Induction of an experimental fanconi syndrome in mice: Its effect on the glomerular filtration function studied by 99mTc-DTPA

Sawas-Dimopoulou, C.; Sigalas, Ilias R.; Margaritis, Loukas H.

doi:10.1016/0969-8051(96)00077-7

Cited by 5 publications

(10 citation statements)

References 24 publications

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“…Verani and others (1982) evaluated the extent of morphological injury in the kidney of rats with MA-induced Fanconi syndrome, and found evidence that the injury and necrosis occurred only in the proximal tubular system, primarily in the medullary rays and outer stripes of the medulla, but not in the distal tubules and collecting ducts. Glomerular filtration rate (GFR) was decreased as has been reported in other forms of idiopathic or acquired Fanconi syndrome (Arend and others 1986, Sawas-Dimopoulo and others 1996). The lowest single dose of MA reported to cause tubular necrosis in dogs was 9 mg/kg, administered to healthy beagle dogs in order to evaluate potential nephrotoxicity of pravadoline maleate (Everett and others 1993).…”

Section: Introductionmentioning

confidence: 65%

Acute kidney injury in three dogs after ingestion of a descaling agent containing maleic acid

Schweighauser

Francey

Gurtner

et al. 2015

Vet Record Case Reports

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Maleic acid (MA) is a common component of descaling products and is widely used in daily life. Accidental ingestion in relevant amounts does not play a major role in human beings; however, it seems to be highly toxic for dogs. It has been commonly used experimentally to induce Fanconi syndrome in dogs or small rodents. Two dogs were presented for acute kidney injury (AKI) after accidental ingestion of a descaling agent containing MA at an estimated amount of 70 mg/kg each. The third dog involved was euthanased by the referring veterinarian, and postmortem pathological analysis revealed severe acute tubular necrosis consistent with toxic nephropathy. The other dogs received symptomatic therapy for AKI including treatment with haemodialysis and showed complete normalisation of serum creatinine at a follow-up after five months. Renal damage can be very severe, but seems to be at least partially reversible and an attempt to treatment is warranted.

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Section: Introductionmentioning

confidence: 65%

Acute kidney injury in three dogs after ingestion of a descaling agent containing maleic acid

Schweighauser

Francey

Gurtner

et al. 2015

Vet Record Case Reports

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“…The present MAL-induced mouse Fanconi syndrome model was described by Dimopoulou et al 27 The model includes urine biochemistry changes similar to those reported for patients with Fanconi syndrome. In the study by Dimopoulou et al, urinary excretion of amino acids was significantly elevated within 30 min after injection of MAL (6 mmol/kg body weight intraperitoneal), and continued to increase with time.…”

Section: Discussionmentioning

confidence: 88%

“…In the study by Dimopoulou et al, urinary excretion of amino acids was significantly elevated within 30 min after injection of MAL (6 mmol/kg body weight intraperitoneal), and continued to increase with time. 27 Dimopoulou et al also reported that 99mTc-DTPA, a radiopharmaceutical freely excreted by glomerular filtration, exhibits significantly delayed pharmacokinetics as a dose-dependent effect. 27 Dimopoulou et al also reported that 99mTc-DTPA, a radiopharmaceutical freely excreted by glomerular filtration, exhibits significantly delayed pharmacokinetics as a dose-dependent effect.…”

Section: Discussionmentioning

confidence: 98%

“…27 Marked aminoaciduria in mice after MAL injection is characterized by multifold increases in levels of most amino acids present in urine of normal mice, and by significant concentrations of neutral amino acids (e.g., phenylalanine, leucine and tyrosine) that are not present in significant quantities in normal urine. 27 Dimopoulou et al suggested that 99mTc-DTPA is an effective marker for early detection of abnormal GFR in Fanconi syndrome. Although 99mTc-DTPA does not accumulate in normal renal cortex, accumulation is seen in the renal cortex of the present model of Fanconi syndrome, suggesting that the renal cortex in the present model is abnormal.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulation of amino acids in the S 1 region of the renal cortex may reflect renal handling of amino acids. 27 Particularly for changes to renal accumulation in the S 1 region of the renal cortex, the results obtained for 125I-IMT were compared with results for 3 clinical renal radiopharmaceuticals: 99mTc-DMSA, 99mTc-mercaptoacetylglycylglycylglycine (99mTc-MAG3), and 99mTcdiethylenetriaminepentaacetic acid (99mTc-DTPA). The present study evaluated use of ~23I-3-iodo-c~methyl-L-tyrosine (J23I-IMT) as a renal functional imaging agent for detection of Fanconi syndrome.…”

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confidence: 99%

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Detection of maleate-induced Fanconi syndrome by decreasing accumulation of125I-3-iodo-a-methyl-L-tyrosine in the proximal tubule segment-1 region of renal cortex in mice: A trial of separate evaluation of reabsorption

et al. 2006

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Aldehyde dehydrogenase 2 alleviates mitochondrial dysfunction by promoting PGC-1α-mediated biogenesis in acute kidney injury

Shi

Chen

et al. 2023

Cell Death Dis

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Renal tubular epithelial cells are one of the high energy-consuming cell types, which mainly depend on mitochondrial energy supply. Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme that is involved in alcohol metabolism and mitochondrial oxidative ATP production; however, its function in mitochondrial homoeostasis in acute kidney injury (AKI) is unclear. Here, we found that ALDH2 expression was predominantly decreased in cisplatin or maleic acid (MA) models both in vivo and in vitro. ALDH2 knockout (KO) mice exhibited exacerbated kidney impairment and apoptosis of tubular epithelial cells after cisplatin injection. In contrast, ALDH2 activation alleviated AKI and tubular cell apoptosis in both cisplatin- and MA-induced models. RNA sequencing revealed that the oxidative phosphorylation pathway was positively enriched in the renal tissues after Alda-1 pre-treatment in MA-induced mice. ALDH2 activation restored mitochondrial structure, mitochondrial membrane potential, and respiration rate, but downregulated glycolysis in MA-induced mice and human renal proximal tubular epithelial (HK-2) cells. Mechanistically, co-immunoprecipitation assays revealed that ALDH2 interacts with peroxisomal proliferator-γ coactivator-1α (PGC-1α), a master regulator of mitochondrial biogenesis, and advanced its nuclear translocation. Subsequently, PGC-1α knockdown almost abolished the improvement of ALDH2 activation on MA-induced tubular epithelial cells damage. Thus, our study revealed that ALDH2 activation alleviated mitochondrial dysfunction in AKI by enhancing PGC-1α-mediated mitochondrial biogenesis. Hence, ALDH2 may act as a potential therapeutic target to prevent AKI progression.

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Induction of an experimental fanconi syndrome in mice: Its effect on the glomerular filtration function studied by 99mTc-DTPA

Cited by 5 publications

References 24 publications

Acute kidney injury in three dogs after ingestion of a descaling agent containing maleic acid

Acute kidney injury in three dogs after ingestion of a descaling agent containing maleic acid

Detection of maleate-induced Fanconi syndrome by decreasing accumulation of125I-3-iodo-a-methyl-L-tyrosine in the proximal tubule segment-1 region of renal cortex in mice: A trial of separate evaluation of reabsorption

Aldehyde dehydrogenase 2 alleviates mitochondrial dysfunction by promoting PGC-1α-mediated biogenesis in acute kidney injury

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