Relation of Distal Nephron Changes to Proximal Tubular Damage in Uranyl Acetate-Induced Acute Renal Failure in Rats

2002 ◽  
Vol 22 (5-6) ◽  
pp. 405-416 ◽  
Author(s):  
Di Fei Sun ◽  
Yoshihide Fujigaki ◽  
Taiki Fujimoto ◽  
Tetsuo Goto ◽  
Katsuhiko Yonemura ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Uranyl Acetate ◽  
Tubular Damage ◽  
Distal Nephron ◽  
Proximal Tubular ◽  
Proximal Tubular Damage

Inhibition of tubular cell proliferation by neutralizing endogenous HGF leads to renal hypoxia and bone marrow-derived cell engraftment in acute renal failure

2008 ◽  
Vol 294 (2) ◽  
pp. F326-F335 ◽  
Author(s):  
Hiroyuki Ohnishi ◽  
Shinya Mizuno ◽  
Toshikazu Nakamura
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Repair Process ◽  
Tubular Cell ◽  
Tubular Damage ◽  
Renal Tubules ◽  
Stromal Cell Derived Factor ◽  
Renal Tubular

During the progression of acute renal failure (ARF), the renal tubular S3 segment is sensitive to ischemic stresses. For reversing tubular damage, resident tubular cells proliferate, and bone marrow-derived cells (BMDC) can be engrafted into injured tubules. However, how resident epithelium or BMDC are involved in tubular repair remains unknown. Using a mouse model of ARF, we examined whether hepatocyte growth factor (HGF) regulates a balance of resident cell proliferation and BMDC recruitment. Within 48 h post-renal ischemia, tubular destruction became evident, followed by two-waved regenerative events: 1) tubular cell proliferation between 2 and 4 days, along with an increase in blood HGF; and 2) appearance of BMDC in the tubules from 6 days postischemia. When anti-HGF IgG was injected in the earlier stage, tubular cell proliferation was inhibited, leading to an increase in BMDC in renal tubules. Under the HGF-neutralized state, stromal cell-derived factor-1 (SDF1) levels increased in renal tubules, associated with the enhanced hypoxia. Administrations of anti-SDF1 receptor IgG into ARF mice reduced the number of BMDC in interstitium and tubules. Thus possible cascades include 1) inhibition of tubular cell proliferation by neutralizing HGF leads to renal hypoxia and SDF1 upregulation; and 2) BMDC are eventually engrafted in tubules through SDF1-mediated chemotaxis. Inversely, administration of recombinant HGF suppressed the renal hypoxia, SDF1 upregulation, and BMDC engraftment in ARF mice by enhancing resident tubular cell proliferation. Thus we conclude that HGF is a positive regulator for eliciting resident tubular cell proliferation, and SDF1 for BMDC engraftment during the repair process of ARF.

New insights into the mechanisms involved in renal proximal tubular damage induced in vitro by ochratoxin A

2004 ◽  
Vol 18 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Alessandra Gennari ◽  
Patricia Pazos ◽  
Monica Boveri ◽  
Robert Callaghan ◽  
Juan Casado ◽  
...  
Keyword(s):  
Ochratoxin A ◽  
Tubular Damage ◽  
Proximal Tubular ◽  
Proximal Tubular Damage ◽  
Renal Proximal Tubular

The roles of apoptosis in uranyl acetate-Induced acute renal failure

Renal Failure ◽  
1998 ◽  
Vol 20 (5) ◽  
pp. 697-701 ◽  
Author(s):  
Koji Sano ◽  
Yoshihide Fujigaki ◽  
Naoki Lkegaya ◽  
Kazuhisa Ohishi ◽  
Katsuhiko Yonemura ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Uranyl Acetate

Glycine attenuates apoptotic cell death in uranyl acetate-induced acute renal failure in rats

2000 ◽  
Vol 4 (1) ◽  
pp. 24-28 ◽  
Author(s):  
H. Zhou ◽  
A. Kato ◽  
T. Miyaji ◽  
Y. Fujigaki ◽  
K. Sano ◽  
...  
Keyword(s):  
Renal Failure ◽  
Cell Death ◽  
Acute Renal Failure ◽  
Apoptotic Cell ◽  
Uranyl Acetate ◽  
Apoptotic Cell Death

Some Aspects of Nephrotoxicity of Paracetamol and Ketoprofen in Patients with Rheumathoid Arthritis

2016 ◽  
Vol 70 (3) ◽  
pp. 118-124
Author(s):  
Dejan Spasovski ◽  
Sonja Genadieva-Stavric ◽  
Tatjana Sotirova
Keyword(s):  
Colorimetric Method ◽  
Initial Therapy ◽  
Tubular Damage ◽  
Moderate Correlation ◽  
Time Intervals ◽  
Number Of Patients ◽  
Proximal Tubular ◽  
Proximal Tubular Damage

Abstract Introduction. To determine the effect of initial therapy with Paracetamol and Ketoprofen on glomerular and tubular integrity in rheumatoid arthritis (RA), to quantify nephrotoxicity of these two drugs by measurement of enzymuria, which correlates with the damage of tubular epithelium. Microalbuminuria is used as a marker for glomerular damage, and urine excretion of N-Acetyl-b-D-glucosaminidase (NAG) as an indicator of proximal tubular damage. Methods. Using colorimetric method for determination of NAG, and immunoturbidimetric method for microalbuminuria, samples of 70 participants were examined (35 RA patients treated with Paracetamol only, 35 RA patients treated with Ketoprofen). The follow-up was in 5 time-intervals in the course of 24 weeks. Results. There was a moderate correlation between NAG and microalbuminuria (r=0.16) in the group of patients treated with Paracetamol only, and a moderate correlation (r=0.28) in the group of patients treated with Ketoprofen. NAG enzymuria in size, by number of patients Registered, and time of appearance, was greater and appeared earlier in the Ketoprofen group compared to the Paracetamol group. Conclusions. Ketoprofen is more potent NAG inductor and provokes greater tubular enzymuria than Paracetamol. Results from our study confirm safety in use of Paracetamol and Ketoprofen in everyday clinical practice.

scholarly journals Possible Involvement of Myofibroblasts in Cellular Recovery of Uranyl Acetate-Induced Acute Renal Failure in Rats

2000 ◽  
Vol 157 (4) ◽  
pp. 1321-1335 ◽  
Author(s):  
Di Fei Sun ◽  
Yoshihide Fujigaki ◽  
Taiki Fujimoto ◽  
Katsuhiko Yonemura ◽  
Akira Hishida
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Uranyl Acetate

Pathogenetic mechanisms in experimental hemoglobinuric acute renal failure

1989 ◽  
Vol 256 (3) ◽  
pp. F446-F455 ◽  
Author(s):  
R. A. Zager ◽  
L. M. Gamelin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Damage ◽  
Iron Chelation ◽  
Proximal Tubular Cell ◽  
Radical Scavenger ◽  
Heme Uptake ◽  
Hydroxyl Radical Scavenger ◽  
Proximal Tubular ◽  
Hemoglobin Production

To evaluate mechanisms in hemoglobinuric acute renal failure (ARF) rats were infused with hemoglobin under aciduric or alkalinuric conditions. Aciduric rats developed azotemia, distal heme casts, and proximal tubular cell (PTC) necrosis, whereas alkalinuric rats developed no renal damage. Aciduria converted hemoglobin to met-hemoglobin, which precipitated, forming distal casts and inducing ARF. Hematin formation was not observed. The importance of met-hemoglobin production was indicated by its greater toxicity than hemoglobin during aciduria and by its ability to induce ARF even under alkalinuric conditions. A link between obstructing casts and PTC necrosis was identified; tubular obstruction induced by various mechanisms (met-hemoglobin casts; ureteral ligation; ischemic ARF) increased PTC hemoglobin uptake, producing lysosomal overload (giant endolysosomes) and PTC necrosis. This worsened ischemic ARF despite an otherwise subtoxic hemoglobin dose being used that had no discernible acute renal vasoconstrictive effect. Iron chelation (deferoxamine)/hydroxyl radical scavenger (Na benzoate) therapy did not mitigate this exacerbation of ischemic injury, suggesting a nonoxidant mechanism. We conclude that H is nephrotoxic, particularly when intratubular obstruction facilitates PTC heme uptake. Thus aciduria-induced met-hemoglobin cast formation and concomitant ischemic renal injury predispose to its nephrotoxic effect.

A COMPARISON OF THE EFFECTS OF PROXIMAL AND DISTAL TUBULAR DAMAGE ON THE ACTION OF DESOXYCORTICOSTERONE AND ALDOSTERONE

1957 ◽  
Vol 35 (1) ◽  
pp. 641-644
Author(s):  
T. F. Nicholson
Keyword(s):  
Left Kidney ◽  
Left Renal Artery ◽  
Tubular Damage ◽  
Normal Kidney ◽  
Significant Drop ◽  
Sodium Tartrate ◽  
Left Ureter ◽  
Proximal Tubular ◽  
Proximal Tubular Damage ◽  
Distal Tubules

The proximal tubules of the left kidney in dogs were damaged by the injection of 0.5% racemic sodium tartrate into the left renal artery. In other experiments the distal tubules were damaged by the injection of 0.05% mercuric chloride up the left ureter. In animals with proximal tubular damage, intravenous infusions of desoxycorticosterone or aldosterone which produced a significant drop in sodium excretion from the normal kidney had no effect on the amount of sodium excreted by the damaged kidney. In animals with distal tubular damage the effect of these hormones on the damaged kidney was as great as on the normal kidney.

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