The term “uremia” was proposed in 1840 by the investigators pierri P., and D. Leriche. Literally translated from Latin it means “mccrobie”. Indeed, the clinical syndrome associated with the transition components of blood in urine.
The pathogenetic mechanisms of the process causing such violations that this pathology is called self-poisoning of the body. Clinical manifestations are confirmed by the signs of accumulation of decomposition products, which are in high concentrations toxic properties.
The symptoms of uremia occur in extreme stages of renal failure. Also designated a separate syndrome of diseases with severe disorders of protein and electrolyte metabolism, the accumulation of nitrogenous substances (azotemia), disorders of acid-base balance and hormonal regulation. Ezoterichesky uremia in any case, is accompanied by dystrophic changes in organs and disruption of their work.
The main cause of uremia – an acute or chronic renal failure. Affects people of different sexes, children and the elderly. Can be caused by three groups of factors.
- different types of shock, especially the combination of pain and traumatic blood loss;
- a serious infectious disease;
- uremia causes of newborn intrauterine hypoxia in the fetus;
- dehydration (fluid loss with prolonged diarrhea, profuse sweating, massive burn surface);
- heart failure.
The pathogenesis of acute uremia and morphological disruption of the structure of the renal parenchyma most often associated:
- violation of the General circulation;
- activation of fibrinolysis;
- massive destruction of red blood cells;
- melting areas of necrosis in the muscle tissue;
- excessive reaction of phagocytosis destruction of its own cells;
- violation vodnoelektrolitnogo hormonal regulation and acid-base balance.
In chronic uremia is more effective renal and postrenal causes.
To renal are:
- malignant tumor of kidney;
- inflammatory diseases (pyelonephritis, glomerulonephritis, tuberculosis of kidney);
- urolithiasis with stone formation in the pyelocaliceal system;
- thrombosis or mechanical compression of renal arteries and veins;
- polycystic disease and hydronephrosis;
In case of poisoning by nephrotoxic substances, in children is dominated by foods in adults – alcohol, drugs, toxic chemicals
Among postrenal causes should be noted:
- kidney disease;
- adenoma of the prostate gland in men;
- malformations of the urinary tract in children at an early age;
- migrated multiple pregnancy in women, hindering the outflow of urine by pressure on the bladder.
What toxic substances accumulate in the blood uremia?
The main culprit of uremic state are the products of protein metabolism. Most of them are toxic in high doses.
- the cyanate;
- uric acid;
- peptides with an average size of the molecules;
- amino acids;
- aliphatic and aromatic amines;
- pyridine derivatives;
- cyclic adenosine monophosphate;
- the lipochromes;
- galactosamine and oxalic acid;
That shows the study of the affected organs uremia?
The severity of pathological changes in organs and tissues reflects the severity and duration of uremia. Full morphological picture of the organ failure study the results of post-mortem autopsies of dead patients.
Among fatal outcomes of diseases in a hospital of General profile uremia is detected in 3.4% of cases
Major diseases that are complicated by this pathology appeared:
- pyelonephritis with symptoms of chronic renal failure (30%);
- tuberculosis of the kidney (26,5%);
- tumor renal tissue (11%);
- hydronephrosis (9%);
- amyloidosis (9%);
- subacute glomerulonephritis and polycystic kidney disease (5.5%);
- diabetes (3.5 per cent).
The study of anatomical changes caused by a violation of functional properties of organs and systems, is conducted through the records about clinical manifestations in the history of the disease, data of additional examinations.
On the function of the heart and blood vessels have the effect of uremia such factors as:
- changes in the renin-angiotensine system;
- the lack of prostaglandins;
- the growth in the volume of extracellular fluid;
- significant fluctuations in sodium excretion;
The most common signs of damage are:
- renal hypertension (observed in nearly 80% of patients);
- uremic myocarditis (18%) against the backdrop of severe degenerative changes and necrosis of cardiomyocytes;
- fibrinous pericarditis (11%).
Secondary cardiomyopathy is found in 71% of deaths from uremia patients, it is caused by hypertension, acidosis, electrolyte disturbances and coronary artery disease
In the myocardium, while histological examination detected a violation of the form of muscle fibers, interstitial edema, the appearance of protein granules, swelling of the walls of the coronary vessels.
Defeat begins in the early stages of uremia. At first they are reversible and do not affect the functional status of the lungs. Further progression starts the pathological mechanisms of kidney failure, leading to the formation of irreversible fibrous changes.
In this case there is a loss of lung tissue’s ability to ventilation and gas exchange (impaired passage of the molecules through the dense wall of the alveoli).
The most frequent morphological changes:
- uremic tracheitis and tracheobronchitis (in 78% of cases);
- hemorrhagic and fibrinous-haemorrhagic pneumonia (40%).
The digestive organs
The high content of urea and other nitrogenous components in plasma leads to their secretion through the mucosa of the mouth, stomach and intestines, salivary glands.
- acute erosive gastritis (in half of the cases);
- fibrinous esophagitis (19%);
- catarrhal stomatitis (5,5%), aphthous (4,5%);
- acute gastric ulcer leading to fatal bleeding;
- uremic mumps.
The liver is formed toxic hepatitis in 95% of patients. On histology – small and globular fatty dystrophy of hepatocytes, inflammatory infiltration, cell necrosis, 28% of patients developed fibrosis.
Clinicians pay attention to the increased probability of viral hepatitis among patients in whom therapy is used for hemodialysis. Pathologists confirm the coincidence of viral hepatitis 2.1% of cases.
Bone lesions, particularly articular surfaces caused a significant reduction in the rate of filtration in the glomeruli, increase in blood salts of phosphates. They contribute to the reduction of the concentration of calcium in the blood.
The subsequent chain reaction, starting with hypocalcemia stimulates increased production of parathyroid hormone and the development of secondary hyperfunction of parathyroid glands. As a result of increased “washout” of calcium from bone. Bone density is reduced.
X-rays confirmed the destruction of the articular surfaces of bones
Diagnosed different forms of osteodystrophy:
- fibrous osteitis;
Clinicians have noted:
- complaints of patients on pain in bones, muscles;
- frequent fractures (5.5% of the cases, edges) without significant physical impact;
- deformation of the skeleton with compression of the vertebrae;
- necrosis of the femoral head;
- in children with uremia delayed growth.
Morphological changes in the kidneys
The detected changes are determined by the dependence on causes and type of kidney failure. In acute renal failure disorders are often associated with the syndrome of “shock kidney” or have features depending on the toxic properties of toxic substances.
In appearance differs in the pale cortical layer with the plethora juxtamedullary zone. Histology reveals foci of infected tubular epithelium with degeneration of the cells. Rarely there is necrosis.
If the shock caused by hemolysis or massive muscle damage during the crush syndrome, the kidneys find nefrozopodobny changes, thrombosis of the capillaries of the glomeruli.
A similar pattern can be detected at:
- bacterial shock and sepsis;
- the disseminated intravascular coagulation;
- embolism amniotic fluid complicating pregnancy.
For a protracted process of kidney failure is typically thinning of the cortical substance. Pathology of pregnancy is accompanied by hemorrhages and necrosis in the cortical layer of the adrenal glands.
Areas of necrosis limited to the demarcation leukocyte shaft. Then they formed calcification or fibrosis.
Changes are determined by the properties of nephrotoxic substances. Under the influence of poisons, blocking the sulfhydryl groups (for example, salts of heavy metals), there is coagulative necrosis of the tubular epithelium. By the end of the first week comes the sloughing starts cell regeneration.
At poisoning with ethylene glycol is formed symmetrical necrosis of the cortex, combined with nephrosis. The kidney increases in size.
- blood clots in the capillaries of the glomeruli;
- degeneration of the tubular epithelium in the proximal and distal nephrons;
- crystals of oxalates inside cells and in the lumen of the tubules.
For poisoning with dichloroethane characteristic fatty degeneration of the epithelial cells of proximal and distal renal tubules. Such poisonous substances as chloroform and carbon tetrachloride cause degeneration of the cells of the convoluted renal tubules.
Hemolytic poisons (acetic acid, arsenic, copper sulfate, amino – and nitro compounds) contribute to the development of acute haemorrhagic nephrosis. On the morphological changes affected by the violation of transportation of hemoglobin in the renal glomerulus. Visually black-brown striations, the renal pyramids on the cut, which is caused by the formation of age of the cylinders.
- the defeat of the epithelial cells of the proximal tubules molecules of hemoglobin;
- rupture of the tubules in the distal;
- the release of content into the surrounding tissue;
- inflammatory reaction around the tubules, with subsequent overlap of the lumen.
Acetic acid is widely used in the food industry for canning, doctors have to deal with its hemolytic properties
Morphological changes in chronic renal failure are accompanied by characteristic abnormalities caused by the underlying disease. Reduces the mass of functioning nephrons, they gradually atrophy, renal parenchyma filled with dysfunctional sklerozirovanie cloth.
The main clinical and laboratory signs of stage uremia in acute and chronic renal failure are the same. Different symptoms in the early stages.
In acute renal failure the course is divided into 4 periods:
- oliguria or anuria;
- recovery of diuresis;
Signs of uremia are manifested in the second period and continue for up to two weeks:
- the patient’s diuresis is reduced to 500 ml or less;
- increases the level of urea in blood;
- at the same time the rise of creatinine, uric acid concentration of salts (sulfates, phosphates);
- the potassium content higher than normal;
- decreases the concentration of calcium, sodium, chlorine;
- anemia increases (decreases the number of red blood cells and hemoglobin).
These changes are violating vodnoelektrolitnogo balance.
Patients complain of:
- lack of appetite;
- nausea and vomiting;
In clinical diagnosis uremic syndrome it is important to distinguish symptoms from other diseases, because patients are shortness of breath, abdominal pain, diarrhea.
Neurological disorders in uremia:
- nystagmus of the eye;
- decreased reflexes;
- memory impairment;
- the excitement gives way to apathy or comatose condition;
- possible convulsions, paralysis, seizures.
Anisocoria of the pupils is known as the sign of focal changes in the brain in trauma, tumors, stroke, but occurs in uremia
Acute renal failure in severe complicated:
- pulmonary edema,
- hypertensive crises.
After the uremic period comes the phase of polyuria, then begins the recovery. Completely normalized renal blood flow, glomerular filtration and reabsorption function. Clinic of chronic renal failure develops gradually. The deterioration of the patient occurs slowly.
For there are two stages: conservative and terminal. But according to the classification of N.. Lopatkina in urologic diseases, resulting in uremic condition, usually considered 4 stage. Persistent uremia develops in the terminal stage. Although earlier may increase the azotemia with hard work, poor diet, infectious diseases.
For the final stage is characterized by reduction in glomerular filtration rate to 10 ml/min and below. While conservative methods of correction of metabolic disorders cannot. Described above symptoms of acute deficiency are exacerbated by the symptoms of multiple lesions of organs and the nervous system.
- the arrhythmia;
- disorders of taste and smell;
- ulcers in the mouth;
- reduced vision;
- dry skin and mucous membranes;
- acting on the face in the form of a white powder urea;
- petechial hemorrhages;
- muscle atrophy;
- acute deterioration in mental status.
Half of the patients develop different forms of pericarditis until the cardiac tamponade. Signs of lesions of the stomach and intestines are in constant pain in the abdomen, diarrhea with blood.
Anemia is observed in almost everyone of patients: the skin is pale, it is possible to yellowness in connection with the liver. Due to the reduction of platelets visible hemorrhage.
Treatment of patients suffering from renal failure, is complex.
- treatment of the underlying disease;
- detoxification in case of poisoning;
- antishock therapy;
- correction of balance disorders of water and electrolytes;
- the appointment of symptomatic drugs for reducing hypertension, compensation of heart failure, toxins from the intestines.
For patients with chronic uremia increases the period of survival at 22 years with regular cleansing of the body
Treatment of uremia requiring hemodialysis and the patient was included in the waiting list for a kidney transplant. To prepare for organ transplant patient can combine hemodialysis with plasmapheresis.
Uremia caused by acute renal failure, it is possible to save by hemodialysis 65-95% of patients.
The causes of death are complications of the various organs:
- pericarditis with cardiac tamponade;
- infectious disease with inflammation of the lungs;
- intestinal bleeding;
- uremic coma.
Currently, uremia refers to the conditions with which medicine can fight only in the early stages. In the future there is a hope for kidney transplantation or the development of new methods of blood purification.