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. OBJECTIVE 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 monitored 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 index (SSI) was evaluated in each patient. In addition, the patients were considered SS when showing an increase > or =5 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 (r2 = 0.592; p = 0.0003) and 350 mmol/day sodium diet (r2 = 0.352; p = 0.01). However, urinary dopamine output varied appropriately throughout the study in SS patients, in agreement with changes in sodium intake. CONCLUSIONS We conclude that in IgA-N patients, a rightward shift in the 'pressure natriuresis' can appear before hypertension and is related with a reduced renal production of dopamine. It is suggested that decreased renal dopamine synthesis in SS IgA-N patients results from acquired tubulointerstitial injury. In contrast to what has been found in SS primary hypertension, renal dopamine may behave appropriately in SS IgA-N patients, as a compensatory hormone.