Influence of erythropoietin treatment on gonadotropic hormone levels and sexual function in male uremic patients.

OBJECTIVE: The purpose of this study was to evaluate whether levels of sex hormones and sexual function differ in renal failure patients with and without uremia and the effect of treatment with recombinant human erythropoietin (rhuEPO). MATERIAL AND METHODS: Fifteen males with chronic renal failure who were not receiving hemodialysis and 25 male renal failure patients with uremia who were undergoing hemodialysis were enrolled before and after rhuEPO therapy. Fifteen male volunteers matched for age and weight were also studied. Levels of various blood biochemicals were measured in all patients before and 1 week after rhuEPO treatment. Sexual function was also studied in all patients before and 6 months after rhuEPO treatment. RESULTS: The control group had significantly higher levels of testosterone (6.21 +/- 1.21 ng/ml) and hematocrit (Hct) (43.2 +/- 2.1%) and significantly lower levels of prolactin (5.27 +/- 1.21 ng/ml), follicular-stimulating hormone (FSH) (7.51 +/- 2.36 mIU/ml) and leutinizing hormone (LH) (4.23 +/- 2.10 mIU/ml) than the two patient groups (p < 0.05 for all comparisons). Patients with renal failure only had significantly lower levels of testosterone and Hct (2.54 +/- 0.53 ng/ml and 21.4 +/- 1.4%, respectively) than those with uremia (3.65 +/- 0.52 ng/ml and 24.3 +/- 2.5%, respectively; p < 0.001 for both comparisons). After rhuEPO therapy, the testosterone and Hct levels of the two patient groups did not reach the level of the control subjects (p < 0.05 for both comparisons). Similarly, the levels of prolactin, FSH and LH were significantly higher in both patient groups than those of control subjects after rhuEPO therapy (p < 0.001 for both comparisons). However, after rhuEPO therapy, significant increases in testosterone and Hct levels were found in both patient groups (p < 0.001 for both comparisons). Sexual function was also markedly improved in the hemodialysis patient group. While 20/25 (80%) male hemodialysis patients reported improved sexual function after rhuEPO treatment, only 3/15 (20%) chronic renal failure patients reported improvement. CONCLUSIONS: In patients with advanced uremia, rhuEPO therapy may result in improved gonadotropic hormone levels and sexual function. Good dialysis quality may contribute to the increase in the incidence of patients with better sexual function.

Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients.

We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremic hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12 months after, the start of combined antihypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHg after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 +/- 70.47 g/m2 to 178.57 +/- 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13 non-responders. Among responders, both the SBP (153.91 +/- 13.24 mmHg vs 134.43 +/- 14.21 mmHg, p < 0.01) and DBP (90.39 +/- 7.89 mmHg vs 79.98 +/- 7.35 mmHg, p < 0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 +/- 72.03 g/m2 to 168.52 +/- 55.53 g/m2, p < 0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 +/- 64.36 g/m2 vs 193.66 +/- 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.

Red blood cell osmotic fragility in chronically hemodialyzed patients.

Chronic renal failure induces anemia and a short erythrocyte life span. Red blood cell (RBC) osmotic fragility is the resistance of RBC hemolysis to osmotic changes that is used to evaluate RBC friability. To find the cause of shortened red cell survival in uremic patients, we evaluated the RBC osmotic fragility in 57 chronic hemodialyzed patients. Each patient had received 12 h of dialysis per week continuously prior to being enrolled in the study. Nineteen healthy volunteers served as a control group. Biochemistry, hemoglobin, electrolyte, osmolarity, beta2-microglobulin, and intact parathyroid hormone were examined before and after the dialysis session. To evaluate the osmotic fragility of RBC, blood samples were collected in heparinized test tubes. Fifty microliters of the RBC of each individual was then incubated in solutions containing a series of various concentrations of NaCl ranging from 0 to 0.6%. The concentration of NaCl at which 50% of RBCs were lysed was considered the median osmotic fragility (MOF). The results showed that the MOF was significantly greater in hemodialyzed patients before dialysis than in the control group (0.41 +/- 0.03 vs. 0.39 +/- 0.02%). The osmotic resistance to hemolysis was also recorded after dialysis (MOF 0.38 +/- 0.03%). Correlation analysis showed that the MOF was significantly correlated with urea nitrogen, serum osmolarity, and intact parathyroid hormone level. In addition, the osmotic fragility was higher in patients who had a predialysis intact parathyroid hormone level > 100 pg/dl. In conclusion, hemodialysis can improve the osmotic fragility. The mechanism underlying this improvement may be the removal of low molecular weight uremic toxins, resulting in normalization of serum osmolarity. Our results indicate that parathyroid hormone is probably a major factor influencing RBC osmotic fragility in chronic renal failure.