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 α₁-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.

Twenty anaemic, normotensive and elderly patients on both haemodialysis and CAPD with left ventricular hypertrophy (LVH) were undergoing systematic echocardiographic analysis during treatment with recombinant human erythropoietin (rHuEPO) for 12 months. Before and after the rHuEPO treatment, M-mode and pulsed Doppler echocardiographic were performed and haemodynamic parameters were closely followed. Partial correction of anaemia resulted in a decrease in the LV end-diastolic diameter (LVEDD) from 56.0$2.0-49.2 f 2.0 mm (PcO.05) in HD patients and 50.5 f 4.M3.6 f 3.0 mm in CAPD patients (P = NS). Concomitantly the calculated mass index (LVMi) was reduced significantly from 232.3 f 21.8-185.9 f 11.4g/m2 in elderly haemodialysis patients. Heart rate and arterial pressure did not change during the study period. However, in CAPD patients there was no significant change in LVMi during the study period. We conclude that long-term amelioration of anaemia in dialysis patients could induce a regression of left ventricular hypertrophy. However, in CAPD patients, both myocardial and haemodynamic effects were less evident. CAPD could possibly modulate the haemodynamic changes associated with the rHuEPO treatment or CAPD itself impose less left ventricular wall stress in these elderly patients.

Abnormalities in circulating lipoprotein concentrations are a characteristic finding in patients undergoing dialytic therapy. A substantial number of these patients display type IV hyperlipoproteinemia. Certain data suggest that secondary hyperparathyroidism may induce disturbances in lipid metabolism. To evaluate the effects of pulse calcitriol therapy on the lipid profile in these patients, we undertook a prospective study in 12 patients on stable bicarbonate hemodialysis. Lipid parameters comprising cholesterol and the low- as well as the high-density lipoprotein subfractions, triglycerides, apolipoproteins A and B, serum parathyroid hormones (iPTH), alkaline phosphatase, calcium, phosphorus, hematocrit, and blood urea were obtained prior to commencement of pulse calcitriol therapy and again 8–10 weeks later. Calcitriol therapy was associated with a decrease in serum iPTH levels (701 ± 103.9 vs. 220.3 ± 50.5 pmol/l; p < 0.001). Significant increases in high-density lipoprotein cholesterol (32.8 ± 2.7 vs. 38.8 ± 2.3 mmol/l; p < 0.05) and apolipoprotein A-I (107.8 ± 6.1 vs. 121.8 ± 5.8 g/l; p < 0.05) were noted during the course of the study. Moreover, serum iPTH correlated inversely with high-density lipoprotein cholesterol and apolipoprotein A-I. There were no changes in other lipid parameters except for low-density lipoprotein cholesterol which showed a tendency to increase. We conclude that in short-term study, pulse oral calcitriol therapy is associated with an improvement in the lipid profile in patients with secondary hyperparathyroidism. However, it remains to be established whether ameliorating the uremic dyslipidemia results in any long-term clinical benefits.