Combined use of dopamine and prostaglandin A1 in patients with acute renal failure and hepatorenal syndrome.

Dopamine and prostaglandin A1 were infused intravenously in 4 patients with the hepatorenal syndrome, in 1 patient with acute tubular necrosis, and 1 patient with cortical necrosis. Large doses of prostaglandin A1 decreased arterial blood pressure preventing increase in dosage; in contrast, high doses of dopamine elevated blood pressure. When the two drugs were administered conjointly, much larger doses of each agent could be administered without change in arterial blood pressure. Significant improvement of renal function was not observed in any of these critically ill patients during or within 24 hours after dopamine and prostaglandin A1 administration. This study demonstrated that extremely large doses of these vasodilating agents can be safely administered conjointly.     

Combined haemodynamic effects of low doses of dopamine and dobutamine in patients with acute infarction and cardiac failure

The haemodynamic effects of an optimal dose of dobutamine (DUo) (6.7 +/- 4.2 micrograms kg-1 min-1) and the combination of this optimal dose minus 2.5 micrograms kg-1 min-1 of dobutamine (DU) plus dopamine 2.5 micrograms kg-1 min-1 (DA) were studied in a first group of 12 consecutive patients with acute myocardial infarction (AMI) and cardiac failure (CF). DUo decreased pulmonary wedge pressure from 23.5 to 16 mm Hg (P less than 0.01), systemic vascular resistance from 1 774 to 1 417 dynes s cm-5 (P less than 0.01). DUo increased cardiac output from 3.21 to 4.55 litres/min (P less than 0.01) and urinary flow (UF) from 20 to 68 ml/h (P less than 0.01). Heart rate and blood pressure did not change significantly. DUo - DU + DA significantly increased UF from 68 to 107 ml/h (P less than 0.05) while the other parameters remained unchanged with respect to DUo. The positive effect of DA on UF was confirmed in a second group of 12 consecutive patients by comparing the successive effects of DA + DUo and DUo + DU : all previously described parameters remained unchanged except UF which decreased from 107 to 65 (P less than 0.01). We conclude that in patients with CF and AMI, association of DA and DUo is useful in obtaining both inotropic and diuretic effects.     

Mechanism of increased renal prostaglandin E2 in uranyl nitrate-induced acute renal failure

We have previously demonstrated that decreased cortical prostaglandin metabolism can contribute significantly to an increase in renal tissue levels and activity of prostaglandin E2 in bilateral ureteral obstruction, a model of acute renal failure. In the present study, we have further investigated whether alterations in prostaglandin metabolism can occur in a nephrotoxic model of acute renal failure. Prostaglandin synthesis, prostaglandin E2 metabolism (measured as both prostaglandin E2-9-ketoreductase and prostaglandin E2-15-hydroxydehydrogenase activity), and tissue concentration of prostaglandin E2 were determined in rabbit kidneys following an intravenous administration of uranyl nitrate (5 mg/kg). No changes in the rates of cortical microsomal prostaglandin E2 and prostaglandin F2 alpha synthesis were noted at the end of 1 and 3 days, while medullary synthesis of prostaglandin E2 fell by 47% after 1 day and 43% after 3 days. Cortical cytosolic prostaglandin E2-9-ketoreductase activity was found to be decreased by 36% and 76% after 1 and 3 days respectively. No significant changes were noted in cortical cytosolic prostaglandin E2-15-hydroxydehydrogenase activity after 3 days. Cortical tissue levels of prostaglandin E2 increased by 500% at the end of 3 days. These data demonstrate that in nephrotoxic acute renal failure, decreased prostaglandin metabolism (i.e., prostaglandin E2-9-ketoreductase activity) can result in increased tissue levels of prostaglandin E2 in the absence of increased prostaglandin synthesis and suggest that alterations in prostaglandin metabolism may be an important regulator of prostaglandin activity in acute renal failure.     

Protection against ischemic acute renal failure by prostaglandin infusion

We have shown that intravenous infusion of epinephrine (4ug/kg/min for 6 hours) into mongrel dogs consistently produces renal hemodynamic and histopathologic characteristics of ischemic acute renal failure (ARF). This study describes renal responses that were modified by intravenous infusion of prostaglandin E (PGE₂)(10 ug/min) one hour before and during a 6 hour infusion of epinephrine (4 ug/kg/min). Two groups of animals were studied: Group I (epinephrine alone) and Group II (epinephrine + PGE₂). Urine volume, glomerular filtration rate, urinary sodium excretion rate, urine osmolality, and serum urea nitrogen were measured. Renal tissues were studied using light and electron microscopy. While urine volume or glomerular filtration rate decreased significantly in both groups, they were slightly but significantly better in Group II than Group I. Urine osmolality significantly decreased in Group I but significantly increased in Group II. Group I animals became azotemic (mean serum urea nitrogen, 27 ± 1 mg/dl), whereas Group II animals showed serum urea nitrogen at the upper limits of normal (mean 20 ± 2 mg/dl). The difference was significant (P <.01). Severe acute tubular lesions were a consistent feature in Group I. Tubular lesions were less severe and infrequent in Group II animals. While mitochondrial dark bodies (electron microscopy) characterized tubular lesions in Group I, fewer mitochondria contained dark bodies in Group II animals. These dark bodies appear to be calcium and constitute a definitive sign of ischemia. Therefore, this study indicates that PGE₂ attenuates epinephrine-induced tubular ischemia and injury and ARF which may be attributed to excessive solute excretion or to inhibition of calcium influx into tubular mitochondria.     

The treatment of the hepatorenal syndrome with intra-renal administration of prostaglandin E1

Three patients with the hepatorenal syndrome were treated with prostaglandin E₁ administered through a selective renal arterial catheter. Prostaglandin E₁ was given in progressively increasing doses (2 to 100 ng/kg/min) over a 60-minute period. Control plasma prostaglandin E levels were elevated in all three patients, 0.98, 0.91, and 0.83 ng/ml, respectively. At the end of the infusion, plasma prostaglandin E levels had risen to 10.4, 2.63, and 10.3 ng/ml in the three patients respectively. Plasma renin activity increased during the course of the infusion in two of the patients. The plasma aldosterone concentration did not change during the prostaglandin E₁ infusion. Intrarenal prostaglandin E₁ failed to increase urine volume or urinary sodium concentration in three patients with the hepatorenal syndrome.     

肾后性急性肾衰诊治临床探讨

目的分析60例肾后性急性肾功能衰竭患者的诊治。方法对60例肾后性急性肾功能衰竭患者的诊治效果进行回顾性分析。结果解除梗阻后,22例患者肾功能恢复正常,38例未完全恢复正常,其中19例行维持性血液透析。结论影象学检查是明确诊断的主要方法,梗阻程度和时间是影响肾功能恢复的关键因素。     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

Mechanism of increased renal prostaglandin E2 in uranyl nitrate-induced acute renal failure

We have previously demonstrated that decreased cortical prostaglandin metabolism can contribute significantly to an increase in renal tissue levels and activity of prostaglandin E₂ in bilateral ureteral obstruction, a model of acute renal failure. In the present study, we have further investigated whether alterations in prostaglandin metabolism can occur in a nephrotoxic model of acute renal failure. Prostaglandin synthesis, prostaglandin E₂ metabolism (measured as both prostaglandin E₂-9-ketoreductase and prostaglandin E₂-15-hydroxydehydrogenase activity), and tissue concentration of prostaglandin E₂ were determined in rabbit kidneys following an intravenous administration of uranyl nitrate (5 mg/kg). No changes in the rates of cortical microsomal prostaglandin E₂ and prostaglandin F_2α synthesis were noted at the end of 1 and 3 days, while medullary synthesis of prostaglandin E₂ fell by 47% after 1 day and 43% after 3 days. Cortical cytosolic prostaglandin E₂-9-ketoreductase activity was found to be decreased by 36% and 76% after 1 and 3 days respectively. No significant changes were noted in cortical cytosolic prostaglandin E₂-15-hydroxydehydrogenase activity after 3 days. Cortical tissue levels of prostaglandin E₂ increased by 500% at the end of 3 days. These data demonstrate that in nephrotoxic acute renal failure, decreased prostaglandin metabolism (i.e., prostaglandin E₂-9-ketoreductase activity) can result in increased tissue levels of prostaglandin E₂ in the absence of increased prostaglandin synthesis and suggest that alterations in prostaglandin metabolism may be an important regulator of prostaglandin activity in acute renal failure.     

Rhabdomyolysis and acute myoglobinuric renal failure following heroin use.

Four life-threatening dermatoses—Stevens-Johnson syndrome, toxic epidermal necrolysis, Kaposi''s varicelliform eruption and purpura fulminans—are unique in their abrupt onset and rapid progress to death, but prompt diagnosis and proper therapy can often cure the condition or prevent undesirable sequelae. Since two of the four conditions can follow the use of a variety of drugs and all may be secondary to an infectious agent, any physician may encounter them in practice and should be aware of their seriousness.     

烧伤合并急性肾功能衰竭的早期指标检测

目的:探讨烧伤合并急性肾功能衰竭(ARF)的早期指标检测以及各种危险因素.方法:选择本院2008年1月～2009年6月收治的75例中重度热烧伤患者.Ⅱ度或ⅡⅢ度烧伤面积累计20%-70%TBSA.所有患者在入院时、入院后3d、7d、14d和21d检测血清肌酐(Scr)、血尿素氮(BUN)、尿微量白蛋白(mALB)和滤过钠排泄分数(FeNa).结果:75例烧伤患者中有14例(18.7%)并发ARF,其中10例进行了血液净化治疗.烧伤合并ARF组烧伤面积和脓毒症发生率均明显高于烧伤未合并ARF组(P均＜0.05).烧伤合并ARF组Scr和BUN水平分别在住院7d和14d后明显高于烧伤未合并ARF组(P均＜0.05).烧伤合并ARF组入院时mALB水平已达到正常值34倍,21d时达到最大值,在观察期间一直高于烧伤未合并ARF组(P均＜0.05).烧伤合并ARF组滤过钠排泄分数均大于2%.烧伤面积与脓毒症是烧伤后ARF发生的主要危险因素(复相关系数R分别为0.52和0.23,P均＜0.05).结论:烧伤合并ARF与烧伤面积与脓毒症相关,mALB是早期监测ARF的有用指标.