A patient with polyuria and hydronephrosis: answer

Jaureguiberry, Graciana; Hoff, William van’t; Mushtaq, Imran; Desai, Divyesh; Mann, Nicholas; Kleta, Robert; Bichet, Daniel G.; Böckenhauer, Detlef

doi:10.1007/s00467-011-1782-4

Pediatr Nephrol

2011

DOI: 10.1007/s00467-011-1782-4

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A patient with polyuria and hydronephrosis: answer

Graciana Jaureguiberry

William van’t Hoff

Imran Mushtaq

et al.

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Cited by 3 publications

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Urinary concentration: different ways to open and close the tap

Böckenhauer

Bichet

2013

Pediatr Nephrol

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Nephrogenic diabetes insipidus (NDI) provides an excellent model for the benefits and insights that can be gained from studying rare diseases. The discovery of underlying genes identified key molecules involved in urinary concentration, including the type 2 vasopressin receptor AVPR2 and the water channel AQP2, which constitute obvious pharmacologic targets. Subsequently developed drugs targeting AVPR2 not only provide potential benefit to some patients with NDI, but are now used for much more common clinical applications as diverse as nocturnal enuresis and heart failure. Yet, the story is still evolving:clinical observations and animal experiments continue to discover new ways to affect urinary concentration. These novel pathways can potentially be exploited for therapeutic gain. Here we review the (patho)physiology of water homoeostasis, the current status of clinical management and potential new treatments.3

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Urinary concentration: different ways to open and close the tap

Böckenhauer

Bichet

2013

Pediatr Nephrol

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Pre- and post-treatment urinary tract findings in children with nephrogenic diabetes insipidus

2013

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Diabetes insípida nefrogénica

Medeiros-Domingo

2014

Boletín Médico del Hospital Infantil de México

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The anti-diuretic hormone arginine-vasopressin (AVP) is released from the pituitary and regulates water reabsorption in the principal cells of the kidney collecting duct. Binding of AVP to the arginine-vasopressin receptor type-2 in the basolateral membrane leads to translocation of aquaporin-2 water channels to the apical membrane of the principal cells of the collecting duct, inducing water permeability of the membrane. This results in water reabsorption in the collecting duct of the nephron following an osmotic gradient. Nephrogenic diabetes insipidus is caused by partial or complete renal resistance to the effects of AVP. Congenital nephrogenic diabetes insipidus is a disorder associated with mutations in either the AVPR2 or AQP2 gene, causing the inability of patients to concentrate their urine. Acquired nephrogenic diabetes insipidus can be caused by electrolyte imbalances (e.g., hypercalcemia, hypokalemia), renal/extra-renal diseases and drugs (e.g., lithium toxicity). This article reviews the causes, clinical manifestations, diagnosis and treatment of patients with nephrogenic diabetes insipidus. Based on more in-depth mechanistic understanding, new therapeutic strategies are current being explored.

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A patient with polyuria and hydronephrosis: answer

Cited by 3 publications

References 16 publications

Urinary concentration: different ways to open and close the tap

Urinary concentration: different ways to open and close the tap

Pre- and post-treatment urinary tract findings in children with nephrogenic diabetes insipidus

Diabetes insípida nefrogénica

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