[Microalbuminuria in hypertensive, non-proteinuric renal transplant recipients: role of previous acute rejection episodes and sodium intake].

Microalbuminuria (Malb: albuminuria: 30-299 mg/24 h) is associated with many cardiovascular parameters (high systolic (SAP) and diastolic (DAP) arterial pressure, total cholesterol, triglycerides, fasting glucose and body weight, low HDL-cholesterol) and may be a marker of cardiovascular and renal risk in the general population. Whether MAlb could be an integrated marker of cardiovascular and renal risk in transplant recipients is unknown.75 hypertensive non-proteinuric renal transplant recipients were selected. Antihypertensive medications were stopped for a month prior to the studies. MAlb (on a 24-hour urine collection), cyclosporine trough levels (CsA-L), fasting glucose and lipids were measured. SAP and DAP were determined with a semi-automatic device.29 patients (12 W/17M) had normal levels of albuminuria (Nalb: albuminuria < 30 mg/24 h) and 46 had MAlb. As compared to Nalb patients, those with Malb were younger (M +/- SD: 44.3 +/- 13 vs 51.2 +/- 9.7 respectively, p = 0.009), had higher SAP (152 +/- 16 vs 146 +/- 15 mmHg, p = 0.09) et DAP (86 +/- 11 vs 81 +/- 10 mmHg, p = 0.01). No difference in smoking habits, serum creatinine (125 +/- 27 vs 119 +/- 28 mumol/L), total-, HDL- and LDL-cholesterol, triglycerides, fasting glucose, CsA-L (142 +/- 29 vs 144 +/- 26 ng/mL), 24 h-urine urea excretion was observed. History of acute rejection episodes (45.7% vs 17.2%, p = 0.01) was more frequent and 24-hour natriuresis (192 +/- 70 vs 152 +/- 79 mmol/24 h, p < 0.01) was higher in Malb than in Nalb.The determinants of microalbuminuria in renal transplant recipients are different from those found in the general population. History of acute rejection episodes was more frequent in renal transplant recipients with Malb than in those with NAlb despite similar renal function, suggesting that Malb may a marker of subclinical renal lesions due to immunological aggression. The relationship between natriuresis and Malb suggests that sodium intake modulates target-organ damage associated with hypertension.