The possible involvement of calcium in renal proximal tubular reabsorptive defect in the rat after release of ureteral obstruction

1990 ◽  
Vol 68 (6) ◽  
pp. 667-670
Author(s):  
V. Chatsudthipong ◽  
S. Sophasan ◽  
S. Jariyawat
Keyword(s):  
Ureteral Obstruction ◽  
Tubular Function ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Control Value ◽  
Proximal Tubular ◽  
Tubular Functions ◽  
Proximal Tubular Function ◽  
Renal Proximal Tubular ◽  
Renal Tubular

The temporal relationship between changes in cytosolic free calcium and proximal tubular function was examined in rats following 24 h of unilateral and bilateral ureteral obstruction. Immediately after release of unilateral ureteral obstruction, proximal tubular functions were found to be normal. Cytosolic free calcium in isolated proximal tubules of the ureteral obstructed and contralateral kidneys were 160 ± 8 and 172 ± 15 nM, respectively. On the 7th day after release, cytosolic free calcium was not different from the sham control value (135 ± 6 vs. 149 ± 7 nM). In contrast, immediately after release of bilateral ureteral obstruction, cytosolic free calcium was increased significantly to 219 ± 6 from 139 ± 9 nM in sham-operated controls. Subsequent declines in cytosolic free calcium to 196 ± 15 and 148 ± 7 nM were observed at 3 and 7 days after release of bilateral ureteral obstruction, respectively. Over this period, renal tubular functions gradually returned to normal. Changes in cytosolic free calcium correlate well with the reported improvement in renal tubular function after release of bilateral ureteral obstruction. Therefore, one possible mechanism for the impairment of tubular function observed in bilateral ureteral obstruction may be an increase in cytosolic free calcium.Key words: ureteral obstruction, cytosolic free calcium, renal proximal tubule, rat.

scholarly journals The soluble intracellular domain of megalin does not affect renal proximal tubular function in vivo

2010 ◽  
Vol 78 (5) ◽  
pp. 473-477 ◽  
Author(s):  
Annabel Christ ◽  
Sara Terryn ◽  
Vanessa Schmidt ◽  
Erik I. Christensen ◽  
Matthew R. Huska ◽  
...  
Keyword(s):  
Tubular Function ◽  
Intracellular Domain ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Renal Proximal Tubular ◽  
Renal Proximal Tubular Function

scholarly journals URINARY PROLACTIN: A NEW MARKER FOR THE RENAL PROXIMAL TUBULAR FUNCTION IN CHILDHOOD

1993 ◽  
Vol 33 ◽  
pp. S34-S34
Author(s):  
C De Felice ◽  
T Tanaka ◽  
J Itoh ◽  
K Hayakawa ◽  
I Hibi ◽  
...  
Keyword(s):  
Tubular Function ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Renal Proximal Tubular ◽  
Renal Proximal Tubular Function

scholarly journals Contrasting short-term effects of nifedipine on glomerular and tubular functions in glomerulonephritic patients.

1994 ◽  
Vol 5 (6) ◽  
pp. 1385-1390
Author(s):  
A Hartmann ◽  
K Lund ◽  
H Holdaas ◽  
P Fauchald ◽  
A Reisaeter ◽  
...  
Keyword(s):  
Tubular Function ◽  
Chronic Glomerulonephritis ◽  
Short Term ◽  
Proximal Tubular ◽  
Glomerular Hemodynamics ◽  
Proximal Tubular Function ◽  
Renal Tubular ◽  
Beta 2 Microglobulin ◽  
Renal Vascular ◽  
Short Term Effects

The short-term effects of nifedipine on glomerular hemodynamics, sieving function, and renal tubular function were assessed in 10 patients suffering from biopsy-verified chronic glomerulonephritis. Three weeks of nifedipine treatment after 2 wk of placebo significantly reduced the blood pressure from 153 +/- 6/90 +/- 3 to 139 +/- 6/84 +/- 4 mm Hg (mean +/- SE; P < 0.05). Renal vascular resistance was reduced from 0.54 +/- 0.10 to 0.46 +/- 0.08 mm Hg/mL per minute. However, GFR (44.3 +/- 7 mL/min), effective RPF (265 +/- 37 mL/min), and filtration fraction (0.17 +/- 0.01) remained unchanged. The excretion of albumin of 1,318 +/- 395 micrograms/min was not affected by nifedipine. The glomerular sieving estimated by use of the fractional dextran clearance technique revealed no significant change by nifedipine compared with placebo in the range of 30 to 60 A of hydrodynamic dextran radius. Fractional proximal reabsorption (lithium clearance method) was reduced by nifedipine from 53 +/- 5 to 46 +/- 4% (P < 0.05). Also, the excretion of beta 2-microglobulin and N-acetyl-beta-glucosaminidase increased from 10.98 +/- 4.62 to 11.86 +/- 4.74 mg/24 h (P < 0.05) and from 19.7 +/- 4.2 to 25.3 +/- 7.0 nmol/h per micromoles of creatinine (P = 0.05), respectively. It was concluded that nifedipine treatment acutely represses proximal tubular function but is without significant effect on glomerular sieving and albuminuria in these patients.

Erythrocyte Sodium/Lithium Countertransport and Renal Lithium Clearance in a Random Sample of Untreated Middle-Aged Men

1989 ◽  
Vol 77 (3) ◽  
pp. 337-342 ◽  
Author(s):  
Pasquale Strazzullo ◽  
Francesco P. Cappuccio ◽  
Maurizio Trevisan ◽  
Licia Iacoviello ◽  
Roberto Iacone ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fractional Excretion ◽  
Tubular Function ◽  
Proximal Tubular ◽  
Erythrocyte Sodium ◽  
Proximal Tubular Function ◽  
Renal Proximal Tubular ◽  
Relationship Of ◽  
The Relationship ◽  
Male Subjects

1. It has been proposed that the enhanced erythrocyte Na+/Li+ countertransport observed in many patients with essential hypertension could be a marker of abnormal renal proximal tubular function. We thus investigated the relationship of blood pressure and Na+/Li+ countertransport to an index of proximal tubular function such as renal Li+ clearance. 2. The study was carried out in a sample of 299 untreated male subjects (aged 21–59 years) randomly selected from a population at work. Na+/Li+ counter-transport was measured in a representative sub-group of 176 men. 3. We did not detect statistically significant correlation of either blood pressure or Na+/Li+ countertransport (Vmax) with fractional excretion of Li+, while confirming the existence of a significant continuous association of blood pressure and body mass index with Na+/Li+ countertransport (P < 0.01). 4. A sub-sample of 57 participants belonging to the lowest or the highest quintiles of Na+/Li+ counter-transport distribution repeated the Li+ clearance study after moderate Na+ restriction. 5. Although fractional excretions of Na+ and Li+ were reduced on the low Na+ diet (both P < 0.001), they did not differ significantly between groups. 6. Our results are at variance with the findings of a recent case-control study in a young age group and suggest that further studies are necessary before a conclusion can be drawn as to the suitability of Na+/Li+ countertransport as a marker of Na+ reabsorption in the renal proximal tubule.

scholarly journals Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice

2021 ◽  
Author(s):  
Stefan Wörner ◽  
Bernhard N. Bohnert ◽  
Matthias Wörn ◽  
Mengyun Xiao ◽  
Andrea Janessa ◽  
...  
Keyword(s):  
Protease Inhibitor ◽  
Serine Protease ◽  
Kidney Injury ◽  
Serine Protease Inhibitor ◽  
Tubular Function ◽  
Proteolytic Activation ◽  
Salt Diet ◽  
Low Salt ◽  
Proximal Tubular ◽  
Proximal Tubular Function

AbstractTreatment with aprotinin, a broad-spectrum serine protease inhibitor with a molecular weight of 6512 Da, was associated with acute kidney injury, which was one of the reasons for withdrawal from the market in 2007. Inhibition of renal serine proteases regulating the epithelial sodium channel ENaC could be a possible mechanism. Herein, we studied the effect of aprotinin in wild-type 129S1/SvImJ mice on sodium handling, tubular function, and integrity under a control and low-salt diet. Mice were studied in metabolic cages, and aprotinin was delivered by subcutaneously implanted sustained release pellets (2 mg/day over 10 days). Mean urinary aprotinin concentration ranged between 642 ± 135 (day 2) and 127 ± 16 (day 8) µg/mL . Aprotinin caused impaired sodium preservation under a low-salt diet while stimulating excessive hyperaldosteronism and unexpectedly, proteolytic activation of ENaC. Aprotinin inhibited proximal tubular function leading to glucosuria and proteinuria. Plasma urea and cystatin C concentration increased significantly under aprotinin treatment. Kidney tissues from aprotinin-treated mice showed accumulation of intracellular aprotinin and expression of the kidney injury molecule 1 (KIM-1). In electron microscopy, electron-dense deposits were observed. There was no evidence for kidney injury in mice treated with a lower aprotinin dose (0.5 mg/day). In conclusion, high doses of aprotinin exert nephrotoxic effects by accumulation in the tubular system of healthy mice, leading to inhibition of proximal tubular function and counterregulatory stimulation of ENaC-mediated sodium transport.

Sign in / Sign up

Export Citation Format

Share Document