Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (640 words), 7 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The amount of plasma that perfuses the kidneys per unit time, approximately 10% greater than effective renal plasma flow (renal plasma flow, effective). It should be differentiated from the renal blood flow; (RBF), which refers to the total volume of blood flowing through the renal vasculature, while the renal plasma flow refers to the rate of plasma flow (RPF).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Plasma Flow, Renal; Flow, Renal Plasma.
Where it fits in the MeSH classification
- Broader topics
- Renal Circulation
Related concepts
Research landscape
PubMed indexes 378 records tagged with the MeSH heading “Renal Plasma Flow” (counts retrieved 2026-10-29). 8 of them (2.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 203 records.
Reviews account for 23 records (6.1%) and meta-analyses for 0. Randomized controlled trials number 40 (10.6%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 203 |
| 2000-2009 | 124 |
| 2010-2019 | 43 |
| 2020 onward | 8 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 23 | 6.1% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 40 | 10.6% |
Method: PubMed query "Renal Plasma Flow"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Renal hemodynamic effects differ between antidiabetic combination strategies: randomized controlled clinical trial comparing empagliflozin/linagliptin with metformin/insulin glargine | 2021 | Randomized controlled trial Design not recorded in structured metadata | 17 | cc by PMID 34481498 · DOI · PMC8418746 |
| Mimicking kidney flow shear efficiently induces aggregation of LECT2, a protein involved in renal amyloidosis | 2024 | Research article Design not recorded in structured metadata | 9 | cc by PMID 38537700 · DOI · PMC11040205 |
| Concerted regulation of renal plasma flow and glomerular filtration rate by renal dopamine and NOS I in rats on high salt intake | 2017 | Research article Design not recorded in structured metadata | 7 | cc by PMID 28351967 · DOI · PMC5371567 |
Renal hemodynamic effects differ between antidiabetic combination strategies: randomized controlled clinical trial comparing empagliflozin/linagliptin with metformin/insulin glargine [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundType 2 diabetes causes cardio-renal complications and is treated with different combination therapies.
- Closing excerpt
- gov (NCT02752113) on April 26, 2016.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (239 words)
BackgroundType 2 diabetes causes cardio-renal complications and is treated with different combination therapies. The renal hemodynamics profile of such combination therapies has not been evaluated in detail.MethodsPatients (N = 97) with type 2 diabetes were randomized to receive either empagliflozin and linagliptin (E+L group) or metformin and insulin glargine (M+I group) for 3 months. Renal hemodynamics were assessed with para-aminohippuric acid and inulin for renal plasma flow (RPF) and glomerular filtration rate (GFR). Intraglomerular hemodynamics were calculated according the Gomez´ model.ResultsTreatment with E+L reduced GFR (p = 0.003), but RPF remained unchanged (p = 0.536). In contrast, M+I not only reduced GFR (p = 0.001), but also resulted in a significant reduction of RPF (p adjust A) (p = 0.116), but diminished resistance of efferent arterioles (RE) (p = 0.001). In M+I group RA was increased (p = 0.006) and RE remained unchanged (p = 0.538). The effects on RA (padjust E (padjust ConclusionsIn patients with type 2 diabetes and preserved renal function treatment with M+I resulted in reduction of renal perfusion and increase in vascular resistance, in contrast to treatment with E+I that preserved renal perfusion and reduced vascular resistance. Moreover, different underlying effects on the resistance vessels have been estimated according to the Gomez model, with M+I increasing RA and E+L predominantly decreasing RE, which is in contrast to the proposed sodium-glucose cotransporter 2 inhibitor effects.Trial registrationThe study was registered at www.clinicaltrials.gov (NCT02752113) on April 26, 2016.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34481498 · DOI · PMC8418746
Mimicking kidney flow shear efficiently induces aggregation of LECT2, a protein involved in renal amyloidosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Aggregation of leukocyte cell-derived chemotaxin 2 (LECT2) causes ALECT2, a systemic amyloidosis that affects the kidney and liver.
- Closing excerpt
- These microfluidic devices may be of general use for uncovering mechanisms by which blood flow induces misfolding and amyloidosis of circulating proteins.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (247 words)
Aggregation of leukocyte cell-derived chemotaxin 2 (LECT2) causes ALECT2, a systemic amyloidosis that affects the kidney and liver. Previous studies established that LECT2 fibrillogenesis is accelerated by the loss of its bound zinc ion and stirring/shaking. These forms of agitation create heterogeneous shear conditions, including air-liquid interfaces that denature proteins, that are not present in the body. Here, we determined the extent to which a more physiological form of mechanical stress-shear generated by fluid flow through a network of narrow channels-drives LECT2 fibrillogenesis. To mimic blood flow through the kidney, where LECT2 and other proteins form amyloid deposits, we developed a microfluidic device consisting of progressively branched channels narrowing from 5 mm to 20 μm in width. Shear was particularly pronounced at the branch points and in the smallest capillaries. Aggregation was induced within 24 h by shear levels that were in the physiological range and well below those required to unfold globular proteins such as LECT2. EM images suggested the resulting fibril ultrastructures were different when generated by laminar flow shear versus shaking/stirring. Importantly, results from the microfluidic device showed the first evidence that the I40V mutation accelerated fibril formation and increased both the size and the density of the aggregates. These findings suggest that kidney-like flow shear, in combination with zinc loss, acts in combination with the I40V mutation to trigger LECT2 amyloidogenesis. These microfluidic devices may be of general use for uncovering mechanisms by which blood flow induces misfolding and amyloidosis of circulating proteins.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38537700 · DOI · PMC11040205
Concerted regulation of renal plasma flow and glomerular filtration rate by renal dopamine and NOS I in rats on high salt intake [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Under high sodium intake renal dopamine (DA) increases while NOS I expression in macula densa cells (MD) decreases.
- Closing excerpt
- HS intake increased natriuresis, diuresis, and urinary DA while it decreased cortical NOS I expression (P P -1, P P P P P 1R, and NOS I in MD cells act in concert to regulate RPF and GFR to stabilize the delivery of NaCl to the distal nephron.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)
Under high sodium intake renal dopamine (DA) increases while NOS I expression in macula densa cells (MD) decreases. To explore whether renal DA and NOS I, linked to natriuresis and to the stability of the tubuloglomerular feedback, respectively, act in concert to regulate renal plasma flow (RPF) and glomerular filtration rate (GFR). Male Wistar rats were studied under a normal sodium intake (NS, NaCl 0.24%) or a high sodium intake (HS, NaCl 1% in drinking water) during the 5 days of the study. For the last two days, the specific D1-like receptor antagonist SCH 23390 (1 mg kg bwt-1 day-1, sc) or a vehicle was administered. HS intake increased natriuresis, diuresis, and urinary DA while it decreased cortical NOS I expression (P P -1, P P P P P 1R, and NOS I in MD cells act in concert to regulate RPF and GFR to stabilize the delivery of NaCl to the distal nephron.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28351967 · DOI · PMC5371567
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone system [4]
- Research article Renal plasma flow and glomerular filtration rate during acute kidney injury in man [5]
- Research article Renal functional reserve in children [6]
- Research article [Paraaminohippuric acid clearance] [7]
References
- Ott C, Jung S, Korn M, Kannenkeril D, Bosch A, Kolwelter J, et al.. Renal hemodynamic effects differ between antidiabetic combination strategies: randomized controlled clinical trial comparing empagliflozin/linagliptin with metformin/insulin glargine. . 2021. PMID 34481498 · DOI · PMC8418746
- Ha JH, Xu Y, Sekhon H, Zhao W, Wilkens S, Ren D, et al.. Mimicking kidney flow shear efficiently induces aggregation of LECT2, a protein involved in renal amyloidosis. . 2024. PMID 38537700 · DOI · PMC11040205
- Ibarra ME, Albertoni Borghese MF, Majowicz MP, Ortiz MC, Loidl F, Rey-Funes M, et al.. Concerted regulation of renal plasma flow and glomerular filtration rate by renal dopamine and NOS I in rats on high salt intake. . 2017. PMID 28351967 · DOI · PMC5371567
- West CA, Sasser JM, Baylis C. The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone system. Am J Physiol Renal Physiol. 2016. PMID 27707703 · DOI · PMC6189751
- Prowle JR, Ishikawa K, May CN, Bellomo R. Renal plasma flow and glomerular filtration rate during acute kidney injury in man. Ren Fail. 2010. PMID 20370451 · DOI
- Anastasio P, Santoro D, Spitali L, Cirillo M, DiLeo VA, De Santo NG. Renal functional reserve in children. Semin Nephrol. 1995. PMID 8525148
- Nagase S, Koyama A. [Paraaminohippuric acid clearance]. Nihon Rinsho. 1995. PMID 8753627
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.