Search PubMed⌕ Search

Biomedical subjects

A Mercado

Publications and source records attributed to A Mercado.

30 records · Page 2Linked to original sources
PubMed1976

Inhibitory effects of hypermagnesemia on the renal action of parathyroid hormone.

Available evidence indicates that serum magnesium (Mg++) levels influence the secretion rate of parathyroid hormone (PTH). Whether serum Mg++ concentrations also modify the action of PTH on its target organs has not been definitively established. The present experiments were designed to study this possibility. The effect of infusing PTH on the urinary excretion of cyclic AMP (cAMP) and PO4= was examined in five normal dogs at two different levels of serum Mg++. At normal serum Mg++ concentrations (1.89 +/- 0.14 mg/100 ml), PTH infusion increased cAMP excretion from 1.76 +/- 0.27 to 4.87 +/- 1.00 nmol/min and fractional PO4= excretion (FEPO4) from 1.58 +/- 0.36% to 23.1 +/- 2.17%. When an identical amount of PTH was given to the same dogs at a serum Mg++ of 4.36 +/- 0.20 mg/100 ml, FEPO4 increased to only 6.02+/-1.89% and cAMP from 1.31 +/- 0.23 to 1.89 +/- 0.39 nmol/min. Identical results were obtained in thyroparathyroidectomized hypermagnesemic dogs. Increased serum Mg++ levels had no effect on the phosphaturia produced by the infusion of dibutyryl cAMP to thyroparathyroidectomized dogs. In vitro studies using rat renal cortical slices revealed a progressive decrease in cAMP production in response to PTH as the Mg++ concentrations were increased in the incubation medium. The overall results indicate that hypermagnesemia inhibits the phosphaturic response to PTH by decreasing the renal production of cAMP. Plasma magnesium, therefore, may participate in a double feedback mechanism, not only controlling the release of PTH, but also altering the biological activity of the hormone at the level of the target organ.

Adenylyl Cyclases↗
PubMed1975

On the mechanisms responsible for the phosphaturia of bicarbonate administration.

Experiments were carried out in normal dogs to characterize the mechanisms by which sodium bicarbonate administration results in increased excretion of phosphate. Infusion of sodium bicarbonate alone increased fractional phosphate excretion from 0.8 to 29.3%. During bicarbonate administration, ionized calcium fell and mean parathyroid hormone values increased from 59.6 to 230.4 muleq/ml. In the same group of dogs, administration of sodium bicarbonate plus calcium prevented the fall in ionized calcium, and parathyroid hormone levels remained unchanged. In these dogs fractional phosphate excretion increased from 2.4 to only 4.9%. Similar results were obtained in thyroparathyroidectomized dogs receiving sodium bicarbonate. In these dogs fractional excretion of phosphate increased from 0.6 to 4.5%. Under all three experimental conditions no differences were observed in sodium or bicarbonate excretion or in urinary or plasma pH. Administration of hydrochloric acid, after phosphaturia had been induced by the infusion of bicarbonate, resulted in a decrease in plasma bicarbonate and an acid urine; however, the phosphaturia persisted even in the presence of an acid urine pH. In five thyroparathyroidectomized dogs infused with parathyroid hormone throughout, administration of identical amounts of sodium as either NaCl or NaHCO3 resulted in a similar degree of phosphaturia despite significant differences in urine pH. These experiments suggest that a rise in parathyroid hormone levels, resulting from a fall in ionized calcium, is the major mechanism by which bicarbonate administration produces phosphaturia. An increased natriuresis per nephron, as a consequence of extracellular fluid volume expansion, contributes to the phosphaturia. On the other hand, alkalinization of the urine does not play a significant role in the phosphaturia seen after bicarbonate administration.

Animals↗
PubMedDate not supplied

Na(+):K(+):ATPase mRNA expression in the kidney during adaptation to sodium intake and furosemide treatment.

Nephron tubular epithelium possesses the capacity of adaptation to any salt ingestion condition. The mechanism of adaptation is due in part to an increase in the activity of Na(+):K(+):ATPase at the basolateral membrane. The goal of the present study was to analyze the long-term regulation of the Na(+):K(+):ATPase alpha(1)-subunit mRNA expression during changes in NaCl metabolism. Male Wistar rats given a normal, high, or low NaCl diet, and intraperitoneal administration of the loop diuretic furosemide from 12 h to 7 days were studied. Rats were kept in metabolic cages 4 days before and throughout the study to determine daily urinary electrolyte excretion and osmolarity. At the end of each experimental period, creatinine clearance and serum electrolytes were also measured. Total RNA was extracted from each individual cortex or outer medulla and from pooled inner medullas using the guanidine/cesium chloride method. Na(+):K(+):ATPase alpha(1)-subunit mRNA expression was assessed by nonradioactive dot-blot analysis. Experimental maneuvers were well tolerated and all groups developed the appropriate renal response to each experimental condition. Urinary sodium excretion was significantly higher in rats administered a high sodium diet or furosemide and lower in rats treated with a low sodium diet after 7 days of treatment. Glomerular filtration rate was similar among all groups. However, the level of expression of the Na(+):K(+):ATPase alpha(1)-subunit did not change in any model. Nephron adaptation to the modification in NaCl intake or furosemide administration over 7 days did not include changes in Na(+):K(+):ATPase alpha(1)-subunit mRNA levels.

Adaptation, Physiological↗
PubMedDate not supplied

[Hepatitis C viral in patients with terminal chronic kidney failure. I. Prevalence].

BACKGROUND: The prevalence of hepatitis C in patients with end stage renal disease, under renal replacement therapy either with hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD), is higher than in the general population. The prevalence of hepatitis C in patients under dialysis, however, is unknown in Mexico. Thus, the major goals of the present study were to determine the prevalence of hepatitis C in our patients on dialysis, and the risk factors associated with it. METHODS: We performed a cross-sectional and comparative study in patients under dialysis in three hospital centers in the south of Mexico City. For every patient we evaluated: age, gender, etiology of the renal failure, modality and time in dialysis, transfusion and surgical history, serum albumin, aminotranferases, BUN, and serum creatinine. The presence of hepatitis C was assessed by ELISA II and qualitative RT-PCR in blood samples. In all patients diagnosed as having hepatitis C, RT-PCR to amplified part of the virus genome was also carried out in the dialysis fluid. RESULTS: We studied 235 dialysis patients that were classified according to their dialysis modality in: 132 patients under CAPD, 17 under CAPD and history of HD (PD/HD) and 86 under HD. The time under dialysis was different between the study groups: CAPD 29.6 +/- 22.3 months, PD/HD 39 +/- 42.3 and HD 14.2 +/- 15.6 (p < 0.01). The presence of hepatitis C was detected in 24 of the 235 patients, for a global prevalence of 10.2%. In no case was viral RNA found in the dialysis fluid. The prevalence varied, however, according to the type of dialysis. It was in the CAPD group 4.5%, 12.7% in the HD group, and 41.1% in the PD/HD group (p < 0.001). The multivariate analysis showed that the risk factors for hepatitis C are transfusions before the year of 1991 (Odds Ratio = 6.4), and history of hepatitis (OR = 4.3). Since less patients are seen with transfusions before 1991, we constructed another model in which this variable was excluded. This new multivariate model showed that history of surgery (OR = 4.4), the use of HD as the dialysis modality (OR = 3.5), and prolonged time under dialysis (OR = 1.01) were all significantly associated with the presence of hepatitis. DISCUSSION: Our results show that the prevalence of hepatitis C is lower in our patients that the prevalence reported by many others (average of other countries 18.5%). Since we found a higher prevalence in HD than in CAPD, even with the lower time under dialysis in the HD group, it is possible that our lower overall prevalence is secondary to the fact that CAPD is the most frequent mode of dialysis in our country. We observed the highest prevalence in the PD/HD group, that is probably due to longer exposure to the risk factors. The association with transfusions before 1991 indicates that the infection was acquired in some patients before dialysis was started. Our results showed that the CAPD is the dialysis technique with lower risk of hepatitis C infection.

Adult↗
PubMedDate not supplied

[Viral C hepatitis in patients with end stage renal disease. II. Viral genotypes].

BACKGROUND: The hepatitis C virus infection is highly prevalent in patients on chronic dialysis. There are more than 10 variants of the hepatitis C virus, with 55 to 72% of identity among them at the amino acid level. However, we do not know the specific genotype in dialysis patients in Mexico. Thus, the aim of the present study was to know the specific genotypes of the C virus in infected dialysis patients, to know the distribution of genotypes in the different dialysis techniques and to know the relation between genotype and hepatic disease stage. METHODS: We performed a prospective, transversal and comparative study in patients in dialysis in three hospital centers in the south of Mexico City. The presence of C-type hepatitis infection was assessed by ELISA II and qualitative RT-PCR in blood samples. The genotype of the hepatitis C virus was determined by analysis of the restriction pattern of the RT-PCR product using Mva I, Hinf I, BstU I and ScrF I restriction enzymes. Variables analyzed were: age, gender, etiology of renal failure, kind and time in substitutive therapy, transfusion and hepatitis history, liver function test, blood urea, serum creatinine and blood cell count. RESULTS: We studied 235 dialysis patients that were divided following their dialysis modality into: 132 in continue ambulatory peritoneal dialysis (CAPD), 17 in CAPD, but with history of hemodialysis (PD/HD) of at least one month and 86 on hemodialysis (HD). The hepatitis infection was detected in 24 of the 235 patients (CAPD = 4.5%, PD/HD = 41.1% and HD = 12.7%; p < 0.001). The most common genotype was 1B (12/24), followed by 1A and 2A (4/24 each one), and finally by 2B and 2C (2/24 each one). We detected no patients with genotypes 3 to 6. The patients with 2A genotype were older than those infected with 1A (p < 0.05). History of surgery, transfusions, and hepatitis was similar in all genotypes. Finally the time in dialysis was longer in patients with 2A genotype than others (2A = 60.5 +/- 71.5 months, vs. 1A = 11.5 +/- 11.3, 1B = 26 +/- 26.4 y 2B/C = 17.5 +/- 13.4), but the difference did not reach statistical significance. The genotype distribution between dialysis techniques showed that 1B genotype was the most frequent in all modalities. The 1A genotype was present in similar proportions in patients of the three dialysis groups, the 2C genotype was present only in patients with CAPD. Finally, the 2B was only found in hemodialysis patients. DISCUSSION: The assessment of viral genotype revealed that 1B is the most common genotype in patients on chronic dialysis in Mexico City. The fact that the 1B and 1A genotypes were the most common types in our dialysis population suggest that transmission was similar to the general population, that is, probably by blood transfusions.

Adult↗