To the Editor,
Albuminuria increases the risk of progression of renal failure (RF), even in advanced stages.1 Renin-angiotensin-aldosterone system (RAAS) inhibitors are the main tool used for reducing albuminuria and slowing the progression of RF, although this treatment is often insufficient.2 Recently, paricalcitol has been proven effective in reducing albuminuria in certain patients.3
The aim of our study was to assess the usefulness of paricalcitol to reduce albuminuria in patients with stage 4-5 RF.
Method: We included all patients referred to the predialysis unit. Patients were administered paricalcitol at an initial mean dose of 1±0.3μg/day orally, adjusted for calcium/phosphorous metabolic parameters. Follow-up continued for at least 6 months, with three visits every 2 months, in which albuminuria, MDRD, and calcium/phosphorous metabolism parameters were registered. Treatment with RAAS inhibitors and hidroferol continued without change. Statistical analysis: we used analysis of variance for comparing the means of quantitative variables, Wilcoxon tests for comparing medians, and chi-square tests to compare percentages.
Results: Our study included a total of 40 patients, 67% males, with a follow-up period of 135-235 days. Baseline MDRD was 19.5±3ml/min, 97.5% of patients had hypertension, and 35% were diabetic. Mean urine albumin-to-creatinine ratio (UACR) was 1932±1641mg/g. Initial calcium-phosphorous metabolism parameters were: calcium: 8.8±0.5mg/dl; phosphorous: 4.5±0.5mg/dl; intact parathyroid hormone (iPTH): 473±143pg/ml. At the start of the follow-up period, 25% of patients received angiotensin-converting enzyme inhibitors, 42.5% angiotensin receptor blockers, 55% hidroferol, and 12.5% calcitriol. During the follow-up period, we observed a significant decrease in MDRD (19.5±3ml/min vs 17.3±3.4ml/min; P=.003). There was also a decrease in iPTH and an increase in calcium, both significant results (473±143pg/ml vs 197±88pg/ml, and 8.84±0.5mg/dl vs 9±0.4mg/dl; P=.00 and P=.01, respectively). We also observed an increase in phosphorous, although this was not significant (4.5±0.5mg/dl vs 4.8±0.6mg/dl; P=.1). UACR decreased over the course of the study from an initial mean value of 1932±1641mg/g to the final mean value of 1417±1284mg/g, a 27% decrease (P=.1). In the group of patients with higher initial UACR values (>3000mg/g), the decrease was significant (4258±944mg/g vs 2786±1630mg/g; P=.03). We observed an increase in patients with normalised albuminuria and a decrease in those with albuminuria >3000mg/g. UACR was not associated with treatment with RAAS inhibitors, hidroferol, or calcitriol. In no cases was suspension of treatment necessary due to altered calcium/phosphorous metabolism or secondary side effects, although 17% of patients required dosage adjustments.
Our study shows that treatment with paricalcitol in this group of patients is associated with a significant decrease in UACR, leading to a higher proportion of patients with normal excretion of albumin, in addition to providing better control of bone metabolism. The effect was greatest and most significant in patients with higher initial albumin excretion levels, which is the group with the highest risk for progression of RF.4
It may be that the small sample in our study was insufficient to demonstrate the antiproteinuric effects of this treatment with a greater level of significance. We may not have observed significant results in the control of renal function deterioration because of this same reason. Although it was not an objective of this study, we should also keep in mind the decreased cardiovascular risk associated with reduced UACR.
Conclusion: Paricalcitol can be effective in halting proteinuria in patients with stage 4-5 chronic renal failure disease and controlling secondary hyperparathyroidism. Its efficacy in preventing the progression of IR must be verified in future studies.
Conflicts of interest
The authors affirm that they have no conflicts of interest related to the content of this article.
