Renal Failure

ISSN: 0886-022X (Print) 1525-6049 (Online) Journal homepage: https://www.tandfonline.com/loi/irnf20

Glomerular Pore Size Corresponding to Albumin

Molecular Size, an Explanation for Underlying
Structural Pathology Leading to Albuminuria at
Nanolevel

Viroj Wiwanitkit

To cite this article: Viroj Wiwanitkit (2006) Glomerular Pore Size Corresponding to Albumin
Molecular Size, an Explanation for Underlying Structural Pathology Leading to Albuminuria at
Nanolevel, Renal Failure, 28:1, 101-101, DOI: 10.1080/08860220500461344

To link to this article: https://doi.org/10.1080/08860220500461344

Published online: 07 Jul 2009.

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Renal Failure, 28:101, 2006
Copyright © Taylor & Francis Group, LLC
ISSN: 0886-022X print / 1525-6049 online
DOI: 10.1080/08860220500461344
BRIEF REPORT
LRNF
Glomerular Pore Size Corresponding to Albumin Molecular Size,
an Explanation for Underlying Structural Pathology Leading
to Albuminuria at Nanolevel
Glomerular Pore Size in Pathology Leading to Albuminuria
Viroj Wiwanitkit, M.D.
Department of Laboratory Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand 10330
The appearance of albumin in the urine has long been
recognized as a cardinal feature of kidney disease.[1] Physi-
ologically, the glomerular capillary wall provides a barrier
to protein in blood not to cross into urine. However, in the
pathological condition, the change in glomerular permeabil-
ity, protein can be detected in the urine. Screening for pro-
teinuria is commonly performed using reagent test strips.[2]
Quantitative measurements of marker proteins can be used
to estimate the extent and the site of damage in the neph-
ron.[2] Basically, glomerulus permeability is influenced by
pore size and the number of pores (pore density). Generally,
due to the diffusion principle, high flux membranes that
have more or larger pores allow more solutes and ultrafil-
trate to move across the membrane. Glomerular hemody-
namic adaptations to glomerular permeability defect are
thought to be the initiating factor of progression to renal
failure.[3] Conti said that the majority of patients with dia-
betic nephropathy reach end-stage renal failure within 10 yr
from the first evidence of albuminuria.[4] The consideration
on the nanostructure of the glomerular correlative to the
albumin can be good information for better understanding
the basic pathology for albuminuria.
Here, the author reviewed the reported glomerular
pore size as well as the molecular size of albumin in the lit-
erature. The glomerular pore size is equal to 4.0–4.5 nm,[5]
and the molecular size of albumin is equal to 6.4 nm × 5.5
nm × 5 nm.[5] Therefore, the molecule of albumin cannot
diffuse across the glomerulus in the physiological condi-
tion. If there is an enlargement of the glomerular pore size
at least by 1.6 times (6.4/4.0), the molecule of albumin can
diffuse across the membrane.
Address correspondence to V. Wiwanitkit, Department of
Laboratory Medicine, Faculty of Medicine, Chulalongkorn Uni-
versity, Bangkok 10330, Thailand; E-mail: wviroj@yahoo.com
101
There are some recent reports on the pore size found
in patients with albuminuria compared to controls. Holmquist
et al. said that change in pore size in the glomerular base-
ment membrane was related to the urinary albumin excre-
tion rate in diabetic patients.[6] Oberbauer et al. reported
that patients with albuminuria above 200 μg/min exhibited
a significant reduction in mean glomerular pore size.[7]
Andersens et al. reported that the glomerular pore size in
patients with early onset albuminuria was about two times
larger than normal,[8] similar to the findings in this study.
According to this report, the pathology underlying albu-
minuria might occur at a very early stage.
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