The objective of our study was to determine the effects of two antihypertensive drug dose schedules (‘PM dose’ and ‘Add on dose’) on nocturnal blood pressure (BP) in comparison to usual therapy (‘AM dose’) in African Americans with hypertensive chronic kidney disease (CKD) and controlled office BP. In a three period, cross-over trial, former participants of the African American Study of Kidney Disease were assigned to receive the following three regimens, each lasting 6 weeks, presented in random order: AM dose (once daily antihypertensive medications taken in the morning), PM dose (once daily antihypertensives taken at bedtime) and ‘Add on dose’ (once daily antihypertensives taken in the morning and an additional antihypertensive medication before bedtime [diltiazem 60–120 mg, hydralazine 25 mg, or additional ramipril 5 mg]). Ambulatory BP monitoring was performed at the end of each period. The primary outcome was nocturnal systolic BP. Mean age of the study population (n=147) was 65.4 years, 64% were male, mean estimated GFR was 44.9 ml/min/1.73 m2. At the end of each period, mean (SE) nocturnal systolic BP was 125.6 (1.2) mm Hg in the AM dose, 123.9 (1.2) mm Hg in the PM dose, and 123.5(1.2) mm Hg in the Add-on dose. None of the pairwise differences in nocturnal, 24-hour and daytime systolic BP were statistically significant. Among African Americans with hypertensive CKD, neither PM (bedtime) dosing of once daily antihypertensive nor the addition of drugs taken at bedtime significantly reduced nocturnal BP compared to morning dosing of anti-hypertensive medications.

Metabolic acidosis is a feature of chronic kidney disease (CKD), but whether serum bicarbonate concentration is influenced by variations in dietary protein intake is unknown. For assessing the effect of diet, data that were collected in the Modification of Diet in Renal Disease study were used. In this study, patients with CKD were enrolled into a baseline period, then randomly assigned to follow either a low-or a usual-protein diet (study A, entry GFR 25 to 55 ml/min) or a low-or very low-protein diet, the latter supplemented with ketoanalogs of amino acids (study B, entry GFR 13 to 24 ml/min). Serum [total CO 2 ] and estimated protein intake (EPI) were assessed at entry (n ‫؍‬ 1676) and again at 1 yr after randomization, controlling for changes in GFR and other key covariates (n ‫؍‬ 723 ]) falls as GFR decreases in chronic kidney disease (CKD) (1,2), but the values vary widely among patients with similar levels of kidney function. Part of this difference may be due to dietinduced differences in endogenous acid production. In individuals with normal kidney function, the effect of diet on serum [total CO 2 ] is small and not detectable unless the influence of Paco 2 is removed (3). Given the impairment in acid excretion that occurs in CKD (4 -6), one might anticipate that differences in diet-induced acid production would have a greater influence on serum [total CO 2 ] than in people with normal kidney function. The major source of endogenous acid production comes from metabolism of dietary protein (7); therefore, protein restriction should result in an increase in serum [total CO 2 ] if this hypothesis is correct. Despite extensive studies on the effects of protein restriction on metabolic parameters and kidney disease progression (8), little attention has been directed to the effect of this intervention on serum [total CO 2 ] in CKD. In one study in humans with severe CKD, serum [HCO 3 Ϫ ] was notably higher when the patients were compliant with a very low-protein diet (0.3 g/kg body weight) supplemented with ketoanalogs of amino acids (9). In two other studies in humans, serum [total CO 2 ] did not increase significantly after a 50% reduction in protein, but both studies contained very few subjects (10,11). The best data supporting an effect of protein restriction on body alkali stores in CKD come from a partial nephrectomy rat model (12). In this model, steady-state serum [HCO 3 Ϫ ] was significantly higher (by 2 mEq/L) in animals that ingested a low-protein diet (6% of total calories/d) as compared with animals that ingested a normal-protein diet (24% of total calories/d).To determine whether systematic changes in dietary protein intake affect serum [total CO 2 ] in a large cohort of patients with CKD, we evaluated the data collected in patients who participated in the Modification of Diet in Renal Disease (MDRD) study, focusing on GFR, protein intake, and serum [total CO 2 ] (13). Our analysis demonstrates that [total CO 2 ] is inversely related to dietary protein intake in this group of patients and that...

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