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C Mora

Publications and source records attributed to C Mora.

At least 37 records · Page 2Linked to original sources
PubMed2000

Amino acid losses during hemodialysis with polyacrylonitrile membranes: effect of intradialytic amino acid supplementation on plasma amino acid concentrations and nutritional variables in nondiabetic patients.

BACKGROUND: Malnutrition is highly prevalent in hemodialysis patients. Amino acid (AA) losses during the dialysis procedure may be a contributing factor. OBJECTIVES: The objectives of this study were 1) to prospectively evaluate AA losses and their effect on plasma AA concentrations during dialysis with polyacrylonitrile at baseline and after administration of AAs by intradialysis and 2) to investigate the effects of intradialytic AA supplementation on nutritional status. DESIGN: Seventeen stable patients without diabetes who were receiving hemodialysis were studied. In the first phase, AA losses were evaluated over 2 wk in 10 patients randomly assigned to receive AA supplementation. AA losses were analyzed during the first week without supplementation and during the second week with AA administration. In the second phase, the patients' nutritional status was investigated after 3 mo of AA supplementation and was compared with those in 7 patients not receiving AAs. RESULTS: Mean +/- SD) AA losses during a 4-h dialysis session were 12 +/- 2 g; there was a significant decrease in plasma AA concentrations (386 +/- 298 micromol/L for essential and 902 +/- 735 micromol/L for nonessential AAs). After administration of AAs, the losses increased to 28 +/- 4 g. However, this procedure produced a positive net balance of AAs (10.6 +/- 5.6 g for total AAs), preventing a reduction in plasma concentrations. After 3 mo of AA administration, there was a significant increase in protein catabolic rate and serum albumin and transferrin. This improvement occurred without any change in the dialysis dose, ruling out the possibility that an increase in dialysis efficiency played a role. CONCLUSIONS: Intradialysis adequately provides AA supplements, prevents reductions in plasma AA concentrations, and favorably affects the nutritional status of patients receiving hemodialysis.

Acrylic Resins↗
PubMed2000

Functional cross talk after activation of P2 and P1 receptors in oviductal ciliated cells.

The presence of ATP and adenosine receptors and their role in controlling ciliary activity in oviductal ciliated cells was studied by measuring the ciliary beat frequency (CBF) in oviductal tissue cultures. ATP, adenosine, and related compounds increased the CBF in a dose-dependent manner. We established that P2 receptors of subtype 2Y(2) and P1 receptors of subtype A(2a) mediated the responses to ATP and adenosine, respectively. We found evidence to suggest that stimulation of ciliary activity by ATP requires D-myo-inositol 1,4, 5-trisphosphate [Ins(1,4,5)P(3)] metabolism, intracellular Ca(2+) mobilization, and protein kinase C activation. On the other hand, the adenosine effect is mediated by activation of a G(s) protein-dependent pathway that enhances cAMP intracellular levels. To study the interaction between P2 and P1 receptors, cells were stimulated simultaneously with both agonists. We observed a synergistic increase of the CBF even at agonist concentrations (100 nM) that did not produce a significant response when added separately to the culture. Furthermore, a blocker of the cAMP pathway produced a reduction of the ATP response, whereas a blocker of the Ins(1,4,5)P(3) pathway also produced an inhibition of the adenosine response. Our evidence demonstrates that both ATP and adenosine receptors are present in a single ciliated cell and that a mechanism of cross talk could operate in the transduction pathways to control ciliary activity.

Adenosine↗
PubMed1999

Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice.

The NOD (nonobese diabetic) mouse is a good animal model for human IDDM. MHC class II-restricted CD4 T cells are necessary for the onset of diabetes in NOD mice. Here, we demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient in MHC class II expression and peripheral CD4 T cells, show significant pancreatic infiltration but do not develop diabetes. CD4 T cell deficiency, then, does not prevent initial pancreatic infiltration, but does stop progression to insulitis. Adoptive transfer studies show that the paucity of CD4 T cells in NOD-CIITA knockout mice is responsible for the absence of diabetes, since the CD8 T cell and B cell compartments are functional. An autoaggressive CD8+ T cell clone can, however, transfer diabetes in CIITA knockout recipient mice without CD4 T cell help, albeit with some delay compared with that in CIITA-sufficient recipients. This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes.

Adoptive Transfer↗
PubMed1999

Relationship between serum magnesium and parathyroid hormone levels in hemodialysis patients.

Acute magnesium (Mg) infusion decreases patathyroid hormone (PTH) secretion. However, the effect of chronic hypermagnesemia on PTH levels in dialysis patients is not well established. We studied 110 hemodialysis patients (mean age, 55 +/- 14 years; time on dialysis, 35 +/- 28 months) not receiving vitamin D and undergoing dialysis with an Mg dialysate concentration of 1.2 mg/dL. The primary phosphate binder was calcium carbonate, and 43% of the patients also needed aluminum hydroxide. During a 6-month period, calcium (Ca), phosphorus (P), and total serum Mg were measured every 2 months; intact PTH and aluminum (Al) were measured every 6 months. The mean value of each parameter was computed. Hypermagnesemia (serum Mg > 2.47 mg/dL) was observed in 73% of the patients. Mg and Ca were inversely correlated with PTH levels (r = -0.48; P < 0.001 and r = -0.21; P < 0.05, respectively). After adjusting for Ca and P (partial correlation analysis), Mg and PTH were inversely correlated (r = -0.58; P < 0.001). A stepwise multiple regression analysis showed that PTH levels were predicted by Mg (P < 0.001), alkaline phosphatase (P < 0.01), and P levels (P< 0.05; multiple R = 0.57; P < 0.001), whereas Ca level, sex (dummy variable), diabetes (dummy variable), time on dialysis, and Al level were not predictive. Patients with inadequately low PTH levels (relative hypoparathyroidism, PTH < 120 pg/mL; n = 52) showed greater serum Mg concentrations than the rest (n = 58; 3.01 +/- 0.33 v 2.63 +/- 0.38 mg/dL; P < 0.001). In conclusion, serum Mg concentrations in dialysis patients are independently associated with PTH levels, suggesting that chronic hypermagnesemia may decrease PTH secretion and/or synthesis. In addition, chronic hypermagnesemia of dialysis patients may have a role in the pathogenesis of adynamic bone disease.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed1999

Urinary protein excretion and serum tumor necrosis factor in diabetic patients with advanced renal failure: effects of pentoxifylline administration.

In 24 diabetic patients with advanced renal failure (creatinine clearance [C(Cr)] < 35 mL/min), we prospectively studied serum tumor necrosis factor-alpha (TNF-alpha) levels, the possible relationship with urinary protein excretion, and the effects of pentoxifylline (PTF) administration. PTF (400 mg daily) was administered for 6 months to 14 patients, and the results were compared with data from a control group (n = 10). Baseline parameters were similar in both groups. At the end of the study, urinary protein excretion and serum TNF-alpha decreased in the active group from 2.7 (1.2 to 5.8) g/d and 569 +/- 285 pg/mL to 1.1 (0.3 to 4.0) g/d and 329 +/- 232 pg/mL, respectively (P < 0.001). By contrast, proteinuria and TNF-alpha did not change in the control group. Regression analysis showed a significant correlation between proteinuria and serum TNF-alpha both at basal (r = 0.55) and at the sixth month (r = 0.57). Furthermore, the reduction of urinary protein excretion was strongly correlated with the decrease of TNF-alpha (r = 0.72, P < 0.01). Serum Cr and C(Cr) remained stable in both groups during the study. Our findings suggest that cytokines might play a role in renal damage in diabetic nephropathy. PTF is effective in reducing proteinuria in diabetic patients with advanced renal failure. The anticytokine activity of PTF may be a further explanation for this antiproteinuric effect.

Aged↗
PubMed1999

Effects of pentoxifylline on the haematologic status in anaemic patients with advanced renal failure.

OBJECTIVE: Erythropoietin (EPO) deficiency is the main cause of renal anaemia. However, inhibition of erythropoiesis by cytokines such as tumour necrosis factor alpha (TNF-a) may play an important role. The aim of this work was to study the effects of pentoxifylline, an agent with anti-TNF-a properties, on the haematologic status in anaemic patients with advanced renal failure. MATERIAL AND METHODS: In a prospective study, 7 anaemic patients with advanced renal disease (creatinine clearance <30 ml/min) were treated with pentoxifylline (400 mg orally daily) for 6 months. The evolution of haemoglobin, haematocrit, creatinine clearance and serum EPO and TNF-a a concentrations were compared with those obtained from an untreated control group. RESULTS: Haemoglobin and haematocrit significantly increased in the pentoxifylline-treated patients (9.9+/-0.5 g/dl and 27.9+/-1.6% at baseline; 10.6+/-0.6 g/dl and 31.3+/-1.9% at the 6th month, respectively, p < 0.01), whereas no variation was seen in the control group. Serum EPO levels remained stable in all patients. However, the serum TNF-a concentration decreased significantly in patients receiving pentoxifylline (basal 623+/-366 pg/ml; 6th month 562+/-358 pg/ml, p < 0.01), but not in the control group. CONCLUSIONS: Our findings suggest that the inhibition of erythropoiesis by cytokines may play a significant role in renal anaemia. The administration of agents with anti-cytokine properties, such as pentoxifylline, can improve the haematologic status in anaemic patients with advanced renal failure.

Aged↗
PubMed1999

Autosomal dominant polycystic kidney disease associated with familial sensorineural deafness.

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by both renal and non-renal disorders. Extrarenal involvement includes noncystic manifestations such as cardiovascular abnormalities, colonic diverticula and intracranial aneurysms. Familial sensorineural hearing loss (SNHL) has been included in the definition of Alport's syndrome. However, other types of nephropathy have been occasionally associated with hereditary deafness. The association of ADPKD with hereditary SNHL has not been previously documented. We report a family with ADPKD associated with bilateral sensorineural deafness in a pedigree of four affected members in four generations.

Deafness↗
PubMed1998

Effect of different membranes on amino-acid losses during haemodialysis.

BACKGROUND: We analysed amino-acid losses during haemodialysis, their influence on plasma amino-acid concentration, and their possible effects on nutritional state. METHODS: Five patients were dialysed with three membranes: cuprophan (CUP), polysulphone (PS), and polyacrylonitrile AN69 (PAN). We compared anthropometric and biochemical parameters after 6 months in patients dialysed with CUP respect to patients with PAN. RESULTS: Total losses of amino acids were higher with PAN than with PS and CUP (6.1 +/- 2.3 vs 3.8 +/- 1.3, P < 0.05, and 3.7 +/- 1.3 g/session, P < 0.01 respectively). Losses of essential amino acids (EAA) and nonessential amino acids (NEAA) were also higher with PAN respect to PS and CUP (1.8 +/- 0.8 vs 1 +/- 0.3 and 0.8 +/- 0.3, and 4.3 +/- 1.6 vs 2.8 +/- 1 and 2.9 +/- 1.1 g/session, P < 0.05). The percentage reduction for plasma EAA and NEAA were lower with CUP respect to PS and PAN (11 +/- 5% and 20 +/- 14% vs 25 +/- 10% and 33 +/- 11%, and 30 +/- 11% and 25 +/- 17% respectively, P < 0.05). There was no difference in the nutritional state between patients with CUP and PAN. However, plasma valine in patients with PAN was lower than in those with CUP (1.88 +/- 0.12 vs 2.13 +/- 0.32 mg/dl) and almost reached statistical significance. CONCLUSIONS: New synthetic membranes are advantageous with respect to conventional ones, but a disadvantage is the higher amino-acid losses, especially with polyacrylonitrile. Long-term studies are necessary to evaluate the impact of amino-acid losses on nutritional state in patients dialysed with these membranes.

Adult↗
PubMed1998

Effects of losartan on the treatment of posttransplant erythrocytosis.

Erythrocytosis is a relatively common complication of renal transplantation. Recent observations indicate that angiotensin-converting enzyme inhibitors correct renal transplant erythrocytosis. Other drugs to inhibit the renin-angiotensin system have been developed recently. The newest of these is losartan, a specific antagonist of the angiotensin II type I receptor. We report three patients in which the use of losartan controlled posttransplant erythrocytosis. Our findings suggest that losartan can be effective and safe in the treatment of posttransplant erythrocytosis.

Adult↗
PubMed1996

Obligatory amino acid exchange via systems bo,+-like and y+L-like. A tertiary active transport mechanism for renal reabsorption of cystine and dibasic amino acids.

Mutations in the rBAT gene cause type I cystinuria, a common inherited aminoaciduria of cystine and dibasic amino acids due to their defective renal and intestinal reabsorption (Calonge, M. J., Gasparini, P., Chillarón, J., Chillón, M., Gallucci, M., Rousaud, F., Zelante, L., Testar, X., Dallapiccola, B., Di Silverio, F., Barceló, P., Estivill, X., Zorzano, A., Nunes, V., and Palacín, M. (1994) Nat. Genet. 6, 420-426; Calonge, M. J., Volipini, V., Bisceglia, L., Rousaud, F., De Sanctis, L., Beccia, E., Zelante, L., Testar, X., Zorzano, A., Estivill, X., Gasparini, P., Nunes, V., and Palacín, M.(1995) Proc. Natl. Acad. Sci. U. S. A. 92, 9667-9671). One important question that remains to be clarified is how the apparently non-concentrative system bo,+-like, associated with rBAT expression, participates in the active renal reabsorption of these amino acids. Several studies have demonstrated exchange of amino acids induced by rBAT in Xenopus oocytes. Here we offer evidence that system bo,+-like is an obligatory amino acid exchanger in oocytes and in the "renal proximal tubular" cell line OK. System bo, +-like showed a 1:1 stoichiometry of exchange, and the hetero-exchange dibasic (inward) with neutral (outward) amino acids were favored in oocytes. Obligatory exchange of amino acids via system bo,+-like fully explained the amino acid-induced current in rBAT-injected oocytes. Exchange via system bo,+-like is coupled enough to ensure a specific accumulation of substrates until the complete replacement of the internal oocyte substrates. Due to structural and functional analogies of the cell surface antigen 4F2hc to rBAT, we tested for amino acid exchange via system y+L-like. 4F2hc-injected oocytes accumulated substrates to a level higher than CAT1-injected oocytes (i.e. oocytes expressing system y+) and showed exchange of amino acids with the substrate specificity of system y+L and L-leucine-induced outward currents in the absence of extracellular sodium. In contrast to L-arginine, system y+L-like did not mediate measurable L-leucine efflux from the oocyte. We propose a role of systems bo,+-like and y+L-like in the renal reabsorption of cystine and dibasic amino acids that is based on their active tertiary transport mechanism and on the apical and basolateral localization of rBAT and 4F2hc, respectively, in the epithelial cells of the proximal tubule of the nephron.

Amino Acid Transport Systems, Basic↗
PubMed1996

The rBAT gene is responsible for L-cystine uptake via the b0,(+)-like amino acid transport system in a "renal proximal tubular" cell line (OK cells).

Several studies have shown that the cRNA of human, rabbit, or rat rBAT induces in Xenopus oocytes sodium-independent, high affinity uptake of L-cystine via a system b0,(+)-like amino acid exchanger. We have shown that mutations in rBAT cause type I cystinuria (Calonge, M. J., Gasparini, P., Chillarón, J., Chillón, M., Gallucci, M., Rousaud, F., Zelante, L., Testar, X., Dallapiccola, B., Di Silverio, F., Barceló, P., Estivill, X., Zorzano, A., Nunes, V., and Palacín, M. (1994) Nat. Genet. 6, 420-425; Calonge, M. J., Volipini, V., Bisceglia, L., Rousaud, F., De Sanctis, L., Beccia, E., Zelante, L., Testar, X., Zorzano, A., Estivill, X., Gasparini, P., Nunes, V., and Palacín, M. (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 9667-9671). Apart from oocytes, no other expression system has been used for transfection of functional rBAT activity. Furthermore, the b0,(+)-like transport activity has not been clearly described in the kidney or intestine. Here, we report that a "proximal tubular-like" cell line derived from opossum kidney (OK cells) expresses an rBAT transcript. Poly(A)+ RNA from OK cells induced by system b0,(+)-like transport activity in oocytes. This was hybrid-depleted by human rBAT antisense oligonucleotides. A polymerase chain reaction-amplified cDNA fragment (approximately 700 base pairs) from OK cell RNA corresponds to an rBAT protein fragment 65-69% identical to those from human, rabbit and rat kidneys. We have also examined transport of l-cystine in OK cells and found characteristics very similar to the amino acid exchanger activity induced by rBAT cRNA in oocytes. Uptake of L-cystine was of high affinity, sodium-independent and shared with L-arginine and L-leucine. It was trans-stimulated by amino acids with the same specificity as rBAT-induced transport activity in oocytes. Furthermore, it was localized to the apical pole of confluent OK cells. To demonstrate that the rBAT protein is functionally related to this transport activity, we have transfected OK cells with human rBAT antisense and sense sequences. Transfection with rBAT antisense, but not with rBAT sense, resulted in the specific reduction of rBAT mRNA expression and b0,(+)-like transport activity. These results demonstrate that rBAT is functionally related to the L-cystine uptake via system b0,(+)-like in the apical pole of the renal OK cell line.

Amino Acid Sequence↗
PubMed1996

Acute cardiovascular effects of intravenous cyclosporine.

The acute effects of intravenous (i.v.) cyclosporine A (CsA) on blood pressure and other haemodynamic parameters were examined in 8 patients with end-stage renal disease on haemodialysis (HD). The study was performed after the mid-week haemodialysis session, when the patients were on their dry body weight. Each patient received an i.v. infusion of 5 mg/kg of CsA in 120 ml of 5% dextrose in water during 2 hours. Heart rate, systolic and diastolic blood pressure (SBP, DBP) were monitored by the Holter system. An echocardiogram (M-mode 2-dimensional and Doppler sonography) was performed using an automatic device (Ultramark 6) before CsA administration, at 30, 60 and 120 minutes during CsA infusion, and at 30 minutes thereafter. SBP, DBP and calculated peripheral vascular resistance (CPVR) increased significantly in respect to basal values at 120 and 150 minutes (SBP: basal 130 +/- 21, 120 min: 136 +/- 20, 150 min: 140 +/- 18, p < 0.05 and p < 0.01, respectively. DBP: basal 80 +/- 9, 120 min: 86 +/- 13, 150 min: 88 +/- 13, p < 0.05 and p < 0.01, respectively. CPVR: basal 1000 +/- 228, 120 min: 1178 +/- 305, 150 min: 1236 +/- 270 dyne/s/cm5, p < 0.01). However, systolic volume (SV) and cardiac output (CO) showed significant decreases from the basal values (SV: basal 103 +/- 29, 120 min: 85 +/- 22, 150 min: 85 +/- 17, p < 0.05. CO: basal 8.2 +/- 2, 120 min: 7.3 +/- 1.1, 150 min: 7 +/- 1.2 l/min, p < 0.05). In conclusion, CsA infusion produces a significant elevation of blood pressure, which seems to be mediated by a direct action on peripheral vascular resistance.

Adolescent↗
PubMed1996

Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy.

Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidification defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities.

AIDS-Related Opportunistic Infections↗