Lercanidipine showed a high antihypertensive effect in CRF patients. It has a good tolerability profile and showed an interesting effect on plasmatic lipids. An improvement in renal function, measured through creatine clearance, was detected.
We have analyzed some parameters of porphyrin metabolism in 60 patients with end-stage renal failure, 20 of them on CAPD and the remaining on HD. In comparison with 56 control subjects, both groups of patients showed the three following findings: low erythrocyte aminolevulinate dehydrase activity, inhibition ability for the activity of this enzyme when their plasma was incubated in vitro with normal erythrocytes, and increased plasma porphyrin levels. Like anemia, these abnormalities were more remarkable in patients on HD who also exhibited increased erythrocyte protoporphyrin levels and compensatory porphobilinogen deaminase activities. Mean weekly porphyrin removal through dialysate was higher in CAPD (90.8 micrograms) than in HD patients (30.4 micrograms). Dialysate and plasma porphyrins were correlated in both circumstances (r = 0.714, P < 0.01 and r = 0.637, P < 0.05, respectively). The less pronounced porphyrin abnormalities found in CAPD patients with respect to HD patients may be due to the more efficient capability of peritoneal dialysis for removing from plasma protein-bound substances, as porphyrins and inhibitors of aminolevulinate dehydrase or other enzymes involved in erythropoiesis. Since no close relationship was found between these abnormalities of porphyrin metabolism and hematocrit values, the anemia of uremia cannot be merely considered as a direct consequence of altered heme biosynthetic pathway.
In patients with chronic renal failure, renal transplantation improves anemia and the production of erythropoietin. In patients undergoing hemodialysis the administration of recombinant human erythropoietin improves anemia with a decrease in bodily iron stores. Therefore, one would expect a similar decrease after kidney transplantation. We followed the ferric parameters to determine the incidence of iron deficiency anemia in 24 consecutive renal transplant patients for an interval long enough to achieve steady state values of hemoglobin (5.1 +/- 0.8 months). Hematological parameters and serum levels of iron, ferritin and erythropoietin were measured. The patients were divided into 2 groups according to the decrease in serum ferritin: group 1--16 with a decrease in respect to basal values (114 +/- 56 ng./ml.) and group 2--those without modifications (720 +/- 320 ng./ml.). Except for the similar values, group 1 showed greater improvement in anemia (red blood cells 4.3 x 10(6) +/- 1.1 x 10(6) versus 3.7 x 10(6) +/- 1.5 x 10(6)/ml., p < 0.01) and hematocrit index (38.5 +/- 5.2 versus 33.0 +/- 5.1%, p < 0.05). Four patients had microcythemia (mean corpuscular volume 76.6 +/- 1.4 fluid) with lower hemoglobin values than the other patients in group 1 (10.77 +/- 0.42 versus 12.79 +/- 0.42 gm./dl., p < 0.05). Among the 16 patients in group 1, 7 of 8 whose basal serum ferritin was less than 150 ng./ml. achieved ferritin levels of less than 30 ng./ml. In conclusion, our data support that renal transplantation produces a rapid decrease in iron stores and in some cases induces iron deficiency anemia. This fact should be evaluated and treated properly.
A retrospective review of 110 consecutive kidney transplants performed during 4 years revealed the development of renal artery stenosis in 9 patients (8.18%). A comparison of this group with a control group similar in patient age and interval elapsed since transplantation revealed no significant differences in donor and recipient ages, degree of HLA compatibility or serum creatinine levels. However, there was a significant difference in the number of acute rejection episodes. In our series only male patients were affected. A sizable proportion of the patients (50%) had no detectable murmur over the graft area despite high blood pressure and increased creatinine levels. The absence of surgical injury during extraction and implantation of the grafts, together with the anatomical site of the stenosis and correlation with the degree of immunological intolerance suggest an immunological factor as the underlying cause in post-transplant renal artery stenosis.
Background: Cinacalcet reduces intact parathyroid hormone (iPTH), Ca and P serum levels in patients with secondary hyperparathyroidism (SHPT). Methods: This Spanish, multicenter, observational, retrospective study collected data from SHPT dialysis patients 12 weeks before and up to 72 weeks after starting cinacalcet in clinical practice. Results: Data from 428 patients with uncontrolled SHPT despite receiving standard of care (29% with baseline iPTH 501–800 pg/ml; 51% with >800 pg/ml) were collected. Percentages of patients within National Kidney Foundation Kidney Disease Outcomes Quality Initiative targets at baseline and 72 weeks were: iPTH, 0 versus 32.5% (p < 0.05); Ca, 40.1 versus 50% (p < 0.05); P, 47.7 versus 53.8% (p = 0.162). Vitamin D sterol use decreased from 53.3% at baseline to 36.7% at 72 weeks (p < 0.05). The mean ± SD cinacalcet dose at 72 weeks was 44.0 ± 25.8, 51.7 ± 31.3 and 57.1 ± 37.0 mg for patients with baseline iPTH 301–500, 501–800 or >800 pg/ml, respectively. The main adverse reactions were nausea (5.4%), dyspepsia (5.1%) and vomiting (3.7%). Conclusions: The introduction of cinacalcet improved the routine clinical management of SHPT in a large cohort of Spanish dialysis patients. Cinacalcet is effective and well tolerated regardless of disease severity, and maintains its efficacy over 72 weeks.
We conducted a retrospective study with 750 peritoneal dialysis (PD) patients in a Spanish multicenter registry between 1993 and 1999 to analyze comorbidity and mortality in type 1 diabetes (T1D), type 2 diabetes (T2D) and nondiabetic (ND) patients. 163 patients (21.7%) were diabetic – 96 T1D (58.8%) and 67 T2D (42.2%) – while 587 were not (78.3%). Different comorbidity factors such as the presence of cardiovascular disease, age over 70 and dyslipidemia at the start of PD were analyzed as well as the incidence of peritonitis, the peritonitis-free interval, need for hospitalization, mortality rate, early mortality rate, survival curves (log rank) and the impact factor (Cox) on mortality for the different variables. The comorbidity index (number of comorbidity factors when starting the treatment) and the peritonitis incidence were higher for T2D. Hospitalization rates were similar, but mortality rates were higher for T2D and early mortality rates (death during the 1st year of treatment) were higher for T1D. The actuarial survival curves showed a higher mortality for T2D with no differences between ND and T1D after adjustment for age. The mortality odds ratio was 1.78 for T2D and 1.13 for T1D, differences which were not significant after adding age over 70 and cardiovascular disease to the variables analyzed. Our results show that associated comorbidity is the most important difference between ND, T1D and T2D. While cardiovascular comorbidity is responsible for the higher percentage of early mortality found in T1D when compared to ND, both age and cardiovascular disease are responsible for the higher comorbidity and mortality found in T2D.
Hyperlipemia is a very frequent complication of the diabetic patient on dialysis. There is difficulty of treatment with the diet, because the dietary restriction already imposed on these patients and the secondary effects and toxicity of the available drugs in uremics aggravate the problem. We have treated 22 diabetic patients on dialysis (8 on hemodialysis and 14 on continuous ambulatory peritoneal dialysis) suffering from hyperlipemia with pantethine, a physiological substance and coenzyme A precursor in the Krebs eycle. With the administration of an oral dose of 900mg/day we obtained a reduction of total cholesterol (275 ± 72 vs. 231 ± 54mg/dl; p < 0.001), very-low-density lipoprotein (VLDL)-cholesterol (66 ± 36 vs. 46 ± 18 mg/dl; p < 0.01) and triglycerides (332 ± 182 vs. 227 ± 90 mg/dl; p < 0.01) at 2 months. High-density lipoprotein (HDL)-cholesterol did not change, but the total cholesterol/HDL-cholesterol ratio decreased significantly (p < 0.05). Total cholesterol, VLDL and triglycerides showed a progressive and significant reduction at 4 and 6 months. No changes were observed in serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, uric acid, blood glucose and glycosylated hemoglobin. Gastric discomfort in 2 patients and pruritus in another one were the secondary effects related. Pantethine was shown to be a very effective hypolipemic agent in diabetic patients on dialysis with a great tolerance.
Using invasive techniques we have studied various hemodynamic and gasometric parameters in the course of hemodialysis (HD) with different buffers in an animal model. HD sessions of 180 minutes at zero ultrafiltration were carried out on three groups of eight uremic dogs each, under anesthesia and constant mechanical ventilation. The three groups differed only in the buffer used: acetate (Group AC), equal proportions of DL-lactate and acetate (Group AC+LA), and bicarbonate (Group BC). No hemodynamic changes were seen in Group BC. In the AC and AC+LA groups we observed on minute 1 a decrease of the mean blood pressure (MBP) and of the systemic vascular resistances (SVR). These parameters returned to baseline values within the first 30 minutes in Group AC+LA. In Group AC the SVR also returned to baseline values after the minute 30, but the MBP remained below baseline throughout the study period, together with cardiac index and left ventricular stroke work index decreases. Only in Group AC did we see a flattening of the ventricular function curves. Only in this Group was there a decrease of the arterial oxygen pressure (PaO2) with an associated increase of the alveolo-arterial and arterio-venous O2 differences. The O2 consumption was not modified in any of the groups. Acetate as a single buffer induces hemodynamic instability through peripheral vasodilation and reduction of myocardial contractility. The myocardial depression induced by acetate, in its turn, causes a reduction in PaO2. The mixed acetate+lactate buffer is hemodynamically better tolerated than acetate as single buffer, as it induces only vasodilation.
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