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Updated: Aug 16, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Microalbuminuria in Rats Treated with D-Nitroarginine Methyl Ether
E V Balbotkina1, T A Karavashkina1, E V Seliverstova1
1I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia.
Abstract:
Microalbuminuria is an early symptom and prognostic marker of the progression of renal pathology. The analysis of the role of anionic components of the renal glomeruli in the albumin retention and the development of a model of minimal changes in the glomerular filter leading to the appearance of microalbuminuria are relevant. The effect of organic cations D-arginine methyl esters (D-AME) and D-nitroarginine (D-NAME) on the excretion of albumin by the kidneys in rats was studied. D-AME had no effect on urinary albumin excretion in rats. D-NAME caused microalbuminuria, which persisted for more than a day and sharply increased after injection of vasopressin. The number of anionic sites labeled with polyethyleneimine decreased in the structures of the glomerular filter. D-NAME-induced microalbuminuria can later serve as a model for studying nephroprotective or damaging factors.
Insights
D-nitroarginine (D-NAME) induces microalbuminuria in rats by reducing anionic sites in the glomerular filter. This finding offers a new model for studying kidney damage and protection.
Area of Science:
- Nephrology
- Renal Physiology
- Pharmacology
Background:
- Microalbuminuria is an early indicator of kidney disease progression.
- Understanding glomerular filter anionic components is key to albumin retention.
- Developing models for minimal change glomerular disease is relevant.
Purpose of the Study:
- To investigate the effect of organic cations D-arginine methyl esters (D-AME) and D-nitroarginine (D-NAME) on albumin excretion in rats.
- To analyze the role of glomerular anionic sites in albuminuria development.
- To establish a rat model for studying microalbuminuria.
Main Methods:
- Administration of D-AME and D-NAME to rats.
- Measurement of urinary albumin excretion.
- Assessment of anionic sites in the glomerular filter using polyethyleneimine labeling.
- Injection of vasopressin to observe effects on D-NAME-induced microalbuminuria.
Main Results:
- D-AME did not affect urinary albumin excretion.
- D-NAME induced persistent microalbuminuria lasting over 24 hours.
- D-NAME administration led to a decrease in glomerular filter anionic sites.
- Vasopressin injection exacerbated D-NAME-induced microalbuminuria.
Conclusions:
- D-nitroarginine (D-NAME) causes microalbuminuria in rats, associated with reduced glomerular anionic sites.
- This D-NAME-induced condition serves as a potential model for studying factors affecting nephropathy.
- Further research can utilize this model to explore nephroprotective and nephrodamaging agents.
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