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Relative Glomerular Hyperfiltration in Primary Aldosteronism

Department of Medicine, Hôpital Lapeyronie, Montpellier, France

Address correspondence to: Dr. Jean Ribstein, Department of Medicine, Hôpital Lapeyronie, 34295 Montpellier cedex 5, France. Phone: +33-467338443; Fax: +33-467338453; j-ribstein{at}chu-montpellier.fr

Received for publication October 22, 2004. Accepted for publication February 21, 2005.

Experimental and clinical data suggest that primary aldosteronism (PA) may be associated with cardiovascular hypertrophy and fibrosis, in part independent of the BP level. Whether PA may also result in specific deleterious effects on the kidneys was less studied. In 25 patients with tumoral PA, renal studies (urinary excretion of proteins, GFR, and effective renal plasma flow [ERPF], as clearances of technetium-labeled diethylene triaminopentaacetic acid and ¹³¹I-ortho iodohippurate, respectively) were performed both before and 6 mo after surgical cure. A control group consisting of patients with essential hypertension (EH) was studied before and after 6 mo of antihypertensive therapy. At baseline, PA and EH patients were similar with respect to demographic data, duration and level of hypertension, and GFR and ERPF. Urinary excretion of albumin and 2 microglobulin were higher in PA than EH (88 ± 26 versus 39 ± 12 and 0.91 ± 0.23 versus 0.26 ± 0.19 mg/24 h, respectively; both P < 0.05). Adrenalectomy was followed by a decrease in arterial BP (by 28 ± 3/13 ± 2 mmHg), urinary excretion of albumin and 2 microglobulin (by 48 ± 19 and 0.53 ± 0.21 mg/24 h, respectively), and GFR and ERPF (by 15 ± 3 and 54 ± 15 ml/min per 1.73 m², respectively). In EH, a similar decrease in pressure was associated with a decrease in albuminuria but no change in GFR or ERPF. In 17 of the 25 PA patients who received a 6-mo treatment of spironolactone, both GFR and ERPF decreased in parallel with BP, similar to what was observed after surgery. These data suggest that PA was associated with relative hyperfiltration, unmasked after suppression of aldosterone excess.

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