Acute diffuse glomerulonephritis postinfectious
Kidney disease is preceded by infectious process (typically the preceding streptococcal tonsillopharyngitis). After a latency period of 2-3 weeks of this form is characterized by abrupt start, strongly marked with the complete clinical picture which corresponds to diffuse lesions glomeruluma: urinary findings, Eden's syndrome, a disorder of homeostasis (increased blood volume, altered electrolyte composition of blood), syndrome of inadequate secretion of renal function nitrogen compounds, changes in the cardiovascular device due to hypertension and diffuse capillary damage.
Acute glomerulonephritis following skin infection
Usually in children, after impetigo, and in adults in relation to infection of the skin burns. Causative germs are usually streptococci, and others.
Various infection-causing germs:
Staphylococcal infection may precede the appearance of glomerulonephritis, often with simultaneous subacute bacterial endocarditis.
Pneumococcal, streptococcal, unlike, latent period between the infectious period and renal disease is longer; arterial hypertension is rare.
Typhoid fever, brucellosis, Rickettsioses, may be accompanied by acute glomerulonephritis.
Leptospirosis ikterohemoragička usually causes kidney lesions in the interstitium, but there are cases with glomerular lesions.
Rheumatic fever
Viral infections
Confluence of the evolution of epidemic mumps, rubella, chickenpox, infectious mononucleosis, acute glomerulonephritis can occur.
Post vaccinal glomerulonephritis
After the vaccine against smallpox, typhoid, diphtheria, BCG and others.
Glomerulonephritis likely infectious origin but the cause is unknown.
War nephritis (Kriegsnephritis, Field nephritis, Trench nephritis). Epidemic occurrence among soldiers, and civilians in extremely occurs. It is more infectious syndrome manifested - chills, fever, headache, loss of appetite, fatigue, and tonzilofaringealne infection rarely precede the disease.
Hemoragički nefrozo-nephritis
It describes the epidemic in Manchuria, Korea, European Russia, the Crimea, at the foreface Omsk, in Uzbekistan, and here. It is spread by flea bites field rodents. It is believed that the viral origin. Russian authors is called endemic hemoragički nefrozonefritis.
Glomerulonephritides noninfectious origin
During serum sickness, allergic phenomena due to hypersensitivity to drugs or food, in the course of rheumatoid purpura, purpura Henoch-Scholein, allergic dermatitis.
No known etiological factors
Not preceded by any infection, and can not find an explanation for the occurrence of glomerulonephritis.
Nefritogene are beta hemolytic streptococci of group A. Most vines belong to type 12 or type 4, is the first cause of epidemics, and other sporadic cases. Nefritogeni are more types 1, "Red Lake" 49, 19, 31 and others.
The anatomical-morphological terms corresponding to acute glomerulonephritis kapilaritisu Malpigijevih particle, ie. glomerulitisu. The kidneys are hyperemic, and glomeralne dilated capillary loops. Later, it occurs in certain loops serofibrinozni spout polinuklearnim rich in leukocytes, endothelial cells are swollen, proliferous and narrow capillary hole. The basal membranes swell, dissociate into strips. Capsular space is filled with red blood cells and epithelial cells deskvamisanim.Tubular epithelium was swollen, containing hyaline granulation and vacuoles.
In clinical terms
There are diffuse acute poststreptococcal glomerulonephritis, subacute, malignant form, with short and rapid evolution to death over the outcome, focal, focal, glomerulonephritis cirkurnskriptni, more anatomical-histological than clinical individuality.
The functional
The forms with preserved function of excretion of nitrogenous products, focal nephritis; forms with impaired secretion, diffuse glomerulonephritis. They are usually with hemodynamic disturbances, increased blood volume, types of congestive heart failure, arterial hypertension and hypertensive encephalopathy.
Diagnosis
Anamnesis
Swelling face, eyelids, and ankles but can the legs and whole body, pain in the buttocks, sometimes with dizuričnim disabilities. The quantity of urine is reduced. The urine is dark in color. The temperature is often elevated. Petechiae, urticaria. Dyspnea. Headache.
One week to three weeks earlier it was an infectious disease: tonsillitis, sinusitis, intestinal catarrh, scarlet fever, sores on the skin, fertilizing the roots of teeth. It is characteristic that no free interval between infection and swelling.
Clinic
Facial pallor. A pale and painless islands face and other body parts: legs, arms, lumbar foreface.
There are various disorders of the heart, especially if the patient over 40 years, and if food containing salt, and urine output was low.
There is often an effort dyspnea, hypertension, the path to the lungs. Systolic murmur at the top of the heart. In severe cases it can perform the expansion of the heart, venous stagnation on the bases of the lungs, liver uvećeanje, dyspnea in the supine position, signs of pulmonary edema, the appearance of a gallop on the heart, even acute pulmonary edema - especially in children.
Venous pressure is elevated. ECG changes can be noted on the T wave (low or inverted), less likely to QRS (extension), or prolonged QT wave. Notwithstanding PR wave is extended, or P is deformed, or are there a variety of arrhythmias.
With the increase in diuresis, losing the clinical and radiological signs of heart failure.
Initially, some patients have a fever. Vomiting, thirst. Absence of sweating.
The children could mark the onset of confusion, transient neurological impairments, for example.blindness.
The appearances of the CNS: Headache, Nausea, vomiting are common symptoms, sometimes the first disturbance of patients. Drowsiness, disturbances of consciousness and even coma. Cramps, usually generalized frequent and continuous nekiput, epileptic status. These phenomena are usually closely associated with hipertenezijom.
Radiological findings: effusion in the pleural space, the path of the lungs, signs of light infiltration into the lung parenchyma Perihilar zones, increased heart rate.
Urine: oliguria, anuria rarely. Specific gravity of urine is high. Rarely there izostenurija, which is then held several months after the disappearance of signs of acute period.
Urine color: dark brown, bloody, muddy.
Proteinuria: usually moderate. Selective. In severe cases, non-selective.
Electrophoresis of urinary proteins: serum albumin prevail. Alfa is one glycoproteins increased.
Macroscopic hematuria, or microscopic.
Leukocyturia usually moderate. Notwithstanding pyuria (excretion of more than one million leukocytes per minute).
Cylinders: granular, epithelial, erythrocyte, leukocyte, hijalni; different sizes.
Antstreptolizinski O titer increased.
Urea: Urea concentration in the blood less likely to have a normal, moderately elevated more frequently, in cases with an oliguria-one can be very high.
Creatinine: movement as well as urea, but increases have been moderate.
Non-protein nitrogen in close correlation with urea.
Electrolytes in the blood: changes in concentration, as well as mutual relations are different: depending on the diuresis and from clinical forms (nephrotic syndrome, hypertensive form).
Sodium: reduced in nephrotic syndrome.
Potassium: increased in anoliguriji, in cases with intense tissue catabolism.
Calcium: expressed a preference for a reduction in concentration.
Magnesium: an increase in koncenetracije-oliguria.
Chlorides: different concentrations.
Bicarbonates: the lower level, that increased in cases with copious vomiting.
Sulfates: in cases with decreased urine output and renal insufficiency have increased.
Phosphate: and sulfates.
Protein: total protein concentrations were normal, but decreased in cases of nephrotic syndrome.Decreased albumin and increased globulin.
Alpha one globulins are increased if a lower serum albumin. Often the increased gamma globulins.Quantities of two alpha and beta globulins were not significantly altered.
Lipidemija and total cholesterol were within normal limits, except in children, in whom may be in increased concentrations.
Haemogram: leukocytosis with lymphopenia.
SE: moderately or very rapid.
Histology
• Diffuse endokapilarna cell proliferation.
Glomerular club is enlarged and has an increased number of cells (cell proliferation endokapilarnih, infiltrovanjem polinukleara and macrophages), the space between klubeta and Bauman's capsule was reduced.
Here and there in ball depots are homogeneous, hyaline mass.
Evolution of histologic changes:
Withdrawal endokapilarne proliferation.
Recanalization long clogged capillary loops.
Hijalinizacija individual glomeruli.
Diffuse proliferation of epithelial cells, especially of visceral part of Bowman's capsule, creating crescents cell infiltration or adhesion interflokulokapsularnih. Complete destruction of the glomerulus.
Hijalni depots and fibrinoid mass glomerulurima.
Maintenance endokapilarne diffuse proliferation in the number of years.
The proliferation of endothelial cells associated with the formation of hyaline subendotelijalno depot - a process called "membranous proliferative glomerulitis."
• exudative glomerulonephritis
Increasing the number of cells in the glomerular klubetu due to increased number of polynuclear leucocytes.
Evolution: the disappearance of infiltration during the 60 days, creating infiltrate crescents in Bowman's capsule, creating sinehija between glomerulus and capsule hijalinizacija individual capillary loops or entire glomerulitisa.
• Focal glomerulonephritis
The lesions were focal (single glomerulus are no changes) and segment (in the affected glomerulus is only one part lediran).
• Necrotizing acute glomerulonephritis.
• haemorrhagic form of acute glomerulonephritis (characterized by the presence of erythrocytes in Bovvman's capsule and the tubule lumen).
• Diffuse membranous acute glomerulonephritis.
Functional testing
Specific gravity of urine is high.
Ability to diluiranje not held, there is a tendency for water retention and sodium.
Clearances may be normal in severe cases there is a reduction in glomerular function (decrease of urea, creatinine, insulin clearance, increased clearance paraaminohipurne acids and decrease filtration fraction. Masses of tubular secretion and reabsorption is reduced.
The sequence of signs, symptoms and parameters of significance for the diagnosis
Anamnesis
The sudden appearance of edema of the eyelids after a free interval of one to three weeks after infection tonzilofaringealne or the other.
Clinic
Edema tendency, if not present. Paleness of skin and mucous membranes in the gaps to the values of blood hemoglobin and erythrocyte counts.
High blood pressure.
The urinary findings: functional impairment (elevated levels of urea and creatinine levels, a reduction in glomerular filtration rate and filtration fraction).
The presence of the causative infection, throat, skin, teeth.
Elevated antistreptolizinski O titer.
Functional characteristics of
In functional terms the hardest hit by the apparatus of glomerular function. Hence there is a complete clinical picture of diffuse glomerular lesions with involvement of the urinary, edemskog, cardiovascular, and biological syndrome with impaired secretion.
Nearly always there are oliguria, azotemia, edema and hypertension.
There are a burden on the heart, the sudden appearance of hypertension.
The program tests of kidney function
Measurement of diuresis: a qualitative proteinuria. Number of cell elements in the urine (leukocyturia and eriturija a minute, that is. Addis's number), to monitor the evolution.
Concentration test. Urea and creatinine clearance. Fenolsulfonftaleinska rehearsals. Control of blood pressure. Fundus examination. Antistreptolizinski O titer.
Forecast
Acute diffuse glomerulonephritis is a disease that can be cured without damage to the residue, the reparabilne nature can not exceed the chronic course, finally, can the acute phase lead to death.Malignant forms quickly end fatally.
Healing can occur quickly, within a few weeks or months, the disease often takes many months, even years, and is completely healed or left behind moderate proteinuria or hematuria.
The disease may go into a chronic form, to maintain one or more leading syndrome, proteinuria, hematuria, renal insufficiency, that evoluiše insuficijenclji to uremia and very fast or very slow with long remissions a decade ago. To estimate forecasts the greatest service gives kidney biopsy because of anatomic changes hijalinoze, renal sclerosis, epithelial proliferation may be stronger than would be concluded by the clinical picture.
Prognosis depends on hypertension and forms of histological lesions: evolution and progression of failure is even faster if blood pressure is fixed, and histological changes in proliferation and diffuse type in all the glomerulus.
The natural course of the disease antibiotics and other medications have little effect. Persistent infection and recurrent episodes of streptococcal infection appears to have no influence on the formation of chronic course.
No sign of the acute period of disease can not be used to provide forecasts. Severe cases can be cured until light and forms may later have a progressive course. Prognosis in children is relatively good.
Mortality in children is 1%, a transition to the chronic course of less than 1% of cases. The mortality of adults is much higher.
Among the factors that influence the disease has an unfavorable development postakutnog poststreptokoknog nephritis should be noted the following: patient age; family predisposition to renal disease, presence of chronic kidney disease. Constantly and rapidly reduce the serum complement biological means to maintain the evolution of the disease.
Subsequent streptococcal infections have no effect on the evolution, because although streptococcal toxins can cause hematuria, it becomes a mechanism different from that which occurs on the basis of hypersensitivity glomerulonephritis.
The criterion for the process evolutivnost
Monitoring the intensity of proteinuria, urinary findings of hematuria.
Blood pressure and maintain it with the sign of the urinary findings evolutivnosti.
Deterioration of functional status.
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