Very Low-Protein Diet (VLPD) Reduces Metabolic Acidosis in Subjects with Chronic Kidney Disease: The "Nutritional Light Signal" of the Renal Acid Load.

BACKGROUND: Metabolic acidosis is a common complication of chronic kidney disease; current guidelines recommend treatment with alkali if bicarbonate levels are lower than 22 mMol/L. In fact, recent studies have shown that an early administration of alkali reduces progression of CKD. The aim of the study is to evaluate the effect of fruit and vegetables to reduce the acid load in CKD. METHODS: We conducted a case-control study in 146 patients who received sodium bicarbonate. Of these, 54 patients assumed very low-protein diet (VLPD) and 92 were controls (ratio 1:2). We calculated every three months the potential renal acid load (PRAL) and the net endogenous acid production (NEAP), inversely correlated with serum bicarbonate levels and representing the non-volatile acid load derived from nutrition. Un-paired T-test and Chi-square test were used to assess differences between study groups at baseline and study completion. Two-tailed probability values ≤0.05 were considered statistically significant. RESULTS: At baseline, there were no statistical differences between the two groups regarding systolic blood pressure (SBP), diastolic blood pressure (DBP), protein and phosphate intake, urinary sodium, potassium, phosphate and urea nitrogen, NEAP, and PRAL. VLPD patients showed at 6 and 12 months a significant reduction of SBP (p < 0.0001), DBP (p < 0.001), plasma urea (p < 0.0001) protein intake (p < 0.0001), calcemia (p < 0.0001), phosphatemia (p < 0.0001), phosphate intake (p < 0.0001), urinary sodium (p < 0.0001), urinary potassium (p < 0.002), and urinary phosphate (p < 0.0001). NEAP and PRAL were significantly reduced in VLPD during follow-up. CONCLUSION: VLPD reduces intake of acids; nutritional therapy of CKD, that has always taken into consideration a lower protein, salt, and phosphate intake, should be adopted to correct metabolic acidosis, an important target in the treatment of CKD patients. We provide useful indications regarding acid load of food and drinks-the "acid load dietary traffic light".

Variability of blood pressure in dialysis patients: a new marker of cardiovascular risk.

BACKGROUND: Hemodialysis patients have a high cardiovascular mortality, and hypertension is the most prevalent treatable risk factor. We aimed to assess the predictive significance of dialysis-to-dialysis variability in blood pressure in hemodialysis patients. METHODS: We performed a historical cohort study in 1,088 prevalent hemodialysis patients, followed up for 5 years. The risk of cardiovascular death was determined in relation to dialysis-to-dialysis variability in blood pressure, maximum blood pressure and pulse pressure. RESULTS: Variability in blood pressure was a predictor of cardiovascular death (hazard ratio [HR] = 1.242; 95% confidence interval [95% CI], 1.004-1.537; p=0.046). Also age (HR=1.021; 95% CI, 1.011-1.048; p=0.049), diabetes (HR=1.134; 95% CI, 1.128-1.451; p=0.035), creatinine (HR=0.837; 95% CI, 0.717-0.977; p=0.024) and albumin (HR=0.901; 95% CI, 0.821-0.924; p=0.022) influenced mortality. Maximum blood pressure and pulse pressure did not show any effect on cardiovascular death. CONCLUSION: Dialysis-to-dialysis variability in blood pressure is a predictor of cardiovascular mortality in hemodialysis patients, and blood pressure variability may be used in managing hypertension and predicting outcomes in dialysis patients.

Ramipril in post-renal transplant erythrocytosis.

BACKGROUND: Posttransplant erythrocytosis (PTE; i.e., hematocrit [Ht] >=51%) may be responsible for cardiovascular events. Angiotensin-converting enzyme inhibitors (ACEIs) are increasingly employed in PTE treatment. Diverse ACEIs have been administered at variable doses and with erratic follow-up. In addition, guidelines recommend the administration of ACEIs as first-line therapy for PTE but do not give information on dosage. In this study the dose-response of a single ACEI was assessed, and patients were followed up for 1 year. The role of ACE gene polymorphism in both prevalence of PTE and successful response to ACEI therapy was also tested. METHODS: At study entry, blood chemistry and ACE-gene polymorphism were measured. ACEI (ramipril) was initiated at 1.25 mg/day; if Ht was still >=51%, ramipril was increased every 6 weeks to ensuing greater dosages. Scheduled dosages were 1.25, 2.5, 5.0, 7.5 and 10 mg/day. Blood chemistry was repeated every 6 weeks. Serum erythropoietin (EPO) concentration was assayed at the start and end of the study. Follow-up was extended for 1 year. RESULTS: PTE developed 12.6 +/- 16.0 months after transplantation in 40 out of 400 patients; 27 patients completed the study. Initial Ht was not correlated with any variable. Final Ht appeared normalized in 26 out of 27 patients. Mean dose (+/- SD) of ramipril was 4.6 +/- 3.6 mg. Mean time for correction of PTE was 135 days, and was not dependent on baseline Ht, hemoglobin or EPO. PTE relapsed in 4 patients. Prevalence of PTE and successful response to ramipril was not dependent on ACE-gene polymorphism. CONCLUSION: Ramipril was effective in PTE; low doses normalized Ht in most patients. No clinical characteristics or biochemical variables predicted the response to ramipril. PTE may relapse; thus long-term follow-up is mandatory.

Coronary artery calcification in patients with CRF not undergoing dialysis.

BACKGROUND: Coronary artery calcification (CAC) correlates with the extent of coronary atherosclerosis and, consequently, with an increased risk for cardiovascular events. CAC is more frequent in uremic patients than in the general population. Nearly all data about CAC relate to patients on dialysis therapy. This study evaluates the prevalence and extent of CAC in patients with chronic renal failure (CRF) not yet on dialysis therapy. METHODS: Consecutive outpatients with CRF not on dialysis therapy were enrolled and compared with controls (ie, healthy volunteers and patients with essential hypertension with normal renal function). Patients and controls were asymptomatic and had no previous history of myocardial infarction, coronary bypass surgery, or angioplasty. Patients with diabetes were excluded. Clinical characteristics, biochemical test results (included homocysteinemia and C-reactive protein level), and serum concentrations of calcium, phosphorus, and intact parathyroid hormone (iPTH) were evaluated in patients and controls. CACs were searched for and scored by means of spiral computed tomography (CT). To assess the CAC progression rate, spiral CT was repeated in some patients. RESULTS: Eighty-five patients and 55 controls were studied. Patients were aged 52 +/- 13 years and had a CRF duration of 6.3 +/- 5.6 years, glomerular filtration rate of 33.0 +/- 16.0 mL/min (0.55 +/- 0.27 mL/s), serum calcium level of 9.5 +/- 0.5 mg/dL (2.37 +/- 0.12 mmol/L), serum phosphorus level of 4.1 +/- 0.9 mg/dL (1.32 +/- 0.29 mmol/L), and serum iPTH level of 143 +/- 121 pg/mL (ng/L). CAC was found in 40% of patients and 13% of controls; calcification scores were 422 +/- 634 in patients and 43.9 +/- 33 in controls. Only age ( P < 0.001) was a predictor of CAC. In patients with a repeated score performed (after a mean of 7.9 months), calcification scores increased (from 383 +/- 627 to 682 +/- 890) in 8 of 10 patients. CONCLUSION: CAC is already present in the early phase of CRF; the prevalence is greater in patients with CRF than in controls, but less than that reported in dialysis patients. Serum concentrations of calcium, phosphorus, iPTH, and inflammation markers do not predict the appearance or progression of CAC.