Mechanism of development of renal edema
Pathogenetically distinguish three factors that cause edema in renal pathology.
1. Hydrostatic (hypervolemic). Reduction of the glomerular filtration rate,leads to a delay in sodium and water in the body development of hypervolemia, which is the cause of increased hydrostatic pressure in the capillaries and causes the development of edema by the mechanism of Starling. This factor plays a major role in the oligoanuric phase of acute and chronic renal failure, with impaired blood circulation of the kidneys.
2. Oncotic (hypoproteinemic). Violation of the glomerular filter causes a massiveproteinuria, as a result of which hypoproteinemia develops and the oncotic blood pressure decreases. This causes the transition of water from the vessels to the tissues by the mechanism of Starling and edema develops. Occurs with nephrotic syndrome.
3. Activation of the renin-angiotensin-aldosterone system. The hypoxia of the juxtaglomerular apparatus causesincreased renin secretion by the kidneys. Renin, being a proteolytic enzyme for angiotensinogen, turns it into angiotensin-1, which under the influence of angiotensin converting becomes angiotensin-2, which, by activating the glomerular zone of the adrenal cortex, leads to an increase in aldosterone synthesis, which leads to sodium retention with an increase in osmotic blood pressure and stimulation development of an antidiuretic hormone, which leads to hypervolemia and edema.
Violations of the acid-base state in renal pathology
The most frequently developed negative acidosis. Depending on the nature of pathological processes in the kidneys, there are three possible variants.
1. Glomerular acidosis (renal azotemic acidosis). It arises from the development of renaldeficiency with a decrease in the glomerular filtration rate below 25 ml / min. It refers to metabolic acidosis with an increased anionic difference. Its development is due to the accumulation of endogenous hydrogen ions, mainly in the form of sulfates, phosphates, uric and other acids.
2. Proximal renal tubular acidosis. Is an
as a result of a disruption in the ability of tubules to reabsorb bicarbonates in the proximal convoluted tubules of nephrons.
3. Distal renal tubular acidosis. It is caused by primary disturbances of processesacidogenesis and ammoniogenesis in distal convoluted tubules, where titration of buffers (preservation of bicarbonate) and acidification (acidification) of urine occur.