Increased sodium-lithium countertransport activity in red cells of IgA nephropathy patients

Increased sodium-lithium countertransport activity in red cells of IgA nephropathy patients. The aim of this work was to analyze Na,Li countertransport activity in the erythrocytes from patients with IgA nephropathy, in relationship with their blood pressure status and lipid profile Forty-nine patients (32 males, 17 females) with biopsy-proven IgA nephropathy and without significant impairment of renal function (serum creatinine ≤ 1.4 mg/dl) and 36 normal subjects (21 males, 15 females) were evaluated Twenty-nine patients with IgA nephropathy were normotensive and 20 hypertensive (diastolic pressure ≥ 95 mm Hg or treated by antihypertensive drugs). Na,Li countertransport was significantly higher in red cells from hypertensive than from normotensive patients (P = 0.002) and normal subjects (P = 0.0001), (values respectively 309 ± 17; 241 ± 12 and 211 ± 11 µmol/liter RBC/hr); normotensive patients with IgA nephropathy did not differ from controls regarding the Na,Li countertransport rate. A multiple stepwise logistic regression analysis with blood pressure status as the dependent variable and Na,Li countertransport activity, age, serum creatinine, proteinuria, cholesterol, triglycerides, plasma potassium and time from onset as independent variables, indicated an independent significant association for Na,Li countertransport (P = 0.002) proteinuria (P = 0.006), plasma potassium (P = 0.006) and age (P = 0.029). Other tested variables were not independently related to blood pressure status. Hyperlipidemic patients (plasma total cholesterol concentration >200 mg/dl and/or plasma triglycerides >172 mg/dl) had an erythrocyte Na,Li countertransport activity significantly higher than normolipidemic (P = 0.005) and controls (P = 0.001) (values respectively 295 ± 14; 226 ± 12 and 211 ± 11 µmol/liter RBC/hr). A high erythrocyte Na,Li counter-transport rate may be a marker of an increased risk of developing arterial hypertension, lipid abnormalities, and perhaps a more severe renal disease in IgA nephropathy.