Safety Of Midodrine Research Articles

Safety of midodrine in patients with heart failure with reduced ejection fraction: a retrospective cohort study.

Background: Heart failure with reduced ejection fraction (HFrEF) poses significant health risks. Midodrine for maintaining blood pressure in HFrEF, requires further safety investigation. This study explores midodrine's safety in HFrEF through extensive matched analysis. Methods: Patients with HFrEF (LVEF <50%) without malignancy, non-dialysis dependence, or non-orthostatic hypotension, were enrolled between 28 August 2013, and 27 August 2023. Propensity score matching (PSM) created 1:1 matched groups. Outcomes included mortality, stage 4 and 5 chronic kidney disease (CKD), emergency room (ER) visits, intensive care unit (ICU) admissions, hospitalizations, and respiratory failure. Hazard ratios (HR) with 95% confidence intervals (95% CI) were calculated for each outcome, and Kaplan-Meier survival analysis was performed. Subgroup analyses were conducted based on gender, age (20-<65 vs. ≥65), medication refill frequency, and baseline LVEF. Results: After 1:1 PSM, 5813 cases were included in each group. The midodrine group had higher risks of respiratory failure (HR: 1.16, 95% CI: 1.08-1.25), ICU admissions (HR: 1.14, 95% CI: 1.06-1.23), hospitalizations (HR: 1.21, 95% CI: 1.12-1.31), and mortality (HR: 1.090, 95% CI: 1.01-1.17). Interestingly, midodrine use reduced ER visits (HR: 0.77, 95% CI: 0.71-0.83). Similar patterns of lower ER visit risk and higher risks for ICU admissions, respiratory failure, and overall hospitalizations were observed in most subgroups. Conclusion: In this large-scale study, midodrine use was associated with reduced ER visits but increased risks of respiratory failure, prolonged ICU stays, higher hospitalizations, and elevated mortality in HFrEF patients. Further research is needed to clarify midodrine's role in hemodynamic support and strengthen existing evidence.

Midodrine reduces new-onset acute kidney injury and hyponatremia in children with cirrhosis and ascites awaiting liver transplantation: Results from an open-label RCT.

Midodrine, an oral α-1-adrenergic receptor agonist, counters arterial hypovolemia and reduces complications in adult patients with cirrhosis. This randomized controlled trial (RCT) aimed to assess the efficacy and safety of midodrine in preventing complications and improving survival in children with cirrhosis and ascites who are awaiting liver transplantation (LT). This open-label RCT conducted from January 2022 to May 2023 included children under 18 years with cirrhosis and ascites. Patients were randomized to receive either midodrine plus standard medical therapies (SMTs) or SMT alone. The primary outcome measure was the incidence of cirrhosis-related complications within 6 months. Thirty-five subjects were enrolled and randomized. Patients in the midodrine arm had a lower incidence of new-onset acute kidney injury (AKI) compared with the SMT arm (11.1% vs. 41.2%). Patients in the midodrine arm showed a decline in serum creatinine and improvement in glomerular filtration rate, whereas no changes were observed in the SMT arm. There was a lower incidence of new-onset hyponatremia in the midodrine arm (20% vs. 56%). Midodrine led to reduction in plasma rennin activity (PRA) and improvement in systemic hemodynamics. There was no difference in the rate of resolution of ascites, recurrence of ascites, requirement of therapeutic paracentesis, cumulative albumin infusion requirement, episodes of spontaneous bacterial peritonitis, and hepatic encephalopathy between the two arms. Midodrine, when added to SMT, was effective in reducing the incidence of new-onset AKI and hyponatremia in pediatric cirrhotics awaiting LT. It also improved systemic hemodynamics and showed a trend towards reducing PRA.

Effect of midodrine on the prognosis of patients with septic shock: a systematic review and meta-analysis.

This study aims to assess the efficacy and safety of midodrine on treating patients with septic shock. Literature search was conducted in PubMed, the Cochrane Library, and Embase. The Mantel-Haenszel method was used to calculate pooled relative risks (RRs) and 95% confidence intervals (95% CI). The mean differences (MD) or standardized mean difference (SMD) were calculated using the inverse variance for continuous variables. Data analysis was performed using Review Manager 5.3. A total of 6 studies were finally included in this meta-analysis. Adding midodrine to patients with septic shock was associated with a reduction in hospital mortality [risk ratio (RR) 0.76; 95% CI, 0.57-1.00; p=0.05] and intensive care unit (ICU) mortality (RR 0.59; 95% CI, 0.41-0.87; p=0.008). However, there were no significant differences in the duration of intravenous vasopressors [standardized mean difference (SMD) -0.18; 95% CI, -0.47-0.11; p=0.23], intravenous vasopressor reinstitution (RR 0.58; 95% CI, 0.19-1.80; p=0.35), the length of ICU stay [mean difference (MD) -0.53 days; 95% CI, -2.24-1.17; p=0.54], and the length of hospital stay (MD -2.40 days; 95% CI, -5.26-0.46; p=0.10) between midodrine group and intravenous vasopressor alone group. The additional use of midodrine might reduce hospital mortality and ICU mortality in patients with septic shock. More high-quality randomized controlled trials are needed to verify this conclusion.

The Use of Midodrine as an Adjunctive Therapy to Liberate Patients from Intravenous Vasopressors: A Systematic Review and Meta-analysis of Randomized Controlled Studies.

Studies evaluating the role of midodrine as an adjunctive therapy to liberate patients with shock from intravenous (IV) vasopressors have yielded mixed results. The aim of our study was to evaluate the efficacy and safety of midodrine as an adjunctive therapy to liberate patients with shock from IV vasopressors. Electronic searches of the MEDLINE, EMBASE, and Cochrane databases through April 2022 for randomized controlled trials (RCTs) that evaluated the use of midodrine versus control in patients with shock and a low dose of IV vasopressors. The primary outcome was total IV vasopressor time, whilethesecondary outcomes includedtime-to-IV vasopressor discontinuation, IV vasopressor restart, intensive care unit (ICU) length of stay (LOS), hospital LOS, and incidence of bradycardia. The final analysis included four RCTs with a total of 314 patients: 158 in the midodrine group and 156 in the control group, with a weighted mean age of 64years (54.2% men). There was no significant difference in the total IV vasopressor time between the midodrine and control groups (standardized mean difference [SMD] - 0.53; 95% confidence interval [CI] - 1.38 to 0.32, p = 0.22; I2 = 92%). Also, there were no significant differences between the two groups in the time-to-IV vasopressor discontinuation (SMD - 0.05; 95% CI - 0.57 to 0.47, p = 0.09), IV vasopressor restart (19.3 vs. 28.3%; risk ratio [RR] 0.74; 95% 0.25-2.20, p = 0.59), ICU LOS (SMD - 0.49; 95% CI - 1.30 to 0.33, p = 0.24), and hospital LOS (SMD 0.01; 95% CI - 0.27 to 0.29, p = 0.92). However, compared with the control group, the midodrine group had a higher risk of bradycardia (15.3 vs. 2.1% RR 5.56; 95% CI 1.54-20.05, p = 0.01). Among patients with vasopressor-dependent shock, midodrine was not associated with early liberation of vasopressor support or shorter ICU or hospital length of stay. Adding midodrine increased the risk of bradycardia. Further large RCTs are needed to better evaluate the efficacy and safety of midodrine in liberating patients from IV vasopressors.

ROLE OF ORAL MIDODRINE IN PATIENTS RECEIVING INTRAVENOUS VASOPRESSORS IN ICU SETTING: A SYSTEMATIC REVIEW

SESSION TITLE: Tuesday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM PURPOSE: Hypotension in patients admitted to ICU who otherwise qualify ICU discharge criteria is challenging as hospitals require IV vasopressors be given in ICU. Oral midodrine has been reported as an option to wean off vasopressors. We performed a systematic review to understand the current evidence regarding the efficacy and safety of midodrine. METHODS: A systematic search of PubMed, Ovid Embase, Web of Science, Cochrane library and clinicaltrials.gov was performed. After removing duplicates from initial 124 articles, 94 articles were screened for relevance by two independent reviewers. 33 articles were screened for eligibility. RESULTS: Seven studies were included with N= 2290, including 953 males and 704 females. Among these, 1582 patients received midodrine while 708 patients served as control group. The reporting of APACHE score was heterogeneous. The midodrine dose ranged from 15 mg to 120 mg per day divided into 2-3 doses. There was significant variability in the reporting of outcomes. The total ICU stay was significantly shorter in midodrine group in one study; Whitson et all: 7.5 vs 9.4 days, p= 0.017. While four studies showed a non-significant difference in ICU LOS between patients receiving midodrine and control group. ICU readmissions data was reported by two studies (Poveromo et al & Roach et al) and showed no significant differences. Similarly, no study showed that midodrine reduces the total hospital stay. Although reported only by three studies with variability in results reporting, midodrine was noticed to significantly reduce the total time vasopressor was administered in two of them while Roach et al showed a longer use of vasopressor in the midodrine arm: Whitson et al(Mean:2.9 days vs 3.8 days, p< 0.001), Poveromo et al (median:1.2 days, 0.5- 2.8 days) and Roach et al(Average:17.9 vs.14.7 days, p< 0.01). The ICU and in-hospital mortality data were reported by three studies. Poveromo et al showed statistically significant reduction of in-hospital mortality (8.5% vs. 22.3%, p= 0.01). However, there was a non-significant trend of reduction in ICU/in-hospital mortality reported by Whitson et al (11% vs. 18.6%, p= 0.8) and Rizvi et al (8% vs. 11%). The drug was well tolerated with a manageable toxicity profile. Bradycardia was the most common side effect, ranging between 12.8-16.5%. Midodrine associated hypertension was reported by only one study (Poveromo et al) as incidence of 6.4%. CONCLUSIONS: Midodrine has potential to decrease ICU length of stay and facilitate early weaning off vasopressors. Current literature is still under powered to illustrate the full benefit of midodrine. CLINICAL IMPLICATIONS: Larger randomized controlled trials are needed to further investigate the full potential for use of midodrine in ICU. DISCLOSURES: No relevant relationships by Muhammad Ahsan, source=Web Response No relevant relationships by Siddique Chaudhary, source=Web Response No relevant relationships by Sana Chaudhary, source=Web Response No relevant relationships by HAFIZ MUHAMMAD FAZEEL, source=Web Response No relevant relationships by Gabriel Patarroyo Aponte, source=Web Response No relevant relationships by Amman Yousaf, source=Web Response

Delayed orthostatic hypotension: Severity of clinical symptoms and response to medical treatment.

Severity of orthostatic intolerance and the benefit of medical treatment in patients with delayed OH have not been elucidated. This study aimed to compare the symptom severity between classic and delayed OH and evaluate the efficacy of midodrine or pyridostigmine in patients with delayed OH. This was an adjunctive study of previously reported randomized, open-label clinical trials evaluating the efficacy and safety of midodrine or pyridostigmine for classic OH. Seventeen patients with delayed OH were enrolled and also received midodrine (2.5 mg twice a day) or pyridostigmine (30 mg twice a day) alone or combined. Result of initial orthostatic vital sign and questionnaires were compared between the patients with delayed OH and previously reported 87 patients with classic OH. Delayed OH patients were followed up at 1 and 3 months post-treatment and the vital sign measurements and questionnaires were repeated during the follow-up period. Questionnaire scores regarding OH-related symptoms, depression and health-related quality of life (HRQOL) were comparable between the classic and delayed OH patients at baseline. OH-related symptoms and depression were significantly improved after 3 months of medical treatment. Patients with delayed OH exhibited orthostatic intolerance similar to that of classic OH. This study shows that these patients may benefit from medical treatment with either midodrine or pyridostigmine.

Midodrine-Induced Bradycardia in the ICU

SESSION TITLE: Shock SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Midodrine, an alpha1 agonist used to decrease or replace IV vasopressors, may cause bradycardia. CASE PRESENTATION: A 60 year old woman was admitted to the ICU for hypothermia and hypotension from the ED. Past medical history included hypothyroidism. BP in the ED ranged from 70-90s systolic with HR 100-120. Labs included WBC 2900/mm3, cortisol 29mcg/dl, TSH 6.35miu/dl, and urinalysis with 2+ leukocyte esterase. Presumptive diagnosis was septic shock due to UTI and she was treated with ceftriaxone, fluid resuscitation and norepinephrine. Norepinephrine was significantly weaned within 24 hours, however off vasopressors MAPs remained in the 50s. Midodrine 10mg TID was started to replace IV vasopressors. Heart rate prior to midodrine ranged 60-120. Nine hours after beginning midodrine she developed sustained heart rates in the 40s and as low as 37. Despite the bradycardia, her MAPs were now in the 70s. Midodrine was discontinued and despite developing recurrent hypotension requiring 3 more days of norepinephrine infusion her heart rate returned to above 60 within 16 hours of the last dose of midodrine and thereafter remained above 60. DISCUSSION: Midodrine is an oral alpha1 agonist indicated to treat orthostatic hypotension. Off-label midodrine in the ICU is used to decrease or replace IV vasopressors.1,2 Midodrine causes bradycardia through the baroreceptor reflex, similar to phenylephrine, another alpha1 agonist. Overdose may cause bradycardia.3 Bradycardia however appears to be an uncommon adverse effect at therapeutic doses. A retrospective analysis of 135 patients who received midodrine in addition to IV vasopressor documented one case of bradycardia necessitating stopping midodrine.1 A prospective study of 20 patients on phenylephrine showed no statistical difference in heart rate before and after addition of midodrine.2 CONCLUSIONS: Midodrine has been shown to be an effective choice to decrease or replace IV vasopressors in the ICU. It may however, cause reflex bradycardia that resolves with discontinuation of the drug. Reference #1: Whitson MR, et al. Feasibility, Utility, and Safety of Midodrine During Recovery Phase From Septic Shock. Chest. 2016 Jun;149(6):1380-3. Reference #2: Levine AR, et al. Oral midodrine treatment accelerates the liberation of intensive care unit patients from intravenous vasopressor infusions. J Crit Care. 2013 Oct;28(5):756-62. Reference #3: Wong LY, et al. Severe Hypertension and Bradycardia Secondary to Midodrine Overdose. J Med Toxicol. 2017 Mar;13(1):88-90. DISCLOSURE: The following authors have nothing to disclose: Dennis Laurence No Product/Research Disclosure Information

Efficacy and Safety of Midodrine in a Cohort of ICU Patients

Efficacy and Safety of Midodrine in a Cohort of ICU Patients

Feasibility, Utility, and Safety of Midodrine During Recovery Phase From Septic Shock

We describe the feasibility, utility, and safety of oral midodrine to replace IV vasopressors during recovery from septic shock. This was a retrospective study performed in a medical ICU. All study subjects had a diagnosis of septic shock requiring at least 24 hours of IV vasopressors and demonstrated clinical stability with stable or decreasing doses of IV vasopressors. The two groups compared were those who received IV vasopressors only and those who received IV vasopressors with adjunctive midodrine. Of the 275 study patients, 140 received an IV vasopressor only and 135 received midodrine in addition to an IV vasopressor. There was no difference between the groups' demographics (age, sex, Acute Physiology and Chronic Health Evaluation 4 score). Mean IV vasopressor duration was 3.8days in the IV vasopressor only group and 2.9days in the IV vasopressor with midodrine group (P< .001). An IV vasopressor was reinstituted after discontinuation in 21 of 140 (15%) patients in the IV vasopressor only group and in 7 of 135 (5.2%) patients in the IV vasopressor with midodrine group (P= .007). ICU length of stay was 9.4days in the IV vasopressor only group and 7.5days in the IV vasopressor with midodrine group (P= .017). There were no complications associated with midodrine use except transient bradycardia in one patient, which resolved upon discontinuation of midodrine. Midodrine may reduce the duration of IV vasopressors during recovery phase from septic shock and may be associated with a reduction in length of stay in the ICU.

Is Midodrine Effective for Orthostatic Hypotension and Recurrent Reflex Syncope

This systematic review was performed to evaluate the efficacy and safety of midodrine in patients with symptomatic orthostatic hypotension (SOH) — defined as a fall in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg within 3 minutes upon standing — and recurrent reflex syncope (RRS). To identify trials of patients with SOH …

Midodrine for orthostatic hypotension and recurrent reflex syncope: A systematic review.

Symptomatic orthostatic hypotension (SOH) and recurrent reflex syncope (RRS) can be disabling. Midodrine has been proposed in the management of patients with these conditions but its impact on patient important outcomes remains uncertain. We performed a systematic review to evaluate the efficacy and safety of midodrine in patients with SOH and RRS. We searched multiple electronic databases without language restriction from their inception to June 2013. We included randomized controlled trials of patients with SOH or RRS that compared treatment with midodrine against a control and reported data on patient important outcomes. We graded the quality of evidence according to the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Eleven trials involving 593 patients were included in this review. Three studies addressed health-related quality of life in patients with RRS, showing improvement with midodrine: risk difference 14% (95% confidence interval [CI] -3.5 to 31.6), very low confidence. Seven studies addressed symptom improvement and provided poolable data showing improvement with midodrine in patients with SOH: risk difference 32.8% (95% CI 13.5-48), low confidence; and RRS: risk difference 63.3% (95% CI 47.6-68.2), very low confidence. Five studies reported syncope recurrence in patients with RRS showing improvement with midodrine: risk difference 37% (95% CI 20.8%-47.4%), moderate confidence. The most frequent side effects in the midodrine arm were pilomotor reactions (33.6%, risk ratio 4.58 [95% CI 2.03-10.37]). Evidence warranting low/moderate confidence suggests that midodrine improves clinical important outcomes in patients with SOH and RRS.

Midodrine for Orthostatic Hypotension: A Systematic Review and Meta-Analysis of Clinical Trials

To perform a systematic review and meta-analysis of clinical trials evaluating the efficacy and safety of midodrine in orthostatic hypotension (OH). We searched major databases and related conference proceedings through June 30, 2012. Two reviewers independently selected studies and extracted data. Random-effects meta-analysis was used to pool the outcome measures across studies. Seven trials were included in the efficacy analysis (enrolling 325 patients, mean age 53 years) and two additional trials were included in the safety analysis. Compared to placebo, the mean change in systolic blood pressure was 4.9 mmHg (p = 0.65) and the mean change in mean arterial pressure from supine to standing was -1.7 mmHg (p = 0.45). The change in standing systolic blood pressure before and after giving midodrine was 21.5 mmHg (p < 0.001). A significant improvement was seen in patients' and investigators' global assessment symptoms scale (a mean difference of 0.70 [95 % CI 0.30-1.09; p < 0.001] and 0.80 [95 % CI 0.76-0.85; p < 0.001], respectively). There was a significant increase in risk of piloerection, scalp pruritis, urinary hesitancy/retention, supine hypertension and scalp paresthesia after giving midodrine. The quality of evidence was limited by imprecision, heterogeneity and increased risk of bias. There is insufficient and low quality evidence to support the use of midodrine for OH.

MP-11.03: Midodrine for the Treatment of Organic Anejaculation but Not Spinal Cord Injury: A Prospective Randomized Placebo-Controlled Double-Blind Clinical Study

Anejaculation is a rare cause of infertility and adversely affects the general sense of well being and perception of sexual life satisfaction. Evidence to support effective and noninvasive treatment for this ejaculatory disorder is lacking. The present study aimed to evaluate the efficacy and safety of midodrine (α1- adrenergic receptor agonist) for the treatment of organic anejaculation but not spinal cord injury (SCI).

Midodrine for the treatment of organic anejaculation but not spinal cord injury: a prospective randomized placebo-controlled double-blind clinical study.

Anejaculation is a rare cause of infertility and adversely affects the general sense of well-being and perception of sexual life satisfaction. Evidence to support effective and noninvasive treatment for this ejaculatory disorder is lacking. This study aimed to evaluate the efficacy and safety of midodrine (alpha(1)-adrenergic receptor agonist) for the treatment of organic anejaculation but not spinal cord injury (SCI). A total of 128 patients were randomly assigned to oral midodrine 7.5-15 mg per day in a stepwise approach (group 1, n=64), or a similar regimen of placebo (group 2, n=64). They underwent a complete physical examination, echocardiography, 12-lead electrocardiogram, transrectal ultrasonography, complete blood count and blood chemistry. Hormonal assays included serum levels of luteinizing hormone, follicle-stimulating hormone, prolactin and testosterone. To rule out other sexual dysfunction, patients also completed the International Index of Erectile Function questionnaire. Psychiatric disorders were excluded by appropriate tests. Outcome measure was reversal of the anejaculation. None of the patients in the placebo group achieved antegrade or retrograde ejaculation. At the end of study, antegrade, retrograde and antegrade+retrograde ejaculation occurred in 18 (29.5%), 8 (13.1%) and 9 (14.8%) patients in midodrine group, respectively (all P=0.01). The most and least favorable responses were among patients with multiple sclerosis and bilateral sympathectomy, respectively. Midodrine improved ejaculation function in a dose-dependent manner. Four participants (6.3%) in midodrine group discontinued this study for reasons of adverse events. In patients with organic anejaculation but without SCI midodrine can reverse anejaculation in more than 50% of patients. Further studies are needed, however, for the evaluation of different treatment regimens in anejaculation therapy.

Midodrine and Octreotide in Treatment of Cirrhosis-Related Hemodynamic Complications

To review studies evaluating the use of midodrine and octreotide in hemodynamic complications of cirrhosis, including ascites and hepatorenal syndrome. Searches of MEDLINE (1966-September 2008) and EMBASE (1974-September 2008) were conducted using the terms midodrine, octreotide, hepatorenal syndrome, ascites, cirrhosis, and paracentesis-induced circulatory dysfunction. Literature review was limited to English-language, human studies. Studies identified from data sources were considered for review. Studies were excluded if primary therapy involved any of the following: transjugular intrahepatic portosystemic shunt procedure, medications other than midodrine or octreotide, or patients included for treatment or prevention of portal hypertension and/or variceal bleeding. Pharmacokinetic/pharmacodynamic studies and studies using retrospective data collection were excluded. Seven studies were included in this review. Midodrine and octreotide in combination or alone have shown conflicting results for systemic and renal hemodynamics and renal function in patients with cirrhosis-related complications. Patients with ascites being treated with midodrine, alone or in combination with octreotide, showed significant changes in systemic hemodynamics, without a correlating change in renal perfusion. Studies comparing the use of midodrine with use of albumin for the prevention of paracentesis-induced circulatory dysfunction (PICD) showed no incidence of PICD in either treatment group. In hepatorenal syndrome, patients using midodrine with octreotide showed significant changes in systemic hemodynamics and improvements in renal perfusion. This regimen's effect on survival is yet to be determined. Available evidence shows inconsistent results for the effectiveness and safety of midodrine and octreotide use in cirrhotic patients. Because of the contradictory results, longer treatment duration and increased number of study participants are necessary to determine the proper use of midodrine and octreotide in these patients.

Efficacy and safety of midodrine in the treatment of dialysis-associated hypotension

Dialysis-associated hypotension is a morbid problem in haemodialysis patients. Employment of midodrine at the start of dialysis has reduced the severity and frequency of hypotensive episodes in these patients. Through selective α1-adrenergic receptor-binding, desglymidodrine, the active metabolite of midodrine, raises blood pressure by enhancing venous and arterial tone. This medication has been demonstrated to be effective and safe in the acute and chronic treatment of haemodialysis-associated hypotension in end stage renal disease patients.

Midodrine for the Treatment of Intradialytic Hypotension

Recurrent intradialytic hypotension is probably the most severely disabling feature in dialysis patients and the etiology is multifactorial. We assessed the efficacy and safety of midodrine, a selective alpha1-adrenergic pressor agent in 12 patients with recurrent intradialytic hypotension. Symptomatic intradialytic hypotension was defined as hypotensive symptoms occurring with a systolic blood pressure < 100 mm Hg or with 25% decrease in systolic blood pressure in those patients with a basal systolic blood pressure of 100 mm Hg. The patients who suffered from symptomatic intradialytic hypotension and failed to improve after cautious body weight adjustment were included into the study. The lowest intradialytic and postdialysis blood pressures were monitored for 18 consecutive dialysis sessions before and after midodrine treatment. Clinical signs and symptoms were also recorded during both periods. With midodrine, the mean (+/- SE) lowest systolic and diastolic blood pressure increased significantly from 68.7 +/- 3.1 and 42.8 +/- 2.0 mm Hg to 84.7 +/- 3.9 and 52.7 +/- 2.7 mm Hg respectively during the study (p < 0.01). Midodrine treatment also significantly increased postdialysis systolic and diastolic blood pressures from baseline values of 90.8 +/- 3.8 and 58.3 +/- 3.0 mm Hg to 113.3 +/- 7.1 and 70.6 +/- 3.1 mm Hg (p < 0.01 and p < 0.01 respectively). In addition, oral administration of midodrine also significantly decreased the total volume of intravenous fluid administered during symptomatic hypotension. The clinical signs and symptoms during dialysis were improved in all patients. There were no differences in hemoglobin, serum albumin, urea, creatinine, fasting blood sugar or volume removed per dialysis between both periods of the study. In conclusion, our study has demonstrated that midodrine is a safe and effective treatment for the prevention of recurrent intradialytic hypotension if routinely premedicated before each dialysis session.

Midodrine hydrochloride in patients on hemodialysis with chronic hypotension.

Chronic hypotension, volume nonresponsive, is not rare in hemodialysis patients and is usually refractory to various therapies. Midodrine hydrochloride is an alpha-mimetic drug acting directly on the peripheral alpha-receptor and increases blood pressure. We studied 10 uremic patients on hemodialysis with chronic hypotension to evaluate efficacy and safety of midodrine. Midodrine hydrochloride was administered at a dose of 2.5 mg twice on the dialytic day, 1.25 mg twice on the nondialytic day. Subjective symptoms and objective parameters were evaluated and compared before and after midodrine treatment. Midodrine significantly increased systolic pressure from 73.0 +/- 10.5 mm Hg to 90.5 +/- 12.3 mm Hg (p < 0.01); and diastolic blood pressure from 44.0 +/- 8.4 mm Hg to 55.4 +/- 7.9 mm Hg (p < 0.01) before dialysis. Orthostasis, dizziness, fatigue, blurred vision, dullness, headache, and depression improved an average of 62%. All patients tolerated midodrine treatment well. Only mild side effects were noted, including flush sensation, neck soreness, and headache. We conclude that midodrine may be another choice for uremic patients on hemodialysis with chronic hypotension which responds poorly to other conventional management.