Causes of reversible nephrogenic diabetes insipidus: a systematic review.

BACKGROUND: In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. METHODS: Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Koch's postulates. RESULTS: One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a "definite" diagnosis of NDI; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. CONCLUSION: Most risk factors for reversible NDI were medications, and their identification and removal resulted in resolution of the condition. Long-term treatment with lithium seemed to result in irreversible NDI.

Naming and grasping common objects: a priming study.

This study examined the effects of priming on response latency when participants named and/or grasped common objects. A repetition-priming paradigm was used. An object was presented during a study phase and then was presented again during testing along with other objects that had not been seen before. In experiment 1, the studied objects were either named twice or grasped twice, named first and then grasped, or grasped first and then named. We found a strong priming effect (i.e., decreased latency) when naming was preceded by naming, as well as by grasping, but no priming effect when grasping was preceded by either naming or grasping. In experiment 2, we investigated the effects of priming in naming-naming and grasping-grasping paradigms, with and without a change in object orientation from study to test. As expected, we found significant priming of naming by naming, and the effect was not reduced by orientation change. Again, we found no evidence of priming in grasping. Experiment 3 was designed to examine how different kinds of perceptual and visuomotor processing (naming, orientation matching, orientation discrimination, simple observation, and grasping) during the study phase affect naming at a later test phase. We found significant priming of naming following all study conditions. Notably, the effect differed depending on how much "perceptual" processing was involved in the study phase. The results clearly indicate that perceptual/semantic processing is more dependent on memory than visuomotor processing, which instead relies more on moment-to-moment computations.