Pathogenetic mechanisms of reduced glomerular filtration rate

Abstract

Relevance. Decreased glomerular filtration rate is a symptom that is diagnosed in kidney pathology and in cardiovascular diseases. The study of the processes of development and progression of decreased glomerular filtration rate will bring closer the solution of problems of nephrology, cardiology and pathological cardiorenal relationships.

Aim. To study the development and progression of decreased glomerular filtration rate.

Material and methods. Using the data of a 6-year prospective follow-up of 22 clinical and anamnestic indicators of a natural group of initially healthy 7,959 men (workers of locomotive crews) aged 18 to 66 years, we found out the origin of decreased glomerular filtration rate and the progression of this pathological symptom. For this purpose, a confusion matrix, a multivariate regression model, relative risk assessment, Kaplan-Meier models and Cox proportional hazards model were used.

Results. Decreased glomerular filtration rate was determined to be due to arterial hypertension, hyperglycemia, aortic sclerosis and creatininemia. These predictors in the types of analyses used showed statistical heterogeneity in assessing their significance. Thus, the predictors have asserted their specific characteristics that can be used for their biochemical or ultrastructural identification at the cellular level and identification of their damage effect.

Conclusion. The course of endothelial dysfunction under the influence of decreased glomerular filtration rate predictors varies considerably and depends on the effect of a particular factor, a set of predictors or all predictors taken together when they are involved simultaneously. These data show the need to find out ultrastructural and biochemical specific markers and their quantitative values of renal endothelial dysfunctions occurring under the influence of decreased glomerular filtration rate predictors during the development and progression of this pathological symptom to restore the normal function of the endothelial cell and the affected organ as long as there is still room for therapeutic efforts.