Antiproteinuric effect of add-on paricalcitol in CKD patients under maximal tolerated inhibition of renin-angiotensin system: a prospective observational study

• Published in: BMC nephrology 2012-11, Vol.13 (1), p.150-150, Article 150
• Main Authors: De Nicola, Luca, Conte, Giuseppe, Russo, Domenico, Gorini, Antonio, Minutolo, Roberto
• Format: Article
• Language: English
• Subjects: Aged; Alfacalcidol; Angiotensin; Angiotensin converting enzyme; Angiotensin converting enzyme inhibitor; Angiotensin II receptor blocker; Antihypertensive Agents - administration & dosage; Antihypertensive drugs; Calcifediol; Care and treatment; Chronic kidney disease; Chronic kidney failure; Colleges & universities; Drug dosages; Drug therapy; Drug Therapy, Combination; Enzyme inhibitors; Enzymes; Ergocalciferols - administration & dosage; Female; Humans; Hypertension; Kidney diseases; Male; Measurement; Medical research; Medicine, Experimental; Middle Aged; Nephrology; Parathyroid hormone; Paricalcitol; Patient outcomes; Patients; Physiological aspects; Potassium; Prospective Studies; Proteinuria; Proteinuria - drug therapy; Proteinuria - epidemiology; Proteinuria - physiopathology; Public speaking; Renal Insufficiency, Chronic - drug therapy; Renal Insufficiency, Chronic - epidemiology; Renal Insufficiency, Chronic - physiopathology; Renin - antagonists & inhibitors; Renin - physiology; Renin inhibitor; Renin-Angiotensin System - drug effects; Renin-Angiotensin System - physiology; Standard deviation; Vitamin D
• ISSN: 1471-2369; 1471-2369
• DOI: 10.1186/1471-2369-13-150

Whether paricalcitol (PCT) reduces proteinuria in the presence of intensified inhibition of Renin-Angiotensin-System (RAS) is poorly studied. We evaluated the antiproteinuric effect of PCT in non-dialysis chronic kidney disease (CKD) patients with proteinuria greater than 0.5 g/24 h persisting despite anti-RAS therapy titrated to minimize proteinuria in the absence of adverse effects. Forty-eight CKD patients were studied in the first six months of add-on oral PCT (1 mcg/day) and three months after drug withdrawal. Males were 87.5%, age 63 ± 14 yrs, systolic/diastolic blood pressure (BP) 143 ± 22/78 ± 11 mmHg, eGFR 29.7 ± 14.5 mL/min/1.73 m(2), diabetes 40%, and cardiovascular disease 38%. At referral in the center (28 months prior to study baseline), proteinuria was 2.44 (95% CI 1.80-3.04) g/24 h with 6 patients not receiving any anti-RAS and 42 treated with a single agent, at low dosage in most cases. At study baseline, twenty patients were under 2-3 anti-RAS drugs while twenty-eight received 1 agent at full dose and proteinuria resulted to be reduced versus referral to 1.23 g/24 h (95%CI 1.00-1.51). Six months of add-on PCT significantly decreased proteinuria to 0.61 g/24 h (95%CI 0.40-0.93), with levels less than 0.5 g/24 h achieved in 37.5% patients, in the absence of changes of BP and GFR. Proteinuria recovered to basal value after drug withdrawal. The extent of antiproteinuric response to PCT was positively associated with diabetes, eGFR and daily Na excretion (R(2) = 0.459, P < 0.0001). PTH decreased from 201 (IQR 92-273) to 83 (IQR 50-189) pg/mL. In CKD patients, add-on PCT induces a significant reduction of proteinuria that is evident despite intensified anti-RAS therapy and larger in the presence of diabetes, higher GFR and unrestricted salt intake.