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Moderate Renal Failure Accentuates T1 Signal Enhancement in the Deep Cerebellar Nuclei of Gadodiamide-Treated Rats

View Article: PubMed Central - PubMed

ABSTRACT

Objectives: The purpose of this preclinical study was to investigate whether moderate chronic kidney disease is a factor in potentiating gadolinium (Gd) uptake in the brain.

Materials and methods: A comparative study was performed on renally impaired (subtotal nephrectomy) rats versus rats with normal renal function. The animals received 4 daily injections of 0.6 mmol Gd/kg a week for 5 weeks (cumulative dose of 12 mmol Gd/kg) of gadodiamide or saline solution. The MR signal enhancement in the deep cerebellar nuclei was monitored by weekly magnetic resonance imaging examinations. One week after the final injection, the total Gd concentration was determined by inductively coupled plasma mass spectrometry in different regions of the brain including the cerebellum, plasma, cerebrospinal fluid, parietal bone, and femur.

Results: After the administration of gadodiamide, the subtotal nephrectomy group presented a significantly higher T1 signal enhancement in the deep cerebellar nuclei and a major increase in the total Gd concentration in all the studied structures, compared with the normal renal function group receiving the same linear Gd-based contrast agent. Those potentiated animals also showed a pronounced hypersignal in the choroid plexus, still persistent 6 days after the last injection, whereas low concentration of Gd was found in the cerebrospinal fluid (<0.05 μmol/L) at this time point. Plasma Gd concentration was then around 1 μmol/L. Interestingly, plasma Gd was predominantly in a dissociated and soluble form (around 90% of total Gd). Total Gd concentrations in the brain, cerebellum, plasma, and bones correlated with creatinine clearance in both the gadodiamide-treated groups.

Conclusions: Renal insufficiency in rats potentiates Gd uptake in the cerebellum, brain, and bones.

No MeSH data available.


Related in: MedlinePlus

Gadolinium concentration determined by ICP-MS in the cortical and subcortical brain, cerebellar parenchyma, DCN (pooled by groups), and brain stem (mean ± SD). The Gd concentration in the gadodiamide + SNx group was significantly greater in all structures compared with the other groups (P < 0.001).
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Figure 10: Gadolinium concentration determined by ICP-MS in the cortical and subcortical brain, cerebellar parenchyma, DCN (pooled by groups), and brain stem (mean ± SD). The Gd concentration in the gadodiamide + SNx group was significantly greater in all structures compared with the other groups (P < 0.001).

Mentions: For gadodiamide-treated rats, renal insufficiency resulted in increased total Gd concentrations in all the brain areas compared with the sham-operated control rats (cortical brain: 5.6 ± 1.5 vs 2.5 ± 0.3 nmol/g [P < 0.001]; subcortical brain: 7.5 ± 2.3 vs 3.4 ± 0.5 nmol/g [P < 0.001]; cerebellar parenchyma: 10 ± 2.8 vs 4.7 ± 0.5 nmol/g [P < 0.001]; brain stem: 5.1 ± 1.2 vs 2.6 ± 0.9 nmol/g [P < 0.001], and pooled DCN: 19.9 vs 12.3 nmol/g) (Fig. 10).


Moderate Renal Failure Accentuates T1 Signal Enhancement in the Deep Cerebellar Nuclei of Gadodiamide-Treated Rats
Gadolinium concentration determined by ICP-MS in the cortical and subcortical brain, cerebellar parenchyma, DCN (pooled by groups), and brain stem (mean ± SD). The Gd concentration in the gadodiamide + SNx group was significantly greater in all structures compared with the other groups (P < 0.001).
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Figure 10: Gadolinium concentration determined by ICP-MS in the cortical and subcortical brain, cerebellar parenchyma, DCN (pooled by groups), and brain stem (mean ± SD). The Gd concentration in the gadodiamide + SNx group was significantly greater in all structures compared with the other groups (P < 0.001).
Mentions: For gadodiamide-treated rats, renal insufficiency resulted in increased total Gd concentrations in all the brain areas compared with the sham-operated control rats (cortical brain: 5.6 ± 1.5 vs 2.5 ± 0.3 nmol/g [P < 0.001]; subcortical brain: 7.5 ± 2.3 vs 3.4 ± 0.5 nmol/g [P < 0.001]; cerebellar parenchyma: 10 ± 2.8 vs 4.7 ± 0.5 nmol/g [P < 0.001]; brain stem: 5.1 ± 1.2 vs 2.6 ± 0.9 nmol/g [P < 0.001], and pooled DCN: 19.9 vs 12.3 nmol/g) (Fig. 10).

View Article: PubMed Central - PubMed

ABSTRACT

Objectives: The purpose of this preclinical study was to investigate whether moderate chronic kidney disease is a factor in potentiating gadolinium (Gd) uptake in the brain.

Materials and methods: A comparative study was performed on renally impaired (subtotal nephrectomy) rats versus rats with normal renal function. The animals received 4 daily injections of 0.6 mmol Gd/kg a week for 5 weeks (cumulative dose of 12 mmol Gd/kg) of gadodiamide or saline solution. The MR signal enhancement in the deep cerebellar nuclei was monitored by weekly magnetic resonance imaging examinations. One week after the final injection, the total Gd concentration was determined by inductively coupled plasma mass spectrometry in different regions of the brain including the cerebellum, plasma, cerebrospinal fluid, parietal bone, and femur.

Results: After the administration of gadodiamide, the subtotal nephrectomy group presented a significantly higher T1 signal enhancement in the deep cerebellar nuclei and a major increase in the total Gd concentration in all the studied structures, compared with the normal renal function group receiving the same linear Gd-based contrast agent. Those potentiated animals also showed a pronounced hypersignal in the choroid plexus, still persistent 6 days after the last injection, whereas low concentration of Gd was found in the cerebrospinal fluid (&lt;0.05 &mu;mol/L) at this time point. Plasma Gd concentration was then around 1 &mu;mol/L. Interestingly, plasma Gd was predominantly in a dissociated and soluble form (around 90% of total Gd). Total Gd concentrations in the brain, cerebellum, plasma, and bones correlated with creatinine clearance in both the gadodiamide-treated groups.

Conclusions: Renal insufficiency in rats potentiates Gd uptake in the cerebellum, brain, and bones.

No MeSH data available.


Related in: MedlinePlus