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S Borrelli, R Minutolo,
L De Nicola,
P Zamboli,
C Iodice,
A De Paola,
E De Simone,
B Zito,
P Guastaferro,
F Nigro, [......],
G Iacono,
A Di Serafino,
L D'Apice,
C Saviano,
A Sarti,
M Capuano,
R Genualdo,
M Auricchio,
M Merola,
G Conte
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ABSTRACT: During hemodialysis, amino acids (AA) are lost in the ultrafiltrate with consequent modification of their plasma profile. The aim of this cross-sectional study was to evaluate intradialytic changes of plasma AA levels during a single session of hemodiafiltration with endogenous reinfusion (HFR) versus acetate-free biofiltration (AFB). 48 patients chronically treated with HFR or AFB were matched 1:1 for age, gender, Kt/V and diabetes. Blood samples were collected at the beginning and the end of dialysis. Baseline plasma levels (μmol/l) of total AA (3,176 ± 722), essential AA (889 ± 221), and branched chain AA (459 ± 140) levels in HFR were similar to those in AFB (3,399 ± 621, 938 ± 277, and 463 ± 71, respectively). Plasma intradialytic AA levels did not change in HFR, while in AFB there was a reduction by about 25%. In conclusion, as compared with AFB, HFR has a sparing effect on AA loss due to the lack of adsorption by cartridge and to their complete reinfusion in blood.
Blood Purification 10/2010; 30(3):166-71. · 2.10 Impact Factor
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ABSTRACT: Blood pressure (BP) is hardly controlled in chronic kidney disease (CKD). We compared the effect of very low protein diet (VLPD) supplemented with ketoanalogs of essential amino acids (0.35 g/kg/day), low protein diet (LPD, 0.60 g/kg/day), and free diet (FD) on BP in patients with CKD stages 4 and 5. Vegetable proteins were higher in VLPD (66%) than in LPD (48%). LPD was prescribed to 110 consecutive patients; after run-in, they were invited to start VLPD. Thirty subjects accepted; 57 decided to continue LPD; 23 refused either diet (FD group). At baseline, protein intake (g/kg/day) was 0.79+/-0.09 in VLPD, 0.78+/-0.11 in LPD, and 1.11+/-0.18 in FD (P<0.0001). After 6 months, protein intake was lower in VLPD than LPD and FD (0.54+/-0.11, 0.78+/-0.10, and 1.04+/-0.21 g/kg/day, respectively; P<0.0001). BP diminished only in VLPD, from 143+/-19/84+/-10 to 128+/-16/78+/-7 mm Hg (P<0.0001), despite reduction of antihypertensive drugs (from 2.6+/-1.1 to 1.8+/-1.2; P<0.001). Urinary urea excretion directly correlated with urinary sodium excretion, which diminished in VLPD (from 181+/-32 to 131+/-36 mEq/day; P<0.001). At multiple regression analysis (R2=0.270, P<0.0001), BP results independently related to urinary sodium excretion (P=0.023) and VLPD prescription (P=0.003), but not to the level of protein intake. Thus, in moderate to advanced CKD, VLPD has an antihypertensive effect likely due to reduction of salt intake, type of proteins, and ketoanalogs supplementation, independent of actual protein intake.
Kidney International 03/2007; 71(3):245-51. · 6.61 Impact Factor
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R Minutolo,
M M Balletta,
F Catapano,
P Chiodini,
G Tirino,
P Zamboli,
G Fuiano,
D Russo,
P Marotta,
C Iodice,
G Conte,
L De Nicola
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ABSTRACT: The greater antiproteinuric efficacy of converting enzyme inhibitor and angiotensin II receptor blocker combination (CEI+ARB), versus monotherapy with either drug, is not a consistent finding. We evaluated the clinicopathologic predictors of response to CEI+ARB in 43 patients with primary glomerulonephritis (GN), never treated with immunosuppressive drugs, and with persistent proteinuria after CEI alone. Main histological lesions were analyzed by obtaining on 557 glomeruli and 165 arteries formal score of mesangial cellularity, glomerulosclerosis, tubulointerstitial damage, mononuclear cell infiltration, arteriosclerosis, and arteriolar hyalinosis. Duration of CEI and CEI+ARB therapy was similar (4.7+/-2.4 and 5.0+/-1.5 months). Proteinuria (g/day) decreased from 3.5+/-2.9 to 2.4+/-2.3 after CEI, and to 1.5+/-1.3 after CEI+ARB (P<0.0001). Reduction of proteinuria after CEI+ARB was greater in proliferative versus non-proliferative GN (-63.3+/-23.4 versus 42.4+/-23.7%, respectively; P=0.006). When patients were categorized in responders and non-responders to CEI+ARB, no difference between the two groups was detected in any demographic or clinical variable, whereas histology showed in responders a greater prevalence of proliferative GN (71.4 versus 31.8%, P=0.009) and higher score of mesangial cellularity (1.76+/-0.53 versus 1.20+/-0.22, P<0.0001). At multiple regression analysis (r(2)=0.476, P=0.001), response to CEI+ARB resulted independently related only to mesangial cellularity (P<0.0001). In conclusion, the best independent predictor of antiproteinuric efficacy of CEI+ARB in patients with primary GN is the degree of mesangial cellularity. This finding supports the experimental evidence that high angiotensin II contributes to proliferation of mesangial cells.
Kidney International 09/2006; 70(6):1170-6. · 6.61 Impact Factor
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L De Nicola, R Minutolo,
P Chiodini,
C Zoccali,
P Castellino,
C Donadio,
M Strippoli,
F Casino,
M Giannattasio,
F Petrarulo,
M Virgilio,
E Laraia,
B R Di Iorio,
V Savica,
G Conte
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ABSTRACT: 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.
Kidney International 03/2006; 69(3):538-45. · 6.61 Impact Factor
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ABSTRACT: We evaluated the levels of atrial natriuretic factor (ANF) in amniotic fluid and in maternal venous blood in pregnancies with fetal cardiac malformations and chromosomal abnormalities.
Between the 16th and 18th week of pregnancy, 151 women were divided into three groups. Group A included patients at lowest risk, carrying a fetus with a normally developing heart and normal karyotype (control group). Group B included women with a fetus suffering from cardiac malformations, with or without associated chromosomal abnormalities. Group C included women carrying a fetus affected with chromosomal abnormalities without congenital cardiopathies. ANF was evaluated by radioimmunoassay.
In maternal venous blood, the mean levels of ANF were 42.1, 53.1 and 38.7 pg/ml in groups A, B and C, respectively. In amniotic fluid, the mean levels of ANF were 34.2, 101.8 and 35.8 pg/ml in groups A, B and C, respectively. In group A (control group) there was no statistical difference in ANF levels across the gestational age range of 16-18 weeks, either in amniotic fluid or in maternal venous blood. A significant difference of ANF content in maternal venous blood was revealed in comparing group A with group B (p < 0.01), and group C with group B (p < 0.01). A statistically significant difference in ANF levels was also found in amniotic fluid between group A and group B (p < 0.01), and between group C and group B (p < 0.01). No statistically significant differences were found between group C and group A in comparing ANF levels in maternal venous blood and amniotic fluid.
ANF levels in amniotic fluid and in maternal venous blood are increased early in the case of fetuses with cardiac malformations, with or without associated karyotype alteration. Chromosomally abnormal fetuses without heart malformations have normal ANF levels. These results could be useful for elucidating fetal pathophysiology mechanisms.
Journal of Maternal-Fetal and Neonatal Medicine 03/2002; 11(3):183-7. · 1.50 Impact Factor
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ABSTRACT: Angiotensin-converting enzyme (ACE) inhibitors and AT1-receptor antagonists (ARAs) are widely administered to reduce urinary protein loss and slow the progression of proteinuric nephropathy to end-stage renal failure. Our group recently observed that the combination of ACE inhibitors and ARAs may have an additive antiproteinuric effect, which may occur because ACE inhibitors do not completely reduce angiotensin II (Ang II) production. Ang II is also produced by chymase. Thus, combination therapy better antagonizes the effects of Ang II. The purpose of this study is to ascertain whether the additive antiproteinuric effect of ACE inhibitors plus ARAs is dose dependent and related to the drug-induced reduction in systemic blood pressure. Therefore, enalapril (E; 10 mg/d) and losartan (LOS; 50 mg/d) were randomly administered alone and then in association; initial dosages were doubled when drugs were administered alone and in association. To determine the influence of the drug-dependent effect on reducing blood pressure and the reduction in urinary proteinuria, both ambulatory and office blood pressures were recorded. E and LOS administered alone reduced proteinuria by the same extent; no further reduction was observed when E and LOS alone were administered at a doubled dose. When E and LOS were coadministered, proteinuria decreased by a greater extent compared with E and LOS alone; an additional reduction in proteinuria was observed when combined therapy doses were doubled. The reduction in proteinuria was not correlated with clinical through blood pressure; however, reductions in diastolic and mean ambulatory blood pressures significantly correlated with the decrease in proteinuria, as well as with creatinine clearance. In conclusion, this study shows that combination therapy with E and LOS has an additive dose-dependent antiproteinuric effect that is likely induced by the drug-related reduction in systemic blood pressure. In normotensive proteinuric patients, it is likely that even a small reduction in systemic blood pressure may affect intraglomerular hemodynamics by a great extent because efferent arteriole regulation is hampered more completely by the coadministration of ACE inhibitors and ARAs.
American Journal of Kidney Diseases 08/2001; 38(1):18-25. · 5.43 Impact Factor
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L De Nicola,
V Bellizzi, R Minutolo,
M Cioffi,
P Giannattasio,
V Terracciano,
C Iodice,
F Uccello,
B Memoli,
B R Iorio,
G Conte
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ABSTRACT: To evaluate the role of plasma tonicity in the postdialysis increment of plasma potassium (p[K(+)]), the outcome of two hemodiafiltration treatments that differed only in the Na(+) level in dialysate (Na(D))-143 mmol/L (high dialysate sodium concentration [H-Na(D)]) and 138 mmol/L (low dialysate sodium concentration [L-Na(D)])-were compared in the same group of uremic patients from the end of treatment (T0) to the subsequent 30 to 120 min and up to 68 h. Kt/V and intradialytic K(+) removal were comparable. At T0, plasma [Na(+)] was 145+/-1 and 137+/-1 mmol/L after H-Na(D) and L-Na(D), respectively (P<0.001). The difference in plasma tonicity persisted from T0 to T68 h. At T120, p[K(+)] was increased from the T0 value of 3.7+/-0.2 to 4.7+/-0.2 mmol/L (P<0.05) after H-Na(D), whereas it was unchanged after L-Na(D). The change of p[K(+)] was still different after 68 h (+76+/-10% and +50+/-7% in H-Na(D) and L-Na(D), respectively; P<0.05). Of note, in the first 2 h after the end of treatment, bioimpedance analysis revealed only in H-Na(D) a significant 11+/-3% decrement of phase angle that is compatible with a decrease of intracellular fluid volume at the expense of the extracellular volume. Similarly, within the same time frame, in H-Na(D), a significant reduction of mean corpuscular volume of red cells, associated with a 2 +/-1% decrease of the intracellular [K(+)], was observed. In contrast, mean corpuscular volume of red cells did not change and erythrocyte [K(+)] increased by 6+/-1% after L-Na(D) (P<0.005 versus H-Na(D)). Thus, hypertonicity significantly contributes to the increase of p[K(+)] throughout the whole interdialytic period by determining intracellular fluid volume/extracellular volume redistribution of water and K(+).
Journal of the American Society of Nephrology 12/2000; 11(12):2337-43. · 9.66 Impact Factor
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ABSTRACT: It is well known that posture affects natriuresis in cirrhosis and heart failure. This study evaluates the role of posture on spontaneous urinary salt excretion (U(Na)V) and diuretic-induced natriuresis in nephrotic patients with mild renal impairment. U(Na)V and plasma concentrations of the main hormones involved in sodium regulation were evaluated at baseline (Baseline) and after furosemide administration (20 mg intravenously at 8:00 AM [Diuretic]) in seven nephrotic patients with mild renal impairment (creatinine clearance, 68.5 +/- 7.6 mL/min) in either the supine or upright position for 6 hours (from 8:00 AM to 2:00 PM). At baseline, U(Na)V was greater in the supine than upright position (sodium, 51.8 +/- 6.2 versus 38.3 +/- 6.1 mEq/d; P: < 0.01). Similarly, furosemide was more effective in increasing U(Na)V in the supine (sodium, 51.8 +/- 6.2 to 87.4 +/- 9.1 mEq/d; P: < 0.005) than upright position (sodium, 38.3 +/- 6.1 to 59.0 +/- 6.8 mEq/d; P: = not significant). Consequently, body weight decreased in the supine but not the upright position (-0.73 +/- 0.15 versus -0.17 +/- 0.22 kg; P: < 0. 05). Peripheral renin activity (PRA) and plasma aldosterone (Aldo) concentrations were greater in the upright than supine position at both Baseline and Diuretic. A similar pattern was observed for hematocrit, used as an index of plasma volume. In addition, a positive correlation was detected between hematocrit and PRA (r = 0.89; P: < 0.001) in the upright position. Postural changes did not influence plasma concentrations of atrial natriuretic peptide. These data indicate that in nephrotic patients with mild impairment of glomerular filtration rate, the upright position causes a reduction in plasma volume; this hypovolemia activates the renin-Aldo system responsible for sodium retention in unstimulated conditions and a blunted natriuretic response to furosemide.
American Journal of Kidney Diseases 10/2000; 36(4):719-27. · 5.43 Impact Factor
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B Memoli,
L Postiglione,
B Cianciaruso,
V Bisesti,
C Cimmaruta,
L Marzano, R Minutolo,
V Cuomo,
B Guida,
M Andreucci,
G Rossi
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ABSTRACT: Interleukin-6 (IL-6) exerts its actions through a cell-surface receptor system that consists of two transmembrane subunits: the IL-6 binding glycoprotein gp 80 (IL-6R) and the signal-transducing component (gp 130). Soluble forms of the IL-6R (sIL-6R) are generated by shedding of the membrane-associated proteins. The sIL-6R binds the ligand IL-6 with comparable affinity as the membrane-associated IL-6R and enhances the actions of IL-6.
Our aim was to evaluate the role of both uremia and different dialysis membranes on peripheral blood mononuclear cell (PBMC) release (either in absence or in presence of mitogen stimulation) and plasma levels of sIL-6R. Ten patients chronically dialyzed with cuprophan membranes (CU), eight patients on regular dialysis treatment with polymethylmethacrylate (PMMA) membranes, 11 uremic nondialyzed patients (UR), and 12 healthy subjects (CON) were included in the study.
PBMCs harvested from CU spontaneously released significantly (P < 0.01) greater amounts of sIL-6R (881.8 +/- 80.1 pg/mL), as compared with CON (267.5 +/- 26.5 pg/mL), UR (258.4 +/- 38.1 pg/mL), and PMMA (288.4 +/- 24.6 pg/mL). Under mitogenic stimulation, the sIL-6R release was significantly (P < 0.01) increased in all groups. The greater PBMC production of sIL-6R in CU was followed by significantly (P < 0.01) higher levels of circulating soluble receptors (48.7 +/- 2.5 ng/mL, 60%), as compared with CON (30.5 +/- 1.9 ng/mL). UR also showed high circulating levels of sIL-6R (53.3 +/- 5.9 ng/mL), probably secondary to an impaired urinary excretion. Circulating levels of sIL-6R in PMMA were comparable to CON (30.3 +/- 3.3 ng/mL). Either the absence of monocyte activation or the adsorption of sIL-6R on the hydrophobic PMMA surface could explain this finding.
These results suggest an important role for poor dialysis biocompatibility of CU on the release of sIL-6R, which increases sIL-6R plasma levels, thereby enhancing the inflammatory effects of IL-6.
Kidney International 08/2000; 58(1):417-24. · 6.61 Impact Factor
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ABSTRACT: Vasodilation of resistance vessels ensues in response to increased perfusion flow to maintain tissue perfusion. The flow-induced vasodilation is mainly dependent on nitric oxide (NO), which also regulates vascular responsiveness to vasoconstrictors. Besides NO, however; high flow increases endothelin-1 (ET-1) production from endothelial cells. It is likely, therefore, that the interaction between NO and ET-1 may play a critical role in the control of arterial vascular tone under high perfusion flow. In this study, the vascular responsiveness (VR) to high flow rate and the role of ET-1 released by vascular smooth muscle cells (VSMC) were evaluated in isolated and in vitro-perfused mesenteric arteries (MA). MA were perfused at constant (3.5 mL/min; CPF) and increased flow rate (4.5, 5.5, 6.5 mL/min; IPF). VR was evaluated by infusing norepinephrine (NE; 5 micromol/L) and potassium chloride (KCl; 80 mmol/L). Mesenteric vascular resistance (MVR), ET-1, and cGMP release were measured under different flow rates. The role of endothelium-derived ET-1 was evaluated by perfusing MA with phosphoramidon (endothelin converting enzyme inhibitor), whereas the role of other endothelium-derived vasoactive substances was excluded by measuring VR in MA without endothelium. Finally, ETA and ETB receptor antagonists were perfused in disendothelized MA. In the IPF group of intact MA, MVR dropped (P<.05) and both ET-1 and cGMP increased in the perfusate (P<.05). VR was enhanced by high flow after NE (101+/-9 v. 56+/-12 mm Hg in CPF, P<.005) and KCl (119+/-12 v. 51+/-10 mm Hg in CPF, P<.005) and it was unaffected by either phosphoramidon or endothelium removal. On the contrary, BQ-610 abolished the flow-dependent increase in VR. No further additive effect was achieved with BQ-788. In conclusion, in MA, high flow reduces MVR and concurrently enhances VR, likely through VSMC-derived ET-1.
American Journal of Hypertension 11/1999; 12(11 Pt 1):1119-23. · 3.18 Impact Factor
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ABSTRACT: Supplementation with L-arginine (ARG) strikingly ameliorates proteinuria and glomerulosclerosis in remnant rats by overcoming nitric oxide (NO) deficiency. Whether or not the same holds true in humans is unknown. This study aimed at evaluating the effects of ARG on the NO system and renal function in proteinuric patients with moderate chronic renal failure (CRF).
We measured plasma arginine, urinary and plasma NO3 (an index of NO synthesis), and urinary cGMP (an intracellular mediator of NO), as well as proteinuria and renal functional reserve (RFR) in CRF patients orally treated for six months with either ARG (0.2 g/kg body wt/day, CRF-A group) or the control vehicle (CRF-C). Normal subjects (NOR) were also included for basal comparisons.
In CRF patients at baseline, plasma arginine was within the normal range; similarly, the urinary excretion of NO3 was comparable to the NOR value (CRF, 0. 440 +/- 0.02; NOR, 0.537 +/- 0.08 micromol/min, P = NS). The plasma NO3 levels were higher than in NOR (CRF, 74 +/- 6; NOR, 27 +/- 2 micromol/liter, P < 0.001), and consequently the renal clearance of NO3 resulted as being reduced. During the six months of treatment, although a remarkable steadiness of ARG and NO3 levels was detected in the CRF-C group, the CRF-A group was characterized by a marked and immediate increase of plasma ARG. This was associated, however, with a delayed increment in urinary and plasma NO3 levels and no change in urinary cGMP. In CRF-A, as in CRF-C, blood pressure, proteinuria, glomerular filtration rate, and renal plasma flow did not vary. Likewise, RFR, which was reduced at baseline in CRF, did not improve after ARG.
In moderate CRF, the tonic release of NO is constant and, likely, not impaired, and ARG supplementation does not lead to an enhancement of NO activity, thus resulting in no renal effect.
Kidney International 09/1999; 56(2):674-84. · 6.61 Impact Factor
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ABSTRACT: We tested the hypothesis that the combination of converting enzyme inhibitor (CEI) with losartan (LOS) produces a more profound antiproteinuric effect than either drug alone in normotensive patients with immunoglobulin A (IgA) nephropathy. Eight normotensive (mean blood pressure, 88.9 +/- 2.1 mm Hg) patients with biopsy-proven IgA nephropathy, nonnephrotic proteinuria (protein, 1 to 3 g/d), and normal or slightly reduced creatinine clearance (range, 69 to 119 mL/min) were studied. Clinical evaluations and laboratory tests were performed (1) before CEI treatment (basal) and after (2) CEI alone (CEI, 12 weeks); (3) the combination of CEI and LOS, the latter at a dosage of 50 mg/d (CEI + LOS, 4 weeks); (4) LOS alone (LOS; 50 mg/d; 12 weeks); (5) the combination of LOS and CEI (LOS + CEI, 4 weeks, at the same dosage as CEI + LOS); and (6) a doubled dose of either CEI alone or LOS alone for 4 weeks. CEI and LOS as monotherapy significantly reduced proteinuria by 38% and 30%, respectively. No further reduction of proteinuria was achieved by doubling the dose of CEI or LOS. Both combinations induced a more remarkable reduction of proteinuria (73%; P < 0.05 v other periods) than either drug administered alone. The antiproteinuric effect of CEI or LOS and the more remarkable effect achieved with both combinations was not dependent on the reduction of blood pressure and/or creatinine clearance. In conclusion, this study provides first-time evidence that the combination of CEI and LOS in normotensive patients with IgA nephropathy produces a more profound decrease in proteinuria than either drug. This additive antiproteinuric effect is not dependent on changes in systemic blood pressure and creatinine clearance. Nevertheless, a larger controlled study is required to confirm this novel observation.
American Journal of Kidney Diseases 05/1999; 33(5):851-6. · 5.43 Impact Factor
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ABSTRACT: Both amount and timing of dietary calcium intake influence the recurrence of renal calcium stones. We have evaluated whether the hardness of extra meal drinking water modifies the risk for calcium stones. The urinary levels of calcium, oxalate and citrate, i.e., the main urinary risk factors for calcium stones, were measured in 18 patients with idiopathic nephrolithiasis, maintained at fixed dietary intake of calcium (800 mg/day), after drinking for 1 week 2 liters per day, between meals, of tap water and at the end of 1 week of the same amount of bottled hard (Ca2+ 255 mg/l) or soft (Ca2+ 22 mg/l, Fiuggi water) water, in a double-blind randomized, crossover fashion. As compared with both tap and soft water, hard water was associated with a significant 50% increase of the urinary calcium concentration in the absence of changes of oxalate excretion; the calcium-citrate index revealed a significant threefold increase during ingestion of hard water as compared with respect to soft water (Fiuggi water), making the latter preferable even when compared with tap water. This study suggests that, in the preventive approach to calcium nephrolithiasis, the extra meal intake of soft water is preferable to hard water, since it is associated with a lower risk for recurrence of calcium stones.
Nephron 02/1999; 81 Suppl 1:66-70. · 13.26 Impact Factor
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ABSTRACT: Left renal vein hypertension, also called "nutcracker phenomenon" or "nutcracker syndrome," is a rare vascular abnormality responsible for gross hematuria. The phenomenon is attributable to the idiopathic decrease in the angle between the aorta and the superior mesenteric artery with consequent compression of the left renal vein. The entrapment of the left renal vein is not easily detectable by ordinary diagnostic procedures. We report two cases of gross hematuria (persistent in one patient and recurrent in the other) caused by "nutcracker phenomenon." In both cases, no remarkable findings were obtained from medical history, urinary red blood cells morphology, repeated urinalysis, pyelography, cystoscopy, or ureteroscopy. Left renal vein dilation in one case was found with a computed tomography (CT) scan performed on the venous tree of left kidney. The diagnosis of "nutcracker phenomenon" was confirmed by renal venography with measurement of pressure gradient between left renal vein and inferior vena cava in both cases. In one case, the diagnosis was complicated by the presence of Mycobacterium tuberculosis in urine. The "nutcracker phenomenon" is probably more common than thought. Early diagnosis is important to avoid unnecessary diagnostic procedures and complications such as the thrombosis of the left renal vein. Many procedures are available to correct the compression of the left renal vein entrapped between the aorta and the superior mesenteric artery: Gortex graft vein interposition, nephropexy, stenting, and kidney autotransplantation. After surgery, gross hematuria ceases in almost all patients.
American Journal of Kidney Diseases 10/1998; 32(3):E3. · 5.43 Impact Factor
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ABSTRACT: Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting > 200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was < 100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 +/- 2 vs. 28 +/- 2 ml/min) and higher proteinuria (2.9 +/- 0.3 vs. 1.5 +/- 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 +/- 2 mm Hg in LSD and 107 +/- 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 +/- 0.07 vs. 0.51 +/- 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.
Mineral and Electrolyte Metabolism 02/1998; 24(4):296-301.
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ABSTRACT: In recent years, different clinical studies have provided new information on the pathophysiological role and diuretic effectiveness of atrial natriuretic peptide (ANP) in subjects with normal renal function and patients with chronic renal disease. Plasma ANP (pANP) was increased by infusion at the lowest doses ever tested in humans who were on low salt diet to the levels that the same subjects gained when on a normal salt diet; ANP accounted for at least 40% of the increase of natriuresis. Similarly, ANP appeared to be mainly involved in the physiological down-regulation of salt excretion (that is, during the shift from a normal to low-sodium diet). Interestingly, data have been also attained on the efficacy of ANP as diuretic agent when administered at a low nonhypotensive dosage in normals as well as CRF patients. Indeed, low-dose ANP promoted a marked increase of sodium excretion in CRF patients to the same levels observed in normals, likely because the renal patients exhibited a more marked pANP increment secondary to the lower renal catabolism of the infused hormone. Moreover, aldosterone suppression was greater in CRF patients with respect to normals. Furthermore, the fractional urinary excretion of cGMP increased more in CRF patients than in normals. Finally, ANP infusion augmented the urinary losses of the main solutes retained in CRF (urea, potassium, phosphorous) with a significant decrease in the plasma levels. Hence, ANP per se not only plays a significant role in the up- and down-regulation of sodium excretion in healthy state and chronic renal disease, but it may also be considered to be a powerful and unique diuretic agent in CRF at nonhypotensive dosages.
Kidney international. Supplement 07/1997; 59:S28-32.
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ABSTRACT: It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP). In this study, plasma ANP (pANP) and renal function were evaluated during stepwise infusion of low ANP doses (2, 4, 8, and 16 ng/kg per min) in glomerulonephritic patients with (CRF) or without (GN) moderate renal failure, and in normal subjects (NOR), kept at low-sodium diet (LSD; 35 mEq NaCl/day). To assess the physiological ANP levels, pANP was also measured in the three groups after normal-sodium diet (NSD; 235 mEq NaCl/day). ANP did not affect systemic and renal perfusion at any of the doses tested; a significant increment of GFR was observed only in NOR and GN. The 2-, 4-, and 8-ng/kg doses increased pANP to values overlapping the physiological concentrations measured at NSD; this was associated with a dose-dependent increment of urinary excretion of sodium (UNaV) that reached analogous levels in the three groups. ANP accounted for approximately 40% of the UNaV increment evoked by NSD in patients and in normal subjects. The 16-ng/kg dose led to supraphysiological levels that induced a similar marked enhancement of UNaV (from the basal value of 0.12 +/- 0.02 to 0.42 +/- 0.08 mEq/min in CRF, from 0.13 +/- 0.02 to 0.73 +/- 0.08 in GN, and from 0.09 +/- 0.02 to 0.49 +/- 0.11 in NOR). In CRF, the normal natriuretic response to the highest dose was caused by a larger increase of fractional UNaV that was strictly dependent on the greater pANP increment, as demonstrated by similar changes in the fractional excretion of cGMP, and, in part, on the greater aldosterone decrease. In all groups, ANP also induced a dose-dependent urinary loss of phosphate, potassium, and urea, resulting in a significant 15 to 25% decrease in the plasma levels. Thus, in GN and CRF patients, ANP plays a significant role in the renal handling of sodium; moreover, the achievement of low supraphysiological pANP levels leads to a conspicuous natriuresis associated with unique extranatriuretic effects.
Journal of the American Society of Nephrology 04/1997; 8(3):445-55. · 9.66 Impact Factor
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ABSTRACT: L-Arginine is a important component of our diet characterized by multiple physiological and pharmacological actions. In the last decade, this amino acid has attracted major interest since it has been identified as the natural substrate of nitric oxide, and is now recognized to play a major role in the regulation of vascular tone. This review, while summarizing the knowledge of the renal actions of the L-arginine/nitric oxide pathway in health and renal disease, focuses on the potential therapeutic implications of the increase in nitric oxide synthesis attained by L-arginine supplementation.
Mineral and Electrolyte Metabolism 02/1997; 23(3-6):144-50.
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Cardiologia (Rome, Italy) 06/1996; 41 Suppl 1:25-9.
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ABSTRACT: The renal response to sodium restriction was evaluated, and the concurrent changes of the plasma levels of aldosterone (ALDO) and atrial natriuretic peptide (ANP), in healthy patients (NOR), in normotensive patients with non-nephrotic chronic glomerulonephritis and normal renal function (GN), and in patients with glomerulonephritis and moderate renal failure (GFR, 41 +/- 4 mL/min; CRF). The three groups were studied for 1 wk after changing from a normal-sodium diet (NSD, 235 mEq NaCl/day) to a low-sodium diet (LSD, 35 mEq NaCl/day). All patients reached a steady sodium balance within the 4th and 5th day of LSD with an analogous cumulative loss of sodium. After salt restriction, the fractional urinary sodium excretion diminished by the same extent in the three groups, whereas the fractional free-water generation, measured during water diuresis, did not vary in NOR and markedly decreased in GN and CRF. Plasma levels of ALDO were similar in all groups at NSD and similarly increased during LSD. In GN and CRF, as compared to NOR, ANP levels were higher at NSD and decreased by a minor extent during LSD. Notably, in GN and CRF, but not in NOR, the attainment of the new sodium balance after sodium restriction was preceded by a significant parallel reduction of blood pressure and GFR; the GFR decline was secondary to a major decrement of RPF so that filtration fraction (FF) increased. It was concluded that in NOR, distal tubular effects of ANP and ALDO account for the attainment of sodium balance during LSD. As a difference, both GN and CRF patients achieve the new sodium balance primarily through hemodynamic changes: the renal hypoperfusion secondary to a decrease in blood pressure that diminishes the filtered load of sodium, and the increase of FF that enhances the proximal tubular sodium reabsorption. This abnormal response seems related to both the minor suppression of ANP and the increased salt-sensitivity of blood pressure that are likely the result of the presence of volume expansion.
Journal of the American Society of Nephrology 03/1996; 7(2):306-13. · 9.66 Impact Factor
