Evidence map›Paper›PMID 18320236›Full record

ReviewPediatric nephrology (Berlin, Germany)2008

Diabetes and chronic kidney disease: lessons from the Pima Indians.

Kevin V Lemley

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Reproducibility of the NEPTUNE descriptor-based scoring system on whole-slide images and histologic and ultrastructural digital images.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  6. Toll-like receptor 2 and type 2 diabetes.Cellular & molecular biology letters · 2016
    Review
  7. Review
  8. Article
  9. Estimating individual glomerular volume in the human kidney: clinical perspectives.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2012
    Article
  10. Article
  11. Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011
    Review
  12. 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

1 author.

Kevin V LemleyDivision of Nephrology, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA. klemley@chla.usc.edu

Funding

EARLY NEPHROPATHY IN NIDDMR01DK054600 · NIDDK · STANFORD UNIVERSITY · PI MYERS, BRYAN DAVID · 1999 to 2003
$1.5M
NIDDK NIH HHS DK 54600
6 · The paper itself

Abstract

Although diabetic nephropathy is a very rare cause of kidney failure during childhood, the underlying events leading to progressive kidney injury begin during childhood in many patients with type 1 diabetes mellitus (T1DM) and in increasing numbers of children with type 2 diabetes mellitus (T2DM). The Pima Indians of Arizona represent an exceptionally thoroughly studied population suffering from very high rates of T2DM and diabetic nephropathy (T2DN). This population well illustrates the often inexorable progression from glomerular hyperfiltration to microalbuminuria to overt proteinuria and loss of glomerular filtration rate (GFR), paralleled by the accumulation of mesangial matrix and basement membrane, glomerular hypertrophy, loss of podocytes and eventual glomerular sclerosis and interstitial fibrosis. Structural changes quantitatively account for the loss of GFR in T2DN. The mechanism of albuminuria (and its relationship to GFR loss) is much less clear. There is strong functional and structural evidence for defects in glomerular size-selectivity (shunts) due to podocyte pathology, but only beginning at relatively high levels of proteinuria (albumin/creatinine ratios > 3000 mg/g). Podocyte loss accompanies, and may underlie, the loss of glomeruli to sclerosis. At this point, most evidence in humans suggests detachment of intact podocytes from the glomerular basement membrane, rather than apoptosis, as the predominant mechanism of podocyte loss.

Indexed as

Indians, North AmericanDiabetic NephropathiesDisease ProgressionHumansRenal Insufficiency, Chronic

Identifiers

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.