ReviewPediatric nephrology (Berlin, Germany)1994
Polycystic kidney disease--a truly pediatric problem.
Review in Pediatric nephrology (Berlin, Germany), 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Functional and therapeutic importance of purinergic signaling in polycystic kidney disease.American journal of physiology. Renal physiology · 2016Review
- Mutations in multiple PKD genes may explain early and severe polycystic kidney disease.Journal of the American Society of Nephrology : JASN · 2011Article
- Diagnosis and management of childhood polycystic kidney disease.Pediatric nephrology (Berlin, Germany) · 2011Review
- The sea urchin sperm receptor for egg jelly is a modular protein with extensive homology to the human polycystic kidney disease protein, PKD1.The Journal of cell biology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic kidney disease (PKD) represents the most common inherited cause of chronic renal failure. PKD is a relatively uncommon cause of chronic renal failure or mortality in childhood and adolescence, but is nevertheless often responsible for symptoms of renal disease. Current research into the pathogenesis of PKD suggests that disturbance of the normal regulation of growth and development of tubular epithelium is intrinsic to cyst formation and growth. Features of cystic epithelium that are analogous to earlier stages of renal development include altered composition of the extracellular matrix, abnormal cell proliferation, and the persistence of a secretory pattern of fluid and electrolyte transport. The potential for early diagnosis and intervention in PKD makes it an area of great interest to the pediatric nephrologist. Animal and in vitro studies have achieved modification of cyst growth by reduction of dietary protein, use of amiloride and its analogs, antagonism of the epidermal growth factor receptor system, anti-inflammatory therapy, and most recently with the use of taxol, an agent that inhibits microtubule assembly. PKD may represent an area in which childhood diagnosis and intervention will have a significant impact on the prevalence of chronic renal failure in adult life.
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What OpenQuestion holds
Registered trials
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.