[Coxitis due to multidrug resistant Mycobacterium tuberculosis in a HIV negative patient]. / Coxitis por Mycobacterium tuberculosis multirresistente en un paciente HIV negativo.

A case of an HIV negative female patient with coxofemoral arthritis of tuberculous etiology, multidrug-resistant strain, and connective tissue disease associated to glucocorticoid therapy is reported. The patient was treated with cycloserine, ethambutol, p-aminosalicylic acid and ofloxacin, with improvement of the joint lesions. Previous publications on this subject are reviewed.

Coxitis por Mycobacterium tuberculosis multirresistente en un paciente HIV negativo. / [Coxitis due to multidrug resistant Mycobacterium tuberculosis in a HIV negative patient]

A case of an HIV negative female patient with coxofemoral arthritis of tuberculous etiology, multidrug-resistant strain, and connective tissue disease associated to glucocorticoid therapy is reported. The patient was treated with cycloserine, ethambutol, p-aminosalicylic acid and ofloxacin, with improvement of the joint lesions. Previous publications on this subject are reviewed.

Transepithelial fate of bilirubin in the isolated rat kidney.

The renal handling of bilirubin in the rat was studied using an isolated kidney preparation by means of the determination of total pigment concentration decay in the perfusion medium and its renal clearance. Unconjugated bilirubin was incorporated in the perfusate at a concentration of about 4 microg/ml. In order to establish the potential role of secretion in renal handling of the pigment, experiments were also performed incorporating in the perfusate different doses of nicotinic acid (NA) (0.1 and 1.0 mM final concentration), which is considered an alternative substrate for the organic anion transport system, or probenecid (Prob) (0.1 and 1.0 mM final concentration), the classical inhibitor of organic anion transport process. The magnitude of pigment uptake from the perfusion medium, estimated by a first order exponential decay constant, was decreased in a dose-dependent way by NA (40 and 76% decrease for 0.1 and 1.0 mM of NA, respectively) and Prob (57 and 88% decrease for 0.1 and 1.0 mM of Prob, respectively). NA and Prob also induced a diminution in the ratio of pigment renal clearance to glomerular filtration rate (24 and 48% decrease for 0.1 and 1.0 mM of NA and 52 and 55% decrease for 0.1 and 1.0 mM of Prob). Based on these findings, it can be proposed that tubular secretion through the proximal cells contributes significantly to renal pigment depuration. In order to establish the possible contribution of cellular metabolism to the secretory process, a different set of experiments was conducted. The content of bilirubin mono and diconjugates (BMC and BDC) were determined in urine, in arterial and venous samples and in renal cortex. Studies performed using either an open or a closed circulating system, revealed that after conjugation in the renal cell, pigment derivatives can be secreted into both the tubule and the venous compartments. Total bilirubin concentration as well as the relative content of BMC and BDC in urine increased over time, representing the sum of both conjugates about 50% of the total pigment excreted by the end of experiments. Consequently, our results support the existence of a tubular transepithelial transport of bilirubin, playing the metabolism of the pigment an important role in this process.

Intrarenal dopamine participation in frusemide diuretic and natriuretic responses to frusemide.

1. Dopamine (DA) involvement in the renal response to frusemide was analysed using the isolated perfused rat kidney preparation. Endogenous DA levels were increased through the infusion of its precursor levodopa (LD) (0.5 or 1 microM) whereas benserazide (50 or 100 microM), an inhibitor of the enzyme L-dopa-decarboxylase, was used to decrease DA synthesis. 2. Frusemide administration (0.3-20 nmols) induced a dose-dependent increase in fractional excretion of water (FE H2O), sodium (FE Na+) and glucose (FEG). FE Na+ elicited by the diuretic was enhanced 30-40% by 0.5 microM of LD (n = 5, P < 0.05), and 60-80% by LD 1 microM (n = 5, P < 0.05). FE H2O produced by the diuretic was enlarged 80-100% by 0.5 microM (n = 5, P = 0.05), and 130-170% by 1 microM of LD (n = 5, P < 0.01). The increase produced by both concentrations of LD on FEG was 200% for the lowest dose of the diuretic (n = 5, P < 0.01), and 90% for the highest (n = 5, P < 0.05). 3. Benserazide (BZ) (100 microM) decreased the F.E. Na+ induced by frusemide (n = 5, P < 0.05) by 32-42%, and completely abolished frusemide effects on FE H2O and FEG (n = 5). 4. In conclusion, our results suggest that endogenous dopamine participates in the frusemide-induced diuresis and sodium excretion within the kidney, and that the participation of extrarenal factors is not essential for this effect. Dopamine may be involved in frusemide-induced inhibition of proximal sodium reabsorption.

[Hypothermic preservation of the liver. Evaluation of Eurocollins solution using rats liver slices]. / Preservación hipotérmica del hígado. Evaluación de la solución Eurocollins utilizando cortes de hígado de rata.

In the present work, we analyze the effects produced by cold ischemia on the liver using Eurocollins solution (EC). This evaluates the function of slices obtained from preserved livers in EC (livers from adult female Wistar rats were used), which were perfused with Krebs-Henseleit solution (KH) for 10 min. and then with cold EC. These livers were stored at 4 degrees C in EC for 7, 24 and 48 hours. At the end of each period of preservation, the livers were sliced and they were incubated 1 hour at 37 degrees C in KH. The following parameters were determined: tissular water distribution and electrolytes content (K+ and Na+), LDH release at the incubation medium, thiobarbituric acid reactive substances (TBARS) and urea synthesis. The slices obtained from preserved livers (7 hours), showed an increase of tissular water, expressed by the expansion of the extracellular space, a progressive diminution of tissular K+ content and an increase in TBARS and the LDH release with the increment of the preservation time. No changes in ureogenesis rate were observed. These results suggest that the cold ischemia in EC, in periods that exceed 5 hours, cause, changes in the membrane permeability and severely affects the mechanism of regulation of the tissular volume and may compromise the functional viability of the organ to be transplanted.

Preservación hipotérmica del hígado. Evaluación de la solución Eurocollins utilizando cortes de hígado de rata. / [Hypothermic preservation of the liver. Evaluation of Eurocollins solution using rats liver slices]

In the present work, we analyze the effects produced by cold ischemia on the liver using Eurocollins solution (EC). This evaluates the function of slices obtained from preserved livers in EC (livers from adult female Wistar rats were used), which were perfused with Krebs-Henseleit solution (KH) for 10 min. and then with cold EC. These livers were stored at 4 degrees C in EC for 7, 24 and 48 hours. At the end of each period of preservation, the livers were sliced and they were incubated 1 hour at 37 degrees C in KH. The following parameters were determined: tissular water distribution and electrolytes content (K+ and Na+), LDH release at the incubation medium, thiobarbituric acid reactive substances (TBARS) and urea synthesis. The slices obtained from preserved livers (7 hours), showed an increase of tissular water, expressed by the expansion of the extracellular space, a progressive diminution of tissular K+ content and an increase in TBARS and the LDH release with the increment of the preservation time. No changes in ureogenesis rate were observed. These results suggest that the cold ischemia in EC, in periods that exceed 5 hours, cause, changes in the membrane permeability and severely affects the mechanism of regulation of the tissular volume and may compromise the functional viability of the organ to be transplanted.

Renal transport of glycine during glutathione replenishment in rats.

Renal transport of glycine was studied in control and glutathione-depleted rats. Diethylmaleate (4.0 mmol/kg body wt, ip) was used as a glutathione depletor agent and the studies were carried out 6 and 10 h post-diethylmaleate injection. Renal transport was measured in isolated rat kidney preparations by means of clearance techniques and in brush border membrane vesicles by a rapid filtration method. Tubular reabsorption of glycine, when compared to glomerular filtration rate, measured at different substrate tubular loads, was higher in treated kidneys. Tissue 14C accumulation was also higher in kidneys from diethylmaleate-treated animals. Studies with brush border membrane vesicles indicated that glutathione depletion induced higher sodium-dependent glycine uptake in contrast with control preparations. This adaptation was not associated with an increment in either tau-glutamyltransferase activity or in protein concentrations. These results could explain in part the replenishment of GSH cellular levels in glutathione-depleted kidneys by means of higher transport capacity for glycine (a glutathione precursor) which was maintained even when GSH levels were restored.

Evidence for a secretory component in the handling of unconjugated bilirubin by the isolated perfused rat kidney.

Previous studies in rats have suggested that the urinary excretion of unconjugated bilirubin (UB) comprises only a small fraction of the pigment that reaches the tubular lumen by glomerular filtration and escapes from tubular cell reabsorption. However, additional data also indicated that UB interacts with renal peritubular cell membranes impairing the secretion of p-aminohippurate (PAH). In this study we examined the possibility of a secretory step which could also be involved in the renal excretory mechanism for UB. An isolated rat kidney preparation was used, and the uptake of UB by renal tissue, the UB appearance in the urine, and the secretion of PAH were analyzed throughout the perfusion. The results indicated that the UB urinary excretion rate changed independently of UB filtered load. The latter remained almost unchanged during the perfusion, whereas the excretion rate of UB and the UB-to-creatinine (Cr) clearance ratio increased significantly. Furthermore, a relationship between the uptake of UB by the kidney, the UB-to-Cr clearance ratio, and the decrease in PAH secretion rate, was proved. In addition, when probenecid was added to the perfusate solution the cumulative uptake of UB by the kidney and the rate of excretion of UB in the urine were diminished. We conclude that the mechanism of UB excretion by the kidney may be considered as the result of a process involving glomerular filtration plus tubular secretion followed by a back diffusion step from the lumen in a similar way to other endogenous compounds, thus explaining the virtual absence of UB from the normal urine.