Renal Tubular Damage (renal + tubular_damage)

Distribution by Scientific Domains


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]


Evaluation of the effect of triterpenes on urinary risk factors of stone formation in pyridoxine deficient hyperoxaluric rats

PHYTOTHERAPY RESEARCH, Issue 6 2002
Lakshminarasimhan Vidya
Abstract Investigations were carried out to evaluate the efficacy of the pentacyclic triterpene, lupeol and its ester, lupeol linoleate, against calcium oxalate urolithiasis in rats. Administration of a pyridoxine deficient diet containing 3% glycollic acid for 21 days led to increased excretion of stone forming constituents such as calcium, oxalate and uric acid. Crystal deposition and subsequent renal tubular damage resulted in increased excretion of the tubular enzymes alkaline phosphatase, lactate dehydrogenase, , glutamyl transferase, , glucuronidase and N -acetyl glucosaminidase along with reduced fibrinolytic enzymes. A reduction in the urinary inhibitory factors magnesium and glycosaminoglycans was also observed. Treatment with lupeol and lupeol linoleate reduced the extent of tubular damage as evidenced from reduced enzymuria and minimized the excretion of stone forming constituents. Copyright © 2002 John Wiley & Sons, Ltd. [source]


Exogenous bone marrow cells do not rescue non-irradiated mice from acute renal tubular damage caused by HgCl2, despite establishment of chimaerism and cell proliferation in bone marrow and spleen

CELL PROLIFERATION, Issue 4 2008
T.-C. Fang
Objective: Various studies have shown that bone marrow stem cells can rescue mice from acute renal tubular damage under a conditioning advantage (irradiation or cisplatin treatment) favouring donor cell engraftment and regeneration; however, it is not known whether bone marrow cells (BMCs) can contribute to repair of acute tubular damage in the absence of a selection pressure for the donor cells. The aim of this study was to examine this possibility. Materials and methods: Ten-week-old female mice were assigned into control non-irradiated animals having only vehicle treatment, HgCl2 -treated non-irradiated mice, HgCl2 -treated non-irradiated mice infused with male BMCs 1 day after HgCl2, and vehicle-treated mice with male BMCs. Tritiated thymidine was given 1 h before animal killing. Results: Donor BMCs could not alleviate non-irradiated mice from acute tubular damage caused by HgCl2, deduced by no reduction in serum urea nitrogen combined with negligible cell engraftment. However, donor BMCs could home to the bone marrow and spleen and display proliferative activity. This is the first report to show that despite no preparative myeloablation of recipients, engrafted donor BMCs can synthesize DNA in the bone marrow and spleen. Conclusions: Exogenous BMCs do not rescue non-irradiated mice from acute renal tubular damage caused by HgCl2, despite establishment of chimerism and cell proliferation in bone marrow and spleen. [source]