Evidence map›Paper›PMID 18550651›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2008

Angiotensin converting enzyme insertion/deletion polymorphism and renoprotection in diabetic and nondiabetic nephropathies.

Piero Ruggenenti, Paola Bettinaglio, Franck Pinares, Giuseppe Remuzzi

Abstract readReview
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Nephroprotective Effect ofInternational journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Role of angiotensin II in aging.Frontiers in aging neuroscience · 2022
    Review
  7. Pharmacogenomics Informs Cardiovascular Pharmacotherapy.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  8. Observational
  9. Article
  10. Review
  11. Achieving remission of proteinuria in childhood CKD.Pediatric nephrology (Berlin, Germany) · 2017
    Observational
  12. Article
  13. Integrative Biology of Diabetic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Piero RuggenentiClinical Research Centre for Rare Diseases Aldo e Cele Daccò, Mario Negri Institute for Pharmacological Research, Villa Camozzi, Ranica, Italy.
Paola Bettinaglio
Franck Pinares
Giuseppe Remuzzi
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the huge amount of studies looking for candidate genes, the ACE gene remains the unique, well-characterized locus clearly associated with pathogenesis and progression of chronic kidney disease, and with response to treatment with drugs that directly interfere with the renin angiotensin system (RAS), such as angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARA). The II genotype is protective against development and progression of type I and type II nephropathy and is associated with a slower progression of nondiabetic proteinuric kidney disease. ACE inhibitors are particularly effective at the stage of normoalbuminuria or microalbuminuria in both type I and type II diabetics with the II genotype, whereas the DD genotype is associated with a better response to ARA therapy in overt nephropathy of type II diabetes and to ACE inhibitors in male patients with nondiabetic proteinuric nephropathies. The role of other RAS or non-RAS polymorphisms and their possible interactions with different ACE I/D genotypes are less clearly defined. Thus, evaluating the ACE I/D polymorphism is a reliable tool to identify patients at risk and those who may benefit the most of renoprotective therapy with ACE inhibitors or ARA. This may guide pharmacologic therapy in individual patients and help design clinical trials in progressive nephropathies. Moreover, it might help optimize prevention and intervention strategies at population levels, in particular, in countries where resources are extremely limited and 1 million patients continue to die every year of cardiovascular or renal disease.

Indexed as

INDEL MutationAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersDiabetic NephropathiesDisease ProgressionGenotypeHumansKidney DiseasesPatient SelectionPeptidyl-Dipeptidase APharmacogeneticsPhenotypeRenin-Angiotensin SystemTreatment OutcomeAngiotensin-Converting Enzyme InhibitorsAngiotensin II Type 1 Receptor BlockersPeptidyl-Dipeptidase A

Identifiers

PMID18550651
PMCPMC4571148
OpenAlexW2125484955

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.