Regulation of urinary calcium excretion by vasopressin

Anastasio, Pietro; Trepiccione, Francesco; Santo, Natale G. De; Capasso, Giovambattista; Viggiano, D.; Capolongo, Giovanna

doi:10.1093/ckj/sfaa134

Cited by 3 publications

(3 citation statements)

References 44 publications

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“…In this context, dopaminergic dysfunction could be important. Among the less known functions of vasopressin in the kidney, the regulation of Ca secretion in the tubules which according to recent studies is increased when the levels of the antidiuretic hormone are low [172]. This alteration of Ca homeostasis might also be relevant for hypercalciuric syndromes such as kidney stones [173].…”

Section: Peripheral Action Of Da and The Role Of Vasopressinmentioning

confidence: 99%

The Dopamine System: Insights between Kidney and Brain

Donato

Buonincontri

Borriello

et al. 2022

Kidney Blood Press Res

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BACKGROUND: Chronic kidney disease (CKD) is one of the most common diseases in adult age and it is typical of older adults. Recent data suggest that almost half of the elders have CKD. It is now clear that CKD is accompanied, in the early stages, by cognitive impairment, together with depression and subtle abnormalities in motor control (such as gait and balance alterations). SUMMARY: Several data suggest a link between brain dopamine and kidney diseases. Metabolic syndrome and diabetes can affect dopamine neuron survival (leading to Parkinson’s Disease). Several uremic toxins in CKD (uric acid, indoxyl sulphate) and trace elements accumulating in CKD (aluminium, manganese) can also modify the dopaminergic system. Hormones produced by the kidney such as vitamin D are neuroprotective for dopamine neurons. Dopaminergic drugs are useful for the treatment of a common sleep disorder in CKD, the restless legs syndrome. However, experiments on animal models of CKD show conflicting results regarding a modification of dopamine neurons. KEY MESSAGES: Several observations suggest a limited relevance of the dopaminergic system in CKD-related cognitive impairment. However, a common sleep disturbance in CKD, the restless leg syndrome, improves with dopaminergic drugs. Therefore, it remains to be established the role of the dopamine system in subtle motor dysfunction observed in CKD, such as tremors, gait alterations, and central sleep apnea.

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Section: Peripheral Action Of Da and The Role Of Vasopressinmentioning

confidence: 99%

The Dopamine System: Insights between Kidney and Brain

Donato

Buonincontri

Borriello

et al. 2022

Kidney Blood Press Res

View full text Add to dashboard Cite

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“…In our patients with SIADH treated with urea at relatively small doses (15 to 30 g/day), the decrease in calciuria is likely due to the normalization of the effective volemia while high doses of urea administered in normal subjects induce an increase in calciuria (osmotic diuresis) [ 24 ]. Interestingly hypercalciuria was recently reported in patients with central diabetes insipidus (CDI) when untreated [ 10 ]. This underscores that urine flow rates and urinary Na handling might be more important than a direct effect of AVP.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic hyponatremia is also associated with sarcopenia [ 5 , 6 , 7 ], which contributes to osteoporosis [ 8 ]. In idiopathic hypercalciuria, osteoporosis is also reported [ 9 ] and in patients with central diabetes insipidus a hypercalciuria is also observed (and attributed to the high diuresis) [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

The Urine Calcium/Creatinine Ratio and Uricemia during Hyponatremia of Different Origins: Clinical Implications

Decaux

Musch²

2023

JCM

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Background: Chronic hyponatremia is known to be associated with osteoporosis. It has been shown that chronic hyponatremia increases bone resorption in an attempt to release body stores of exchangeable sodium by different mechanisms. We wanted to know the calciuria of patients with hyponatremia of different origins. Material and Methods: We made a retrospective study of 114 consecutive patients with asymptomatic hyponatremia of different origins with the usual serum and urine chemistry. Result: In hyponatremia due to SIADH, we had a high urine calcium/creatinine ratio of 0.23 ± 0.096 while in patients with salt depletion the UCa/UCr ratio was low (0.056 ± 0.038), in patients with hyponatremia secondary to thiazide intake the value was also low (0.075 ± 0.047) as in hypervolemic patients (0.034 ± 0.01). In hyponatremia due to polydipsia, the value was high (0.205 ± 0.10). Correction of hyponatremia in the euvolemic patients was associated with a significant decrease in the UCa/UCr ratio. In patients with hyponatremia secondary to thiazide intake, we noted that in the patients with low uric acid levels (<4 mg/dL, suggesting euvolemia) we also observed a low UCa/UCr (<0.10). In nine patients with chronic SIADH (SNa 125.1 ± 3.6 mEq/L), the 24 h urine calcium excretion was 275 ± 112 mg and decreased to 122 ± 77 mg (p < 0.01) after at least 2 weeks of treatment. Conclusions: Patients with chronic hyponatremia due to SIADH usually have a high UCa/UCr ratio (>0.15). This is also observed in hyponatremia secondary to polydipsia. Patients with thiazide-induced hyponatremia usually have low UCa/UCr levels and this is the case even among those with a biochemistry similar to that in SIADH (uric acid < 4 mg/dL).

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