ReviewDrugs1993
Nephroprotective effect of ACE inhibitors.
Review in Drugs, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 22 citations in OpenAlex.
- Effects of Zofenopril and Thymoquinone in Cyclophosphamide-Induced Urotoxicity and Nephrotoxicity in Rats; The Value of Their Anti-Inflammatory and Antioxidant Properties.Journal of inflammation research · 2025Article
- Reduced renal function strongly affects survival and thrombosis in patients with myelofibrosis.Annals of hematology · 2020Article
- A Lanosteryl Triterpene (RA-3) Exhibits Antihyperuricemic and Nephroprotective Effects in Rats.Molecules (Basel, Switzerland) · 2020Article
- Review
- Determinants of coronary vascular disease in patients with type II diabetes mellitus and their therapeutic implications.Clinical cardiology · 1997Review
- Formulary management of ACE inhibitors.PharmacoEconomics · 1996Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In most cases of renal disease, progression of renal failure occurs via nonspecific mechanisms that can be dissociated from the primary cause of renal damage. Progression of disease is accompanied by glomerulosclerosis and tubulointerstitial fibrosis. Loss of autoregulation and afferent renal vasodilation renders the glomerular microcirculation particularly susceptible to systemic hypertension. Glomerular growth is an ancillary factor permitting the development of glomerulosclerosis. Experimental and clinical studies indicate that angiotensin converting enzyme (ACE) inhibitors may prevent progressive renal deterioration. Furthermore, it appears that this effect can be dissociated, at least in part, from the haemodynamic effects of ACE inhibitors. Some evidence indicates that the renal-protective effects of ACE inhibitors results from their effects on glomerular growth and glomerular permselectivity. The role of reduced generation of angiotensin II or accumulation of kinins in the renal effects of ACE inhibitors is under investigation. Prospective clinical trials have demonstrated that ACE inhibitors reduce proteinuria and interfere with progression of renal disease to a greater degree than can be explained by their blood pressure lowering effects alone.
Indexed as
Identifiers
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.