Elevated arterial pressure is a major risk factor for progression to ESRD in diabetic nephropathy. However, the component of arterial pressure and level of BP control for optimal renal outcomes are disputed. Data from 1590 hypertensive patients with type 2 diabetes in the Irbesartan Diabetic Nephropathy Trial (IDNT), a randomized, double-blind, placebo-controlled trial performed in 209 clinics worldwide, were examined, and the effects of baseline and mean follow-up systolic BP (SBP) and diastolic BP and the interaction of assigned study medications (irbesartan, amlodipine, and placebo) on progressive renal failure and all-cause mortality were assessed. Other antihypertensive agents were added to achieve predetermined BP goals. Entry criteria included elevated baseline serum creatinine concentration up to 266 mol/L (3.0 mg/dl) and urine protein excretion >900 mg/d. Baseline BP averaged 159/87 ؎ 20/11 mmHg. Median patient follow-up was 2.6 yr. Follow-up achieved SBP most strongly predicted renal outcomes. SBP >149 mmHg was associated with a 2.2-fold increase in the risk for doubling serum creatinine or ESRD compared with SBP <134 mmHg. Progressive lowering of SBP to 120 mmHg was associated with improved renal and patient survival, an effect independent of baseline renal function. Below this threshold, all-cause mortality increased. An additional renoprotective effect of irbesartan, independent of achieved SBP, was observed down to 120 mmHg. There was no correlation between diastolic BP and renal outcomes. We recommend a SBP target between 120 and 130 mmHg, in conjunction with blockade of the renin-angiotensin system, in patients with type 2 diabetic nephropathy.

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Overweight patients with uncomplicated essential hypertension were followed up biweekly for six months: 24 not receiving antihypertensive-drug therapy (Group I) and 83 on regular but inadequate (despite drug manipulation) antihypertensive-drug therapy (Group II). All patients in Group I and 57 randomly selected patients from group II (IIa) participated in a weight-reduction program. The remaining 26 from Group II (IIb) did not receive a dietary program. Salt intake was in the normal range in all three groups. All patients on the dietary program lost at least 3 kg (mean, 10.5 kg), and all but two showed a meaningful reduction in blood pressure; 75 per cent of Group I and 61 per cent of Group IIa returned to normal blood pressure. The weight and blood-pressure reductions were highly significant (P less than 0.001), were present in both sexes and all ages, and were directly associated. In Group IIb, no significant change in blood pressure or weight occurred (P greater than 0.30).

Elevated serum uric acid concentration is a common laboratory finding in subjects with metabolic syndrome/obesity, hypertension, kidney disease and cardiovascular events. Hyperuricemia has been attributed to hyperinsulinemia in metabolic syndrome and to decreased uric acid excretion in kidney dysfunction and is not acknowledged as a main mediator of metabolic syndrome, renal disease, and cardiovascular disorder development. However, more recent investigations have altered this traditional view and shown by providing compelling evidence to support an independent link between hyperuricemia and increased risk of metabolic syndrome, diabetes, hypertension, kidney disease and cardiovascular disorders. However, despite these new findings, controversy regarding the exact role of uric acid in inducing these diseases remains to be unfolded. Furthermore, recent data suggest that the high-fructose diet in the United State, as a major cause of hyperuricemia, may be contributing to the metabolic syndrome/obesity epidemic, diabetes, hypertension, kidney disease and cardiovascular disorder. Our focus in this review is to discuss the available evidence supporting a role for uric acid in the development of metabolic syndrome, hypertension, renal disease, and cardiovascular disorder; and the potential pathophysiology mechanisms involved.

Hypertension is common, difficult to diagnose, and poorly controlled among patients with ESRD. However, controversy surrounds the diagnosis and treatment of hypertension. Here, we describe the diagnosis, epidemiology, and management of hypertension in dialysis patients, and examine the data sparking debate over appropriate methods for diagnosing and treating hypertension. Furthermore, we consider the issues uniquely related to hypertension in pediatric dialysis patients. Future clinical trials designed to clarify the controversial results discussed here should lead to the implementation of diagnostic and therapeutic techniques that improve long-term cardiovascular outcomes in patients with ESRD. Hypertension is common among patients with ESRD. In this review, we discuss the diagnosis, epidemiology, and management of hypertension among dialysis patients. We also review areas of existing controversies and briefly discuss the issue of hypertension in pediatric dialysis patients. EPIDEMIOLOGYThe prevalence, treatment, and control of hypertension among people on hemodialysis (HD) have used varying definitions to diagnose hypertension. The epidemiology differs based on how BP is measured: either before and after dialysis or using ambulatory BP recordings. Epidemiology with Routine BP MeasurementsThe prevalence of hypertension (defined as 1-week average predialysis systolic BP [SBP] measurements .150 mmHg or diastolic BP [DBP].85 mmHg or the use of antihypertensive medications) was 86% among 2535 clinically stable adult HD patients participating in a multicenter trial. 1 Among hypertensive patients, 12% did not receive antihypertensive drugs, 58% were treated but not controlled, and only 30% were controlled. The use of antihypertensive drugs has been reported to vary from 59% to 83%. [2][3][4][5] Furthermore, even among children on long-term HD, similar findings have been reported. 6 Several studies have confirmed greater antihypertensive drug use to be associated with poorer control. 7,8 It should be noted that antihypertensive drug use per se do not lead to worse BP control; in the absence of adequate volume control, increasing antihypertensive drug use may simply reflect difficult-to-control BP. Epidemiology Using Ambulatory BP MeasurementsThe prevalence of hypertension (defined by either a 44-hour interdialytic ambulatory BP of $135/85 mmHg or the prescription of any antihypertensive agent) was 86% among 369 chronic HD patients. 8 Although hypertension was being treated with antihypertensive drugs in 89% of patients, it was adequately controlled only in 38%. The independent determinants of poor control were the use of antihypertensive drugs and an expanded extracellular volume state. If patients were volume overloaded, nearly 80% became hypertensive when medications were Published online ahead of print. Publication date available at www.jasn.org.