Subclinical functional and structural renal abnormalities predict new onset type 2 diabetes in patients with primary hypertension.

Recent studies suggest a close relationship between renal dysfunction and new onset diabetes (NOD). The aim of the study was to investigate the association between subclinical functional and structural renal abnormalities and NOD in primary hypertension (PH). This observational prospective study (9.1 ± 2.2 years follow-up) includes 231 consecutive untreated non-diabetic patients with PH and without overt nephropathy. The primary end point was NOD. Albuminuria (albumin to creatinine ratio, ACR), glomerular filtration rate (eGFR), and renal structure and hemodynamics (ultrasound scan and Doppler) were evaluated at baseline. During 2106 person-years of follow-up, 10 patients developed diabetes (incidence rate 4.7/1000 person-years). Patients with NOD showed a higher body mass index, serum uric acid, serum creatinine and ACR, and lower eGFR and renal volume (RV) to resistive index (RI) ratio (RV/RI) at baseline, as compared with the 221 controls that did not develop diabetes. When all renal variables were taken into consideration, RV/RI was the only variable significantly related to diabetes (hazard ratio 1.04, P=0.0342). Patients in the lowest tertile of RV/RI were more likely to develop diabetes (10.4 vs 2.6 vs 0%, P=0.0044). For each s.d. decrease of RV/RI, the risk of NOD increased by 68% (P=0.0012). Subclinical functional and structural renal abnormalities are independent predictors of diabetes in PH.

Sub-clinical organ damage in hypertension and obesity.

BACKGROUND: The development of sub-clinical organ damage precedes and predicts the occurrence of cardiovascular (CV) events in hypertensive as well as in obese patients. AIM AND METHODS: We investigated the prevalence and clinical correlates of organ damage (OD), namely carotid atherosclerosis (US scan) and urine albumin to creatinine ratio (three non-consecutive first morning samples) in a group of 164 obese patients and in an age- and gender-matched group of non-obese hypertensive patients. RESULTS: There was a significantly greater prevalence and severity of OD in obese patients as compared to non-obese hypertensive patients. In particular obese patients more frequently had microalbuminuria (16 vs 7%, χ(2) 5.8, P=0.0157) and carotid abnormalities (53 vs 10%, χ(2) 69.5, P<0.0001) as well as higher urinary albumin excretion rate (-0.05 ± 0.52 vs -0.28 ± 0.43log ACR, P<0.0001) and carotid intima-media thickness (0.955 ± 0.224 vs 0.681 ± 0.171, <0.0001). Notably, the coexistence of hypertension and obesity did not entail a greater prevalence and severity of OD. Moreover, after adjusting for potentially confounding factors including blood pressure levels, diagnosis of diabetes, and lipid profile, morbidly obese patients showed a 5-fold, and 22-fold higher risk of having microalbuminuria, and carotid atherosclerosis, respectively. CONCLUSIONS: Sub-clinical OD is highly prevalent in obese patients, even in the absence of high blood pressure. Hypertension and obesity seem to exert an independent, possibly non-additive role on the occurrence of organ damage.