GLOMERULONEPHRITIS

From Big Medical Encyclopedia

GLOMERULONEPHRITIS (glomerulonephritis; lat. glomerulus a ball + nephrite) — bilateral diffusion immunological - an inflammatory disease of kidneys with preferential defeat of balls. Distinguish acute and chronic G.

History

For the first time in 1726 J. Morganyi pointed to communication of hypostases with changes of kidneys; it described the changed kidneys at the patient who had hypostases. The first mentioning of detection of protein in urine belongs to Kotunyo (D. Cotugno, 1770). Krukshenk (Cruickshank, 1798) distinguished an edema with curtailed under heating effect and nitric to - you urine and an edema, at a cut urine had no these properties. However only R. Brayt in 1827 established that the general edema with protein in urine is connected with diffusion diseases of kidneys, described clinic of these diseases and morfol, changes of kidneys. R. Brayt along with an edema and an albuminuria observed at patients blood in urine, increase in heart, firm pulse, headaches, back pains. It allocated three types of anatomic damage of kidneys: the increased spotty yellow kidney, a big red granular kidney and the wrinkled rough kidney. In 1933. Osman on the basis of studying of the remained drugs described them as an amyloidosis, malignant nephrite and a nephritic contracted kidney. R. Brayt's works were a basis for creation of the doctrine about diseases of kidneys. A big contribution to the doctrine about G. were researches Folgarda, Farah (F. Volhard, Th. Fahr, 1914). Based on kliniko-anatomic parallels, they created the classification of diseases of kidneys close to modern. Three groups of damage of kidneys were allocated: primary and degenerative changes of tubules — nefroza; primary and inflammatory changes of balls — nephrites; scleroses with arterial hypertension — a primary contracted kidney with division on high-quality and malignant.

S. S. Zimnitsky (1924) considered a lipoid nephrosis option hron., denied existence of primary epithelial disease of kidneys. Later the lipoid nephrosis began to be carried not to canalicular, and to glomerular diseases [to a glomerulonefroz — Headlights, 1934; to hymenoid G. — Bell (E. T. Bell), 1929, 1946] with secondary canalicular defeats.

An etiology

the Diseases and influences preceding G.'s emergence are very various. Most often — from 21,5% (M. S. Vovsi, G. F. Blagman, 1955) to 51% [H. Sarre, 1968] — G. develops after quinsy, tonsillitis and diseases of upper respiratory tracts. Less often it is preceded by other reasons: pneumonia, food toxicoinfections, cooling, introduction of a vaccine, serums, medicines etc.

Typing of the streptococci allocated from sick G.' pharynx showed that in 78% of cases type 12 of a beta and hemolitic streptococcus of group A is found. Dominance 12 like a streptococcus is noted both in sporadic cases, and at disease outbreaks.

In tropical countries to G.'s development it is especially frequent [in 85% of cases, according to Dillon (N. S. Dillon), 1967] skin diseases (a pyoderma, impetigo, an ugly face) precede; at such patients piogenic streptococci are, as a rule, sown. In blood serum of sick G. antibodies to type 12 of a streptococcus most often are found. Almost streptococcal antigens are found in 51% of patients with acute G. in blood and come to light in balls at immunofluorescent microscopy [Segal (V. S. of Seegal), 1965; G. A. Andres et al., 1966]. Often are found also antistreptolysin - Oh, anti-hyaluronidase and anti-Streptokinasa. However post-streptococcal acute G. from 50th began to meet less often that is connected substantially using powerful antibacterial drugs. It is more closely connected with a streptococcal infection of G. at a subacute septic endocarditis that can be shown not only classical focal embolic nephrite [Leleyn (M. by H. F. Lohlein), 1910], but also diffusion damage of kidneys. Frequency of damage of kidneys at a subacute septic endocarditis can be high — to 50%, at rheumatism (according to section data) — to 10,5%. G. is described and at a staphylococcal endocarditis. Pneumonia is complicated by G. in 1 — 3% of cases. The role belly and a sapropyra, malaria in G.'s development is small. At malarial nephrite find adjournment of malarial antigen in balls; as a part of a cell-bound immune complex along with immunoglobulins, a complement, fibrin. At tuberculosis the wedge, a picture G. can be the leader.

According to V. V. Sur, A. M. Vikhert (1966), hymenoid G. easily is reproduced at animals at administration of mikobakterialny adjuvant, i.e. a stimulator of processes of an immunogenesis (see. Adjuvants ). At tuberculosis at the person it is described by B. M. Kovaliv and V. F. Podugovsky (1957). At syphilis, proceeding usually on nephrotic type, it is rare.

Carry also poorly studied virus G. at measles, chicken pox, a viral hepatitis, an enteroviral infection to infectious and immune group G.

G. developing after a number of antigenic influences (serum, a vaccine, pollen of plants, poison of insects, medicinal and other chemical substances, foodstuff enters into group G. of a noninfectious and immune origin at individual intolerance), and also G. arising at disturbance of venous outflow (the partial thrombosis of renal veins, the lower vena cava squeezing a pericardis, insufficiency of the three-leaved valve).

Cooling, especially at high humidity, can promote G.'s emergence or its aggravation.

A pathogeny

the Standard pathogenetic classification does not have a G. yet. The most reasonable is the immunoallergic concept confirmed a wedge., immunol., experimental and immunogistokhy. data.

Arises usually after an infection or other influence (vaccination etc.) with various duration of stage of latency though also its intrainfektsionny development [Rammelkamp is known (Page H. Rammelkamp), 1963]. In blood serum of sick G. rather often find antirenal antibodies, However their credits not always correlate about a wedge, acute G.'s manifestations that allows a number of authors to consider these antibodies as the satellites of process which do not have pathogenetic value. The caption of a complement at G. is almost constantly lowered that demonstrates consumption of a complement in the course immunol, reactions.

Easily is reproduced in an experiment by means of the heterologous anti-renal serums received at immunization of animals by renal antigen of animal other look [V. K. Lingdemang, Masugi (M. of Masugi)]. As showed experiences with marked antirenal serum, its binding on a basal membrane of balls happens within several minutes [D. Pressman, 1948], emergence kliniko-morfol, G.'s manifestations is connected with complement deflection in balls and depends on complement-linked ability of the entered antirenal serum.

For experimental G.'s reproduction across Masugi the antirenal serum of birds which does not have ability to connect a complement of mammals is used. Between administration of serum and G.'s emergence there passes the stage of latency (6 — 8 days) necessary for formation of complement-linked antirenal autoantibodies. In a pathogeny of this option of experimental G. it is possible to allocate two immunol, phases — fixing of exogenous antibodies in kidneys and the subsequent formation of the autoantibodies capable to connect a complement.

Experiments with use of adjuvants like Freynd [Heymann] show 1959 value of the general immunol, reactivity for emergence of. If introduction by an animal of homologous renal antigen does not cause in them G.'s development, then introduction as a part of a mikobakterialny stimulator allows to reproduce it.

The immunoallergic hypothesis of a pathogeny of G. is confirmed also by the data obtained during the studying of a role of streptococci in its emergence. As showed Kavelti's experiences (R. of A. Cavelti, F. S. Cavelti, 1945), G. is possible to cause introduction animal mixes from tissue of a kidney and streptococci. Perhaps, the streptococcus changes properties of proteins of tissue of kidney, doing them antigenic; also its adjuvant action is not excluded. Antigen of a streptococcus (M-protein) by the chemical nature belongs to glycoproteins. Antigenic affinity of a basal membrane of capillaries of balls and covers of streptococci of nephrogenic strains is proved. Part of the M-protein is fixed in balls, a part circulates in a blood channel, causing antibody formation. The complexes which are formed as a result of reaction antigen — an antibody, are late the glomerular filter with complement deflection. Formation of cell-bound immune complexes can happen to complement deflection and directly in balls. Cell-bound immune complexes injure a kidney. At immunomorfol. immunocomplex G.'s studying accumulations of a complex are found subendotelialno or subepitelialno in a look glybok. Find a linear arrangement of deposits (deposits) of cell-bound immune complexes less often that is peculiar for some forms of proliferative G., nephrite of a transplantirovanny kidney. Further irrespective of an arrangement of deposits as a result partly hemotaksichesky actions of C3 complement of system (see. Complement ) segmentoyaderny leukocytes are fixed on capillary loops, exfoliate or remove an endothelium, closely contact to a basal membrane. Lizosomalny enzymes of leukocytes influence a basal membrane and cause its damage.

Participation of cellular mechanisms of immunity in G.'s pathogeny more characteristic of hymenoid G. is confirmed by a possibility of transfer of experimental adjuvant nephrite lymphocytes (but not serum) a sick animal [E. V. Hess et al., 1962] to the healthy recipient. The mechanism of such transfer is explained by a cytopathic effect of lymphocytes in an experiment [G.Holm, 1966], including in culture of renal fabric (T. G. Troyanova with soavt, 1973, 1974).

Along with immune mechanisms the change of processes of coagulation which is combined with them matters; use of anticoagulants prevents severe defeat of balls at Masugi-nefrite.

Pathological anatomy

Morfol, changes of kidneys at G. differ in a big variety and are observed in all of them structural elements, but the leader is the diffusion glomerulitis, to-rogo the inflammation of usually immune nature is the cornerstone.

Changes of balls at G. were in detail studied after implementation in a wedge, practice of a puncture biopsy of a kidney with use of methods of a histochemistry (see. Histochemical methods of a research ), submicroscopy (see), an immunohistochemistry (see. Immunomorphology ), autoradiography (see) etc. On the basis of studying of renal punctate [V. V. Serov, H. Noltenius, P. Dittrich, Bruer (D. Century of Brewer)] at, distinguish the following changes of balls: minimum, hymenoid, proliferative (intra-and ekstrakapillyarny), exudative (intra-and ekstrakapillyarny), membranoznoproliferativny, fibroplastic. In this classification of glomerular changes, edges also Bella is further development of schemes of A. Ellis (E. T. Bell), proliferative, hymenoid and fibroplastic changes — the main.

The minimum changes (at light microscopy) come down to an insignificant focal thickening of basal membranes of capillaries of balls and a hyperplasia of cells of an endothelium only in separate loops. The submicroscopy finds initial changes in a type of a reduction of small shoots of podocytes without the expressed changes of a basal membrane of capillaries of balls [foot process type, according to J. Churg]. Immunogistokhim. the research yields negative takes. About the nature of these changes there is no consensus. One researchers consider them as G.'s manifestation, others — as an independent disease (a lipoid nephrosis of children).

Fig. 1. Microdrugs (and, c) and the diffraction pattern (b) of a kidney at a hymenoid glomerulonephritis: and — fixing of 131jgamma-globulin of cell-bound immune complexes on a basal membrane of a ball (a direct method of Koons); — hymenoid transformation, a thickening of a basal membrane (1) of the glomerular filter in the field of subepithelial deposits (deposits) (2) cell-bound immune complexes, the basal membrane is soldered to small shoots (4) podocytes (3), an endothelium (5) vakuolizirovan; x 13 500; in — a ball at a hymenoid glomerulonephritis (coloring hematoxylin-eosine); X 200.

Hymenoid G. (the II type according to Ellis) is described for the first time by Bell. He suggested to carry to hymenoid G. a wedge, cases of a lipoid nephrosis (an idiopathic nephrotic syndrome) at which the thickening (fig. 1, c) and splitting of basal membranes of capillaries of the balls with existence of «Friday peaks» revealed by method of silvering in the absence of proliferation of cells of a ball histologically is found. Further hymenoid changes were found at gistol, a research of kidneys (biopsy) not only at an idiopathic nephrotic syndrome, but also at others a wedge, Forms.

A starting point in damages of a basal membrane of capillaries of balls consider fixing on it autologous cell-bound immune complexes (rice, 1, a) that is proved by methods of an immunohistochemistry (on basal membranes immunoglobulins and a complement) and a submicroscopy (detection of deposits on the epithelial party of a membrane come to light). At the hymenoid G. designated as a diffusion hymenoid glomerulopatiya (perimembranozny or ekstramembranozny, G., a lipoid nephrosis of adults) on the outer side of a basal membrane there are granular deposits (fig. 1,6) of cell-bound immune complexes and adjournment of plasma proteins whereas the interior of a membrane has usual contours. Deposits are separated from each other by the ledges of lamina densa directed towards an epithelium therefore the membrane has an appearance of a crest (hymenoid transformation across Chergu). As a result of «washing away» of deposits the basal membrane becomes uneven density. Over time between deposits and legs of podocytes crossing points are formed, they merge and condensed. The membrane is thickened at the expense of a neogenic layer of a knaruzha from deposits which are incorporated, exposed to a resorption and become less osmiofilny. At the expressed hymenoid changes proliferation of cells of a ball is absent.

Hymenoid changes are considered morfol, an equivalent of an idiopathic nephrotic syndrome. However the proteinuria at hymenoid G. is connected not only with changes of balls, but also with an insufficient resorption of protein in renal tubules. The morphology of this insufficiency is presented by dystrophy and an atrophy of an epithelium of tubules, a sclerosis of a stroma. Over time dystrophic changes of renal tubules accrue, the hyalinosis of membranes not only balls, but also tubules comes to light.

Fig. 2. Microdrug (b) and the diffraction pattern (a) of a kidney at a proliferative glomerulonephritis: and — in a gleam of a glomerular capillary (1) a granulocyte (2); behind a basal membrane (3) endothelia (4) are visible the cytoplasmatic shoots of proliferating mezangialny cells (5) surrounded with membranopodobny substance; X 13 500; — a histologic picture of a proliferative glomerulonephritis, significant increase in quantity of kernels of an endothelium of capillaries of a ball (coloring hematoxylin-eosine).

At proliferative G., development to-rogo is usually connected with influence of a streptococcus, proliferation of endotheliocytes and mesangiocytes is, as a rule, combined with exudative changes, infiltration of a ball polymorphonuclear leukocytes. Otslaivy the endothelium, leukocytes get to a basal membrane of capillaries and migrate in a mezangiya (fig. 2). They can constantly be found near the granular subepithelial deposits in the form of humps («humps») containing heterological cell-bound immune complexes which part are a streptococcus, immunoglobulin and a complement.

At a submicroscopy deposits of cell-bound immune complexes are found in biopsionny material from a kidney in 2 — 4 weeks from the beginning of a disease, but meet in 6 weeks and more. Infiltration of a ball by leukocytes, development of an immune inflammation in its connecting fabric — mezangiya is connected with leykotaksichesky effect of a complement of these complexes. Damages of a basal membrane of glomerular capillaries are also caused by lytic action of a complement of cell-bound immune complexes and lizosomalny enzymes of leukocytes. As a result of damage of a basal membrane and processes of intravascular coagulation to capillaries of balls blood clots are formed, and also reactive proliferation of cells of a ball is observed. Proliferation of endotheliocytes is combined with the expansion a mezangiya connected with increase in quantity of mesangiocytes and accumulation of membranopodobny material — a mezangialny matrix that is characteristic of proliferative intracapillary diffusion G. (mesangioproliferative G.). A wedge, intracapillary G.'s manifestations are various, however a certain dependence between a hamaturia and expressiveness of proliferative glomerular reaction is unconditional.

Fig. 3. Microdrug (a) and the diffraction pattern (b) of a kidney at an ekstrakapillyarny productive glomerulonephritis: and — proliferation a nefroteliya with formation of characteristic «semilunums» (1) in a cavity of the glomerular capsule (coloring hematoxylin-eosine); x 200; — in cytoplasm of a podocyte (1) a large number of phagolysosomes (2); X 20 000.

At dominance of proliferation of an epithelium of the capsule of a ball there is proliferative ekstrakapillyarny G. which is considered as morfol, an analog of the malignant «subacute» or progressing acute G. [Jennings (R. Century of Jennings), D. P. Earle]. This type of G. has rather characteristic morphology in the form of so-called semilunums from proliferating cells (fig. 3, a) which fill a gleam of the capsule and squeeze capillary loops of a ball. Proliferation of cellular elements of balls is usually combined with exudative ekstrakapillyarny processes, emergence among cells of threads of fibrin. At the same time phagocytal function of podocytes in which cytoplasm by means of a submicroscopy it is possible to find a set of phagolysosomes (fig. 3,6) comes to light: processing products of proteinaceous disintegration. Ekstrakapillyarny proliferation arises as reaction to sharp damage kapillyartsy, loops of a ball, a cut for ekstrakapillyarny forms G. is the rule. Early enough cells of «semilunums» undergo fibroplastic transformation. In proliferat connecting fabric from the capsule grows, there is a cicatricial obliteration of a cavity of the capsule that leads to death of a ball.

Exudative (intra-and ekstrakapillyarny) G. as an independent form meets extremely seldom that, most likely, is connected with early treatment of G. steroid drugs. Usually exudative changes in a type of accumulation of exudate (serous, fibrous, hemorrhagic) in a cavity of the capsule accumulate on morfol, manifestations of other form G., reflecting sharpness of process. In some cases they are combined with a fibrinoid necrosis of capillary loops of balls that allows to speak about exudative and necrotic.

Fig. 4. Microdrug (b) and the diffraction pattern (a) of a kidney at a hymenoid and proliferative glomerulonephritis: and — proliferation of mezangialny cells (1), emergence of shoots of these cells (2) near deposits (3) cell-bound immune complexes in a basal membrane. (4); expansion mezangiya (5); fleecy transformation of podocytes; x 20 000; — a histologic picture of a hymenoid and proliferative glomerulonephritis (coloring hematoxylin-eosine); x 200.

Hymenoid and proliferative G., chronic latent or subacute nephrite, gipokomplementarny persistent, the chronic lobulyarny, mixed, mezangiokapillyarny G. — the same form, for a cut proliferation of mesangiocytes and a thickening of walls of capillaries of a ball [J. S. Cameron and soavt are morphologically characteristic., 1970], and clinically — hron, the current, a proteinuria, is more rare a hamaturia and in some cases lack of effect at treatment by steroid hormones. Though behind this type G. the term «hymenoid and proliferative» was also approved, it is more correct to call it mesangioproliferative [N. N. Mandalenakis and soavt., 1971] since glomerular changes at it, including and hymenoid, are connected first of all with proliferation of mezangialny cells and interposition a mezangiya. By means of a submicroscopy (fig. 4, a) sharp expansion a mezangiya due to proliferation of its cells and increase in a matrix is defined. The mezangiya leads expansion to its interposition [Arakawa and Kimmelstil (M. of Arakawa, P. Kimmelstiel), 1969] — the shoots of mesangiocytes surrounded with membranopodobny substance go beyond connecting fabric of a ball and, extending along a basal membrane to the periphery of a capillary loop, remove an endothelium. At light microscopy the phenomenon of a thickening (fig. 4,6) and splitting of a membrane comes to light. The proliferation of mesangiocytes observed, as a rule, near deposits of cell-bound immune complexes can be limited to an endothelial vystilka (at the same time the gleam of a capillary remains free), or proliferating cells break through an endothelial vystilka and fill partially or completely a gleam of a capillary. Hypersecretion proliferating mesangiocytes of tropocollagen leads to accumulation of membranopodobny substance in a wall and a gleam of capillaries that is the cornerstone of a sclerosis and a hyalinosis of balls. Narrowing of a gleam of capillaries is promoted also by proliferation of an endothelium, however it considerably concedes to proliferation of mezangialny cells. Changes of podocytes are various from the hyperplasia of ultrastructures reflecting the raised functional load to deep dystrophy in the form of a reduction of small shoots, vacuolation of cytoplasm, fleecy transformation of cells.

Hymenoid and proliferative G. is divided on several kliniko-morfoimmunol. options (forms): hymenoid and proliferative G. with subendothelial or dense deposits, lobulyarny G., IgA-glomerulopatiya (Berger's disease).

Hymenoid and proliferative G. with subendothelial deposits is characterized by a hyperplasia of cells a mezangiya, splitting of basal membranes of glomerular capillaries (mezangiokapillyarny G.), the subendothelial deposits (containing a large amount of immunoglobulins, early fractions of a complement, properdin), a gipokomplementemiya.

At hymenoid and proliferative G. with dense deposits («a disease of dense deposits») a hyperplasia the mezangiya is presented slightly, and the thickening of walls of capillaries is caused by electronic and dense deposits in a basal membrane. In deposits find a large number of C'3 of fraction of a complement, contents a cut in blood serum it is reduced; immunoglobulins in deposits are absent.

About lobulyarny G. which, as a rule, is immunocomplex, speak when proliferation of mesangiocytes happens within a segment and is followed by its early sclerosis and a hyalinosis.

The main sign of IgA-glomerulo-patii, or Berger's disease — dominance in subendothelial and mezangialny deposits of cell-bound immune complexes of IgA and S'Z of fraction of a complement. Histologically find focal or diffusion proliferation of mezangialny cells.

Fig. 5. Microdrug (b) and the diffraction pattern (a) of a kidney at a fibroplastic glomerulonephritis: and — an obliteration of a gleam (1) and fall of a glomerular capillary; thickening of a basal membrane (2); mezangialny cells (3); legs of a podocyte (4); x 7500; — a histologic picture of a fibroplastic glomerulonephritis (coloring by Nitrofunginum according to Van-Gizona); X 200.

Fibroplastic G. should be considered as a collective evolutive form of proliferative, hymenoid and hymenoid and proliferative. At all these forms G. in development of a sclerosis and hyalinosis of balls the main role belongs to mezangialny transformation: proliferation of mesangiocytes, the hyperproduction of membranopodobny substance and interposition a mezangiya conducting to an obliteration of a gleam of capillaries (fig. 5, a). Proliferation and fibroplastic transformation of an endothelium in development of a glomerulosclerosis play a smaller role. At fibroplastic G. balls take a web-footed form (fig. 5,6), is frequent between capillary loops and an outside leaf of the capsule of a ball synechias appear. Nek-raya a part of balls is completely replaced with connecting fabric (a glomerulosclerosis, glomerulogialinoz). At the same time in an epithelium of the main departments of tubules dystrophic and subatrophic changes develop, there is an angiosclerosis and stromas of a kidney. More often fibroplastic G. is result is long the current nephrotic or hypertensive nephrite and, as a rule, meets at an end-stage of a disease.

Morfol, forms, as well as wedge., are not stable. They in some cases reflect morphology of phases and Options. Repeated biopsies of a kidney prove a possibility of transition of one form G. in another.

At G., except changes in balls, there are dystrophic and atrophic changes in tubules. At the same time dystrophy prevails in an epithelium proximal, and an atrophy — in an epithelium of distal department of nephron. Different types of proteinaceous dystrophy (granular, hyaline and drop, vacuolar) and fatty dystrophy meet. Increase in permeability of the glomerular filter, the raised reabsorption, infiltration of renal tubules and blockade of various groups of enzymes of an epithelium is the cornerstone of its development. Different types of dystrophy of an epithelium of tubules reflect, thus, different degree and various quality of the developing fermentopatiya. In this regard granular dystrophy of an epithelium of tubules, at a cut the nature of distribution respiratory, glycoclastic and hydrolases in nephron do not change, and their activity increases, do not carry to patol, to processes at all. It is considered that granular dystrophy of an epithelium of tubules reflects morphologically increased reabsorbtsionny function of a tubule of hl. obr. concerning protein. Hyaline and drop, vacuolar and fatty dystrophies at which disturbance of distribution of enzymes in nephron y decrease in their activity is noted are morfol, equivalents of rezorbtsionny insufficiency of tubules (relative or absolute). Accumulation in cytoplasm of an epithelium of tubules of protein, water or lipids conducts to a necrobiosis and desquamation of an epithelium. The desquamated epithelium, as well as components of an ultrafiltrate, forms a basis of formation of cylinders, occlusive distal departments of nephron are more often that leads to increase in intra canalicular pressure, formation kistozno of expanded tubules. At the same time regeneration of an epithelium of the whole pieces of tubules is quite often noted.

The atrophy of Tubules expressed in a varying degree usually supplements their dystrophic changes. Most often it is an atrophy of distal department of nephron or group of nephrons at which balls are hyalinized, sclerosed. Around the atrofichny, replaced with connecting fabric nephrons there is a regeneration hypertrophy of the next nephrons which can provide a long time function of a kidney. However in process of G.'s progressing even more often there is «a separation tubul» renal tubules from balls to formation of so-called aglomerulyarny functionally defective nephrons. Over time atrophic processes in renal tubules begin to prevail over dystrophic, an increasing number of nephrons is exposed to fibrous substitution, a net result to-rogo is wrinkling of kidneys.

Considerable changes happen both in circulatory, and in limf, vessels of a kidney. In blood vessels distinguish several types of changes [A. I. Abrikosov, H. U. Zollinger]: 1) the proliferative endarteritis concerning arterioles and small arteries, connected probably with a renal allergy at G. [F. Volhard]; in the result of this process the sclerosis of an internal cover of vessels with sharp narrowing or an obliteration of a gleam of vessels develops; 2) plasmorrhagias), arteriolonekroz and arteriolosclerosis (see), caused by arterial hypertension; these changes are most brightly presented at hypertensive G.; 3) a hyperplasia of an internal cover, progressing intimofibroz average and large arteries of a kidney, it is frequent with a secondary lipoidosis, an atrophy of an average (muscular) cover and the centers of aneurysmal expansion of a gleam of arteries; these changes consider as adaptation of arteries to switching off of arterioles and balls — «a peripheral bed of a kidney».

Changes of blood vessels conduct to a reduction of a vascular bed, emergence of «short ways» of a blood-groove. In cortical substance the quantity of the short branches connecting bypassing a ball the bringing and taking out arterioles increases, the number of post-glomerular (peritubulyarny) capillaries of bark, as well as the false direct arteries feeding marrow of a kidney decreases. Zapustevayet not only circulatory, but also limf, system. Insufficiency limf, systems comes for the second time, first of all in connection with disturbances of renal blood circulation. The reduction circulatory and limf, beds of kidneys promotes development in them sclerous and atrophic changes.

In a stroma of kidneys hypostasis, a sclerosis, lipoid and cellular infiltration develop. Hypostasis is more sharply expressed in marrow and forms a basis early of the coming hyalinosis of pyramids, especially their nipples (see. Hyalinosis ), what matters in development of disturbances of the counterflow mechanism of a kidney. The sclerosis, as well as swelled, comes is more sharply expressed earlier in marrow of kidneys where it has diffusion character. In cortical substance, in addition to diffusion fibrosis of a stroma, note the centers of a sclerosis, substituting groups of the switched-off nephrons. Over time the centers of a sclerosis merge, forming fibrous fields in which the hyalinized balls and atrophied tubules are immured. On the periphery of such fields hypertrophied nephrons (a regeneration hypertrophy) remain. In some cases (at a nephrotic syndrome) in the sclerosed stroma of kidneys find birefringent lipoida (lipoid infiltration of a stroma) in a large number.

The sclerosis of a stroma is, as a rule, combined with the cellular infiltration presented by gnezdny accumulations of lymphoid elements, histiocytes, plasmocytes. It is considered that gistiolimfotsitarny infiltrates of a stroma can reflect the immune responses (the slowed-down hypersensitivity) developing in kidneys at. In favor of this assumption ability of cells of infiltrates to the cytopathic action which is shown a lysis of membranes and an epithelium of Tubules testifies. It is not excluded that lymphoid infiltrates of a stroma only adaptive reaction of cells of a mesenchyma to the developing resorption and mechanical insufficiency limf, systems of a kidney.

At an acute glomerulonephritis in the first days of a disease the hyperemia of balls is observed, to-ruyu leukocytic infiltration the mezangiya and diffusion intracapillary proliferation of cells (intracapillary exudative and proliferative G.), thrombosis of separate capillary loops, plasmatic treatment y quickly enough replace fibrinoid changes of arterioles. Further ekstrakapillyarny exudative changes in the form of a serous and desquamative, fibrinous or hemorrhagic exudate in a cavity of the glomerular capsule (exudative ekstrakapillyarny G.) or proliferation a nefroteliya join at sharp damage of a basal membrane of capillaries of balls. In more hard cases (death in the first weeks of a disease) acute necrotic G. is observed, for to-rogo the fibrinoid necrosis of loops of capillaries of a ball and the bringing arteriole along with thrombosis of capillaries and infiltration by neutrophilic leukocytes is characteristic. Very seldom typical hymenoid develops.

Fig. 5. «A motley kidney» (acute glomerulonephritis): small hemorrhages on the surface of a kidney and in fabric (are visible on a section).

Kidneys at acute G. are a little increased, bulked up, dryablovata, motley — «a motley kidney» (tsvetn. fig. 5). Pyramids are dark red, bark of grayish-brown color with small red impregnations on a surface and a section — at a hemorrhagic form or with grayish translucent points — at proliferative and fibrinous exudative forms. However in some cases (death in the first days of a disease) kidneys during the opening can seem not changed at all, and only gistol. the research reveals diffusion. On the basis of studying of repeated biopsies it is revealed that the changes of kidneys characteristic of acute G. can be completely reversible. But in some cases even at full a wedge, recovery gistol, changes, inherent G., can remain for years.

Fig. 7. «A big motley kidney» in a section (a subacute glomerulonephritis): the bast layer with small hemorrhages is well delimited from plethoric marrow.

For the subacute glomerulonephritis which is quickly progressing, or malignant, the combination ekstrakapillyarny productive (more rare exudative) changes of balls with heavy dystrophic changes of tubules (subacute G. with a nephrotic component, on old authors) and edematous and infiltrative changes of a stroma is characteristic. Kidneys at the same time are considerably increased, flabby, a bast layer wide, bulked up, yellow-gray, dim, with small red impregnations and is well delimited from dark red marrow of a kidney — «a big motley kidney» (tsvetn. fig. 7) — or it red also merges with plethoric pyramids — «a big red kidney».

The morphology of a chronic glomerulonephritis is very various, intracapillary proliferative, minimum, hymenoid, hymenoid and proliferative, and also fibroplastic changes in various combinations to changes of tubules, vessels and a stroma are found. Accurate dependence between a wedge, options and morfol, forms at hron. Is not present. However it is possible to consider that for a hamaturia (gematurichesky option G.) intracapillary productive processes in balls, of a proteinuria (nephrotic option hron are most characteristic.) — the minimum and hymenoid changes, to the Crimea tubulointerstitsialny insufficiency, and for arterial hypertension joins (hypertensive option hron.) and combinations of a nephrotic syndrome to hypertensia — fibroplastic reaction in balls and secondary vascular and intersticial changes.

Fig. 6. «A big white kidney» (nephrotic option of a glomerulonephritis).

The most characteristic macro - microscopic changes of kidneys are observed at nephrotic option hron. And in an end-stage of a disease. At nephrotic option G. in some cases dystrophic changes of tubules and a stroma of kidneys, especially fatty infiltration, dominate over the minimum or hymenoid changes of balls. Kidneys at the same time become increased, flabby, white-yellow or white — «a big white kidney» (tsvetn. fig. 6), and it is difficult to distinguish them from a lipoid nephrosis (an idiopathic nephrotic syndrome).

Fig. 8. Microdrug of a kidney (a chronic glomerulonephritis from the outcome in wrinkling): 1 — a sclerosis and a hyalinosis of balls; 2 — an atrophy of tubules; 3 — growth of connecting fabric in a stroma; coloring hematoxylin-eosine.
Fig. 9. A kidney (a chronic glomerulonephritis from the outcome in wrinkling): the dense fine-grained surface which is formed as a result of alternation of sites of a sclerosis and an atrophy with sites of a hypertrophy.
Fig. 10. A kidney in a section (a chronic glomerulonephritis from the outcome in wrinkling): the anemic the sclerosed fabric of gray color, in a bast layer is visible a cyst (it is specified by shooters).

For an end-stage hron. Development of secondary (nephritic) wrinkling of kidneys is characteristic. At the same time kidneys decrease in sizes, become dense, a surface their fine-grained, seldom smooth — at uniform wrinkling (tsvetn. fig. 9). Granularity of a surface of kidneys is explained by the fact that sites of a sclerosis and atrophy (sticking) alternate with sites of hypertrophied nephrons (protrusion). On a section a layer of renal fabric thin, and cortical substance is especially thinned; tissue of a kidney is dry, anemic, gray color (tsvetn. fig. 10). At microscopic examination in the sunk-down sites the atrophy of balls and tubules and substitution are noted by their connecting fabric (tsvetn. fig. 8). Balls turn into scars (glomerulosclerosis) or hyaline balls (glomerulogialinoz). In eminating sites balls of a sokhranna, some of them are hypertrophied. The capsule of such balls is thickened, capillary loops are sclerosed (Web-footed balls), the sclerosed «semilunums» meet here and there, tubules are expanded, their epithelium is thickened. Arterioles are sclerosed and hyalinized. In small, average arteries fibrosis and a hyalinosis of an internal cover are observed, the sclerosis and histiocytic infiltration of a stroma are sharply expressed.

The clinical picture

the Acute glomerulonephritis can develop at any age, however up to 2 years it meets seldom [Fison (T. N. Fison), 1956].

Indicators of incidence fluctuate from 0,55 to 0,71, and among various children's age groups from 0,08 to 0,85 on 1000 people. The maximum incidence among children is the share of age from 7 to 10 years (N. A. Chistenkov, 1969). Among adults there are indicators of incidence on average 0,62 for 1000 (A. M. Shukhtina and A. N. Butts, 1963); patients more young make than 40 years 75 — 90% [V. V. Pozharskaya, M. S. Babitskaya, 1936; Addis (T. Addis), 1948]; patients are more senior than 60 years make no more than 3%. Distinctions of incidence of men and women are not revealed.

A wedge, acute G.'s manifestations are very various — from extremely scanty (only accidentally in the course of inspection the revealed changes of urine) to extremely bright, with violently developing classical triad of symptoms: hypostases, hypertensia, hamaturia. Weakness, thirst, an oliguria can precede these symptoms. At the developed picture of a disease of the patient an asthma, heartbeat, a headache, nausea, vomiting, back pains, hypostases of different degree of manifestation disturbs. Urine at a gross hematuria can be red or brownish because of transition of hemoglobin to hematin at acid reaction of urine.

Hypostases — one of the most precursory and frequent symptoms of G. — are noted at 70 — 90% of patients, approximately at a half they are considerable. Preferential localization of hypostases on a face, pallor of skin and swelling of cervical veins allow to speak (at a part of patients) about facies nephritica. Hypostases can begin and standing. In edematous liquid of protein to 1 — 2%.

The pathogeny of hypostases at acute G. is difficult and up to the end is not clear. Their prime cause is the defeat of balls leading to reduction of glomerular filtering that is followed by decrease diuresis (see). The reabsorption of sodium (and waters) in tubules raises. At the same time it is difficult to exclude a role of a hyper aldosteronism; though secretion of Aldosteronum is usually not increased, but the natriuretic and diuretic effect of antagonists of Aldosteronum is obvious. In developing of hypostases significance is attached to increase in vascular permeability.

Arterial hypertension is registered at 70 — 90% of patients (see arterial hypertension). Its degree considerably fluctuates, the frequency of emergence and weight increase with age. Hypertensia, as well as other symptoms of acute G., can be «tranzitorny». Decrease in the ABP to datum level happens usually over the first 3 weeks in parallel with reduction of other symptoms. Long and permanent increase in the ABP predictively is adverse. The leading significance in a pathogeny of hypertensia at acute G. is attached to a delay of sodium and water, increase in volume of the circulating blood and a stroke output of heart. Increase in the ABP on hyperkinetic type with increase in cordial emission is combined with decrease in peripheric resistance in the first days of a disease. Further in process of decrease in the ABP peripheric resistance is normalized (M. I. Frankfurt, A. K. Merzon, 1968). At a heavy current of G. permanent increase in peripheric resistance comes to light.

Value of system a renin — angiotensin in developing of hypertensia at acute G. is exposed to studying. Big sensitivity of a vascular wall to pressor agents in connection with a delay of sodium in it is not excluded.

Frequency of hemodynamic disturbances increases with age. The phenomena of heart failure, an acute fluid lungs are the main reason for death of patients acute G. Obychna characteristic signs left ventricular (an asthma, an orthopnea, a pneumorrhagia, the cardiac asthma reaching considerable degree) and right ventricular insufficiency (swelling of cervical veins, increase in venous pressure). Increase in mass of the circulating blood is the cornerstone of emergence of hemodynamic disturbances, 7 — 9 l can reach edge. In the absence of a hypervolemia hemodynamic shifts are usually insignificant. Developing of hypertensia can aggravate an overload of heart though symptoms of heart failure can appear also without increase in the ABP.

Damages of a cardiac muscle in the form of serous myocarditis are found in 10% of cases.

Sharply arising hypervolemia (see Blood) leads to expansion of cardial cavities; its sizes are normalized gradually after recovery of a diuresis and fall of hypostases. Force of an apical beat depends on an anasarca (the general edema), expansion of cardial cavities, existence hydrocardia (see). At auscultation easing of the first tone, emphasis of the second tone on an aorta, systolic noise on a top quite often is found at relative insufficiency of the mitral valve, in hard cases — a cantering rhythm (see. Gallop rhythm ). Changes of an ECG are various and are defined by expressiveness of hemodynamic and electrolytic disturbances. The low voltage of an ECG, lengthening of an interval of PQ, two-staging and flattening of a tooth of T, sometimes shift of an interval of ST are often observed. The acute disorders of blood circulation in peripheral arteries leading to a focal necrosis on extremities are occasionally observed.

The expressed changes of an eyeground find at 5% of patients [H. Sarre, 1967]. At a severe disease with permanent increase in the ABP the vasospasm, sometimes dot hemorrhages in a retina is observed (see. Eyeground , tab.). As a result of a papilledema and a spot of a retina the amaurosis can develop (see. Blindness ).

From a nervous system there are subjective and objective disturbances. Complaints to a headache, weight in the head are characteristic. The severe headache in combination with nausea and vomiting, decrease in sight and flashing of «front sights» before eyes can precede angiospastic encephalopathies (see). Sometimes muscular and mental irritability increases. Predecessors of encephalopathy and its typical attacks can develop at a sufficient diuresis and even a polyuria; The ABP at the same time sharply raises (it can remain normal with children), pulse urezhatsya. Attacks of encephalopathy remind epilepsy: pupils are expanded (but are not narrowed, as at uraemia), consciousness is absent, spasms of clonic and tonic character, are followed by tongue biting, an involuntary otkhozhdeniye a calla and urine; pressure of cerebrospinal liquid sharply increases. During attacks there can come the amaurosis. Renal encephalopathy usually comes to an end favorably, however the hematencephalon is possible. Disturbance of cerebral circulation is the cornerstone of these phenomena (vasomotor spasm) and wet brain (see. Swelled also swelling of a brain ).

Also other manifestations of acute are observed. Pains in a waist of different degree of manifestation, a thicket symmetric (at 34% of patients), depend on swelling of kidneys and stretching of their capsule, disturbance of urodynamic. The dysuric phenomena arise seldom; they are connected probably with high concentration and a hyperoxemia of urine. Oliguria (see) and even anury , (see) are possible more often in the first days of a disease and 2 — 3 days proceed usually. More long oliguria is observed seldom. High specific weight of urine is characteristic of an oliguria at acute G. A long oliguria, especially at elderly patients — a bad predictive sign though favorable outcomes at the oliguria proceeding to 8 weeks are described [D. Perscoff, 1965].

Changes of function of kidneys are various and depend on weight of process. At developed a wedge, a picture glomerular filtering and filtrational fraction of a renal plazmotok decreases, function of proximal tubules on the maximum reabsorption of glucose and secretion paraaminobenzaminoacetic to - you or a diotrasta decreases. Decrease in secretion paraaminobenzaminoacetic to - you is connected rather with obstruction of renal tubules proteinaceous masses, than with their defeat. The renal blood stream is normal or increased, except for the most hard cases; function of distal departments of tubules is usually kept; azotovydelitelny function is not broken, except for the hard cases which are followed by an oliguria and an anury.

Proteinuria (see) it is noted almost at all patients, except for exceptional cases of analbuminurichesky G., and can reach high figures (to 90 per milles). The massive proteinuria remains usually no more than 1 — 2 week, moderate several months can last. The proteinuria can be the selection with allocation of hl. obr. albumine or non-selective when at an electrophoretic research find in urine also other serum proteins. In urine of patients the factor of the unspecified nature causing cellular phenomena comes to light: A LE phenomenon and a phenomenon leucio-and an erythrophagocytosis — at influence by urine of patients on leukocytes of healthy donors. The same phenomena are observed at an aggravation latentno flowing hron. (JI. V. Kozlovskaya et al., 1976).

A microhematuria (see. Hamaturia ) — the symptom is almost so constant, as well as the proteinuria, but keeps usually longer. The gross hematuria is observed at 12 — 18% of patients. Leukocyturia (see), though meets, of G. it is not characteristic.

In blood moderate anemia, usually normokhromny and normotsitarny is observed. Decrease in an erythrogenesis, but not a hypervolemia is its main reason. Changes of level of leukocytes and a leukocytic formula are changeable. Acceleration of ROE is frequent, and is sometimes considerable also above (to 50 mm/hour). Level of a serum protein is normal or slightly reduced that is connected generally with a hydremia and in a smaller measure with loss of protein with urine. Albumin-globulinovy coefficient (see) the hl decreases. obr. due to increase alfa2-and gamma-globulins. Acidosis, as a rule, compensated. The hyperpotassemia is observed only at a severe disease. Content of sodium and uric to - you is more often a little increased.

A malignant glomerulonephritis (subacute, ekstrakapillyarny, quickly progressing hron.) it is characterized by the galloping current without stage of latency and remissions; during the period from 6 months to 2 years leads to development hron, a renal failure. In a wedge, all symptoms — hypostases, hypertensia, a proteinuria, a hypoproteinemia, a hypercholesterolemia usually are considerably expressed to a picture. Quite often heart failure develops. Signs of disturbance of functional capacity of a kidney can already appear in especially hard cases on 4 — to the 6th week of a disease, at the same time changes of an eyeground quickly progress. At a part of patients hypostases, hypertensia can be absent. Bystry and resistant depression of function of kidneys in these cases gains crucial diagnostic importance.

The chronic glomerulonephritis on an etiology, a pathogeny, a patomorfologiya, clinic and a current is heterogeneous that causes difficulty of its classification. Contrary to the doctrine dominating to the middle of 20 century Folgarda and Farah (F. Volhard, Th. Fahr), according to Krom hron. Represents only post-streptococcal G.'s acute, as a rule, outcome, from 60th considerable number of cases carry to primary hron. Without initial acute stage. Becomes obvious that exists, in addition to infectious and immune group, and noninfectious and immune group G. (serumal, medicinal, etc.).

Wedge, manifestations hron. Are characterized by hypostases, increase in the ABP, a proteinuria and other changes of urine, a hypoproteinemia, a hypercholesterolemia, signs of chronic renal failure (see) in far come cases. At separate options hron. Symptoms are expressed to these in various degree and combinations.

Depending on dominance of these or those a wedge, manifestations hron. It can be divided into four main options: nephrotic, hypertensive, mixed and latent.

Chronic G. with a nephrotic syndrome is characterized by massive hypostases and a proteinuria, hypercholesterolemia, hypoproteinemia, especially due to decrease in level of albumine; The ABP normal or lowered. The current is usually gradual: the hypostases arising on a face and legs extend to a trunk, an edema of cavities joins. Develop a fluid lungs with an asthma, wet brain with spasms, hypostasis of a retina with a blindness less often. Hypostases can be very persistent or have recurrent character. For the developed picture of a disease an oliguria with release of urine of high specific weight, considerable loss of protein with urine (Zgi more in days), a proteinuria the selection are ordinary or non-selective. The last is more often observed at heavier morfol. changes of kidneys. Signs of canalicular insufficiency can join. At the same time come to light glycosuria (see), aminoaciduria (see). A cholesterinemia (see. Hypercholesterolemia ) can reach 1000 mg of % and above, the content of albumine in blood serum decreases sometimes to 1 — 2 g of %. Dystrophic changes of skin and skeletal muscles are frequent.

The hypertensive glomerulonephritis proceeds, as a rule, latentno in the beginning, is characterized by long development (up to 20 — 30 years), well or well transferable arterial hypertension and little changes in urine. In the compensated stage the disease quite often is diagnosed accidentally (at medical examination, a research of urine, etc.). Severe defeat of brain or coronal vessels is observed less than at an idiopathic hypertensia. The ABP even more raises at development hron, a renal failure when there can be symptoms of heart failure — cardiac asthma, a pneumorrhagia, increase in a liver etc. Klin, manifestations during this period are similar to a picture of a malignant hypertension. At sharp increase in the ABP the gross hematuria is possible.

The mixed glomerulonephritis (classical otechnogipertonichesky nephrite) is characterized by hypostases, usually persistent, and hypertensia. Duration of a current from the beginning of a disease of 3 — 5 years.

The latent glomerulonephritis comes to light unexpectedly, sometimes at a dispensary or accidental research of urine when the proteinuria or a hamaturia comes to light. Quite often the disease is not distinguished up to development of uraemia (see). The beginning of nephrotic can be latent. This G. can proceed 20 and more years and to end hron, a renal failure.

The end-stage of a chronic glomerulonephritis finishes any option hron. G. Complaints of patients are caused by intoxication and defeat of cardiovascular system. The arterial hypertension which is quite often accruing or developing for the first time at approach of a renal failure sometimes gains lines malignant. Deterioration in sight occurs usually at obviously expressed azotemias (see). Big hypostases remain seldom and carry mixed — cardiorenal character. It is characteristic isosthenuria (see), the polyuria, edges at the end of a disease can be replaced by an oliguria. The proteinuria is usually small, in draft the «wide» cylinders coming from expanded tubules of the remained hypertrophied nephrons.

Complications are various and are defined a wedge, a form and the course of a disease, therapeutic actions. The last, napr, a hemodialysis, owing to lengthening of an end-stage of a disease led to emergence few complications known earlier (heavy an osteopathy, polyneurites, etc.).

At malignant G. can be observed amotio of a retina (see), a hematencephalon (see. Stroke ), phenomena heart failure (see). The complications at nephrotic G. caused by immune disturbances inherent in it — loss of immunoglobulins, a complement and the phenomena of hypercoagulation are especially numerous: peritonitis, an erysipelatous inflammation with a bakta riyemichesky shock and falling of functional capacity of kidneys («nephrotic crisis»). Their emergence can be promoted by therapy by corticosteroids, as a result the cut is suppressed formation of mast cells — the main source of heparin. Coronary heart disease (see) meets more often at nephrotic. The complications characteristic are inherent to hypertensive G. for idiopathic hypertensia (see).

The diagnosis

Difficulties in acute G.'s diagnosis arise in cases of the monosimptomny and erased forms. Differential diagnosis with focal embolic nephrite, hron is necessary. In the period of its aggravation, a congestive kidney at heart failure, an amyloidosis of kidneys, an acute nekronefroz, acute pyelonephritis.

Focal embolic nephrite arises, as a rule, at patients with sepsis or subacute septic endocarditis; renal hypertensia, hypostases are not characteristic of it.

Diagnosis of an aggravation hron. It is put if in carefully collected anamnesis there is an instruction on a disease of kidneys in the past, the patient has signs is long the existing hypertensia, at terminal G. there are signs hron, a renal failure with reduction of the sizes of kidneys. «Congestive kidney» from acute G. is distinguished by the anamnesis, signs of organic lesion of heart, dynamics of changes of urine at successful therapy of heart failure.

Rough progressing is earlier hidden the proceeding amyloidosis (see), arisen after the postponed infections, surgeries, vaccination, sometimes reminds acute.

The greatest value in differential diagnosis with an amyloidosis has the anamnesis (data about hron, suppurative diseases, tuberculosis, a pseudorheumatism), identification of the increased dense liver and a spleen, and also these biopsies of kidneys and a rectum.

Developing of an acute renal failure owing to a nekronefroz is preceded usually by influence of nephrotoxic agents, incompatible blood transfusion, depressed and kollaptoidny cases etc. Difference from acute G. are the low specific weight of urine, absence of hypertensia, heart failure.

At acute pyelonephritis there are no hypostases, the ABP more often normal, fever, back pains, a dysuria are observed.

Diagnosis hron. In typical cases comes easy. Differential diagnosis with nephrite at general diseases at which hypostasis can be almost only manifestation throughout more or less long time is more difficult. Nephrites at a hemorrhagic vasculitis are that (see. Shenleyna — Genokh a disease ), when other symptoms (damage of joints, skin rashes, abdominal pains etc.) can be expressed a little. Unlike G. developing of nephrite at young women and communication of a disease with insolation, fever, even short-term, allow to suspect small joint pains system lupus erythematosus (see).

Other general diseases able to proceed with nephrite — a nodular periarteritis (see. Periarteritis nodular ), scleroderma (see), Wegener granulomatosis (see), Gudpaschera a syndrome (a necrotizing alveolitis with proliferative or necrotic nephrite), Moshkovich disease (see), are characterized by brighter, than at G., and are easily distinguished by the general manifestations. Rheumatic nephrite usually is followed by other manifestations rheumatism (see).

Hron, pyelonephritis (see) it is distinguished according to the anamnesis: periodic as if unmotivated oznoba, the dysuric phenomena, existence the Urals, diseases is frequent (a nephrolithiasis etc.). The proteinuria at pyelonephritis is usually small, in draft leukocytes prevail. The nephrotic syndrome is extremely rare. Asymmetric damage of kidneys, change of pyelocaliceal system in late stages of a disease is characteristic.

The idiopathic hypertensia leads to falling of functional capacity of kidneys with the considerable duration of a disease. Besides, the malignant idiopathic hypertensia, and also renovascular hypertensia, are characterized by bigger expressiveness of cardiovascular symptomatology. Identification in the anamnesis of existence of changes of an urocheras is important for G.'s diagnosis.

Anemia, sharp acceleration ROE, a paraproteinemia, a paraproteinuria — Bens-Jones's protein are characteristic of a renal form of a multiple myeloma (see. Bens-Jones of squirrels ).

Diabetic G. is diagnosed on the basis of the anamnesis, a characteristic retinopathy and other displays of diabetes.

Damage of kidneys at gout is diagnosed taking into account displays of a disease and existence of high concentration uric to - you in blood — a hyperuricemia (see. Lithemia ).

Treatment

At an acute glomerulonephritis the main therapeutic actions — a high bed rest, a diet and drug treatment. In the presence of hypostases, hypertensia, the phenomena of heart failure, a hamaturia of the patient the bed rest for 3 — 4 weeks shall observe, and at an adverse current and more long term. The bed rest needs to be observed before total disappearance of hypostases, normalization of the ABP, elimination of heart failure; it promotes increase in functional capacity of kidneys. Careful observance of a bed rest, according to some authors [H. Sarre, 1968], interferes with acute G.'s transition to chronic. The insignificant proteinuria and a microhematuria are not the indication to preservation of a bed rest if transition to more free mode does not worsen a condition of the patient.

After the postponed acute G. patients within a year and more shall avoid overfatigue, long stay in vertical position, coolings. Introduction of vaccines and serums is contraindicated. A diet at acute G.

restriction in food of sodium, water and partly is the cornerstone of protein. Treatment by hunger and thirst, as a rule, shall not be applied because of a possible eksikoz (see. Toxic syndrome ), leading to deterioration in function of kidneys and disintegration of an internal protein. In the first days of a disease food depending on the ABP and hypostases shall contain no more than 0,5 — 2 g of sodium chloride, and amount of the drunk liquid to exceed a diuresis for the last days on 400 — 500 ml for compensation of extrarenal losses. At the expressed hypostases and hypertensia the amount of liquid in the first days is admissible to reduce to 400 — 500 ml a day. The general caloric content of food shall be satisfied with hl. obr. at the expense of carbohydrates and fats. During the first 3 — 4 weeks restriction of protein to 0,5 g/kg of weight a day is reasonable.

Antibacterial therapy is reasonable in the first days of development of postinfectious G., especially in the presence of the active center of an infection (an exacerbation of tonsillitis, sinusitis etc.) or at G. which is closely connected with an infection, napr at a subacute septic endocarditis. Least nefrotoksichen penicillin and its semi-synthetic derivatives, erythromycin. Penicillin is appointed usually in a dose of 1 million. Piece a day within 7 — 10 days. At decrease in glomerular filtering the dose of penicillin shall be reduced. Neomycinum, Monomycinum, Kanamycinum and to a lesser extent drugs of a tetracycline number of a nefrotoksichna.

Treatment of heart failure is directed first of all to elimination of its main reason — a hypervolemia and partly to arterial hypertension. Essential value can have bloodletting of 400 — 500 ml of blood and more, a cut prevents also spasms. Use of cardiac glycosides, especially strophanthin and digitoxin is shown. Use diuretic [is more preferable lasixum (furosemide) on 40 — 160 mg a day, ethacrynic to - that (Uregitum) of 50 — 200 mg a day] in combination with antagonists of Aldosteronum in the absence of a hyperpotassemia reasonablly at the expressed hypostases and arterial hypertension. Special treatment of arterial hypertension is necessary at high figures of the ABP, symptoms of heart failure; especially active it shall be at threat of renal encephalopathy. For this purpose intravenously enter rausedyl. For achievement of bystry effect in the absence of an oliguria and symptoms of a renal failure enter intravenously ganglioblokator (Pentaminum) on 0,2 — 0,4 ml of 5% of solution divorced in 20 ml of 5% of solution of glucose.

At the first symptoms of encephalopathy — bloodletting (500 ml and more), introduction of 25 mg of aminazine in the form of 2,5% of solution intramusculary, osmotically active agents (200 — 250 ml of 20 — 40% of solution of glucose, the same dose of solution of Polyglucinum) during 20—30 min., osmotic diuretics (Mannitolum of 0,5 — 1,5 g of nonvolatile solid on 1 kg of body weight) intravenously.

Spinal puncture (see) it is carried out at the proceeding spasms and an amaurosis; liquid shall be extracted slowly in order to avoid infringement of brain fabric in a big occipital opening, pressure is reduced to 150 mm w.g.

Hemodialysis (see) it is necessary at the expressed oliguria which is followed by a hyperpotassemia, an azotemia.

Efficiency of glucocorticoids at acute G. is doubtful. Only at a prolonged current if the therapy which is earlier carried out during 6 — 8 weeks was unsuccessful, carrying out a prednizolonoterapiya is reasonable (60 mg a day for 3 — 4 weeks with the subsequent gradual reduction of a dosage).

At a chronic glomerulonephritis regime of the patient, a diet and to lay down. actions are under construction on the basis of the analysis of function of kidneys, activity of process, a condition of cardiovascular system. The centers of an infection shall be revealed, pyelonephritis is excluded, portability of drugs, foodstuff, influence physical is found out. loadings. At purpose of a diet it is necessary to consider that aggravations hron. With the phenomena of a hypervolemia, heavy arterial hypertension, hypostases of renal and cardiorenal genesis demand sharp restriction of sodium in food, and in an end-stage of a disease it is necessary to limit protein, to avoid excess of potassium and magnesium and not to allow a lack of calcium of food.

At sufficient functional capacity of kidneys, normal or easily adjustable ABP, in the absence of a hypervolemia and hypostases the usual diet is recommended. The patient shall receive 1 — 1,5 g of protein on 1 kg of weight, from them 2/3 — full animal origin (eggs, meat, dairy products); caloric content of food shall correspond to the performed work and weight. Fried meat, stewed vegetables is admissible. It is not necessary to use a lot of fruit and tomato juice because of high content of potassium in them. Sodium chloride at a tendency to hypostases and hypertensia is limited.

Anti-infectious therapy is carried out during the developing of infectious diseases, at the mixed damages of kidneys (nephrite pyelonephritis), after operative measures, and also with the preventive purpose at corticosteroid therapy. Preference is given to semi-synthetic derivatives of penicillin of a broad spectrum of activity. Antibiotics are shown to a thicket in case of a nephrotic hron. Because of tendency of these patients to infectious complications, preferential coccal (pneumonia, etc.). Diuretics, hl are widely applied. obr. saluretics (furosemide to 80 — 160 mg a day and more; Uregitum to 200 mg a day and more, etc.) in combination with antagonists of Aldosteronum (veroshpiron) and osmotic diuretics (Polyglucinum to 250 ml; Mannitolum on 200 — 400 ml of 10 — 20% of solution). Seralbumin on 100 — 200 ml or plasma on 150 — 200 ml with various intervals is recommended. It is necessary to control the level of potassium in blood serum and an ECG in connection with potassiumuretic effect of saluretics.

Antihypertensives apply at substantial increase of the ABP; at the same time it is necessary to try to obtain its slow decrease in order to avoid deterioration in a functional condition of kidneys. The combination of drugs of Rauwolfia and Methyldopa (usually in average doses) with saluretics is reasonable. If decrease in the ABP is followed by increase in content of creatine in plasma, it is necessary to refuse hypotensive drugs. Especially carefully it is necessary to appoint diuretics at the phenomena hron, a renal failure not to break a water-salt homeostasis and not to cause hypostasis of little or hypovolemic shock.

Glucocorticoids (steroid hormones) are most effective at nephrotic G. with the minimum defeat of balls and are much less effective at others a wedge, forms. Prednisolonum in doses of 40 — 60 mg a day during 3 — 4 weeks with a gradual dose decline is more often used.

Immunodepressants, first of all Azathioprinum (imuran), in a dose of 1,5 — 2 mg on 1 kg of body weight a day are applied in combination with doses of Prednisolonum (10 — 20 mg), necessary for prevention of a haemo-cytopenia, within 2 — 3 and more months. They are reasonable at G.'s aggravation, resistant to steroid hormones, or in the presence of contraindications for use of high doses of glucocorticoids (high the ABP, etc.).

Anticoagulants are most widely applied in the period of an exacerbation of a disease, especially the heparin having ability to suppress immune responses of the immediate and slowed-down type. They are entered usually in a dose of 15 — 25 thousand. Piece a day within 1 — 2 month; the combination of heparin to glucocorticoids, cytostatics is possible. Anticoagulants of indirect action are used less often.

4-Aminokhinolinovye drugs — delagil (Resochinum, chloroquine), plaquenil possess an insignificant immunodepressive effect, stabilization of lysosomes promote and interfere with release of lizosomalny enzymes. Are applied also more) on 0,25 g a day is long (about one year. Increase in a dose can cause a leukopenia, dyspepsia, defeat of a cornea and a retina.

Indometacin on 75 — 100 laid down in days is applied at various a wedge, options G. within 1 — 2 and more months. Sometimes it causes clear decrease in a proteinuria, hamaturia; at a part of patients during the easing of activity of G. the ABP decreases.

Anti-lymphocytic serum and anti-lymphocytic globulin did not find broad application yet.

Dignity. - hens. treatment is shown for patients without disturbance of functional capacity of kidneys and without high arterial hypertension; in a complex to lay down. actions it promotes recovery or maintenance of working capacity. Resorts with climate of deserts (A Bayram Alya, etc.), the Southern coast of the Crimea are recommended.

The forecast

the Lethality at acute G. is usually small and connected by hl. obr. with complications of a disease — a hematencephalon, an acute heart failure, infectious complications and fibrinferments. The renal failure seldom leads to death.

In 50% of cases acute G. passes into chronic. It is conditionally possible to speak about acute G.'s transition in chronic if within a year hypertensia or hypostases remains, or the proteinuria is higher than 1%, however cases of recovery later from the beginning of development of these symptoms are known 2 years.

Working ability of patients depending on a form and G.'s weight is recovered in various terms, usually in 2 months. It is necessary to be careful physical. loadings; return to the profession connected with cooling is undesirable.

At timely treatment by corticosteroids, immunodepressants, Resochinum patients hron. Can recover. But the individual forecast is difficult. It is defined by a progrediyentnost of a disease, immune activity of process, depth of disturbances of renal blood circulation. Transition hron is most often observed. In a final stage with wrinkling of kidneys. This process can proceed as within several years, and decades. The forecast at an azotemia at patients with arterial hypertension is especially serious (diastolic pressure more than 120 mm of mercury.) and fluid lungs.

Prevention

Prevention consists in early and vigorous treatments of a streptococcal infection of a nasopharynx, adnexal bosoms and skin. The persons which are in contact with the patients having a streptococcal infection are inspected and carry out preventive treatment. Preventive sanitation of the centers of an infection is obligatory; the hardening of an organism is reasonable. It is important to consider individual intolerance of medicines, foodstuff, instructions on heavy inoculative reactions.

The glomerulonephritis at pregnant women

Is observed no more than 1 — 2 cases on 1000 pregnant women. Influence of pregnancy on G.'s current substantially depends on a form of a disease. Only at hron. Without renal failure and hypertensia pregnancy does not cause exacerbations of a disease. Perhaps, it is promoted by the hypersecretion of glucocorticoids inherent to the period of pregnancy. Also acute G.'s rarity is explained by the same circumstance partly during pregnancy. That pregnancy does not worsen G.'s current with safe function of kidneys, satisfactory condition of women in the remote terms after the delivery demonstrates. If G. proceeds with azotemia (see), the impaired renal function during pregnancy worsens even more. Normal at pregnancy such indicators of function of kidneys as a renal blood stream, glomerular filtering, filtrational fraction, are increased in the first trimester of pregnancy and gradually decrease by its end. At patients hron. The nature of changes of these indicators remains; at its aggravation considerably the reduced level of glomerular filtering and filtrational fraction by the end of pregnancy becomes even less and increases uraemia (see).

Burdens the course of pregnancy: often there is late toxicosis of pregnant women (11 — 35%), perinatal mortality (14 — 17%) is high and quite often there is premature amotio of normally located placenta to massive blood loss (see. Premature placental detachment), an afibrinogenemiya that leads to death of the woman and child. Frequency of these complications depends on a form hron. G.: if the disease is followed by increase in the ABP, late toxicosis of pregnant women (see) it is observed by 4 times, and perinatal mortality (see) by 12 times more often than at the normal ABP [Felding (Page F. Felding)].

For G.'s diagnosis at pregnant women use usual methods, but in connection with a possibility of an adverse effect on a fruit restrictedly apply rentgenol., angiographic, tracer techniques of a research of kidneys, puncture biopsy of kidneys. Microscopic examination of an urocheras, definition of a clearing coefficient of endogenous creatinine is of great importance (see. Clearance test ). For differential diagnosis of G. with nephropathy of pregnant women (see) important identification of communication with recently postponed streptococcal diseases and the sensibilizing factors (vaccination and so forth) and detection of the raised credits of antistreptococcal antibodies (antistreptolysin-0 and anti-hyaluronidase).

G.'s treatment at pregnant women is limited to purpose of a diet, diuretic, antihypertensives, cardiac glycosides and so forth. Active pathogenetic therapy of G. at pregnant women is impossible since the high doses of corticosteroids applied to this purpose, cytostatic means and immunodepressants are contraindicated because of their embriotoksi-chesky action. Therefore acute G. and aggravation hron. Are the indication for abortion in any terms.

A wedge, observations and morfol, a research of tissue of the kidney received by a puncture biopsy several years later after the delivery confirmed the assumption of an outcome of late toxicosis of pregnant women existing earlier in G. Vozmozhnost of G.'s development after a nephropathy or eclampsias (see) it is caused immunol. reactions between a fruit, a placenta and an organism of the pregnant woman.

The glomerulonephritis at children

In children's nephrology of G. is considered as an immunoinflammatory disease, on the immunol, and morfol, by entities inclined to a long current. The classification offered in 1966 by N. Speransky et al. is most widespread. The scheme of the developed G.'s diagnosis provides allocation of a form and character of a current, degree of activity of process, a functional condition of kidneys and so forth.

At children distinguish the gematurichesky, nephrotic and mixed forms G. with an acute, chronic (long) or wavy current. Besides, in each form allocate active and inactive phases.

For a wedge, pictures the combination of hypertensia, hypostases and changes of urine which degree of manifestation varies at different forms of a disease is typical. Changes of urine can be three types: gematuricheskiya — it is characterized by the expressed erythrocyturia at a small proteinuria (to 1 g of protein in daily amount of urine); proteinuricheskiya — differs in big loss of protein with urine (Z and more per day) at a considerable cylindruria and a microhematuria; mixed — is noted a proteinuria, a hamaturia, a cylindruria, quite often a leukocyturia, as a rule, not connected with an infection.

Moderate hypertensia, unsharply expressed hypostases and a hamaturia is inherent in the Gematurichesky form G., edges remains also after disappearance of extrarenal symptoms of a disease. From a pharynx at patients in most cases sow nefritogenny strains of a hemolitic streptococcus; in blood the high caption of anti-streptococcal antibodies is noted. During the acute period of G. at children note small acceleration of ROE, a disproteinemia at the normal content of crude protein in serum. On excretory Urogramums either aberrations are not noted, or there is a picture of a prelum of cups infiltrate around them. At gistol, studying of biopsy material of a kidney the proliferative glomerulitis usually is found. This form G. occurs at children of school, is more rare than preschool age.

Hypostases, a proteinuria, hypo - and a disproteinemia, and also a hyperlipemia are inherent to a nephrotic form G. At the same time quite often there are ascites, a hydrothorax. During the acute period of a disease of ROE it is sharply accelerated, considerable disturbances of electrolytic balance, a secondary hyper aldosteronism are noted. On excretory Urogramums increase in the sizes of kidneys, infiltrative type of changes of pyelocaliceal system comes to light. At a biopsy of kidneys quite often reveal the minimum changes of balls, however it is possible to observe a hymenoid or hymenoid and proliferative glomerulitis. To morfol, researches of kidneys regarded a disease as an idiopathic nephrosis (see. Nephrotic syndrome ). The nephrotic form G. — the main reason for a nephrotic syndrome at children and, on the majority of observations, arises within the first three years of life.

The mixed form G. is characterized by existence at the child of persistent hypertensia, hypostases, permanent changes of urine, resistance to therapeutic actions, tendency to early depression of function of kidneys. Shifts in indicators of exchange are similar to changes at a nephrotic form of a disease, but a proteinuria usually more moderate. Sometimes the protein secreted with urine in character approaches blood protein, i.e. selectivity of a proteinuria is broken that speaks about heavy destructive process in kidneys. On Urogramums changes of infiltrative) type are often observed. Histologically define a fibroplastic glomerulitis, the expressed changes in tubules and connecting fabric. The mixed form G. develops at children of the advanced school age more often.

The acute current of G. at children is characterized by the rough beginning with pronounced extrarenal manifestations which can disappear quickly enough under the influence of treatment. At a part of patients within 1,5 — 2 months from the beginning of a disease changes in urine completely disappear. Such favorable cyclic current is characteristic of a gematurichesky Form. Quickly progressing malignant G. occurs at children seldom, usually at the mixed form of a disease. If extrarenal manifestations of G. are unsharply expressed, but changes of urine do not disappear many months, it is possible to speak about a long current of. Consecutive change of a recurrence and remissions is characteristic of a wavy current. Remissions can be full or incomplete when at good shape at the patient laboratory signs patol, process remain. The wavy current, even at timely begun treatment, is most characteristic of a nephrotic Form.

When the disease is revealed accidentally, napr, at dispensary inspection, and has no extrarenal manifestations, is carried out careful clinical laboratory, rentgenol., the Urals, and morfol, (biopsy) a research for an exception of hereditary and inborn nefropatiya.

Activity patol, process at the child is defined by degree of manifestation of hypertensia, hypostases, changes of urine and the nature of exchange disturbances. It is possible to speak about inactive process at normalization of urine, main types of exchange and immunol. indicators.

At children's age seldom comes to an end with an end-stage of a renal failure. At sharply proceeding G. at children the perversion of a day-night rhythm of filtering early enough is noted. Disorders of function of renal tubules join later during the progressing of a disease or in the early period of G. proceeding with a tubulointerstitsialny component.

Children with G. need consecutive treatment: in a hospital, policlinic, local nefrol, sanatoria. The bed rest is necessary during 3 — 4 weeks from the beginning of acute displays of a disease. Further the mode is defined by expressiveness of extrarenal manifestations. To children, unlike adults, at G.'s treatment it is inexpedient is long to limit protein in food. In the first days it is necessary to reduce salt, to exclude chlorides and to limit protein content; at favorably developing process it is recommended to expand a diet due to addition of protein of animal origin. At a gematurichesky form G. drugs of calcium, redoxons, PP are appointed. At the nephrotic and mixed forms also A, D, B vitamins are necessary 6 and B 15 . Antibacterial therapy is carried out by everything to children with G.: during the acute period of a disease the antibiotics suppressing growth of nefritogenny strains of a streptococcus apply not less than 1 — 1,5 month. It is obligatory sanitation of an oral cavity (see). In the presence hron, tonsillitis during remission carry out a tonsilectomy against the background of antibacterial and antihistaminic therapy (see. Tonsillitis ). Prednisolonum appoint at a nephrotic form G. in a dose 1,5 — 2 mg, and in certain cases to 4 mg to 1 kg of weight a day for 3 — 4 weeks with gradation at development of remission on a maintenance therapy by a discontinuous course. Except steroids, cytostatics (leukeranum, cyclophosphamide) are applied, Azathioprinum,

6 Mercaptopurinum, drugs of a 4-aminoquinolinic row (Resochinum and its analogs) is more rare. Also heparin and indometacin are used. Anabolic steroid drugs (Nerobolum, retabolil) are appointed to children very seldom and only during the subsiding of the acute phenomena.

At considerable hypostases. antagonists of Aldosteronum in a dose to 5 — 20 mg on 1 kg of weight of the child are necessary, at the expressed hypertensia apply Reserpinum and its combinations with dopegity, Isobarinum. Lack of hypotensive effect gives the grounds to assume an abnormal structure of renal vessels or a renal dysplasia. The Gormonorezistentny nephrotic syndrome can be manifestation of a combination of two diseases — G. and pyelonephritis (see). The mixed form G. should be differentiated with a renal syndrome at to a system lupus erythematosus (see) and Shenleyn's diseases — Genokh (see. Shenleyna — Genokh a disease ). In case of torpidno the proceeding nefropatiya it is necessary to exclude hereditary diseases of kidneys. In particular, hereditary nephrite (see) quite often reminds a gematurichesky form of diffusion. The forecast and G.'s prevention at children essentially same, as well as at adults.



Bibliography Alekseev G. I. and Storozhenko of A. A. Sostoyaniye of lipidic exchange at an acute and chronic diffusion glomerulonephritis, Klin, medical, t. 52, No. 1, page 70, 1974, bibliogr.; Diseases of kidneys, under the editorship of G. Mazhdrakov and N. Popov, lane with bolg., Sofia, 1973; Bondarenko B. B. The malignant glomerulonephritis, Works of the 9th congress rubbed. USSR, page 126, Kiev, 1974; And r to about K. P., Bilchenko O. S. idundich A. A. Renografiya and immunological researches at patients with a glomerulonephritis, the Doctor, business, JsTs 6, page 54, 1973; Clem and - N and I. K. Titr of a complement and renal autoantibodies at diffusion diseases of kidneys, Rubbed. arkh., t. 38, JsTs 12, page 93, 1966; Kozlovskaya L. V., etc. Assessment of nuclear pathology in a kidney during the uses of the LE cellular test Induced by urine, in the same place, t. 48, JVe 7, page 35, 1976; The Multivolume guide to pathological anatomy, under the editorship of A. I. Strukov, t. 7, page 80, M., 1964; Moiseyeva O. I. and Yaroshevsky A. Ya. Anemiya at diseases of kidneys, Rubbed. arkh., t. 41, No. 7, page 44, 1969; Fundamentals of nephrology, under the editorship of E. M. Tareeva, t. 1, page 350, M., 1972, bibliogr.; V. V. sirs. Morphological bases of an immunopathology of kidneys (nephrite, nephrosis), M., 1968, bibliogr.; Serovv. EL d river Elektronnomikroskopichesky characteristic of histologic types and Morphogenesis of a glomerulonephritis, Arkh. patol., t. 35, No. I, page 3, 1973, bibliogr.; Frankf at rt M. I., etc. Myocarditis at a diffusion glomerulonephritis, Works of the 9th congress of therapists of USSR, page 95, Kiev, 1974; Shekhtman M. M., Ivanov Nominative and F at to about M. A. Glomerulonefrit and pregnancy, Akush, and ginek., No. 11, S. 49, 1973, bibliogr.; Yu N d and I. F. and Imshchinetskaya L. P. Function of bark of adrenal glands at a glomerulonephritis, Kl*n. medical, t. 52, M 10, page 79, 1974, bibliogr *; Yaroshevsky A. Ya. Clinical nephrology, page 168, L., 1971; Addis T. Glomerular nephritis, N. Y., 1948; Allen A. Page of The kidney, p. Yu8, N. Y., 1951; A n d r e s G. A. a. o. Electron microscopic studies of human glomerulonephritis with ferritin-conjugated antibody, J. exp. Med., y. 123, p. 399, 1966; B e 11 E. T. Renal diseases, Philadelphia, 1946; Brewer D. B. Renal biopsy, L., 1964; Burkholder P.M. Atlas. of human glomerular pathology, Hagerstown, 1974; Ellis A. Natural history of Bright’s disease, Lancet, v. 1, p. 1 a. o., 1942; Feldi ngC. F. Obstetric aspects in women with histories of renal disease, Acta obstet, gynec. scand., v. 48, suppl. 2, p. 1, 1969; F rank 1 i n W.A., Jennings R. B. a.Earle D.P. Membranous glomerulonephritis, Kidney Int., v. 4, p. 36, 1973; Gabriel R, Postqraduate nephrology, L., 1974; G e k 1 e D. Akute diffuse Glomerulonephritis, Med. Klin., S. 121, 1974; Hedner U., Ekberg M. N i 1 s-s o n M. Urinary fibrin/fibrinogen degradation products (FDP) of and glomerulonephritis, Acta med. scand., v. 195, p. 8i, | 974; Nephrologie, Urologie, hrsg. v. H. Losse, S. 27, §7, B. u. a., 1975; Nierenkrankheiten, hrsg., v. H. Sarre, S. 223, 251, Stuttgart, 197ken D. E. Chronie renal diseases and pregnancy, Amer. J. Obstet. Gynec., v. 94, p. 1023, 1966, bibliogr.; R a m m e 1-kamp C. H. a. Weaver R. S. Acute glomerulonephritis, J., clin. Invest., v. 32, p. 345, 1953; Renal disease, ed. by D. A. K. Black, Oxford, 1973; S e e g a 1 B. G. a. o. Studies on the pathogenesis of acute and progressive glomerulonephritis in man by immunofluorescein and immunoferritin techniques, Fed. Proc., v^24, p. 100, 1965; Structural basis of renal disease, ed. by E. L. Becker, p. 132, N., - Y, 1968, bibliogr.

At children — Valentinovich A. A. and Vitebsk E. M. A diffusion glomerulonephritis at children, L., 1973, bibliogr.; Ignatova M. S. and Veltishchev Yu. E. Diseases of kidneys at children, M., 1973, bibliogr.; Fundamentals of children's urology and nephrology, under the editorship of S. D. Goligorsky, Kiev, 1973; Speransky G. N., etc. About the diagnosis of a glomerulonephritis at children, Pediatrics, No. 2, page 3, 1966; Yuryeva E. A., etc. Correction by a dietotherapy of disturbances of transport of amino acids at diseases of kidneys at children, Vopr. okhr. mat. also it is put., No. 3, page 42, 1971; Royer P. e. a. Nephrologie pediatrique, P., 1973.

E. M. Tareev, V. V. Sura; M. S. Ignatova (ped.), V. V. Serov (stalemate. An.), M. M. Shekhtman (academician).

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