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It was observed that glomerular hyperfiltration (GHF) is associated with progression of kidney disease in diabetics, patients in stage 1 hypertension (HT), and we found previously that eGFR decreased faster also in prehypertensives (PHT) with GHF. Here we analyzed whether GHF in PHT is associated with other biomarkers of early renal impairment.

Design and Method:

From 954 subjects enrolled in ENAH follow-up study, 371(137 m;mean age = 46years) were eligible for further analysis:100 with optimal,72 with normal BP,70 with PHT(high normal BP),and 129 with newly diagnosed untreated HT. Exclusion criteria were treatment with antihypertensive drugs, diabetes, pregnancy, eGFR < 60 ml/min (CKD-Epi),CV or cerebrovascular incident, chronic terminal diseases, dementia, immobility and missing data. CKD was defined as eGFR < 60 ml/min, albuminuria as ACR > 30 mg/g, HT as BP >  = 140/90 mmHg and/or taking antihypertensive drugs, and PHT as high-normal BP. Various kidney biomarkers were analyzed: alpha1CR (proximal tubule dysfunction), LAP (brush border enzyme), NAG (lyzosomal enzyme), TGF-beta (marker of fibrosis). Glomerular hyperfiltration (GHF) was defined as 5th quintile of the group.


eGFR and prevalence of GHF were higher in PHT vs. OBP and HT (25.5% vs.21.8% vs.18%). ACR showed linear trend accords the BP categories. Neither of PT dysfunction marker nor TGF beta differ among PHT vs. other BP categories. Subjects with GHF were younger, visceral obese and had signs of sympathetic overactivity (higher leptin and heart rate). Neither metabolic disturbances nor renal dysfunction were found in GHF group.


GHF is first sign of renal impairment in our PHT group, sympathetic overactivity being the most important driving force. Higher values of ACR could be attributed to the general endothelial damage. None of other analyzed biomarkers of renal impairment were found to be increased in PHT. Therefore, we could conclude that PHT is not the consequence of renal damage. PHT subjects with GHF should be monitored more closely.

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