Correspondence and offprint requests to: Geoffrey Douglas Braatvedt; E-mail: g.braatvedt@auckland.ac.nz Abstract Background. In this study, our main goal was to determine whether an integrated, community-based model of care using culturally appropriate health-care assistants to manage hypertension in Māori and Pacific patients with diabetes and chronic kidney disease (CKD) is more effective than conventional care in achieving blood pressure (BP) targets and delaying progression of cardiac and renal end-organ damage. Methods. Sixty-five Māori and Pacific patients (aged 47-75 years) with type 2 diabetes, moderate CKD (>0.5 g proteinuria/day, serum creatinine 130-300 μmol/l) and hypertension were randomized to usual care (n = 32) or community/intervention care (n = 33) for 12 months. Community care patients were visited monthly by a nurse-led health-care assistant for BP measurement. Antihypertensives were adjusted using a stepwise protocol, aiming for a BP <130/80 mmHg. Office BP and renal and echocardiographic parameters were measured at baseline and 12 months.Results. Baseline characteristics including office BP, renal and echocardiographic parameters, and number of antihypertensives were well matched in both groups. By 12 months, the community care patients had achieved a significantly greater reduction in office systolic BP (−21 ± 26 mmHg vs −12 ± 20 mmHg, P = 0.04) and in 24-h urine protein (−1.4 ± 2.6 g vs +0.1 ± 2.8 g, P = 0.04). The number of prescribed antihypertensives was greater in these patients at 12 months (3.4 ± 1.1 vs 2.3 ± 1.0, P < 0.01). Left ventricular (LV) mass and left atrial (LA) volume progressed in the usual care group, but not in the intervention group (P < 0.05).Conclusion. This novel model of care is more effective than conventional care in lowering systolic BP and reducing cardiac and renal end-organ damage in these highrisk patients.

Our studies have detected ARMC5 mutations in 4 of 5 BMAH families tested, confirming that these mutations are a frequent cause of BMAH. Two of the 4 families had novel mutations, indicating allelic heterogeneity. Preclinical evaluation did not predict mutation status. The ARMC5-negative family had unusual prominent hyperaldosteronism. Further studies are needed to determine the penetrance of BMAH in ARMC5 mutation-positive relatives of affected patients, the practical utility of genetic screening and genotype-phenotype correlations.

Adrenal nodules, suppressed ACTH and increased VP sensitivity may represent preclinical disease, allowing early detection, and treatment, of affected individuals. In AIMAH-01, increased VP sensitivity may be due to adrenal VP receptor overexpression. In these kindreds, VPs-AIMAH is familial, and autosomal dominant inheritance is most likely.