Literature DB >> 11380812

Glomerular cell number in normal subjects and in type 1 diabetic patients.

M W Steffes1, D Schmidt, R McCrery, J M Basgen.   

Abstract

BACKGROUND: The number of cells in glomeruli has been a challenging measure, especially in human kidneys, with only a small amount of tissue obtained by biopsy. However, the number of cells and their function are important determinants of renal function in health and disease.
METHODS: Modern morphometric techniques have now provided the means to determine the numerical density (Nv) and number (with a measure of glomerular volume) of endothelial cells, mesangial cells, and podocytes in plastic-embedded renal tissue biopsied from nondiabetic subjects (N = 36) and type 1 diabetic patients (N = 46) over an extended age range from childhood through late adult.
RESULTS: Nv values for all glomerular cells varied only slightly with age and did not change within the range of glomerular lesions of diabetes studied. Thus, the increase in glomerular volume during childhood to a steady level thereafter was the primary determinant of total glomerular cell number. The number of mesangial cells and endothelial cells increased with age, reflecting the increase in all cells, while the podocytes remained unchanged in number over all ages studied (10 to 69 years). Numbers of total glomerular cells, mesangial cells, and endothelial cells were not changed with diabetes, while podocytes were fewer in number in diabetic patients of all ages, with reduced podocyte numbers even in diabetes of short duration.
CONCLUSIONS: The essentially constant glomerular cell density in nondiabetic and diabetic subjects under different circumstances possibly indicates an underlying propensity for the glomerulus to regulate its architecture to maintain a constant number of cells per volume, no matter the size of the glomerulus or the severity of diabetic nephropathy studied in this set of patients. The reductions in podocyte numbers in both younger and older diabetic patients indicate a significant risk for functional abnormalities as diabetic nephropathy progresses. Moreover, these observations do not support the suggestion of marked increases in glomerular cell number (and especially mesangial cells) with the development and progression of diabetic nephropathy.

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Year:  2001        PMID: 11380812     DOI: 10.1046/j.1523-1755.2001.00725.x

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  149 in total

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4.  Growth-dependent podocyte failure causes glomerulosclerosis.

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Review 6.  Pathophysiology of diabetic kidney disease: impact of SGLT2 inhibitors.

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Review 7.  The renin-angiotensin system in glomerular podocytes: mediator of glomerulosclerosis and link to hypertensive nephropathy.

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8.  A small-molecule inhibitor of TRPC5 ion channels suppresses progressive kidney disease in animal models.

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Journal:  Science       Date:  2017-12-08       Impact factor: 47.728

9.  A novel mouse model of podocyte depletion.

Authors:  L Wang; Y Tang; D N Howell; P Ruiz; R F Spurney
Journal:  Nephron Exp Nephrol       Date:  2012-10-19

Review 10.  Signaling in regulation of podocyte phenotypes.

Authors:  Peter Y Chuang; John C He
Journal:  Nephron Physiol       Date:  2009-01-13
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