Renal dopamine and salt sensitivity of blood pressure in IgA nephropathy.
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.
Pestana
Manuel
M
Department of Nephrology, Faculty of Medicine, Porto, Portugal. mvasconcelos@hsjoao.min-saude.pt
Santos
Joana
J
Santos
Alejandro
A
Coroas
Andreia
A
Correia
Flora
F
Serrão
Paula
P
Valbuena
Carmen
C
Soares-da-Silva
Patrício
P
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects*; D018660:Blood Pressure Monitoring, Ambulatory; D003404:Creatinine / Q000378:metabolism; D004298:Dopamine / Q000096:biosynthesis* / Q000652:urine; D004351:Drug Resistance; D005260:Female; D005922:Glomerulonephritis, IGA / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000652:urine; D006801:Humans; D006973:Hypertension / Q000209:etiology; D007668:Kidney / Q000378:metabolism*; D008297:Male; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*
D017673:Sodium Chloride, Dietary; D003404:Creatinine; D011188:Potassium; D004298:Dopamine