Nephritic syndrome is a complex of signs of renal pathology, which includes edema, hematuria and arterial hypertension. It occurs in various forms of glomerular disorders: postinfectious and rapidly progressing glomerulonephritis, IgA nephropathy, hereditary and autoimmune nephropathies. The syndrome is manifested by swelling of the face and lower extremities, urine discharge of the color of “meat slops”, severe headaches. Ultrasound and CT of the kidneys, puncture biopsy, laboratory blood and urine tests are prescribed for diagnosis. Treatment of glomerular pathology includes glucocorticoids, immunosuppressants, hypotensive and nephroprotective drugs.
ICD 10
N05 Nephritic syndrome, unspecified
Meaning
Acute nephritic syndrome (ANS) associated with glomerulonephritis occupies the 3rd-4th place in the structure of renal pathology. The disease mainly occurs in children and young people, men get sick 2 times more often than women. ANS is recognized as one of the most dangerous conditions in practical nephrology, because it is fraught with a rapid decline in renal function, severe cardiovascular complications. The development of new methods of treatment and effective measures for the prevention of the disease does not lose relevance.
Causes
The syndrome is formed in all variants of glomerulonephritis – primary inflammation of the renal glomeruli, which proceeds with the involvement of the interstitial process, tends to progress. Among the acute forms of the disease, post-streptococcal glomerulonephritis prevails, enterococci, herpesviruses, toxoplasmas and schistosomes also act as pathogens of the disease. Other causes of glomerular disorders:
- IgA-nephropathy. The most common form of nephritic syndrome, which occurs when immune complexes accumulate in the glomeruli. The disease is characterized by a gradual and steadily progressive development. The risk group includes adolescents and young men, representatives of the Caucasian and Asian races.
- Rapidly progressive glomerulonephritis. The disease develops with the defeat of more than 50-60% of the glomeruli, the formation of characteristic half-moons in their membranes. Typically, the rapid formation of an expanded ANS, its progression to the terminal stage of renal failure in a few months.
- Lupus is jade. Renal pathology is a typical manifestation of systemic lupus erythematosus, which is caused by nonspecific autoimmune damage. Nephritic symptoms develop against the background of thickening of the glomerular basement membranes, fibrin deposits, and the appearance of hyaline thrombi.
- Hereditary jade. Pathology develops with a mutation of the COL4A3 gene, which is mainly inherited by the X-linked mechanism. Manifestations of ANS occur in childhood, by the age of 20-30, most people have signs of chronic kidney disease.
- Rheumatological diseases. In addition to lupus erythematosus, damage to the renal glomeruli is provoked by rheumatoid arthritis, systemic scleroderma, dermatomyositis. The cause of pathology is also vasculitis: nodular polyarteritis, nonspecific aortoarteritis.
- Other reasons. ANS is a clinical variant of the onset of nephropathy in 29% of cases of antiphospholipid syndrome, in 25% of patients with cryoglobulinemia. About 20% of patients with Schenlein-Genoch purpura have recurrent forms of kidney damage. Sometimes clinical and laboratory syndrome develops with alcoholic nephropathy.
Nephritic syndrome is observed in non-infectious kidney damage by chemical agents. The nephrotoxic effect has pollen of poisonous plants, insect poisons, organic solvents. Immune inflammation of the glomeruli in rare cases develops after vaccination and administration of therapeutic serums. Endogenous tumor antigens also have a toxic effect.
Pathogenesis
The key link in the development of nephritic syndrome is considered to be the deposition of immune complexes in the renal glomeruli in the gap between the basement membranes and the processes of podocytes. There is a pronounced inflammatory reaction, the glomerular filtration rate decreases, water and salts are retained in the body. Elevated sodium levels and activation of RAAS provoke an increase in the volume of extracellular fluid.
Under conditions of hyperhydration, cardiac output increases, vascular walls swell and their sensitivity to catecholamines increases, prostaglandins and kinins production decreases. Such mechanisms cause persistent arterial hypertension. The redistribution of fluid with preferential deposition in loose fiber causes edema.
The inflammatory process damages the glomerular capillaries and disrupts filtration processes, as a result of which erythrocytes and large-molecular plasma proteins enter the primary urine. Cylinders appear in the urinary sediment, micro- or macrohematuria occurs. With nephrotic syndrome, aseptic leukocyturia, moderate proteinuria is possible, the degree of which correlates with the severity of damage to the glomerular membranes.
Symptoms
Brown or pinkish-gray color of urine is a specific sign of nephritic syndrome, which causes patients to immediately consult a doctor. It is accompanied by aching lower back pain, general weakness and malaise, and a decrease in diuresis. At the same time, dense nephritic edema appears, which are most pronounced on the face in the morning. When the heart is affected, swelling also occurs on the legs.
The defeat of the cardiovascular system manifests compressive headaches, shortness of breath, unpleasant sensations in the heart area. With a sharp increase in pressure, patients experience tinnitus, dizziness, nausea. Damage to the fundus is manifested by the flickering of “flies”, blurred vision. The clinical picture is complemented by sleep disorders, increased muscular and mental excitability.
The features of the course of nephritic syndrome depend on its root cause. With rapidly progressing glomerulonephritis, deterioration occurs rapidly: oliguria develops, nausea and vomiting, lethargy and other disorders of consciousness. In severe cases, uremic gastroenterocolitis is associated, which often causes profuse gastrointestinal bleeding.
Complications
A natural consequence of untreated nephritic syndrome is renal failure, which in 15-20% of cases ends in death. The defeat of the cardiovascular system is fraught with pulmonary edema, cardiac asthma. A critical increase in blood pressure increases the risk of hemorrhagic strokes, blindness due to retinal detachment.
With the development of nephritic syndrome against the background of nephropathy of pregnant women, there is a risk of eclampsia ‒ severe gestosis, occurring with convulsions, loss of consciousness, disorders of uteroplacental hemodynamics. Against the background of generalized convulsive syndrome, it is possible to develop brain edema and a comatose state, which is difficult to correct.
Diagnostics
Finding out the root cause of nephritic syndrome is handled by a nephrologist. At the initial examination, pallor and pasty skin, pronounced edema, auscultative signs of cardiac pathology are determined. Recent acute infections and contacts with chemicals have diagnostic value. The plan of the extended examination of the patient includes the following methods:
- Ultrasound of the kidneys. Sonography is used to assess the structural features of the organ, to exclude cavities and volumetric formations. To study the speed of blood flow in the renal vessels, Dopplerography is performed.
- Radiation diagnostics. According to the indications, the study program is supplemented with overview and intravenous urography, CT of the kidneys. Diagnostics of the functional activity of the organ is performed by isotope renography.
- ECG. Electrocardiogram results show signs of left ventricular hypertrophy. To clarify the degree of decrease in cardiac output, echocardiography is performed.
- Kidney biopsy. Puncture biopsies are examined using light and electron microscopy for morphological diagnosis of glomerulonephritis. Immunofluorescence analysis of cells is used to clarify the diagnosis.
- Examination of the fundus. Vascular damage in arterial hypertension is manifested by the phenomenon of “crossroads”, narrowing of arterioles. In severe cases, there is swelling of the optic disc and retinal hemorrhage.
- Urine tests. The pathognomonic sign of ANS is hematuria with the appearance of glomerular leached erythrocytes. Leukocyturia, nonselective proteinuria, hyaline and erythrocyte cylinders are also diagnosed. In the Zimnitsky sample, a decrease in the relative density of urine is determined.
- Blood test. Biochemical examination reveals dysproteinemia, hyperglobulinemia, increased activity of fibrinogen and plasmin. Immunological diagnostics reveals circulating immune complexes, increased complementary activity of serum.
Differential diagnosis
When a nephritic syndrome is detected, a differential diagnosis is made between acute and chronic glomerulonephritis, acute medicinal nephritis, renal pathology against the background of systemic connective tissue diseases. Questionable laboratory data require the exclusion of pyelonephritis, tubulointerstitial pathologies, tuberculosis and amyloidosis of the kidneys.
Treatment
The reverse development of renal pathology is achieved by eliminating the etiological factor, if possible. In case of intoxication, extracorporeal methods of blood purification are prescribed, antidotes are used, nephrotoxic drugs are canceled. With paraneoplastic syndrome, complex treatment of oncopathology is carried out. However, the etiological approach is implemented in a small part of patients.
Pathogenetic and symptomatic therapy is most often used in clinical nephrology. In the acute period of nephritic syndrome, bed rest is necessary. To reduce edema, it is recommended to reduce the use of table salt and control the volume of liquid consumed, the amount of protein in the diet should not exceed 0.75-1 g / kg of weight. The pharmacotherapy scheme includes:
- Glucocorticoids. Hormones suppress immune inflammation, they are recognized as the drugs of choice for glomerular lesions. With their insufficient effectiveness, cytostatics and other types of immunosuppressants are used.
- Blood-thinning drugs. To improve the rheological properties of blood and prevent thrombosis, a combination of direct anticoagulants and antiplatelet agents is prescribed. Taking medications is carried out under the control of coagulogram indicators.
- Nephroprotectors. A good effect is provided by antihypertensive drugs that affect the RAAS and vascular tone. In nephritic syndrome, ACE inhibitors and their more modern analogues, angiotensin II receptor blockers, are prescribed. Calcium antagonists are used less often.
- Antibiotics. Antimicrobials are prescribed for proven streptococcal etiology of the disease and the presence of microorganisms in the blood. In renal tuberculosis, long-term specific chemotherapy is indicated.
Prognosis and prevention
The outcome of the disease depends on the morphological variant of kidney damage, the timeliness of therapy, and the development of chronic renal failure. Due to the complexity of the etiopathogenesis of nephritic syndrome, most patients require long-term pathogenetic therapy, dispensary observation by a nephrologist, and regular monitoring of kidney function. Prevention consists in early initiation of nephropathology treatment to prevent the development of acute kidney failure and CRF.