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Biomedical subjects

A Purroy

Publications and source records attributed to A Purroy.

At least 19 recordsLinked to original sources
PubMed2003

Autosomal-dominant polycystic kidney disease: high prevalence of graft loss for death-related malignancies and cardiovascular risk factors.

Autosomal-dominant polycystic kidney disease (ADPKD) is a systemic disease with multiple extrarenal manifestations. It accounts for 7% to 11% of patients receiving dialysis or renal transplantation (RT) for end-stage renal disease (ESRD) in Europe. We analyzed retrospectively the causes of death, the prevalence of cardiovascular risk factors (CVRF) and the patient and graft survivals in 62 consecutive ADPKD patients who received 63 cadaveric grafts (29 men and 34 women), of the 600 RTs performed between 1980-2001. The diagnosis of ADPKD was established by family history and ultrasound techniques. At present, 50 patients (79.4%) have functioning grafts, with a mean follow-up of 84.7 months (range, 12-255), and 13 patients have lost their grafts. The main cause of failure was patient death with a functioning graft (9 cases). Malignancies occurred in 5 patients, including 2 lymphomas, 1 renal carcinoma, 1 pancreas sarcoma, and 1 lung cancer associated with infection. Three patients died of cardiocerebrovascular events, and 1 patient of pneumonia. One patient lost the graft after decreasing the immunosuppression for an obstructing colon cancer. Three additional patients now on dialysis lost their grafts due to chronic rejection in 2 cases and primary nonfunction in 1 case. The prevalence of cardiovascular risk factors among the 50 patients with functional grafts were: hypertension, 70%; hypercholesterolemia, 62%; hyperhomocysteinemia, 30%; hyperfibrinogenemia, 68%; increased lipoprotein (a), 18%; microalbuminuria, 22%; hyperuricemia, 48%; hyperparathyroidism, 24%; overweight status, 24%; and nonlethal myocardial infarction, 10%. We conclude that ADPKD patients have good graft and patient survivals, and that the presence of malignancy is the main cause of death and graft failure at our center.

Blood Pressure↗
PubMed2003

Treatment of hyperhomocysteinemia after renal transplantation.

INTRODUCTION: Several epidemiologic prospective studies have provided strong evidence that hyperhomocysteinemia (HHC) is a risk factor for cardiovascular disease (CVD) due to its role in producing endothelial damage due to oxidation stress. Several studies show that combined folic acid (FA) and vitamin B12 (B12) treatment decreases fasting total homocysteine (HC) levels in renal transplant recipients (RTR). The aim of the study was to determine the efficacy and safety during one year of combined FA and B12 treatment in 89 RTR, as well as the relationship between HHC with other known risk factors for CVD and the intrinsic characteristics of the transplantation. METHODS: Among 193 RTR in whom we determined the baseline levels of HC, FA, B12, creatinine, and CV risk factors, 81 had normal (HC < 14 micromol/L) and 112 elevated (HC > or = 14 micromol/L) HC levels, 89 of whom were included in a treatment group (23 nontreated). Analytic measures were performed at baseline and 1, 3, and 12 months. RESULTS: We observed a decrease in HC levels among the treatment group (P<.05) after 12 months without differences in the other groups. There were no differences in age, hypertension, hypercholesterolemia, smoking, presence of diabetes, or type of immunosuppression between the groups. There was a significant correlation between basal creatinine and HC level (P<.05). A higher prevalence of CVD was observed in the HHC group (P<.05). CONCLUSION: HHC is associated with worse renal function and a higher prevalence of CVD. FA and B12 treatment normalize HC levels, representing a safe treatment that could improve the long-term vascular prognosis of RTR.

Adult↗
PubMed2003

Lipogenic enzyme activities in different adipose depots of Pirenaican and Holstein bulls and heifers taking into account adipocyte size.

The effects of sex, genotype, and adipose depot on lipogenic enzyme activity have been investigated in Holstein and Pirenaican bulls and heifers, taking into account differences in adipocyte size. Fifteen Pirenaican bulls and 15 heifers and 15 Holstein bulls and 13 heifers were fattened until slaughter (12 to 13 mo old and 450 to 500 kg of body weight). During the fattening period, animals had ad libitum access to commercial concentrates and straw. The 10th rib was dissected to determine the fat content. Adipocyte size and activities of the following lipogenic enzymes were determined: glycerol 3-phosphate dehydrogenase, fatty acid synthase, nicotinamide adenine dinucleotide phosphate (NADP)-malate dehydrogenase, glucose 6-phosphate dehydrogenase, and NADP-isocitrate dehydrogenase, in the omental, perirenal, subcutaneous, and intermuscular adipose depots, respectively. Because adipocyte mean cell volume varied with sex, breed, and depot, regression analyses of log(e) activity per cell and log(e) cell volume were used to compare activities per unit volume. Sex, breed and depot had no effect (P > 0.05) on the gradients of regressions, which did not differ significantly from 1. Thus, activity per unit volume did not vary with cell size. Consequently, sex, breed, and depot effects on the regression analyses were equivalent to effects on activity per unit volume. Females had greater amounts of fat in the 10th rib (P < 0.001), larger adipocytes (P < 0.001) and, in general, greater (P < 0.05) lipogenic activity per cell, even when adjusted for cell size, than males. These findings suggest that differences in adiposity between sexes are mainly due to females having a greater capacity for lipid synthesis, and hence, hypertrophy, than males. When adjusted for differences in carcass weight, Holsteins had larger adipocytes than Pirenaicans. The abdominal depots, omental and perirenal, had a greater adipocyte size (P < 0.001) and, in general, greater lipogenic enzyme activities per cell (P < 0.05) than the subcutaneous and intermuscular carcass depots. However, when activity per cell was adjusted for cell size, subcutaneous depots had greater fatty acid synthae, glucose 6-phosphate dehydrogenase, and NADP-malate dehydrogenase activities than omental and perirenal, indicating that other factors such as nutrient supply may restrict hypertrophy of carcass adipocytes.

Adipocytes↗
PubMed2000

Hemostatic disturbances in patients with systemic inflammatory response syndrome (SIRS) and associated acute renal failure (ARF).

Endothelial damage plays a central role in the development of an SIRS-related Multiple Organ Dysfunction Syndrome (MODS) as a consequence of the establishment of a hemostatic imbalance between coagulation and fibrinolysis systems. Until now, sepsis is the SIRS model that has been most studied. The aim of this study was to assess the endothelial damage and the hemostatic imbalance in early stages of an SIRS of different origins, and to study if there are any differences in these disturbances between infectious and noninfectious SIRS. The endothelial damage and hemostatic changes were studied in 40 patients with SIRS (with less than 12 h of evolution) and an acute renal failure. Infectious SIRS was diagnosed in 19 cases and noninfectious SIRS in the remaining 21 patients. Patients with SIRS presented significantly higher values (p<0.001) for factors related to endothelial damage [von Willebrand factor (vWF), thrombomodulin, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor type 1 (PAI-1) antigen], hypercoagulability [prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TAT)], and fibrinolysis (D-dimer and PAI activity) with respect to the control group. However, although the group with infectious SIRS presented higher values for all the factors except for the t-PA and D-dimer with respect to SIRS of other origins, none of these differences reached statistical significance (p>0.05). Our data show that patients with SIRS and associated acute renal failure, irrespective of the origin (infectious or noninfectious), show signs of intense endothelial damage and hypercoagulability throughout the process.

Acute Disease↗
PubMed2000

Characteristics of Lacha and Rasa Aragonesa lambs slaughtered at three live weights.

A study was made of differences in the quality of meat from Lacha (L) and Rasa Aragonesa (RA) lambs slaughtered at 12, 24, or 36 kg live weight. Lambs from both breeds were weaned at 25 to 57 d, approximately 11.5 to 18.5 kg live weight, and fed concentrate and barley straw until slaughter at 24 and 36 kg live weight. Hot carcass weight, cold carcass weight, conformation, color, firmness, and thickness of backfat and color of rectus abdominis muscle were recorded on the carcass. Final pH (pHu), instrumental color (L*, a*, b*), myoglobin concentration, chemical composition, and water-holding capacity (WHC) of the longissimus muscle, shear force of the biceps femoris muscle, and iodine values and fatty acid composition of the i.m. and s.c. fat depots were determined. The percentage of fat in the longissimus muscle increased with live weight, and values for RA lambs were higher than those for L lambs. The WHC of meat from RA lambs was lower at 24 kg than at 12 or 36 kg slaughter weight. Live weight and breed had no effect on the shear force of the biceps femoris muscle. There was an increase in myoglobin concentration in the longissimus muscle with increased live weight in both breeds. The fatty acid content of s.c. and i.m. fat, which was not affected by breed, declined with the increase in slaughter weight. The polyunsaturated fatty acid content of the s.c. fat depot increased, whereas that of the i.m. fat depot decreased, with the increase in slaughter weight in both breeds. Subcutaneous fat had a higher content of heptadecanoic acid (17:0) than i.m. fat, and this increased with the increase in slaughter weight. In both depots, there was an increase in oleic acid (18:1) at 12 kg in RA lambs and at 24 kg in L lambs. In the s.c. fat depot, there was a progressive increase in linoleic acid (18:2) content with the increase in live weight in both breeds. There was a higher degree of unsaturation in the s.c. fat of RA lambs than in that of L lambs, which was reflected in the iodine value.

Animals↗
PubMed1999

Intracerebroventricular infusion of hypertonic NaCl increases urinary CGMP in healthy and cirrhotic rats.

Implication of serum atrial natriuretic peptide (ANP) and endothelin-1 (ET1) in the central nervous system (CNS)-induced natriuresis and hypertension respectively, was investigated in healthy and cirrhotic rats. Both healthy and nonascitic CCl(4)-induced cirrhotic rats under pentobarbital anesthesia received either normotonic (140 mmol/L) or hypertonic (320 mmol/L) NaCl artificial cerebrospinal fluid into the CNS lateral ventricle at a rate of 8.3 microl/min for 120 min. A sham operated group, but not centrally infused, served as matched control. Hypertonic NaCl solution significantly increased mean arterial pressure (MAP) similarly in both healthy (n = 5) ((MAP: 16 mm Hg, 13%) and cirrhotic rats (n = 6) ((MAP: 20 mm Hg, 15%) (ANOVA, p <.001) although the latter showed a slower increment. Under hypertonic NaCl infusion, natriuresis was also significantly increased in a similar manner in both healthy (U (Na) V: baseline: 0.38 +/- 0.22 micromol/min x 100 g; experiment: 2.36 +/- 0.90 micromol/min x 100 g; mean +/- SD) and cirrhotic rats (0.69 +/- 0.48 vs. 3.16 +/- 0.87; p <.001). By contrast, central hypertonic NaCl solutions did not show a significant modification of serum ANP in neither healthy (62 +/- 18 fmol/ml vs. 51 +/- 17 fmol/ml) nor cirrhotic rats (126 +/- 61 vs. 115 +/- 30). Likewise, ET-1 was not significantly modified under central hypertonic NaCl infusion in neither healthy (352 +/- 46 pg/ml vs. 344 +/- 39 pg/ml) nor cirrhotic rats (287 +/- 58 vs. 277 +/- 61). Despite no modification in serum ANP, there was a significant increment in urinary excretion of cGMP under central hypertonic NaCl infusions in bo th healthy (6.8 +/- 4.1 pmol/min x 100 g vs. 13.0 +/- 6.5 pmol/min x 100 g; p <.05) and cirrhotic rats (8.6 +/- 1.7 vs. 11.1 +/- 1.3; p <.05). Our data indicate the preservation of the mechanisms of central natriuresis in a model of non-ascitic CCl(4 )-induced cirrhosis in rats. An increment in urinary cGMP could potentially be implicated in the natriuretic response obtained by intracerebroventricular hypertonic NaCl stimulus in both healthy and cirrhotic rats. The lack of modification of serum ANP and ET-1 does not appear to support a systemic implication of these peptides in the natriuretic and hypertensive responses respectively induced by this manoeuvre.

Animals↗
PubMed1996

Verapamil deleterious effects in chronic renal failure.

Three hypertensive patients with chronic renal failure treated with slow-release verapamil at the recommended doses for high blood pressure experienced acute deleterious effects shortly after treatment (6 h to 3 days). Patients developed slow cardiac rhythms (junctional bradycardia or atrial fibrillation), hypotension and hyperkalemia. Consequently they also had oliguria and worsening of the renal function. Inotropic support, fluid therapy and potassium-lowering measures were able to restore the renal function and sinus rhythm after 10-12 h. Only 7 similar cases have been described so far. It is suggested that slow-release formulations of verapamil must be used with caution in hypertensive patients with impaired renal function.

Aged↗
PubMed1993

[Relationship between genetic markers and serum enzymatic activity in fighting bulls].

The relationships between 41 genetic markers (blood groups and biochemical polymorphisms), 3 environmental factors (season, management before the Lidia ("encierro"), punishment suffered), body constitution, and pedigree on the one hand, and the activity of muscular enzymes in serum, creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST)) on the other, were analyzed in 179 fighting bulls. The C system of cattle blood groups and the "encierro" were significantly related to the activity of the muscular enzymes of the studied animals. The fighting bulls with the W1 and C1 antigens had a higher CK and LDH activity respectively, whereas the fighting bulls with the X1 antigen as well as those that participate in the "encierro" had a lower AST activity. This results could suggest a lesser degree of muscular injury during the Lidia in animals with X1 antigen, in those that participate in the "encierro", and in those without W1 and C1 antigens.

Animal Husbandry↗
PubMed1992

[Muscular lesions and enzymatic activities in fighting bulls].

The aim of this study was to determine whether some muscular pathology existed in fighting bulls, in relation or not to the weakness shown in these animals during the bullfight (corrida for males and tienta for females). Creatinine kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) serum enzyme activities were increased after the corrida or the tienta. Most of the fighting bulls (78%) had some histological lesions in the skeletal or cardiac muscle, with predominance of chronic lesions. Clinical signs of these chronic lesions could only be seen after some trigger-effect, such as physical, exercise or stress, as shown after the corrida or tienta.

Animals↗
PubMed1991

Enhanced responsiveness to CNS-induced natriuresis in anesthetized nonascitic cirrhotic rats.

Central nervous system (CNS)-induced natriuresis was investigated in nonascitic rats with CCl4-induced cirrhosis (CTC rats) under pentobarbital anesthesia. At baseline, urine sodium output (UNa+V, in mumol.min-1.100 g body wt-1) (-30%, P less than 0.01) and mean arterial pressure (MAP, in mmHg) (-12%, P less than 0.001) were significantly reduced in CTC rats (n = 32) compared with matched controls (n = 34). In response to intracerebroventricular infusion of sodium-rich (349 mM) artificial cerebrospinal fluid (Na(+)-CSF infusion), UNa+V was significantly higher in CTC rats (2.8 +/- 0.3; n = 15) than in controls (1.7 +/- 0.2; n = 17; P less than 0.01); no differences were found in pressor changes (24 +/- 3 vs. 19 +/- 2). A similar but normal sodium CSF (150 mM) infusion did not influence UNa+V or MAP in any group (n = 12, both). In contrast, CTC rats (n = 5) showed, compared with controls (n = 5), significantly reduced natriuretic (UNa+V, 6.9 +/- 0.5 vs. 12.4 +/- 0.9; P less than 0.001) and pressor (+16 +/- 3 vs. +31 +/- 2; P less than 0.01) responses to an intravenous hypertonic sodium overload. Natriuresis induced by Na(+)-CSF infusion was related to increases in creatinine clearance (similar in both groups) and in fractional sodium excretion, which was significantly higher in CTC rats (5.90 +/- 0.15%) than in controls (3.65 +/- 0.14%; P less than 0.01). In summary, CNS-dependent efferent natriuretic mechanisms were preserved in CTC rats and were able to reverse renal tubular sodium retention in these animals. It is proposed that Na(+)-CSF infusion may be a useful tool for the study of renal sodium retention in experimental liver cirrhosis.

Animals↗
PubMed1990

Loss of renal graft due to recurrent IgA nephropathy with rapidly progressive course: an unusual clinical evolution.

Recurrence of IgA nephropathy following renal transplantation has been described in 40-50% of patients, and it usually has a good outcome. We present the case of a 54-year-old man with IgA nephropathy who developed terminal renal failure in 1985, 3 years after the onset of the disease. In March 1986 he received a cadaveric renal allograft following treatment with ciclosporin and steroids. Eight months later he developed microhaematuria and proteinuria and 10 months later he developed acute nephritic syndrome and rapidly progressive renal failure. Renal biopsy disclosed an IgA nephropathy with epithelial crescents in 60% of glomeruli. Treatment with plasma exchange and cyclophosphamide was unsuccessful and the patient lost his graft and returned to regular haemodialysis 15 months after renal transplantation.

Acute Kidney Injury↗