Rise In Urinary Levels Research Articles

Changes in urinary kidney injury molecule-1 levels after blood transfusions in preterm infants

Literature supports an association between transfusions and gut injury in preterm infants. We hypothesized that packed red blood (PRBC) transfusions are associated with kidney inflammation marked by a rise in urinary levels of Kidney Injury Molecule 1 (KIM-1). Prospectively, KIM-1 levels were measured before and then at 6, 12 and 24 h after a PRBC transfusion. Results are presented as mean (± SD) and median (IQR). Thirty-four infants, birth weight 865 (± 375) g, had higher pretransfusion KIM-1 levels of 2270 (830, 3250) pg/mg than what is normal for age. These were not associated with hematocrit levels. KIM-1 levels peaked between 6 and 12 h after the transfusion. Levels peaked to 3300 (1990, 6830) pg/mg; levels returned to pretransfusion levels of 2240 (1240, 3870) pg/mg by 24 h, p < 0.01. The 24-h post-transfusion KIM-1 levels were similar to pretransfusion levels, p = 0.63. PRBC transfusions in preterm infants are associated with an elevation in urinary KIM-1 levels. The mechanism of this association may be important in studying transfusion associated organ injury. KIM-1, as an inflammatory marker, may be helpful in assessing the effect of different transfusion volumes or in evaluating operational thresholds of anemia in premature infants.

The effects of rhodium on the renal function of female Wistar rats

In recent years, the increased use of rhodium (Rh) as an active catalyst material in modern three-way automobile catalytic converters has led to a parallel rise in environmental levels of this metal. In spite of this, the literature contains few studies of the effects of Rh on human health.The aim of this study is to assess the effects of Rh on the renal function of female Wistar rats.Our findings show that sub-acute exposure to six increasing concentrations, ranging from 0.001 to 1mgL−1, of Rh (III) chloride hydrate in drinking water does not induce alterations in urinary albumin levels, while, at concentrations from 0.1 to 1mgL−1, a significant rise in urinary levels of Retinol Binding Protein is evident and an increasing trend in urinary β2-microglobulin, which becomes significant at 1mgL−1, is observed. These results therefore demonstrate a nephrotoxic action of Rh at tubular level in a wide range of doses. Interestingly, because of the recent increase in environmental Rh levels, these findings may have relevant implications both for occupationally exposed subjects and for the general population, especially children.

Differential response of angiotensin peptides in the urine of hypertensive animals

Urinary excretion rates of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin-(1–7) [Ang-(1–7)] were determined in normotensive Sprague Dawley (SD), spontaneously hypertensive (SHR), and mRen-2 transgenic hypertensive animals before and following blockade of Ang II synthesis or activity for two weeks. This study was performed to determine for the first time whether inhibition of Ang II alters the excretion of angiotensin peptides in the urine. Rats were given either tap water or water medicated with lisinopril, losartan or both agents in combination. Blood pressure was monitored at regular intervals during the experiment by the tail-cuff method, and once again at the end of the study with a catheter implant into a carotid artery. Metabolic studies and 24 h urinary excretion variables and angiotensin peptides were determined before and during the procedures. While all three treatments normalized the blood pressure of hypertensive animals, therapy with either lisinopril or the combination of lisinopril and losartan had a greater antihypertensive effect in both SHR and [mRen-2]27 transgenic hypertensive rats. In the urine, the concentration of the angiotensins (normalized by 24-h creatinine excretion) was several-fold higher in the untreated hypertensive animals than in normotensive SD rats. In SD rats, lisinopril or lisinopril and losartan produced a sustained rise in urinary levels of Ang-(1–7) without changes in the excretion of Ang I and Ang II. In contrast, Ang I and Ang-(1–7) were significantly elevated in SHR medicated with lisinopril alone or in combination with losartan. Only losartan, however, augmented urinary levels of Ang II in the SHR. The antihypertensive effects of the three separate regimens had no effect on the urinary excretion of angiotensin peptides in [mRen-2]27 transgenic hypertensive rats. These data show that Ang I and Ang-(1–7) are excreted in large amounts in the urine of SD, SHR and [mRen-2]27 hypertensive rats. The unchanged Ang-(1–7) excretion in transgenic hypertensive (Tg +) rats after inhibition of the renin–angiotensin system agrees with the previous finding of a reduced plasma clearance of the peptide in this model of hypertension. The data suggest that this form of hypertension may be associated with increased activity of an endogenous converting enzyme inhibitor.

Involvement of thromboxane A2 and prostacyclin in the early pulmonary hypertension after porcine meconium aspiration.

Severe perinatal aspiration of meconium is frequently complicated by unsuccessful neonatal adaptation with associated pulmonary hypertension. This vascular complication is supposedly related to pulmonary release of vasoconstrictory agents, including metabolites of arachidonic acid. Thus, to investigate the role of prostanoids on these meconium-induced circulatory changes in the lungs, the hemodynamic response to meconium instillation was studied in acetylsalicylic acid-pretreated juvenile pigs. Twelve 10-wk-old pigs with adapted lung circulation received 3 mL/kg of 65 mg/mL human meconium via the endotracheal tube. Six of them were medicated with 10 mg/kg acetylsalicylic acid 30 min before meconium insufflation. Hemodynamic parameters and urinary excretion of stable metabolites of thromboxane A2 and prostacyclin were measured serially for 6 h after the insult. Meconium administration induced a biphasic increase in mean pulmonary artery pressure and pulmonary vascular resistance, and a rapid rise in urinary levels of prostanoid metabolites. Acetylsalicylic acid pretreatment prevented the initial (0-1 h) pulmonary hypertensive response and increase in prostanoid excretion. During the second phase (1-6 h), acetylsalicylic acid did not attenuate the progressive increase in mean pulmonary artery pressure and pulmonary vascular resistance nor did it affect the longitudinal distribution of the pulmonary resistances. Our results thus show that in adapted porcine lungs, arachidonic acid metabolites contribute to the early hypertensive response, but have only minor effects during the second phase vascular hypertension.

Elevation in urinary levels of pyridinium cross-links of collagen following chymopapain-induced degradation of articular cartilage in the rabbit knee provides evidence of metabolic changes in bone

To measure urinary levels of two pyridinium cross-links of collagens at various times, rabbits were injected in the left knee with 0.2 mg (N = 11) or 2.0 mg chymopapain (N = 11). Urinary levels of the bone-specific deoxy-pyridinoline cross-link and of the hydroxylysyl pyridinoline cross-link, found in large amounts in articular cartilage and bone, were measured by high performance liquid chromatography (HPLC). The urinary levels were correlated with histological evidence of progressive articular cartilage destruction in animals injected with 2.0 mg chymopapain and of successful repair in rabbits injected with the lower dose. Rabbits injected with 2.0 mg chymopapain showed a very large increase in urinary levels of deoxy-pyridinoline during the first 30 days after the injection. This rise was not seen in animals injected with the lower dose. A rise in urinary level of the hydroxylysyl pyridonline cross-link was observed in all rabbits but was more pronounced and lasted longer in animals receiving the higher dose. The failure of rabbits injected with 2.0 mg chymopapain to repair the damaged articular cartilage was strongly associated with a marked increase in the catabolism of the bone-specific deoxy-pyridinoline cross-link and to a lesser extent with the catabolism of the hydroxylysyl pyridinoline found in bone and in articular cartilage.

The role of the adrenal cortex in the normal adaptation to dietary sodium deprivation.

During short periods of rigid dietary sodium deprivation, there was no significant change in the urinary output of total 17-hydroxycorticoids in a normal subject and in a patient with intact adrenals given a constant quantity of cortisone orally. The urinary excretion of cortisol and cortisone was also unaffected under these circumstances. The administration of a constant dose of prednisone or deoxycorticosterone to patients with Addison's disease did not permit normal adaptation to acute dietary sodium deprivation, although the latter was much more effective than the former. These observations tend to emphasize the physiologic importance of a rise in the urinary excretion of aldosterone in the adaptation to sodium restriction, and it would appear that the rise in urinary levels of aldosterone during a low sodium diet is a reflection of an increased secretion of this hormone rather than a result of alteration in its intermediary metabolism.

Urinary excretion of oestrogens during pregnancy, lactation, and the re-establishment of menstruation.

A new chemical method for estimating the urinary excretion of estriol estrone and estradiol 17beta during conception pregnancy puerperium lactation and resumption of menstruation postpartum is described and used to measure these levels in women; the results of 4 are presented here. 2 subjects were studied for levels of urinary estrogens over a period which included a complete menstrual cycle and the cycle in which pregnancy started. In both women the urinary estrogen levels were similar in the 2 cycles up to about Day 24 showing ovulation peaks and subsequent luteal rise. In the first cycle estrogen levels then decreased before onset of menstruation but in the second pregnancy cycle estrogen concentrations continued to increase increasing rapidly about 7 weeks after the last menstrual period. In all 4 subjects (results are presented both in a logarithmic scale and in tabular form) there was a rapid rise in urinary levels of the 3 estrogens throughout pregnancy which was greatest from Weeks 6-12. The estrone and estradiol levels at labor were 100 times higher than those during the luteal phase of the menstrual cycle with the estradiol levels being about one-third of the estrone levels. The urinary estriol levels rose about 1000-fold during this time. 1 subject followed after delivery showed that during the first menstrual periods after delivery ovulation did take place but the luteal phases were abnormally short.