肝硬化失代偿期并发低钠血症的治疗

目的探讨肝硬化失代偿期患者合并低钠血症的治疗。方法对我院128例肝硬化失代偿期患者监测血钠,110例血钠下降,随机分为补钠组(57例)与限钠组(53例),进行肝功能、血钠、尿量、腹水消退的监测,同时观察肝肾综合征、肝性脑病等并发症及死亡率的发生情况。结果肝硬化失代偿期发生低钠血症的发生率为85.94%(110/128),补钠组尿量增加、腹水消退时间缩短、肝肾综合征发生率、肝性脑病发生率、死亡率等均好于限钠组(P<0.05)。结论对于肝硬化腹水并发低钠血症患者补充氯化钠有利于肝功能的改善。     

不限钠饮食与限钠饮食对肝硬化腹水消退影响的研究

目的比较不限钠饮食与限钠饮食对肝硬化腹水消退的影响。方法将60例肝硬化腹水患者随机分为两组:不限钠饮食组30例,饮食中不限钠。限钠饮食组30例,予低盐饮食。在治疗前、治疗后10 d测定血钠、血氯、尿钠、尿氯、血浆肾素活性(PRA)、血管紧张素Ⅱ(AⅡ)、醛固酮(ALD)、肾有效血流量,比较腹水消退情况。结果治疗后10 d不限钠饮食组血钠、肾有效血流量高于治疗后10 d的限钠饮食组。治疗后10 d不限钠饮食组PRA、AⅡ、ALD均显著低于限钠饮食组;至出院时腹水消失,不限钠饮食组20例(66.67%)多于限钠饮食组(11例,占36.67%);腹水消失时间,不限钠饮食组短于限钠饮食组。结论肝硬化腹水患者在使用利尿剂同时不应限钠饮食,以防低血钠而影响利尿剂效果,影响腹水消退,并能防止低血钠诱发肾功能损害,改善预后。     

补钠佐治肝硬化腹水并低钠血症32例的临床观察

目的 :探讨肝硬化腹水并低钠血症的治疗方法。方法 :选择 62例肝硬化腹水并低钠血症的患者 ,随机分为限钠组和不限钠组。观察肝性脑病、肝肾综合征的发生率 ,病死率 ,腹水消退时间。结果 :不限钠组患者肝性脑病、肝肾综合征的发生率 ,病死率均低于限钠组患者 ,且腹水消退时间短。结论 :肝硬化腹水并低钠血症患者适量补充钠盐可以改善患者的预后。     

慢性重型病毒性肝炎低钠血症的临床分析

目的:探讨慢性重型病毒性肝炎患者低钠血症的治疗"方法"对41例慢性重型病毒性肝炎中重度低钠血症患者随机分为限钠组(20例)和不限钠组(21例)观察腹水消退时间,肝性脑病发生率,死亡率"结果"不限钠组患者在腹水消退时间,肝性脑病发生率,死亡率均低于限钠组患者"结论:对慢性重型病毒性肝炎低钠血症患者适量补充钠盐是一项重要的辅助治疗措施"     

补钠与限钠交替治疗肝硬化腹水的临床意义

目的 探讨补钠与限钠交替方法治疗肝硬化腹水的意义.方法 将120例肝硬化腹水患者随机分为治疗组(57例)和对照组(63例),2组常规治疗(保肝、利尿、补充白蛋白)相同,治疗组监测血钠,＜130 mmol/L者给予静脉补钠盐,血纳≥130 mmol/L者给予限钠;对照组均取限钠治疗,观察治疗后病情的转归情况.结果 治疗组24 h尿量增加,腹水消退,与对照组比较差异有统计学意义[尿量:治疗组(1936±53)ml,对照组(1365±63)ml,t=53.4239;腹围:治疗组(83.5±3.4)cm,对照组(88.3±4.0)cm,t=16.4376;P均＜0.05].结论 肝硬化腹水根据血钠情况交替补钠与限钠治疗,可提高利尿效果,减轻腹水,防止肝性脑病及低渗性脑病的发生.     

肝硬化腹水限钠治疗的弊端及其对策

１引言对肝硬化腹水患者进行限钠、利尿治疗已沿用一百余年，并为国内外所公认。通过近十余年的临床研究，我们发现，限钠、利尿治疗易导致血钠及渗透压下降，出现稀释性低钠血症，利尿药作用减弱或消失，产生所谓耐药（抗药）现象，腹水消失时间延长及诱发肝肾综合征（hepatorenalsyndrome，HRS）、低渗性脑病、低渗性休克等严重后果，但至今未引起广泛重视。目前对肝硬化腹水患者应用利尿药时多重视钾的补充，而忽视补钠，使肝硬化腹水患者在治疗过程中发生低钠血症者（８６．３％）明显多于低钾血症（１９．２％）。而低钠血症后果严重…     

肝硬化腹水并发低钠血症的临床分析

目的探讨肝硬化腹水患者不同血清钠水平与病情严重程度的关系。方法回顾分析2008年7月-2010年6月收治47例肝硬化腹水并发低钠血症患者,根据其入院时血清钠水平分为低钠血症轻(A组)、中(B组)、重(C组)3组。比较肝硬化腹水患者不同血钠水平的腹水程度及疗效的关系、以及低钠程度与肝性脑病、肝肾综合征和死亡发生率的关系。结果与A组比较,B、C两组腹水量、肝性脑病、肝肾综合征及病死率明显增高,差异有统计学意义(P<0.05);对治疗的效果明显降低(P<0.05)。结论肝硬化腹水患者的血清钠水平与其病情程度具有紧密相关性,监测血清钠的水平可作为判断病情严重程度的重要指标之一,提示在临床上需重视预防、及时发现并治疗低钠血症。     

重度低钠血症与肝肾综合征的关系研究

目的:通过研究肝硬化腹水伴重度低钠血症患者的临床资料及实验室指标,探讨重度低钠血症与肝肾综合征(HRS)的关系.方法:纳入我院2009年1月至2011年5月肝硬化腹水伴重度低钠血症患者40例(Na＜ 125.0 mmol/L)为研究对象,随机选取同期肝硬化腹水正常血钠患者52例为对照组,分析两组患者肝功能、肾功能、醛固酮(ALD)水平,并分析两组的HRS发病情况.结果:肝硬化重度低钠血症组血钠平均水平为122.2 mmol/L,对照组血钠平均水平为139.8 mmol/L.肝硬化重度低钠血症组HRS发生率26.9％,显著高于对照组(3.4％)(P＜0.05).肝硬化重度低钠血症组ALD水平为(48.21±29.85) ng/dL,高于对照组的(23.81±17.29)ng/dL (P＜ 0.05).肝硬化重度低钠血症组BUN、Crea水平均高于对照组(P＜0.05),而两组的肝功能酶学指标比较差异无显著性.结论:肝硬化重度低钠血症患者经肾素-血管紧张素-醛固酮系统分泌高水平醛固酮,醛固酮强烈的肾动脉收缩作用引发肾小球滤过率降低,从而导致肾功能减退.本研究结果提示:重度低钠血症可能是HRS发生的重要因素.     

慢性重型病毒性肝炎低钠血症的治疗体会

慢性重型病毒性肝炎低钠血症的治疗。本文对103例慢性重型病毒性肝炎中、重度缺钠患者随机分成限钠组51人和非限钠组52人，观察腹水吸收时间、肝性脑病发生率及病死率，发现不限钠组上述三指标明显低于限钠组。故对慢性重型病毒性肝炎低钠血症患者适当补充钠盐是一项重要的辅助治疗措施。     

肝硬化腹水不限钠治疗的疗效观察

目的 评价肝硬化失代偿期不限钠治疗腹水的疗效观察。方法 对照组23例患者采用严格的限钠治疗，治疗组24例患者不限钠或纠正低钠血症，其余保肝、利尿等治疗方法两组一致。结果 治疗组较对照组腹水消退快而明显，且并发症少，P〈0．05。结论 不限钠或纠正低钠血症治疗肝硬化腹水疗效显著。     

Renin, aldosterone and arginine vasopressin in patients with liver cirrhosis: the influence of ascites retransfusion

Plasma renin activity (PRA), and concentrations of aldosterone (PAL) and arginine vasopressin (AVP) in plasma were determined in 15 patients with ascites due to cirrhosis. The concentrations in ascites were analyzed simultaneously. Six patients were studied during extracorporeal ascites retransfusion. All but one patient with ascites showed elevated PAL (642 +/- 255 pg ml-1) and PRA (43 +/- 26 ng ml-1 h-1); all had increased AVP (7.3 +/- 5.1 pg ml-1). A low ascites to plasma ratio was found for aldosterone (0.023 +/- 0.023), but not for AVP (0.71 +/- 0.82). Retransfusion resulted in a normalization of central venous pressure (CVP), urinary volume, sodium/potassium ratio in urine, PAL and PRA, but not of AVP, serum sodium concentration and urinary sodium excretion. PRA and PAL increased again after cessation of treatment, while urinary output, CVP and sodium/potassium ratio in urine decreased. The results support the 'underfilling' concept, but give evidence that, in addition, other factors must be involved in the impaired natriuresis in cirrhotic patients. They further support the concept of volume expansion and increased renal perfusion as reason for the therapeutic efficacy of ascites retransfusion. Previous diuretic treatment seems not to be of importance for altered hormone metabolism in liver cirrhosis. Storage in a third compartment may be a factor in the persistently elevated AVP levels.     

慢性心力衰竭患者血钠水平对血浆肾素活性、醛固酮和N末端前脑钠肽水平的影响

目的探讨慢性心力衰竭（心衰）患者血钠水平对血浆。肾素活性（PRA）、醛固酮（ALD）和N末端前脑钠肽（NT．proBNP）水平的影响。方法91例慢性心衰患者,根据治疗前血钠水平分正常血钠组和低血钠组,均在人院第二天清晨卧位采血测定PRA、ALD和NT．proBNP水平,常规治疗心衰及低钠血症一周后以同样的方法采血复查血钠、PRA、ALD和NT-proBNP水平,对上述指标进行统计分析。结果入院时低血钠组PRA、ALD和NT-proBNP比正常血钠组高,差异有统计学意义（P〈0．05l低血钠组患者常规治疗心衰及低钠血症一周后,PRA、ALD和NT-proBNP水平较入院时降低．差异有统计学意义（P〈O．05）正常血钠组常规治疗心衰一周后PRA、ALD和NT．proBNP水平较入院时降低,差异有统计学意义（P〈0．05）;而两组患者治疗前后PRA、ALD和NT．proBNP水平下降值有明显差异（p〈O．05）,低血钠组下降史明显。结论低钠血症可能促进慢性心衰患者PRA、ALD和NT-proBNP分泌增加,心衰伴低钠血症患者的神经内分泌水平激活更明显。低钠血症经治疗血钠水平恢复正常后,神经内分泌激素水平明显降低。     

Renal prostaglandins in cirrhosis of the liver

Urinary prostaglandin excretion was studied in 42 patients with liver cirrhosis and in nine control subjects on restricted sodium intake and on bed rest. Creatinine clearance (CCr), sodium excretion (UNaV), plasma renin activity (PRA) and plasma aldosterone were also evaluated. Patients without ascites and ascitic patients without renal failure showed increased urinary excretion of immunoreactive 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha), prostaglandin E2 (iPGE2) and thromboxane B2 (iTXB2) when compared with controls, while immunoreactive PGF2a (iPGF2 alpha) levels did not differ from those in the control group. Patients with functional renal failure (FRF) presented a significant reduction of vasodilator prostaglandins but urinary excretion of iTXB2 was higher than in controls. On the whole, cirrhotic patients with higher urinary excretion of prostaglandins had normal or nearly normal PRA and aldosterone levels. i6-keto-PGF1 alpha and iPGE2 inversely correlated with PRA and aldosterone. The relationship between i6-ketoPGF alpha alpha and CCr was found to be highly significant in cirrhotic patients but not in the control group. On the other hand, iPGE2 significantly correlated with UNaV and with the fractional excretion of sodium (FENa). We concluded that: (a) enhanced renal prostaglandin synthesis in cirrhosis, inversely related to PRA and aldosterone, may be dependent on volume status; and (b) preserved renal function in these patients is associated with the ability to synthesize prostacyclin and PGE2.     

Effects of plasma expansion with albumin and paracentesis on haemodynamics and kidney function in critically ill cirrhotic patients with tense ascites and hepatorenal syndrome: a prospective uncontrolled trial

Introduction  

Circulatory dysfunction in cirrhotic patients may cause a specific kind of functional renal failure termed hepato-renal syndrome (HRS). It contributes to the high incidence of renal failure in cirrhotic intensive care unit (ICU) patients. Fluid therapy may aggravate renal failure by increasing ascites and intra-abdominal pressure (IAP). This study investigates the short-term effects of paracentesis on haemodynamics and kidney function in volume resuscitated patients with HRS.     

Renal haemodynamics in patients with liver cirrhosis assessed by colour ultrasonography

Colour Doppler flow imaging was used in this prospective, cross-sectional study to analyse renal haemodynamics in 50 cirrhotic patients and 15 healthy controls. Mean renal arterial resistive index (RI) was higher in cirrhotic patients than in healthy controls. Mean RI was also higher in cirrhotic patients with non-refractory ascites than in those without ascites, suggesting that the degree of renal vasoconstriction varies with the severity of ascites. A gradient of RI values across the main renal artery, interlobar artery and interlobular renal artery was retained in cirrhotic patients even in the decompensatory stage with non-refractory ascites but was not present in the decompensatory stage with refractory ascites. The disappearance of this gradient may be an important prognostic factor in the development of hepatorenal syndrome (HRS). An inverse correlation between creatinine clearance and interlobular arterial RI was shown for all cirrhotic patients suggesting that even patients with refractory ascites are in a prophase of HRS.     

Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.     

Atrial natriuretic factor, cyclic 3'',5''-guanosine monophosphate and prostaglandin E2 in liver cirrhosis: relation to blood volume and changes in blood volume after furosemide

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic 3',5'-guanosine monophosphate (cGMP) were measured in 11 cirrhotic patients with ascites, 11 cirrhotic patients without ascites and 15 control subjects. The following were determined in 15 of the cirrhotic patients and in all the control subjects: blood volume (BV) and furosemide-induced changes in BV, plasma values of ANF, cGMP, angiotensin II (AII), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion rates of cGMP, prostaglandin E2 (PGE2), water and sodium. Basal plasma levels of ANF and cGMP were higher in patients with cirrhosis than in controls, but were the same in both groups of cirrhotics (ANF: cirrhosis with ascites 12.7, without ascites 13.4, and in controls 5.8 pmol l-1 (medians); cGMP: 7.7, 7.4 and 4.3 nmol l-1, respectively). BV was less reduced after furosemide in the cirrhotic patients (6.0%) than in the healthy subjects (10.1%), but basal BV did not differ. Urinary sodium excretion rates after furosemide were significantly lower in the cirrhotic patients than in the controls. PGE2 excretion rate increased after furosemide in the cirrhotic patients (0.29 to 0.66 pmol min-1; P less than 0.01) but not in the controls (0.31 to 0.38 pmol min-1). After furosemide ANF and cGMP decreased slightly in both groups whereas AII and Aldo increased; AVP increased in the controls, but not in the cirrhotic patients. In conclusion, plasma values of ANF and cGMP are increased in liver cirrhosis both with and without ascites. This and the elevated PGE2 excretion after furosemide may be compensatory phenomena in order to facilitate renal sodium excretion.     

Comparison of two aquaretic drugs (niravoline and OPC-31260) in cirrhotic rats with ascites and water retention

kappa-Opioid receptor agonists (niravoline) or nonpeptide antidiuretic hormone (ADH) V2 receptor antagonists (OPC-31260) possess aquaretic activity in cirrhosis; however, there is no information concerning the effects induced by the chronic administration of these drugs under this condition. To compare the renal and hormonal effects induced by the long-term oral administration of niravoline, OPC-31260, or vehicle, urine volume, urinary osmolality, sodium excretion, and urinary excretion of aldosterone (ALD) and ADH were measured in basal conditions and for 10 days after the daily oral administration of niravoline, OPC-31260, or vehicle to cirrhotic rats with ascites and water retention. Creatinine clearance, serum osmolality, ADH mRNA expression, and systemic hemodynamics were also measured at the end of the study. Niravoline increased water excretion, peripheral resistance, serum osmolality, and sodium excretion and reduced creatinine clearance, ALD and ADH excretion, and mRNA expression of ADH. OPC-31260 also increased water metabolism and sodium excretion and reduced urinary ALD, although the aquaretic effect was only evident during the first 2 days, and no effects on serum osmolality, renal filtration, and systemic hemodynamics were observed. Therefore, both agents have aquaretic efficacy, but the beneficial therapeutic effects of the long-term oral administration of niravoline are more consistent than those of OPC-31260 in cirrhotic rats with ascites and water retention.     

Management of hyponatremia

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.