The nutritional treatment of chronic renal failure with a low-protein low-phosphorus diet (conventional low-protein diet, CLPD) is effective in reducing uremic intoxication, slowing the progression of renal failure and preventing secondary hyperparathyroidism. Unfortunately, in some patients, the poor palatability and the high cost of the protein-free substitutes, together with difficulties in following the diet away from home, can make good compliance difficult, possibly causing low energy intake and malnutrition. Here the results are reported of an attempt we made to overcome these drawbacks, using a diet supplying only natural foods of plant origin in definite proportions to give an essential amino acid supply satisfying the recommended dietary allowance. This is possible thanks to an appropriate cereal-legume mixture, supplying proteins complementary for essential amino acids. Additional positive features of this special vegan diet (SVD) are the high ratio of unsaturated to saturated fatty acids, the absence of cholesterol, and the lower net acid production in comparison with a mixed diet. This study indicates that the results obtained with the SVD are similar to those obtained with the CLPD. Therefore the SVD can be a substitute for the CLPD in the management of patients with mild chronic renal failure. The SVD is the diet of choice when products made of starch are not available or poorly tolerated.

—Intimal-medial thickening of the carotid wall is considered an early marker of atherosclerosis. Endothelial function is impaired in the presence of various cardiovascular risk factors that are implicated in the pathogenesis of atherosclerosis. To evaluate the relationship between vascular reactivity and carotid intimal-medial thickening, in 44 (mean±SD age, 45.7±8.8 years; range, 28 to 60 years; 31 men and 13 women) patients with essential hypertension who had never been treated and whose history of increased blood pressure was no longer than 12 months, we evaluated several parameters: intimal-medial thickening of the common carotid arteries (by B-mode ultrasound); forearm vascular response (by strain-gauge plethysmography) to intrabrachial infusion of acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 μg/100 mL forearm tissue per minute), an endothelium-dependent vasodilator, or sodium nitroprusside (1, 2, and 4 μg/100 mL forearm tissue per minute), an endothelium-independent vasodilator; calculated minimal forearm vascular resistances (the ratio between mean arterial pressure and maximal forearm vasodilation induced by 13 minutes of ischemia and 1 minute of exercise); and left ventricular mass index (on echocardiography profile). Carotid wall intimal-medial thickening showed a significant ( P <0.001) inverse correlation with vasodilation to acetylcholine ( r =−0.58) and age ( r =−0.40), whereas no correlation was observed with the response to sodium nitroprusside or with minimal forearm vascular resistances, left ventricular mass index, systolic and diastolic blood pressures, and plasma cholesterol and glucose levels. Moreover, vasodilation to acetylcholine showed no correlation with minimal forearm vascular resistances or left ventricular mass index. Although comparison of different vascular “districts,” such as the forearm microcirculation and carotid artery, does not allow for a conclusive interpretation, the present data indicate that in patients with essential hypertension, carotid wall thickening is associated with reduced endothelium-dependent vasodilation and suggest that endothelial dysfunction might be involved in early arterial structural alterations.

Studies have demonstrated a positive correlation between fluid overload (FO) and adverse outcomes in critically ill patients. The present study aims at defining the impact of hyperhydration on the Intensive Care Unit (ICU) mortality risk, comparing Bioelectrical Impedance Vector Analysis (BIVA) assessment with cumulative fluid balance (CFB) recording. We performed a prospective, dual-centre, clinician-blinded, observational study of consecutive patients admitted to ICU with an expected length of ICU stay of at least 72 hours. During observational period (72–120 hours), CFB was recorded and cumulative FO was calculated. At the admission and daily during the observational period, BIVA was performed. We considered FO between 5 % and 9.99 % as moderate and a FO ≥10 % as severe. According to BIVA hydration scale of lean body mass, patients were classified as normohydrated (>72.7 %–74.3 %), mild (>71 %–72.7 %), moderate (>69 %–71 %) and severe (≤69 %) dehydrated and mild (>74.3 %–81 %), moderate (>81 %–87 %) and severe (>87 %) hyperhydrated. Two multivariate logistic regression models were performed: the ICU mortality was the response variable, while the predictor variables were hyperhydration, measured by BIVA (BIVA model), and FO (FO model). A p-value <0.05 was considered to indicate statistical significance. One hundred and twenty-five patients were enrolled (mean age 64.8 ± 16.0 years, 65.6 % male). Five hundred and fifteen BIVA measurements were performed. The mean CFB recorded at the end of the observational period was 2.7 ± 4.1 L, while the maximum hydration of lean body mass estimated by BIVA was 83.67 ± 6.39 %. Severe hyperhydration measured by BIVA was the only variable found to be significantly associated with ICU mortality (OR 22.91; 95 % CI 2.38–220.07; p < 0.01). The hydration status measured by BIVA seems to predict mortality risk in ICU patients better than the conventional method of fluid balance recording. Moreover, it appears to be safe, easy to use and adequate for bedside evaluation. Randomized clinical trials with an adequate sample size are needed to validate the diagnostic properties of BIVA in the goal-directed fluid management of critically ill patients in ICU.

Chronic kidney disease (CKD) includes all clinical features and complications during the progression of various kidney conditions towards end-stage renal disease (ESRD). These conditions include immune and inflammatory disease such as: primary and hepatitis C virus (HCV)-related glomerulonephritis; infectious disease such as pyelonephritis with or without reflux and tuberculosis; vascular disease such as chronic ischemic nephropathy; hereditary and congenital disease such as polycystic disease and congenital cystic dysplasia; metabolic disease including diabetes and hyperuricemia; and systemic disease (collagen disease, vasculitis, myeloma). During the progression of CKD, ultrasound imaging and color Doppler imaging (US–CDI) can differentiate the etiology of the renal damage in only 50–70% of cases. Indeed, the end-stage kidney appears shrunken, reduced in volume (Ø < 9 cm), unstructured, amorphous, and with acquired cystic degeneration (small and multiple cysts involving the cortex and medulla) or nephrocalcinosis, but there are rare exceptions, such as polycystic kidney disease, diabetic nephropathy, and secondary inflammatory nephropathies. The main difficulties in the differential diagnosis are encountered in multifactorial CKD, which is commonly presented to the nephrologist at stage 4–5, when the kidney is shrunken, unstructured and amorphous. As in acute renal injury and despite the lack of sensitivity, US–CDI is essential for assessing the progression of renal damage and related complications, and for evaluating all conditions that increase the risk of CKD, such as lithiasis, recurrent urinary tract infections, vesicoureteral reflux, polycystic kidney disease and obstructive nephropathy. The timing and frequency of ultrasound scans in CKD patients should be evaluated case by case. In this review, we will consider the morpho-functional features of the kidney in all nephropathies that may lead to progressive CKD.

Background. The effect of cinacalcet on the structural pattern of hyperplastic parathyroid glands was evaluated, using high-resolution colour Doppler (CD) sonography, in haemodialysis patients with severe, inadequately controlled, secondary hyperparathyroidism (sHPT). Methods. Nine patients (6 males, 3 females; mean age ± SD, 55.5 ± 12.6 years) received cinacalcet, with adaptation of existing concomitant therapies. Biochemical parameters and the morphology and vascular pattern of hyperplastic parathyroid glands were measured at baseline and every 6 months thereafter, for a follow-up period of 24–30 months. Results. At baseline, 28 hyperplastic glands were identified. Cinacalcet led to a reduction in glandular volume during the course of the study: 68% in glands with a baseline volume <500 mm ³ and 54% in glands with a baseline volume ≥500 mm ³ . The mean volume ± SD of glands <500 mm ³ changed significantly from the baseline (233 ± 115 mm ³ ) to the end of follow-up (102 ± 132 mm ³ , P = 0.007). Levels of mean serum phosphorus, calcium and calcium–phosphorus product decreased, but not significantly, whereas there were significant decreases in mean parathyroid hormone ± SD levels (1196 ± 381 pg/ml versus 256 ± 160 pg/ml; P < 0.0001) and alkaline phosphatase ± SD levels (428 ± 294 versus 223 ± 88 IU/l; P = 0.04), accompanied by an improvement in a subjective clinical score. Conclusions. Cinacalcet, in combination with conventional treatments, led to an improvement in biochemical and clinical parameters of sHPT and reduced glandular volume in patients with severe sHPT. Volume reduction was more evident in smaller glands. Longer term, larger, randomized clinical trials are needed to confirm these preliminary findings and to further define a more systematic approach in the treatment of sHPT.