Nephrotic edema mechanism

· Excess oral intake of table salt

</ b> Pathophysiological mechanisms of edema arelowering of the oncotic pressure (ie, the pressure formed due to the osmotic activity of albumin) and the osmotic pressure of the blood plasma (pressure due to the osmolality of the plasma, one of its components is the oncotic pressure). Also, edema develops with an increase in hydrostatic blood pressure in the capillary. The opposing forces of the P guide are Panc, P osm and Pt. Tissue pressure is composed of the osmolarity of the interstitial space and the pressure of the interstitial tissue on the wall of the capillary. An important factor in the appearance of edema is an increase in the permeability of the capillary wall, which develops during hypoxia, hypercapnia, acidosis, inflammation, an increase in P guide.

In connection with the above, the listedpathological processes trigger different pathophysiological mechanisms of edema development. This is reflected in the nature of differential diagnosis and treatment. The diagnostic task for the appearance of edema is formed on the basis of the listed main causes of edema, pathophysiological mechanisms and clinical classification. In order to determine whether a particular pathophysiological mechanism is appropriate, it is necessary to bear in mind the diagnostic algorithm. Of course, each of the pathological conditions leading to the formation of edema, has its clinical picture, which is reflected in the algorithm means to make it cumbersome and non-functional.

2. Causes of edematous syndrome</ b>

</ i> Genesis of edema in nephrotic syndrome is associated witha decrease in the oncotic pressure of blood plasma due to a decrease in albumin concentration. These swelling are also called protein-free. Characteristic are their symmetry, as well as localization on the lower limbs. The latter is observed in patients who spend most of their time standing or sitting with their legs lowered. Edematous tissues have the property to form in those parts of the body, the venous blood pressure in which is positively elevated. Edema can position migrate, i.e. depending on the position of the patient's body, the hands, face and neck, body can swell. With a long lying position, swelling of the lower extremities decreases, edema of the upper limbs and face appear. Often, the intensity of edema is asymmetric. With prolonged lying on the side, extremities of the lateral side swell more. Mandatory satellites of edema in nephrotic syndrome are high proteinuria and hypoalbuminemia. The absence of one of these signs casts doubt on the nephrotic syndrome.</ b>

</ i> With nephritic syndrome, most often swellinglocated on the face, namely in the periorbital zone, as well as in the phalanges of the fingers and forearms. This is because the nephritic syndrome reduces urinary sodium excretion, which is accompanied by the development of hypernatremia. Compensatory reaction is the redistribution of sodium with its transition from vascular space to extravascular. Thus, tissue hypernatriosis is formed, leading to an increase in the osmolality of the interstitial tissue and an increase in Pt, which leads to the transition of water into the interstitial space. This process is observed in all parts of the body, but the loose hydrophilic regions of the cellulose swell more. This explains the localization of edema. Edema is mild and more noticeable on the face. It should be remembered that nephritic syndrome in addition to edema includes urinary and hypertensive syndromes. In order to remind you of the clinical manifestations of nephritic syndrome, you need to remember the math:

Nephritic Syndrome = Urinary Syndrome + Hypertensive Syndrome + Hyperhydration

Urinary Syndrome = Erythrocyturia and / or Proteinuria <3.5 g / day

Hypertensive syndrome = AH (with a chronic nephritic syndrome) or an acute hypertensive reaction (in acute nephritic syndrome)

Hyperhydration = Peripheral, hollow and parenchymal edema Hypervolaemia</ i>

</ i> Hyperaldosteronism is often found inclinical practice and is mainly associated with three main problems: the use of diuretics, CHF and nephrotic syndrome. In this case, hyperaldosteronism is designated as secondary. There is also a syndrome of Cohn caused by a benign tumor of the adrenal gland (aldosterome) with hyperproduction of aldosterone. In this case, there is primary hyperaldosteronism. Removal of the tumor is accompanied by a cupping of the clinic of the disease.

In the diagnosis of hyperaldosteronism,determination of blood aldosterone level. When taking blood in the prone position, the aldosterone concentration is normally 8-172, while in the standing position it is 30-355 mg / ml.

With primary hyperaldosteronism, the concentrationaldosterone in the blood exceeds the normal 5-10 times. There is a delay in sodium and water, potassium excretion in the urine increases. Edema is symmetrical. The face, limbs are swollen. Often develops hypertension.

Unlike primary hyperaldosteronismsecondary does not lead to the development of hypertensive syndrome. Significantly less pronounced edematous syndrome (pastosity of the face, fingers and toes). Hyperaldosteronism is not an independent cause of anasarka, however, pronounced swelling, for example, with nephrotic syndrome or chronic heart failure, usually occurs with the phenomena of secondary hyperaldosteronism. This is due to many reasons. The main among them are the use of loop diuretics for the control of edema with the development of hyponatremia, the formation of hypovolemia (nephrotic syndrome), circulatory hypoxia (chronic heart failure). They are a potent stimulant of renin secretion, which activates the conversion of angiotensinogen into angiotensin I, which leads to an increase in the concentration of angiotensin II and aldosterone. The secretion of aldosterone is also amplified directly by the action of these factors.

When taking diuretics, especially loop(furosemide, torasemide, ethacrynic acid), there is hyponatriosis, which is a powerful stimulant for the secretion of aldosterone. In this regard, daily intake of furosemide in the same dose is accompanied by a gradual decrease in diuresis, despite the absence of complete relief of the phenomena of hyperhydration. With pseudosyndrome Bartter, the main pathogenetic link of developing changes due to prolonged abuse of furosemide is hyperaldosteronism.

</ i> With chronic heart failure, edemaare associated with an increase in P guide and an increase in the permeability of the vascular wall due to circulatory hypoxia. Since the growth of P guide is due to a decrease in the contractile activity of the right ventricle, hypertension in the system of hollow veins leads to an increase in pressure in the venules and capillaries of the microcirculatory bed. Peripheral edema is caused by isolated right ventricular heart failure or its combination with left ventricular. In addition to hemodynamic reasons, it should be noted that secondary hyperaldosteronism develops with water and sodium retention in heart failure, which is a self-causing or exacerbating factor.

Since in the genesis of edema the main role is played byhydrostatic component, they are observed in those parts of the body in which the positioning guide is higher (lower limbs). Swelling of the legs have the property of decreasing in the prone position, while swelling of the face and upper limbs is aggravated. Usually, edema decreases with therapy with loop diuretics. Perhaps the development of an anasarca, as well as cavitary and parenchymal edema, often accompanying peripheral edema. Edema in heart failure is always accompanied by its other symptoms in the form of general weakness, dyspnea, malaise. In the anamnesis, as a rule, there is a chronic cardiac pathology (arterial hypertension, ischemic heart disease, cardiomyopathy, congenital or acquired heart disease, etc.). Dyspnea increases with walking and decreases at rest. In echocardioscopy, signs of systolic left ventricular myocardial dysfunction are revealed in the form of a decrease in the ejection fraction, an increase in the end systolic and diastolic volumes, and a decrease in the stroke volume. In the study of blood, there is no hypoalbuminemia, and in the study of urine - proteinuria, which excludes nephrotic syndrome or protein starvation as the causes of edematous syndrome. However, the phenomenon of a congestive kidney that develops in chronic heart failure is known and manifests itself as a small proteuria with a decrease in renal function, which is wavy in nature and grows or decreases as the signs of heart failure decompensate. This pathological condition is not always easy to differentiate with glomerulonephritis on the background of heart failure. With a congestive kidney (secondary nephropathy in the background of chronic heart failure) there is no nephrotic syndrome, extremely rare hematuria, and the explanation of its appearance often lies in the plane of iatrogenic pathology (drug interstitial nephritis). The latter also needs to be differentiated from a stagnant kidney. The presence of an isolated erythrocyturia, the lack of swelling, the presence of a causative drug or a combination thereof (NSAIDs, analgesics, aminoglycosides), as well as the restoration of renal function after the abolition of these medicines allow differential diagnosis.

Not all pathological conditions are accompanied by the development of edema, but their appearance against the background of chronic heart failure explains their combination with edematous syndrome.

Moreover, in some cases, the genesis of edematous andurinary syndrome is due to a single disease. For example, in a patient suffering from infective endocarditis, valvular heart disease develops with the development of severe heart failure and, as a consequence, edematous and urinary syndromes (congestive kidney), kidney damage proceeds according to the type of glomerulonephritis caused by the immunocomplex mechanism, leading to the formation of a urinary syndrome and contributing contribution to the development of edema. In this case, carrying out puncture nephrobiopsy does not always allow for differential diagnosis, and due to the severity of the condition and the presence of contraindications to biopsies, the latter seems hardly possible.

</ i> One of the possible causes of edema isbecome alimentary hypervolemic hypernatremia, which develops as a result of consuming a large number of products containing a lot of table salt and liquid (for example, salted fish with a lot of water or beer). Light swelling appears after several hours and pass independently for 1-2 days. There is swelling of the face (periorbital edema), less often - fingers and toes (a symptom of a tight ring). Swelling occurs more often in individuals with hereditary predisposition to retention of sodium with kidneys (salt-sensitive). Often edema accompanied by a sharp increase in blood pressure in normotonics or hypertensive crisis in people with hypertension.

In some healthy people the appearance of puffinessunder the eyes (periorbital edema) may be a consequence of the excess fiber in this area and is not a pathology. Usually this physiognomic trait is inherited. We conducted a family analysis of 20 healthy persons with periorbital edema and 20 persons without such. In families with proband with periorbital edema among relatives of the first degree of kinship, similar edema occurred with a frequency of 80% on the maternal or paternal line. In relatives of probands without edema, the prevalence of edema does not exceed 5%. According to our data, the prevalence of these edemas in the regional population was 37% (n = 300). At the same time, in a screening study, only 7% had a urinary tract pathology. Thus, in our opinion, it is expedient to allocate family periorbital edema, which is not a symptom of somatic pathology.

</ i> This cause of edema lies in the plane of iatrogenia. In the forensic medical examination of the patient's case of 18 years old, suffering from diabetes mellitus and died of cerebral edema, we found that death was due to excess infusion of crystalloid solutions. For ten days the patient was infused with saline solution, Ringer-Lok solution in a volume of 10 to 13 liters / day.

On the second day there was swelling of the feet andshins, which, despite the use of loop diuretics, did not disappear. The edema of the optic nerve and pulmonary edema, the increase in central venous pressure were noted on the 7th day of treatment, brain symptoms appeared in the form of a constant diffuse headache, hyperreflexia. There was also swelling of the soft tissues of the oropharynx, regarded by the otorhinolaryngologist as tonsillitis, despite a history of tonsillectomy. There was also an acute increase in blood pressure, polyuria, thirst and hypernatremia. In this case, almost all the symptoms associated with high-volume infusions are described. At the basis of edema is hypervolemic hypernatremia. In Russia, there is no data on this kind of iatrogenia, as in most other iatrogenia.

In a selective analysis of patient records,treated in the departments of therapy and cardiology (n = 177), unjustified infusions of crystalloid solutions were made in 76% of cases. At the same time, excessive infusions, capable of leading to the development of water-electrolyte disorders, were carried out in half of cases of their unmotivated appointment. When talking with doctors, the most frequent arguments in the appointment of infusion therapy was the need to conduct detoxification and provide the proper level of treatment, as tableted therapy patients can receive in outpatient settings. In our opinion, the decision to conduct routine infusion therapy should be made by a consultation of doctors, and cases of unjustified infusion therapy are accompanied by special attention of experts of insurance medical companies.

</ i> Edema and hypoalbuminemia in protein starvationare interrelated. Edema occurs in the case of protein or complete starvation, provided free fluid intake. In this case, edema may appear on the 3rd-5th day.

When conducting differential diagnosisgreat importance is the questioning of the patient with the construction of a diary, as well as the presence of hypoalbuminemia in the absence of proteinuria. Edema is symmetrical. They are often located on their feet. Normalization of food or intravenous drip in severe cases of albumin solution is accompanied by the coping of edema. The action of furosemide is low and increases only after the infusion of the albumin solution.

</ i> With hepatic failure, edema occursdue to a decrease in the protein's protein function and a drop in serum albumin levels. Also, edema can worsen in patients with hepatorenal syndrome due to the development of hyperhydration and a sharp increase in the permeability of the vascular wall. In the case of maintaining an adequate diuresis, administration of albumin solutions or liver transplantation can reduce swelling.

1.</ b> Nephrology. Keys to a difficult diagnosis / MM Batyushin - Elista: ZAOR NPP "Janahar", 2007.

2. Nephrology. Fundamentals of Diagnostics / Ed. Bustard. VP Terentyev. (Series "Medicine for You.") - Rostov n / a: Phoenix, 2003.