173. Glomerulonephritis: principles of classification, morphological characteristics, leading clinical symptoms, complications.

Glomerulonephritis is a disease of an infectious—allergic or unidentified nature. It is based on bilateral diffuse or focal non-purulent inflammation of the glomerular apparatus of the kidneys (glomerulitis) with characteristic renal and extrarenal symptoms.

Classification:

According to the situation:

Primary,

secondary;

Downstream:

Acute (up to 1 year),

subacute (up to 2 years old),

chronic (for many years);

By etiology:

postinfectious,

non-infectious,

unknown;

By pathogenesis: antibodies, immunocomplex, Ig A, toxic, etc.

Morphological characteristics:

According to morphology, glomerulonephritis is divided into:

Alterative - fibrinoid necrosis

Exudative - serous, fibrous, hemorrhagic.

Proliferative - intracapillary, extracapillary, mixed.

According to the localization of inflammation, intra- and extracapillary forms of glomerulonephritis are distinguished, according to the nature of inflammation — exudative, proliferative (productive) and mixed glomerulonephritis.

Intracapillary glomerulonephritis, which is characterized by inflammation in the vascular glomerulus, can be exudative, proliferative or mixed.

• In intracapillary exudative glomerulonephritis, the mesangium and capillary loops of the glomeruli are infiltrated by neutrophils.

• In intracapillary proliferative (productive) glomerulonephritis, endothelial and especially mesangial cells proliferate, while the glomeruli are enlarged and become "paw-like".

Extracapillary glomerulonephritis, in which inflammation develops in the glomerular capsule cavity, can also be exudative or proliferative. Extracapillary exudative glomerulonephritis can be serous, fibrinous or hemorrhagic. Extracapillary proliferative glomerulonephritis is characterized by proliferation of glomerular capsule cells (nephrotelium and podocytes) with the formation of characteristic half-moons. According to the prevalence of inflammation in the glomeruli, diffuse and focal glomerulonephritis are distinguished.

Morphological changes in the kidneys in glomerulonephritis concern not only the glomerular apparatus, but also other structural elements — tubules, stroma, vessels. In this regard, glomerulonephritis is isolated with a tubular, tubulointerstitial or tubulointerstitial vascular component.

Clinical symptoms:

Swelling of body tissues (edema)

Increased blood pressure

Decrease in urine volume

The presence of red blood cells in the urine (hematuria)

Drowsiness and confusion

Nausea, vomiting

Weakness, fatigue

Fever (fever)

Complications:

Chronic renal failure

Chronic heart failure

Chronic liver failure

Uremic pleurisy

Pericarditis

Peritonitis

174. Acute tubular necrosis: etiology, pathogenesis, macro- and microscopic characteristics, manifestations and complications.

Acute tubular necrosis (Acute renal failure, necrotic nephrosis) is a syndrome whose morphological characteristics are necrosis of the tubular epithelium and profound disorders of renal blood and lymph circulation.

Etiology.

The main causes are intoxication and infection. Poisoning can lead to necrotic nephrosis:

– salts of heavy metals (mercury, lead, bismuth, chromium, uranium);

– acids (sulfuric, hydrochloric, phosphoric, oxalic);

– polyatomic alcohols (ethylene glycol, or antifreeze);

– narcotic substances (chloroform, barbiturates);

– sulfonamides (sulfonamide kidney).

Pathogenesis:m (at least read part of the pathogenesis)

Acute renal failure develops in a number of severe infections (cholera, typhoid fever, paratyphoid, diphtheria, sepsis). It can complicate liver diseases (hepatorenal syndrome) and kidney diseases (glomerulonephritis, amyloidosis, urolithiasis). Necronephrosis occurs with traumatic injuries (prolonged crushing syndrome), after surgery, with extensive burns, massive hemolysis (hemolytic kidney), dehydration and deschlorination (chlorohydropenic kidney).

Acute renal failure is closely related to the mechanisms of shock of any etiology — traumatic, toxic, hemolytic, bacterial. Any shock stimulus that can cause acute circulatory disorders, hypovolemia and a drop in blood pressure can cause the development of acute renal failure. In this regard, violations of renal hemodynamics become the main link in its pathogenesis. They reflect the general hemodynamic shifts in shock: vasospasm of the cortical layer and discharge of the bulk of blood at the border of the cortex and medulla into the veins via a renal shunt. Reduced blood circulation in the kidneys determines progressive ischemia of the cortical substance and impaired renal lymph flow with the development of interstitial edema. Due to the increase in cortical ischemia, deep dystrophic and necrotic changes in the tubules of the main sections develop with rupture of the tubular basement membrane (tubulorexis). In the development of tubular dystrophy and necrosis, the direct action of nephrotoxic substances circulating in the blood plays an important role on the epithelium of mainly proximal tubules. Tubule necrosis and ruptures of their basement membrane determine the possibility of inadequate tubular reabsorption, the entry of glomerular plasma ultrafiltration into the renal interstitium. This contributes to an increase in edema of the renal tissue, an increase in intrarenal pressure. Tubular necrosis, rupture of their basement membrane, tubulovenous reflux is associated with blockage of tubules with pigment detritus, myoglobin crystals, and dead cells. Tubular obstruction and progressive interstitial edema are the main causes of increased intrarenal pressure, exacerbating the condition of tissue hypoxia and anoxia. The destructive processes in the tubules are replaced by reparative ones. However, complete recovery of the renal parenchyma does not occur: focal nephrosclerosis develops, therefore recovery with structural damage occurs.

Macro- and microscopic characteristics:

During histological examination, various changes are found in the kidneys at different stages of the disease. The dynamics of these changes can be traced with puncture biopsies of the kidney.

In the initial (shock) stage, there is a sharp, predominantly venous fullness of the intermediate zone and pyramids with focal ischemia of the cortical layer, where the glomerular capillaries are in a dormant state. Interstitial edema is accompanied by lymphostasis, most pronounced in the intermediate zone. The epithelium of the tubules of the main departments is in a state of hyaline drip, hydropic or fatty dystrophy. The lumen of the tubules is unevenly expanded, contains cylinders, sometimes crystals of myoglobin.

In the oligoanuric stage, focal necrosis of the tubules of the main departments is expressed with the destruction of the basement membranes of mainly distal tubules — tubulorexis. The cylinders contour the nephron at different levels, which leads to stagnation of the glomerular ultrafiltrate in the cavity of the glomerular capsule. Interstitial edema is increased, leukocyte infiltration and hemorrhages join it. Venous stagnation is also significantly pronounced, against which venous thrombosis often occurs.

At the stage of restoration of diuresis, many glomeruli are full-blooded, and edema and infiltration of the kidney are significantly reduced. Areas of tubular epithelial necrosis alternate with islets of regenerators from light epithelial cells. Necrotized tubules, the membrane of which is preserved, regenerate completely. In areas where tubular necrosis is accompanied by destruction of the basement membrane, connective tissue grows in place of the deceased nephron, foci of sclerosis are formed.

The morphology of the kidneys in acute renal failure of different etiologies is the same, although it has some specifics depending on the cause. The kidney is enlarged, weighing 200-250 g, of a flabby consistency, the bark is thickened to 2 cm, yellow-gray, dull, matte, wraps over the capsule, the cerebral layer is sharply delimited from the cortex (the red line of Juxtamedullary blood flow), the cerebral layer is full-blooded, the capsule is easily removed, the surface of the kidney is smooth, gray-yellow.

Manifestations:

Edema, anemia, congestive HF, hypertension, encephalopathy, hyperazotemia, oligoanuria, headache, vomiting.

Complications:

Azotemic uremia, pulmonary edema, cerebral edema, rupture or rupture of the kidney capsule, anemia, hypertension, sepsis, pneumonia.