Original Paper Kidney Blood Press Res 2004;27:78–87 DOI: 10.1159/000076022 Kidney Blood Pressure Research & Renal Dopamine and Salt Sensitivity of Blood Pressure in IgA Nephropathy Manuel Pestana a,c Joana Santos a Alejandro Santos c Andreia Coroas a Flora Correia b Paula Serra ˜o c Carmen Valbuena d Patrı´cio Soares-da-Silva c a Department of Nephrology, Faculty of Medicine, Porto, b Faculty of Nutrition Sciences, University of Porto, c Institute of Pharmacology and Therapeutics, and d Department of Pathology, Faculty of Medicine, Porto, Portugal Accepted: September 5, 2003 Published online: January 12, 2004 Manuel Pestana Department of Nephrology, Faculty of Medicine PT–4200 Porto (Portugal) Tel./Fax +351 2 5502023 E-Mail mvasconcelos@hsjoao.min-saude.pt ABC Fax + 41 61 306 12 34 E-Mail karger@karger.ch www.karger.com © 2004 S. Karger AG, Basel 1420–4096/04/0272–0078$21.00/0 Accessible online at: www.karger.com/kbr Key Words Dopamine W Sodium sensitivity W IgA nephropathy W Twenty-four-hour ambulatory blood pressure monitoring Abstract Background: Patients with chronic glomerulonephritis exhibit salt-sensitive (SS) hypertension. In the early stage, however, the exact characteristics are still unclear. A decrease in renal dopamine production under basal conditions or after a sodium load has been reported in a subset of patients with SS primary hypertension. Aims: The present study examined 17 untreated IgA-N patients with near-normal renal function, to determine whether salt sensitivity appears before hypertension and whether this sensitivity is related to renal dopamine production. Methods: Daily urinary excretion of dopamine, the amine precursor – L-DOPA, and metabolites was moni- tored in conditions of basal sodium ingestion, followed by three consecutive 5-day periods of 100, 20 and 350 mmol/day sodium intake. The sodium sensitivity in- dex (SSI) was evaluated in each patient. In addition, the patients were considered SS when showing an increase 65 mm Hg in 24-hour mean BP when they changed from a 20- to a 350-mmol/day sodium diet. Results: Urinary dopamine output was lower in SS than in salt-resistant patients throughout the study (p ! 0.001). This was accompanied by lower creatinine clearance values and higher urinary protein excretion in SS IgA-N patients. A strong negative relationship was observed in these 17 IgA-N patients between the SSI and the daily urinary excretion of dopamine in conditions of both 20 mmol/ day sodium intake (r 2 = 0.592; p = 0.0003) and 350 mmol/ day sodium diet (r 2 = 0.352; p = 0.01). However, urinary dopamine output varied appropriately throughout the study in SS patients, in agreement with changes in sodi- um intake. Conclusion: We conclude that in IgA-N pa- tients, a rightward shift in the ‘pressure natriuresis’ can appear before hypertension and is related with a re- duced renal production of dopamine. It is suggested that decreased renal dopamine synthesis in SS IgA-N pa- tients results from acquired tubulointerstitial injury. In contrast to what has been found in SS primary hyperten- sion, renal dopamine may behave appropriately in SS IgA-N patients, as a compensatory hormone. Copyright © 2004 S. Karger AG, Basel Introduction Immunoglobulin A nephropathy (IgA-N) is the most common glomerular disorder worldwide and a major cause of chronic renal parenchymal disease. In this condi- tion, hypertension is frequently present in association with normal renal function and its prevalence increases as