Effect of renal ischemia on urinary excretion of lithium in rats

Uwai, Yuichi; Suzuki, Tomoyuki; Kondo, Ryota; Kawasaki, Tatsuya; Nabekura, Tomohiro

doi:10.1002/bdd.2163

Cited by 3 publications

(5 citation statements)

References 16 publications

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“…The plasma concentrations of lithium were in the therapeutic range (Table 2). The renal clearance and the fractional excretion of lithium of the control group (Table 2) were comparable to our previous values that were obtained from the experiments with the lithium injection as a bolus [15,16]. Fanconi syndrome decreased the renal clearance of lithium, and no effect on the fractional excretion of lithium was recognized (Table 2).…”

Section: Discussion/conclusionsupporting

confidence: 85%

“…In the previous and the present studies, we showed that the renal clearance of lithium was decreased by S-flurbiprofen, renal ischemia, and Fanconi syndrome in rats [15,16]. And, S-flurbiprofen decreased the fractional excretion of lithium, and no effect of renal ischemia and Fanconi syndrome on the ratio was recognized [15,16]. Our animal studies indicate the heterogeneity in the effects of renal failures on the renal handling of lithium, suggesting that it is significant to examine effect of each renal failure on the lithium reabsorption as well as glomerular filtration.…”

Section: Discussion/conclusionsupporting

confidence: 57%

“…The correlation coefficient between creatinine clearance and lithium clearance of 303 data from 90 patients was calculated to be 0.4548 [25], and it is suggested that creatinine clear-ance may be a poor surrogate for the renal clearance of lithium exceptionally. In the previous and the present studies, we showed that the renal clearance of lithium was decreased by S-flurbiprofen, renal ischemia, and Fanconi syndrome in rats [15,16]. And, S-flurbiprofen decreased the fractional excretion of lithium, and no effect of renal ischemia and Fanconi syndrome on the ratio was recognized [15,16].…”

Section: Discussion/conclusionsupporting

confidence: 55%

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Effect of Experimental Fanconi Syndrome on Tubular Reabsorption of Lithium in Rats

Uwai¹,

Nabekura²

2021

Pharmacology

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Lithium, administered to patients of bipolar disorders, is mainly excreted into urine, and tubular reabsorption at the proximal tubule is involved in the renal handling of lithium. In this study, we examined the renal excretion of lithium in rats with Fanconi syndrome, characterized by defects of transports of various compounds at the proximal tubules, induced by maleic acid. After maleic acid was intravenously injected, mannitol and lithium chloride were infused in turn. Using samples of plasma and bladder urine during the mannitol infusion, renal parameters were determined. Pharmacokinetic parameters of lithium were obtained using samples during the lithium chloride infusion. Maleic acid decreased creatinine clearance and increased the fractional excretion of glucose and phosphate, suggesting the induction of Fanconi syndrome. In rats with Fanconi syndrome, plasma concentration of lithium was increased, and its renal clearance was decreased. No effect on the fractional excretion of lithium was exhibited. This study represents that the tubular reabsorption of lithium was impaired to the same degree with glomerular filtration in rats with experimental Fanconi syndrome and that the dysfunction of the tubular reabsorption of glucose and phosphate was more severe. It is possible that Fanconi syndrome inhibited the reabsorption of lithium at the proximal tubule and facilitated the reabsorption of lithium from the loop of Henle to the collecting duct.

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Section: Discussion/conclusionsupporting

confidence: 85%

Section: Discussion/conclusionsupporting

confidence: 57%

Section: Discussion/conclusionsupporting

confidence: 55%

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Effect of Experimental Fanconi Syndrome on Tubular Reabsorption of Lithium in Rats

Uwai¹,

Nabekura²

2021

Pharmacology

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“…Lithium salts serve as mood-stabilizing and psychotropic agents (Dangana et al, 2019;Hart et al, 2020;Menshanov et al, 2016;Vosahlikova et al, 2020;Zhang et al, 2021) in patients with bipolar disorders (BDs) (Gehrmann et al, 2021;Luu & Rodway, 2018;Sung et al, 2019;Uwai et al, 2018), mania (Manto, 2012) and chronic depression (Medi c et al, 2020;Zhang et al, 2021). Lithium salts are also found in groundwater and drinking water, as recorded in the USA (Lindsey et al, 2021) and China (Shanghai) (Shen et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Maternal LiCl exposure disrupts thyroid–cerebral axis in neonatal albino rats

Mohammed

Ahmed

2021

Intl J of Devlp Neuroscience

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This work aimed to elucidate whether maternal lithium chloride (LiCl) exposure disturbs the thyroid-cerebral axis in neonatal albino rats. 50 mg of LiCl/ kg b.wt. is orally given for pregnant Wistar rats from gestational day (GD) 1 to lactation day (LD) 28. The maternal administration of LiCl induced follicular dilatation and degeneration, hyperplasia, lumen obliteration and colloid vacuolation in the maternal and neonatal thyroid gland at postnatal days (PNDs) 14, 21 and 28. Neuronal degeneration (spongiform), gliosis, nuclear pyknosis, perivascular oedema, and meningeal hyperaemia were observed in the neonatal cerebral cortex of the maternal LiCl-treated group at examined PNDs. This disturbance appears to depend on intensification in the neonatal cerebral malondialdehyde (MDA), nitric oxide (NO), and hydrogen peroxide (H 2 O 2 ) levels, and attenuation in the glutathione (GSH), total thiol (t-SH), catalase (CAT), and superoxide dismutase (SOD) levels. In the neonatal cerebrum, the fold change in the relative mRNA expression of deiodinases (DII and DIII) increased significantly at PNDs 21 and 14, respectively, in the maternal LiCltreated group. These data suggest that maternal LiCl may perturb the thyroidcerebrum axis generating neonatal neurodevelopmental disorder.

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“…Lithium salts are psychotropic mood-stabilizing agents (Dangana, Michael, Omolekulo, Areola, & Olatunji, 2019;Hart, Perlis, & McCoy, 2020;Menshanov, Bannova, & Dygalo, 2016;Zhang, He, Yang, Li, & Cai, 2019) used for treating bipolar disorders (Luu & Rodway, 2018;Sung et al, 2019;Uwai, Suzuki, Kondo, Kawasaki, & Nabekura, 2018). Lithium salts are found in some natural mineral water (Dawson, 1991), vegetables and grains (0.5-3.4 mg/kg), meat (0.012 mg/kg) and dairy products (0.5 mg/kg) (Laurie Mischley, 2014).…”

Section: Introductionmentioning

confidence: 99%

Maternal lithium chloride exposure alters the neuroendocrine‐cytokine axis in neonatal albino rats

Mohammed

Ahmed

2020

Intl J of Devlp Neuroscience

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The aim of this work was to clarify whether maternal lithium chloride (LiCl) exposure disrupts the neonatal neuroendocrine‐cytokine axis. Pregnant Wistar rats were orally administrated 50 mg LiCl/kg b.wt. from gestational day (GD) 1 to postpartum day 28. Maternal administration of LiCl induced a hypothyroid state in both dams and their neonates compared to the control dams and neonates at lactation days (LDs) 14, 21 and 28, where the levels of serum free triiodothyronine (FT3) and free thyroxin (FT4) were decreased and the level of serum thyrotropin (TSH) level was increased. A noticeable depression in maternal body weight gain, neonatal body weight and neonatal serum growth hormone (GH) was observed on all examined postnatal days (PNDs; 14, 21 and 28). A single abortion case was recorded at GD 17, and three dead neonates were noted at birth in the LiCl‐treated group. Maternal administration of LiCl disturbed the levels of neonatal serum tumor necrosis factor‐alpha (TNF‐α), transforming growth factor‐beta (TGF‐β), interleukin‐1 beta (IL‐1β), interferon‐gamma (INF‐γ), leptin, adiponectin and resistin at all tested PNDs compared to the control group. This administration produced a stimulatory action on the level of neonatal cerebral serotonin (5‐HT) at PND 14 and on the level of neonatal cerebral norepinephrine (NE) at PNDs 21 and 28. However, this administration produced an inhibitory action on the level of neonatal cerebral dopamine (DA) at all examined PNDs and on the level of neonatal cerebral NE at PND 14 and the level of neonatal cerebral 5‐HT at PNDs 21 and 28 compared to the corresponding control group. Thus, maternal LiCl exposure‐induced hypothyroidism disrupts the neonatal neuroendocrine‐cytokine system, which delay cerebral development.

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Effect of renal ischemia on urinary excretion of lithium in rats

Cited by 3 publications

References 16 publications

Effect of Experimental Fanconi Syndrome on Tubular Reabsorption of Lithium in Rats

Effect of Experimental Fanconi Syndrome on Tubular Reabsorption of Lithium in Rats

Maternal LiCl exposure disrupts thyroid–cerebral axis in neonatal albino rats

Maternal lithium chloride exposure alters the neuroendocrine‐cytokine axis in neonatal albino rats

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