gender, BMI, MAP, Ccr, TG and FA are independent correlation factors of UA. Glucose-lowering,antihypertensive, lipemia-regulating combined treatments were of advantage to decline of SUA of T2DM. 展开更多
关键词 diabetes mellitus serum uric acid blood glucose fractional excretion of uric acid INSULIN
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