Evidence map›Paper›PMID 23408166›Full record

ReviewAmerican journal of physiology. Renal physiology2013

Lithium: a versatile tool for understanding renal physiology.

Bellamkonda K Kishore, Carolyn M Ecelbarger

Abstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  18. Genetic Deletion of P2YFrontiers in physiology · 2018
    Article
  19. Article
  20. Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Bellamkonda K KishoreNephrology Research (151M) VA SLC Health Care System, 500 Foothill Dr, Salt Lake City, UT 84148, USA. BK.Kishore@hsc.utah.edu
Carolyn M Ecelbarger
Individual Differences · USVA Salt Lake City Healthcare System · US

Funding

Role of Insulin Receptors in the KidneyR01DK082507 · NIDDK · GEORGETOWN UNIVERSITY · PI ECELBARGER, CAROLYN MARY · 2010 to 2013
$1.3M
P2U(P2Y2)-PURINOCEPTOR AND WATER TRANSPORT IN RAT KIDNEYR01DK061183 · NIDDK · UNIVERSITY OF UTAH · PI KISHORE, BELLAMKONDA K · 2001 to 2004
$883k
Potential Therapeutic Applications of Ecto-Nucleotidases in Lithium-induced NDIR21DK081041 · NIDDK · WESTERN INSTITUTE FOR VETERANS RESEARCH · PI KISHORE, BELLAMKONDA K · 2009 to 2010
$375k
NIDDK NIH HHS DK-061183NIDDK NIH HHS DK082507NIDDK NIH HHS DK81041NIDDK NIH HHS R01 DK082507
6 · The paper itself

Abstract

By virtue of its unique interactions with kidney cells, lithium became an important research tool in renal physiology and pathophysiology. Investigators have uncovered the intricate relationships of lithium with the vasopressin and aldosterone systems, and the membrane channels or transporters regulated by them. While doing so, their work has also led to 1) questioning the role of adenylyl cyclase activity and prostaglandins in lithium-induced suppression of aquaporin-2 gene transcription; 2) unraveling the role of purinergic signaling in lithium-induced polyuria; and 3) highlighting the importance of the epithelial sodium channel (ENaC) in lithium-induced nephrogenic diabetes insipidus (NDI). Lithium-induced remodeling of the collecting duct has the potential to shed new light on collecting duct remodeling in disease conditions, such as diabetes insipidus. The finding that lithium inhibits glycogen synthase kinase-3β (GSK3β) has opened an avenue for studies on the role of GSK3β in urinary concentration, and GSK isoforms in renal development. Finally, proteomic and metabolomic profiling of the kidney and urine in rats treated with lithium is providing insights into how the kidney adapts its metabolism in conditions such as acquired NDI and the multifactorial nature of lithium-induced NDI. This review provides state-of-the-art knowledge of lithium as a versatile tool for understanding the molecular physiology of the kidney, and a comprehensive view of how this tool is challenging some of our long-standing concepts in renal physiology, often with paradigm shifts, and presenting paradoxical situations in renal pathophysiology. In addition, this review points to future directions in research where lithium can lead the renal community.

Indexed as

LithiumAldosteroneAnimalsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansKidneyModels, AnimalProstaglandinsSignal TransductionVasopressinsAldosteroneGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, ratLithiumProstaglandinsVasopressinsaldosteronearginine vasopressindiabetes insipidusglycogen synthase kinase-3prostaglandinspurinergic signaling

Identifiers

PMID23408166
PMCPMC3651632
OpenAlexW2161135180

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.