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R Peces

Publications and source records attributed to R Peces.

85 records · Page 5Linked to original sources
PubMed1981

Pathogenesis of hyperprolactinemia in uremic rats.

Experiments have been carried out in order to clarify to what extent the absence of PRL renal catabolism in experimental renal insufficiency is responsible for the high PRL circulating levels. Furthermore, the relative contribution of the glomerular filtration rate and peritubular degradation to PRL renal clearance have been assessed. Circulating PRL basal levels were measured by RIA in sham-operated and intact control rats and in three uremic rat models: urine autoinfusion, bilateral ureteral ligation, and bilateral nephrectomy. Plasma PRL basal levels (nanograms per ml; mean +/- SEM) were increased in sham-operated rats (30.3 +/- 5.1) with respect to control animals (18.5 +/- 2.7; P less than 0.05). Bilaterally nephrectomized animals (66.4 +/- 16.4) and those with bilateral ureteral ligation (69.3 +/- 15.9) developed similar hyperprolactinemia, in contrast to urine-autoinfused rats (20.2 +/- 2.1; P less than 0.005) whose hormone levels were similar to those of control animals. Creatinine levels were markedly elevated and comparable in the three uremic rat groups. The results suggest that: 1) hyperprolactinemia in rats in acute renal insufficiency is due primarily to reduced renal function; 2) PRL renal catabolism in the rat requires a certain rate of glomerular filtration; and 3) PRL peritubular degradation does not seem to be relevant in PRL catabolism by rat kidney.

Acute Kidney Injury↗
PubMed1981

Study on the natriuretic activity in the suprahepatic plasma after portal hypertonic NaCl infusion in dogs.

The involvement of the liver in the control of the renal excretion of water and sodium can be deduced from some recent investigations. Hypertonic or isotonic sodium chloride infusion into the hepatic portal vein enhanced renal sodium excretion when compared with identical infusions into a systemic vein. It has been suggested that a humoral factor produced by the liver could be a functional link between the liver and the kidney. In order to test this hypothesis, the present experiments were carried out in two groups of anesthetized dogs. Animals from group I were infused with NaCl (855 mmol/l) at a rate of 0.05 ml/min/kg b.w. during 30 min, into the portal vein. Blood samples were withdrawn from the suprahepatic vein, before (SH1) and coinciding with the maximal natriuresis after hypertonic saline infusion (SH2). Plasma from SH1 and SH2 were infused into the left renal artery (LRA) of dogs from group II. Two 20 min clearance periods were performed before and after each SH-infusion. After both SH-infusions urinary sodium excretion (UNaV) was significantly increased from preinfusion values in both kidneys, and these increases were significantly greater after SH2 than after SH1. No significant differences were found in UNaV between left and right kidney. After both plasma infusions the increases in urinary volume and osmolar clearance were higher in the infused than in the not infused kidney. These results suggest that the plasma leaving the liver contains a substance with natriuretic activity and that the infusion of hypertonic NaCl into the portal vein could induce either a higher secretion of the same substance or the presence of other different substance.

Animals↗
PubMedDate not supplied

[Association of hypercalcemia, elevated levels of calcitriol and tuberculosis in patients on hemodialysis].

Hypercalcemia is associated with numerous chronic granulomatous processes and chronic infections. Increased production of calcitriol by activated macrophages has been shown to be the cause in most cases. In this article, we describe three cases of hypercalcemia associated with inappropriately elevated calcitriol levels and suppressed PTH in hemodialysis. In addition to conventional techniques for tuberculosis diagnosis we used Ligase Chain Reaction (LCR) to detect mycobacterial DNA in pleural effusion with acid-fast stain and culture negativity. Antituberculous therapy was associated with a decrease in the levels of calcium, as well as in serum calcitriol concentrations, and a substantial increase in the levels of iPTH. The serum levels of 25(OH)D3 remained unchanged. These findings suggested ectopic production of calcitriol. The discussion reviews the previously reported cases of hypercalcemia and tuberculosis that occurred during hemodialysis, and concludes that ectopic production of calcitriol by tuberculous granulomas is extremely unusual and its demonstration requires a high index of suspicion. Molecular techniques are a potentially useful approach for early and rapid diagnosis of tuberculous infection in dialysis patients.

Adult↗
PubMedDate not supplied

[Hemolytic anemia caused by graft-versus-host reaction in ABO-nonidentical renal transplants from blood group O donors].

Acute hemolytic anemia is one of the side effects associated with cyclosporin and tacrolimus therapy, and three mechanisms have been described to account for hemolytic anemia in patients receiving these drugs: drug induced hemolysis, autoimmune hemolysis and alloimmune hemolysis resulting from donor lymphocytes derived from the allograft (passenger lymphocyte syndrome). We report four cases of renal transplant recipients who developed alloimmune hemolytic anemia due to minor ABO incompatibility while under treatment with cyclosporin (two) and tacrolimus (two). The anti-erythrocyte antibodies responsible for hemolysis were of the IgG isotype and showed anti-A or anti-B specificity. These findings suggest that the hemolysis could be related to alloantibodies derived from the clonal development of donor B lymphocytes in the recipients (microchimerism). In summary, hemolytic anemia due to ABO-minor incompatibility occurs infrequently after renal transplantation. Risks are higher for patients A, B or AB blood group receiving an O blood group graft under treatment with cyclosporin or tacrolimus. Follow-up of these patients is warranted for the early detection and optimal management may be achieved by reduction of immunosuppression and change to mycophenolate mofetil.

ABO Blood-Group System↗
PubMedDate not supplied

[Polycystic liver disease without autosomal dominant polycystic kidney disease].

Polycystic liver disease is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. The natural history and clinical manifestations of polycystic liver disease are based on the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD). The occurrence of polycystic liver disease independently from polycystic kidney disease has been known for a long time. More recently, a gene for autosomal dominant polycystic liver disease has been identified on chromosome 19p 13.2-13.1. Isolated polycystic liver disease is underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with similar pathogenesis and clinical manifestations. We report here two men with polycystic liver disease no associated with ADPKD. Ultrasound and computed tomography imaging were effective in documenting the underlying lesions non-invasively.

Adult↗