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Renal Tubular Function (renal + tubular_function)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Renal tubular function in children with ,-thalassemia minor

NEPHROLOGY, Issue 5 2005
SÜLEYMAN KALMAN
SUMMARY: Background: , -thalassemia minor is a common heterozygous haemoglobinopathy that is characterized by both microcytosis and hypochromia. It requires no treatment. It has been postulated that low-grade haemolysis, tubular iron deposition and toxins derived from erythrocytes might cause renal tubular damage in adult patients with , -thalassemia minor. Our aim was to investigate the renal tubular functions in children with ,-thalassemia minor and to determine its possible harmful effects. Methods: The study was conducted on 32 children (14 female and 18 male) at the age of 5.8 ± 3.1 years (range 2,14 years) with , -thalassemia minor. The patients were classified as anaemic (haemoglobin (Hb) , 11 g/dL) (Group 1, n = 14) and non-anaemic (Hb > 11 g/dL) (Group 2, n = 18). A control group was formed with 18 healthy children whose ages and sexes match those in other groups (Group 3, n = 18). Fractional excretion of sodium (FENa, %), fractional excretion of magnesium (FEMg, %), fractional excretion of uric acid (FEUA, %) and tubular phosphorus reabsorption (TPR,%) were calculated with standard formulas. Urinary calcium excretion (mg/kg per 24 h), zinc (Zn) (µg/dL), glucosuria (mg/dL), , -2 microglobulin (mg/dL) and N -acetyl- ,,D-glycosaminidase (NAG, U/mmol creatinine) levels were measured through biochemical methods. Results: There was no statistically significant difference among the three groups in terms of the results of FENa (%), FEMg (%), FEUA (%), TPR (%), calciuria (mg/kg per 24 h), NAG, urine Zn, proteinuria, glucosuria or urine , - 2 microglobulin levels (P > 0.05). Conclusion: On the contrary of children with , -thalassemia major, renal tubular dysfunction has not been determined in children with , -thalassemia minor in the present study. [source]

Clinicopathology of childhood-onset renal systemic lupus erythematosus

NEPHROLOGY, Issue 4 2007
WASIU A OLOWU
SUMMARY: Aims: To determine the clinicolaboratory renal manifestations; glomerular, extra-glomerular histopathologic lesions; renal tubular dysfunction (RTD) frequency and outcome of a short-term renal follow up in Nigerian children with systemic lupus erythematosus (SLE). Methods: A non-randomized prospective study of consecutive cases of childhood-onset SLE with nephropathy was conducted. Baseline/follow-up clinicolaboratory data were collected. Each patient was followed up for 12 months. Results: Seven of the 11 children studied were girls. The median age at diagnosis was 11.0 years. Median diagnosis time interval (1.9 years) and median time of renal disease onset (1.0 year) were similar. Hypertension, nephrotic syndrome and acute renal failure (ARF) occurred in 45.5%, 54.5% and 63.7% of the patients, respectively. The glomerular lesions were non-proliferative lupus nephritis (LN) in 9.0% (class II LN); focal (class III LN) and diffuse (class IV LN) proliferative LN (PLN) in 27.0% and 64.0%, respectively. Tubulointerstitial nephritis (TIN, 91.0%) and RTD (64.0%) were common. ARF (P = 0.033) and RTD (P = 0.015) were significantly associated with severe TIN. Complete renal remission rate at end-point was 71.4%. Relapse and renal survival rates were 14.3% and 86.0%, respectively. RTD was persistent in 43.0%. Conclusion: Renal function disorders, diffuse PLN and extra-glomerular lesions were frequent. Significant association of ARF and RTD with severe TIN in this series suggests the need for early renal tubular function (RTF) assessment in our SLE patients. Deranged RTF may be marker of severe TIN in SLE warranting early confirmatory renal biopsy and aggressive interventional treatment. [source]

Evaluation of renal tubular function in children taking anti-epileptic treatment

NEPHROLOGY, Issue 6 2006
BULENT UNAY
SUMMARY: Aim: To assess the effects of anti-epileptic drugs on renal tubular function. Methods: Urinary N-acetyl-,-D-glucosaminidase activity was measured in 114 epileptic children (mean age 5.6 ± 1.1 years) who were undergoing monotherapy with valproate (n = 46), carbamazepine (n = 34), lamotrigine (n = 13) and combined therapy with valproate+carbamazepine (n = 21). Results: The urinary N-acetyl-,-D-glucosaminidase index of valproate (P < 0.01), carbamazepine (P < 0.05) and polytherapy group (P < 0.01) were significantly elevated when compared with that of the control group. No significant difference in N-acetyl-,-D-glucosaminidase levels was found between the lamotrigine group and the control subjects. We found that the distribution of the N-acetyl-,-D-glucosaminidase values of patients depended significantly on the length of therapy (P < 0.01). The level of urinary excretion of N-acetyl-,-D-glucosaminidase was significantly higher in the patients who were taking long-term treatment (>10 years) with valproate, carbamazepine and combined therapy than those taking therapy shorter than 10 years (P < 0.01). The mean serum concentrations of valproate and carbamazepine were 68.7 ± 17.44 µg/mL and 5.41 ± 1.23 µg/mL, respectively. There was a significant correlation between the serum concentration of valproate and urinary N-acetyl-,-D-glucosaminidase levels (r = 0.44, P < 0.01). There was also a significant correlation between the serum concentration of carbamazepine and N-acetyl-,-D-glucosaminidase excretion (r = 0.52, P < 0.01). Conclusion: The present study demonstrated that in patients treated with valproate and carbamazepine, an impairment of tubular function can be present, whereas lamotrigine does not cause any significant change. [source]

Increased Hepatic and Decreased Urinary Metallothionein in Rats after Cessation of Oral Cadmium Exposure

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2010
Yihuai Liang
Wistar rats of both genders were given CdCl2 in drinking water at daily doses of 0, 2.5, 5.0 or 10.0 mg Cd/kg body-weight for 12 weeks. Half of the animals were then killed; the others were given Cd-free water for the following 16 weeks, i.e. until 28 weeks after start of the experiment (28-week rats). We observed dose-dependent increases in the levels of MT in the tissues of rats 12 weeks after beginning the experiment (12-week rats). After the exposure ceased, levels of MT in the 28-week rats changed in three ways: an increase in the liver, persistence in the kidney cortex and a decrease in the medulla, relative to those levels in their 12-week counterparts. Biomarkers of kidney dysfunction were determined to be urinary MT (UMT) and urinary N -acetyl-,- d -glucosaminidase (UNAG). After 12 weeks, we observed dose-related statistically significant increases in UMT and UNAG in all of the Cd-exposed groups. A statistically significant decrease for UNAG between the 12- and 28-week rats occurred among males at the lowest Cd dose and for UMT in all of the Cd-exposed groups. The unchanged tissue levels of MT in the kidney cortex suggest that decreased UMT is a sign either of (i) decreased transport of Cd-MT from the liver via blood plasma to the renal tubules or (ii) increased tubular reabsorption and recovery of renal tubular function. [source]