Normal Hemodynamic and Coagulation Responses to 1-Diamino-8-D-Arginine Vasopressin in a Case of Lithium-Induced Nephrogenic Diabetes Insipidus. Results of Treatment by a Prostaglandin Synthesis Inhibitor (Indomethacin).
| Title: | Normal Hemodynamic and Coagulation Responses to 1-Diamino-8-D-Arginine Vasopressin in a Case of Lithium-Induced Nephrogenic Diabetes Insipidus. Results of Treatment by a Prostaglandin Synthesis Inhibitor (Indomethacin). |
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| Authors: | Hober, Christine; Vantyghem, Marie-Christine; Racadot, Andre; Cappoen, Jean-Pierre; Lefebvre, Jean |
| Publisher: | Hormone Research |
| Date Published: | January 01, 1992 |
| Reference Number: | 310 |
This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Lithium (Li) is a drug widely used to treat certain psychological disorders. One side effect of Li is that it can cause nephrogenic diabetes insipidus (NDI) in people who use it, especially those who use it over a long time. Hober, et al., examined a 33-year-old woman with Li-induced NDI to determine her hemodynamic and coagulation responses to DDAVP. Extended use of Li can inhibit the antidiuretic action of AVP by impairing the cAMP system which must be activated by AVP once it binds with V2R. Therefore, the authors suspected that Li may interact with V2Rs.
The patient showed normal hemostatic and coagulation responses to DDAVP, which indicated that her V2Rs outside the kidney were working fine. However, her V2Rs in the kidney were not working fine as indicated by the symptoms of Li-induced NDI: polyuria (chronic passage of large volumes of urine) and polydipsia (chronic, excessive thirst). The authors suspect that Li causes structural damage to kidney tubules and tissue. (V2Rs reside in the principal cells of the kidney collecting ducts, which are part of the tubules.)
The authors found that the patient's NDI caused an increase in her urinary prostaglandin (PGE2). (This PGE2 increase has also been documented in cases of congenital NDI.) In this case, the increase was due to volume depletion in the kidney due to a low kidney blood flow, high levels of plasma renin activity (PRA), and a high volume of urine flow. Because PGE2 exacerbates NDI, the authors treated their patient with a prostaglandin synthesis inhibitor (PSI) called indomethacin. They also placed her on a low osmotic diet (LOD), which meant consuming low amounts of sodium and protein. This decreased her urine volume by about half and improved the rate at which sodium cleared from her blood and solute-free water moved from her blood to her urine. The patient's urine osmolality (her relative concentration of osmotically active solids to liquid in her urine) rose by 42%, but remained very low when compared to healthy individuals, perhaps in part because of her LOD.



