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Objectives: Several donor and recipient factors are known to be associated with graft loss in a kidney transplant. In this retrospective single-center study, we analyzed the effect of clinical and immunologic factors on kidney transplant outcomes in our region in Italy. Materials and Methods: The study included 245 transplanted recipients from deceased donors at Federico II University of Naples, Kidney Transplant Centre, between the years 2000 and 2006. Age, cause of death, history of hypertension, hypotension or cardiac arrest, length of time spent in the intensive care unit, serum creatinine levels and human leukocyte antigen typing all were evaluated in the donors. Age, time spent on the wait list, human leukocyte antigen typing, antibody sensitization, and allocation were evaluated in the recipients. Age, donor/recipient matching, and human leukocyte antigen mismatches also were evaluated. Results: Cox regression analysis showed that in recipients, time spent on the wait list increased the risk of restarting dialysis (OR 1.019, 95% CI: 1.000-1.038; P =.050) and dying (OR 1.017, 95% CI: 1.000-1.038; P =.032). Patients who received a kidney from a donor with a history of hypertension presented a major risk of death (OR 3.212, 95% CI: 1.190-8.668; P =.021), while human leukocyte antigen-A mismatch increased the risk of restarting dialysis (OR 3.137, 95% CI: 1.255-7.842; P =.014). Conclusions: In our study, in recipients, time spent on the wait list, and a history of hypertension were associated with a greater risk of death. Human leukocyte antigen-A mismatch is associated with a greater risk of restarting dialysis.

A large body of evidence supports the validity of decreasing blood pressure to target levels in patients with essential hypertension to prevent cardiovascular disease. This issue becomes even more critical in chronic kidney disease because of the remarkably greater risk for cardiovascular fatal and nonfatal events. Indeed, renal patients should maintain blood pressure levels less than those suggested for the general population. Paradoxically, management of hypertension in this high-risk patient population is far from optimal and certainly worse with respect to essential hypertension. The Target Blood Pressure Levels in Chronic Kidney Disease (TABLE-CKD) study, performed in Italian patients with mild to advanced chronic kidney disease regularly followed-up by nephrologists, has shown that the prevalence of patients at target blood pressure is less than 20%. The assessment of antihypertensive strategy in these patients, however, suggests that there is room for improvement; in particular, a more aggressive treatment of volume expansion may ameliorate hypertension control in this population characterized by a high salt sensitivity of blood pressure.

The current implementation into nephrology clinical practice of guidelines on treatment of cardiovascular (CV) risk factors in chronic kidney disease (CKD) is unknown. We designed a cross-sectional analysis to evaluate the prevalence and treatment of eight modifiable CV risk factors in 1058 predialysis CKD patients (stage 3: n =486; stage 4: n =430, stage 5: n =142) followed for at least 1 year in 26 Italian renal clinics. The median nephrology follow-up was 37 months (range: 12–391 months). From stages 3 to 5, hypertension was the main complication (89, 87, and 87%), whereas smoking, high calcium-phosphate product and malnutrition were uncommon. The prevalence of proteinuria (25, 38, and 58%), anemia (16, 32, and 51%) and left ventricular hypertrophy (51, 55, and 64%) significantly increased, while hypercholesterolemia was less frequent in stage 5 (49%) than in stages 4 and 3 (59%). The vast majority of patients received multidrug antihypertensive therapy including inhibitors of renin–angiotensin system; conversely, diuretic treatment was consistently inadequate for both frequency and dose despite scarce implementation of low salt diet (19%). Statins were not prescribed in most hypercholesterolemics (78%), and epoietin treatment was largely overlooked in anemics (78%). The adjusted risk for having a higher number of uncontrolled risk factors rose in the presence of diabetes (odds ratio 1.29, 95% confidence interval 1.00–1.66), history of CV disease (odds ratio 1.48, 95% confidence interval 1.15–1.90) and CKD stages 4 and 5 (odds ratio 1.75, 95% confidence interval 1.37–2.22 and odds ratio 2.85, 95% confidence interval 2.01–4.04, respectively). In the tertiary care of CKD, treatment of hypertension is largely inadequate, whereas therapy of anemia and dyslipidemia is frequently omitted. The risk of not achieving therapeutic targets is higher in patients with diabetes, CV disease and more advanced CKD.

Postdialytic rebound (PDR) of plasma solutes is a relevant drawback of intermittent hemodialysis, but its pathophysiological process remains undefined. We assessed the independent effects of efficiency and length of dialytic session on PDR of urea, phosphate, and potassium.Uremic patients were evaluated at the beginning and end of dialysis and after 180 minutes in 2 randomized crossover studies. In study 1, we compared the effect of standard versus higher efficiency acetate-free biofiltration (AFB) while maintaining the same duration of 4 hours. In study 2, we compared the effect of 3- versus 5-hour AFB sessions while maintaining similar efficiency.In study 1, greater Kt/V (1.49 +/- 0.20 versus 1.22 +/- 0.15; P0.0001) was coupled with significant increases in both absolute removal and PDR of urea and phosphate (PDR of urea, +45% versus +29%; PDR of phosphate, +79% versus +52%), but not of potassium. Similarly, in study 2, shortening the AFB session while maintaining similar absolute removal and Kt/V (1.28 +/- 0.09 versus 1.31 +/- 0.09) significantly increased PDR of urea and phosphate (PDR of urea, +32% versus +19%; PDR of phosphate, +63% versus +36%), but not of potassium. In both studies, greater PDRs of urea and phosphate were associated with estimated greater removal of these solutes per hour.The rate of removal of phosphate and urea is a critical determinant of their PDR; conversely, potassium is not influenced by removal rate, likely because of its marked cell compartmentalization.

Maximal suppression of renin-angiotensin system in nonproliferative glomerulonephritis. Background Elimination of residual proteinuria is the novel target in renoprotrection; nevertheless, whether a greater suppression of renin-angiotensin system (RAS) effectively improves the antiproteinuric response in patients with moderate proteinuria remains ill-defined. Methods We evaluated the effects of maximizing RAS suppression on quantitative and qualitative proteinuria in ten patients with stable nonnephrotic proteinuria (2.55 ± 0.94 g/24 hours) due to primary nonproliferative glomerulonephritis (NPGN), and normal values of creatinine clearance (103 ± 17 mL/min). The study was divided in three consecutive phases: ( 1 ) four subsequent 1-month periods of ramipril at the dose of 2.5, 5.0, 10, and 20 mg/day; ( 2 ) 2 months of ramipril 20 mg/day + irbesartan 300 mg/day; and ( 3 ) 2 months of irbesartan 300 mg/day alone. Results Maximizing RAS suppression was not coupled with any major effect on renal function and blood pressure; conversely, a significant decrement in hemoglobin levels, of 0.8 g/dL on average, was observed during up-titration of ramipril dose. The 2.5 mg dose of ramipril significantly decreased proteinuria by 29%. Similar changes were detected after irbesartan alone (-28%). The antiproteinuric effect was not improved either by the higher ramipril doses (-30% after the 20 mg dose) or after combined treatment (-33%). The reduction of proteinuria led to amelioration of the markers of tubular damage, as testified by the significant decrement of α 1 microglobulin (α 1 m) excretion and of the tubular component of proteinuria at sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Conclusion In nonnephrotic NPGN patients, standard doses of either ramipril or irbesartan lead to significant reduction of residual proteinuria and amelioration of the qualitative features suggestive of tubular damage. The enhancement of RAS suppression up to the maximal degree does not improve the antiproteinuric response and is coupled with a decrement of hemoglobin levels.

The present paper reports a numerical-experimental study on the dynamic behaviour of a compression system based on a multi-stage centrifugal blower and fitted with an innovative device for the dynamic suppression of surge instability. The control device is of passive type and is based on the aeroelastic coupling of the basic compression system with a hydraulic oscillator. The controlled system is modelled at first by using a non-linear lumped parameter approach. The simulated system dynamics within a wide range of operating conditions allows a parametric analysis to be performed and the optimal values of the control parameters to be singled out. Such optimal values are then used to design the hydraulic oscillator, which results in a technically feasible and very simple configuration. Finally, experimental tests are carried out on the compression plant with and without the passive control device, which demonstrate the effectiveness of the proposed control system in suppressing surge instabilities, at least within the limits predicted by the numerical simulation.Copyright © 2000 by ASME

Maintenance hemodialysis (HD) patients were studied to assess the effect on hemoglobin (Hb) concentration induced by the cyclic variation in hydration status.Forty-nine HD patients were examined in three consecutive HD sessions in a 1-week treatment period. In a subgroup of 23 patients, Hb levels also were investigated during the long interdialytic interval.Hb levels at the end of the long interdialytic interval were significantly lower by 0.5 to 0.6 g/dL (5 to 6 g/L) than those at the end of short intervals. Among all pre-HD and post-HD Hb values, levels measured at the end of short intervals were closest to the mean Hb value of the week, derived from calculation of the area under the curve (12.0 +/- 0.2 g/dL [120 +/- 2 g/L]). Intradialytic Hb increments were different in the three sessions (+1.6 +/- 0.1 g/dL [+16 +/- 1 g/L] after the long interval, +1.1 +/- 0.1 g/dL [+11 +/- 1 g/L] and +1.1 +/- 0.1 g/dL [+11 +/- 1 g/L] after short intervals [P0.001] and proportionate to weight loss [-3.4 +/- 0.1, -2.7 +/- 0.1, and -2.6 +/- 0.1 kg, respectively; P0.001]). Hb level increment and weight loss correlated directly (r = 0.527; P0.0001); each 1 L of ultrafiltration (UF) led to an increase in Hb level of approximately 0.4 g/dL (4 g/L). Plasma refilling accounted for an approximately 45% decrement in the intradialytic increase in Hb level 2 hours post-HD.This study suggests that: (1) the end of the short interdialytic period is the most appropriate timing for anemia assessment, and (2) the remarkable hemodiluting effect of post-HD plasma refilling protects against excessive increments in Hb levels induced by UF.

The present paper deals with several problems arising in the stabilisation of surge in compression systems. From a theoretical standpoint the system requires a high gain type controller to be stabilised. On the other hand, the real system is affected by persistent measurement noise whose negative effect on stability is strongly amplified by the high gain. Therefore, a suitable filtering of the system output is necessarily required. The bandwidth of the filter is subject to opposite constraints: if it is too large it affects the attenuation property; if it is too narrow, the large phase-lag introduced at low frequencies may compromise the system stabilisation, which requires a fast actuator reaction. This paper analyses all these aspects concurring in the stabilisation problem and the consequent trade-off in the control design. The results of experimental and numerical studies are provided with reference to the active control of surge in a multistage centrifugal compressor.Copyright © 2002 by ASME

At the beginning of this century, the diagnosis of various renal diseases was made with relative accuracy although neither plasma markers of glomerular filtration nor renal biopsy nor imaging were available. Renal edema was identified by high albuminuria, hyalin cylinders, high urine density and oliguria. Renal hematuria was detected by cylinders of erythrocytes. Hallmarks of chronic renal insufficiency, recognized at autopsy by atrophic kidneys, were hyposthenuria, polyuria and slight albuminuria without edema associated with arterial hypertension, anemia, retinopathy and left ventricular hypertrophy. The detection of increased plasma volume in experimental toxic nephritis by St. Moscati proposed the underlying mechanism of arterial hypertension. Experimental and clinical research in the preinsulin era indicated the central role of the kidney in the functional alterations induced by diabetes. Indeed, glucosuria was known to appear only when glycemia was relatively high. The kidney appeared enlarged and hyperemic, i.e. the so-called glomerular hyperfiltration. Glucosuria was directly correlated with diuresis but it markedly decreased in renal insufficiency. In diabetes complicated by nephropathy, tolerance to carbohydrates improved. Correction of glucosuria by dietary treatment was followed by a prompt rise in body weight, due to retention that counterbalanced the previous losses. Diabetic ketoacidosis, determined by the measurement of urinary ketonic body excretion, was treated with sodium bicarbonate (30–50 g/day in severe acidosis) up to achieving an alkaline urine pH. It was known that high doses of sodium bicarbonate might induce edema which gradually disappeared with a reduction in the alkaline administration. Clinical significance of sodium balance was, in fact, recognized: the external NaCl balance between alimentary ingestion and urinary excretion was neutral in normal conditions and became positive at high body temperature or negative during reabsorption of exudates.