1/7. lithium-induced nephrogenic diabetes insipidus.BACKGROUND: lithium can cause nephrogenic diabetes insipidus in up to 20 to 40 percent of patients currently taking the medication, and a subset of these patients will have a persistent concentrating defect long after lithium is discontinued. They are at risk for serious hypernatremia when fluid intake is restricted for any reason. methods: medline as used to search the key words "nephrogenic diabetes insipidus" and "lithium" from 1990 to the present. A case report describes a patient who had been off lithium for 8 years and who developed hypernatremia after she was transferred to a new long-term facility and the staff attempted to control the patient's polydipsia. The diagnosis and treatment of nephrogenic diabetes insipidus are also discussed. RESULTS: This case of persistent nephrogenic diabetes insipidus 8 years after discontinuing lithium is the longest ever reported. Certainly, a number of patients have varying degrees of persistent lithium-related nephrogenic diabetes insipidus. Although pathologic changes are associated with persistent nephrogenic diabetes insipidus, the exact mechanism of the persistent defect is unknown. The mechanism of acute lithium-induced nephrogenic diabetes insipidus while the patient is on lithium is related to changes in intracellular cyclic adenosine monophosphate. CONCLUSIONS: patients currently taking lithium and patients with a remote history of lithium treatment need to be monitored for signs and symptoms of nephrogenic diabetes insipidus. physicians need to be aware of the potential for nephrogenic diabetes insipidus in these patients and care for them appropriately.- - - - - - - - - - ranking = 1keywords = hypernatremia (Clic here for more details about this article) |
2/7. Possible liposomal amphotericin b-induced nephrogenic diabetes insipidus.OBJECTIVE: To report the development of nephrogenic diabetes insipidus (NDI) associated with the use of high-dose liposomal amphotericin b. CASE SUMMARY: A 38-year-old white man with relapsed acute myelogenous leukemia underwent a matched unrelated donor allogeneic bone marrow transplant with adequate engraftment and mild graft-versus-host disease responding to corticosteroids. Approximately 11 months after transplant, the patient was admitted to the hospital with suspected fungal pneumonia and started on liposomal amphotericin b (baseline serum creatinine 1.4-1.5 mg/dL). The dose was increased due to his immunosuppression and poor response, as the fungal etiology was identified as Torulopsis glabrata. The patient required mechanical ventilation due to biopsy-proven bronchiolitis olbiterans organizing pneumonia. Additionally, he developed diffuse alveolar hemorrhage and received intravenous desmopressin, with a reduction in bloody secretions. He also developed hypernatremia (serum sodium 155 mEq/L) on day 3 of the desmopressin and had an inappropriately increased urine output consistent with NDI. The most likely etiology for the NDI was liposomal amphotericin b and its associated hypokalemia. DISCUSSION: The observation of worsening hypernatremia (serum sodium increased from 135 to 164 mEq/L) with polyuria was associated with an increasing cumulative dosage of liposomal amphotericin b for fungal pneumonia despite the concurrent use of intravenous desmopressin. Aggressive water replacement was an effective treatment option in this patient. The Naranjo probability scale classified this as a possible adverse reaction because of the temporal sequence of NDI after high-dose liposomal amphotericin b and previously reported cases of NDI associated with amphotericin b desoxycholate. CONCLUSIONS: amphotericin b desoxycholate has been implicated as an etiology for NDI, and the use of the newer liposomal amphotericin b reportedly avoids this rare complication. We observed the development of NDI despite the use of liposomal amphotericin b in a critically ill patient with bone marrow transplant.- - - - - - - - - - ranking = 1keywords = hypernatremia (Clic here for more details about this article) |
3/7. Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.- - - - - - - - - - ranking = 3.5keywords = hypernatremia (Clic here for more details about this article) |
4/7. A novel deletion mutation in the arginine vasopressin receptor 2 gene and skewed x chromosome inactivation in a female patient with congenital nephrogenic diabetes insipidus.X-linked nephrogenic diabetes insipidus (NDI) is a rare inherited disorder caused by mutations in the arginine vasopressin receptor 2 (V2R) gene. The clinical phenotype is fully expressed in hemizygous male patients and is usually asymptomatic in heterozygous females. In the present study, a 51-yr-old Japanese female with congenital NDI and her family members were examined. The patient developed severe hypernatremia accompanied by hypoosmotic polyuria after gynecological surgery, and was unable to concentrate urinary osmolality in response to exogenous vasopressin. Direct sequencing analysis of the propositus and her two affected sons revealed a two-nucleotide deletion change at codon 30 (g.452-453delAC) in the V2R gene, resulting in a frameshift and premature termination in translation at codon 190. The x chromosome inactivation pattern was investigated in the propositus using methylation analysis of the polymorphic CAG repeat in the androgen receptor gene, and the value for relative x chromosome inactivation of one allele was 70.2%. In conclusion, we identified a novel V2R gene mutation in a female patient and her sons with congenital NDI, and her phenotype may be caused by skewed x chromosome inactivation.- - - - - - - - - - ranking = 0.5keywords = hypernatremia (Clic here for more details about this article) |
5/7. Nephrogenic diabetes insipidus presenting with developmental delay and intracranial calcification.A one-year-boy presented with constipation, fever, failure to thrive and developmental delay from the neonatal period. Investigations revealed persistent hypernatremia and deranged renal functions. Diagnostic work-up was suggestive of nephrogenic diabetes insipidus (NDI). Computerized tomography of head revealed calcification in the frontal, thalamic and basal ganglia region. The rare association of NDI and intracranial calcification is discussed.- - - - - - - - - - ranking = 0.5keywords = hypernatremia (Clic here for more details about this article) |
6/7. Nephrogenic diabetes insipidus secondary to lithium therapy in the postoperative patient: a case report.Nephrogenic diabetes insipidus (NDI) presents a rarely encountered but challenging fluid management problem in the perioperative period. This case is that of a patient with a perforated duodenal ulcer and previously undiagnosed NDI who received standard preoperative and postoperative hydration with normal saline, causing hypernatremia and an inappropriate diuresis. The resulting hypernatremia and hyperosmolality required aggressive hypotonic fluid replacement to return to preoperative values. Though refractory to 1-desamino-8-D-argenine-vasopressin (dDAVP), thiazide diuretics and nonsteroidal anti-inflammatory agents have a role in managing selected patients. early diagnosis with careful fluid and electrolyte management are critical in successful management of these patients in the perioperative period.- - - - - - - - - - ranking = 1keywords = hypernatremia (Clic here for more details about this article) |
7/7. Mutations in the vasopressin V2 receptor gene in two families with nephrogenic diabetes insipidus.Congenital nephrogenic diabetes insipidus (CNDI) is a rare X-linked disorder in which the renal collecting duct is unresponsive to arginine vasopressin, and thus, the urine is consistently hypotonic to plasma. As a result, affected individuals are unable to concentrate urine and suffer from episodes of severe dehydration and hypernatremia. Recently, the association between arginine vasopressin V2 receptor gene mutations and CNDI has been demonstrated. In this report, two additional novel molecular defects of the arginine vasopressin V2 receptor gene in CNDI families are described. In one family, the affected individual demonstrated a G-->T transversion causing a nonsense mutation in codon 231. This mutation results in a glutamic acid becoming a termination codon, causing premature termination and truncation of the encoded receptor protein. This mutation causes a NciI site within the gene to be abolished and a BsaWI site to be created. In the second family, affected individuals showed a 28-basepair duplicating insertion in the very beginning of exon 2 down-stream of the splice acceptor site. It was hypothesized that an insertion mutagenesis mechanism involves the formation of a stem-loop structure within the newly synthesized dna strand, followed by a slipped mispairing. This may be a general mechanism for the deletion or insertion of repeated sequences within the genome. Recent data show that G-protein-coupled receptors are susceptible to many different mutations that often result in the loss of function, causing a similar clinical phenotype.- - - - - - - - - - ranking = 0.5keywords = hypernatremia (Clic here for more details about this article) |