Renal dopamine, salt sensitivity of blood pressure and histological damage in IgA nephropathy

• Tipo: Artigo em Revista Científica Internacional
• Data: 2004

Autores

Manuel Pestana (Autor) FMUP; Joana Santos (Autor) FMUP; Alejandro Santos (Autor) Outra; Andreia Coroas (Autor) Outra; Flora Correia (Autor) Outra; Paula Serrão (Autor) FMUP; Carmen Valbuena (Autor) Outra; Patrício Soares da Silva (Autor) FMUP

Revista

Título: Kidney and Blood Pressure Research

Vol. 27

Páginas: 78-87

ISSN: 1420-4096

Editora: Karger

Classificação Científica

CORDIS: Ciências da Saúde

Outras Informações

Abstract (EN): 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 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 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. Conclusion: 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.

Idioma: Português

Tipo (Avaliação Docente): Científica