Why seniors need phlazine in chronic kidney disease

Chronic kidney disease is easy to diagnose but leads to premature death in 95% of patients. 80,000 patients die annually. Approximately 4 - 4.5 million Polish women and men suffer from this condition in Poland. 11% of adults have already lost more than half of their active kidney parenchyma and 18% of the Polish population has kidney function below physiological norm.

Chronic renal failure is a disease with a long and slow disease progression.

The cause of kidney disease can be hypertension, diabetes - diabetic nephropathy, congenital diseases, autoimmune diseases, kidney interstitial diseases - primary or secondary glomerular diseases and tubular interstitial kidney diseases.

If unrecognized and untreated, it always leads to chronic kidney failure.

Acceleration of chronic kidney disease is influenced by age, gender , family burden, hypertension, smoking, hyperglycemia, obesity. Dangerous complications include anemia, mineral and bone complications and protein and calorie malnutrition.

Chronic renal failure is diagnosed by a simple laboratory diagnosis, we test the level of creatinine, urea then GFR or glomerular filtration rate.

It determines the amount of glomerular filtrate in the kidneys.

Based on the abnormalities observed, we perform uACR, which is the determination of the ratio of albumin to creatinine in the urine.

Flozins or sodium glucose cotransporter 2 or SGLT 2 inhibitors.

We have six of them in the world but not all in Poland.

In Poland, dapagliflozin is the most popular.

They are commonly used in diabetes but act with their nephro and cardioprotective mechniism on the overworked kidneys and jaded hearts.

In chronic hyperglycemia, the activity of the glucose-sodium cotransporter increases, leading to an increase in the amount of reabsorbed glucose and sodium.

Less sodium reaches the macula densa, the tension of the ductus arteriosus decreases because it dilates which leads to increased blood flow through the glomeruli.

Intrathoracic pressure increases and GFR increases.

Mechanism of nephroprotective action of SGLT2 inhibitor

Administration of an SGLT2 inhibitor to a patient preserves glucose and sodium reabsorption.

More sodium ions reach the dense macula

Dense spot stimulated orders the arteriole to increase tension, blood flow through the glomeruli decreases.

SGLT2 inhibitor lowers intraglomerular pressure, increases natriuresis, osmotic diuresis, arterial pressure.

The SGLT2 inhibitor improves neurohormonal balance, reduces inflammation and fibrosis, and decreases renal hypoxia.