v 3 v & & disease “ Cc eo y Se “SChapter 15. Main symptoms and of 18.1. Main symptoms of urinary system diseases s. . rT During questioning (ollectin ifyi history of th Z @ complaints and clarifying the disease and life) in adult patients with diseases of the oe 4 i h t organs, the follo symptoms characteristic of diseases of the urinary system can be identified, Pain in the lumbar region. There are Several options for pain in the lumbar region, Constant symmetrical pains of dull and aching nature in the Jumbar region — Observed in acute glomerulonephritis, but statistically much more 0 with dorsopathies (pathclogy of the Iumbar spine). Sharp, acute unilateral pain in the lumbar region. Characterized by renal infarction, acute pyelonephritis and chronic pyelonephritis (pain syndrome of the renal capsule or sprs the pelvis are the basis of pain in these diseases Tn addition. these pains occur in spinal hernia. Attacks of pain in the area of the ki ;, ureters and bladder or an a "renal colic". —These pains are provoked by drinking plenty of water and driving road. As a rule, these pains are one-sided. ~~" An attack of "renal golic” is a characteristic symptom of the presenee in the kidneys, urinary tract and bladder. Violation of the process of urination. ne The following types of urination disorders are distinguished: (ishuria), urinary incontinence, Frequent “urination (pollakiuria), diffi ‘stranguria) “These types of disorders of the process of urination are observed ma syndrome. ‘Nocturia. : nace tia This is an increase in urine excretion at.night, ie. excretion of evening and at night more than in the daytime. Nocturia is one of the earliest signs of chronic renal fai CR a in chronic heart failure, and can also occur in healthy individual taking amounts of Tiuid in the evening, rohematurid. ae vee condition in which urine contains sanall_amounts of blood, guanlity is too low to change the color of urine. -254-Protenwete-bn) alhurbwuorte fic pave. ~ dinbetts bene Microhematuria Boe gla. ReciFolsy > Sb- a rg ane . ining Of Urine in red col : ie in red col (more often the color of “meat slops"), s kidney infarction, ation in s possible to identify the f system. Forced position on the patient's side, with and led to the stomach on the side of the lesion. This position is characteristic of paranephritis, 4 Swelling on the face, then on the feet and legs, and in severe cases throughout the body (anasarea). r These edemas are characteristic of renal edema and nephrotic syndrome. Unpleasant smell of ammonia from the mouth and from the skin of the patient. Itis detected in the final (uremic) stage of chronic renal failure (CRF), as well as in acute renal failure (ARF), cee adult patients with diseases of the urinary organs ollowing symptoms charactetistic of disen eased ses of the urinary the leg bent at the hip and knee During palpation in adult patients with diseases of the urinary organs it is possible to identify the following symptoms characteristic of diseases of the urinary system 2 Nephroptosis (kidney prolapse). Nephroptosis is a variant of the norm and does not require treatment. But in some cases it can lead to a violation of the outflow of urine, then the treatment is carried out, including surgery. Unilateral increase in kidneys. ; 5 Observed in kidney cancer and in the presence of cysts in the kidney Bilateral enlargement of the kidneys. : al his is the case for polyeystic kidney disease and renal isis Soreness ii jection of the kidneys during palpation. ie ate ‘served with the syndrome of the presence ea urinary tract and bladder, acute and chronic pyelonephritis and Kidney cancer, but more often With dorsopathies (pathology of the lumbar spine). ee tients with diseases of the urinary ey toms characteristic of diseases of system. i jectic kidneys). Pain when tapping in the back (in the projection oft a se Boe *B - io 9 a - (2 Prokenwtor see ce oppinersts Une GPOrr— + Chrer During percussion in adult pat possible to identify the following symp! nep-4 AES ~ Bo. nae x Oliguria (daily diuresis less than 500 ml). ¢ é POLE Yolen B00 ml Jos Y P er Yor” Observed with the syndrome of the presence of stone j tract and bladd te and chronic pyelonephritis and stone in the kidneys, urinary Aor an Kidney cancer, but statistically much more often (as mentioned above) is found in Goi “ ly $3 lumbar spine), dorsopathies (pathology of the SJ During auscultation in adult patients with diseases of the urin on; is possible to identify the following symptoms characteristic of diseases of the ‘cea system, Systolic (stenotic) noise during auscultation of the renal region. ‘This is characterisifo of renal artery stenosis, Renal arterial hypertension. It is a variant of secondary arterial hypertension and is associated with increased \renin_production, and activation of the \fenin-angiotensin-aldosteroney system. The features of renal arterial hypertension are gharply high blood pressure numbers, a predominant increase in diastolic blood pressure, severe course, efficacy of antihypertensive drugs and frequent complications (primarily pa heart, brain a = sae a Renal arterial hypertension occurs with the same syndrome. “ During laboratory studies in adult patients with diseases of the urinary” S organs it is possible to identify the following symptoms characteristic of diseases J the urinary system. Pathological changes in the study of the physical properties of urine. ~ It is characteristic of renal failure syndrome (oligoanuric stage of acute failure and late-stage chronic renal failure). failure and late-stage chronic rena! Anuria (lack of wine). ‘Occurs with renal failure syndrome (oligoanuric stage of acute renal fai the final stage of chronic kidney disease). Polyuria (daily diuresis more than 2 Ii . : Observed with zenal failure syndrome (in the initial stage of chronic disease and the stage of polyuria or conve et acute renal failure), as well as edema, diuretics and polydipsia (increased thirst). oh "Dark color of tine ("color of Beer. 2 +0 ‘ExUvaptn This is due to the appearance of bilirubin in the urine. Observed (as indicated above) with cholestasis syndrome. Red color of urine (urine of the colo¥ of ary 7 iris associated with the appearance in it of a large number and is called macrohematuria (see above, “Inquity”). i Significant jurbidity of urine. of -256-Due to the content in it of a 1 and epithelial cells ae with acute and chronic pyelonephritis, Decrease in urine density (hypostemuria) Characteristic of renal failiire syndrome is MIE (is one of th Increase in urine sp a 5 arliest signs of CRF) Specific gravity yperstonuri Observed in diabetes Grete the oe seemiria. ii fhe presence in the urine of a large amount of glucose (seg’chapter "The main Symptomy’and syndromes‘of thé endocrine system of an adult patient”), aed 4 Pathological changes in the study large number of : Of Teukoeytes, bacteria, salts, mucus of the chemical properties of urine. ‘rvical properties of uri Increased urine acidity (pH> 9.0 Observed with diabetes mellitus, chronic kidney disease, kidney tuberculosis and agidosis._ | ue oie pre gee eee Alkaline urine (pH <4.5). ‘ay occur with vomiting and chronic urinary tract infections, Se ane eAronie urinary tract infection The appearance of glucose in the urine (glycosuria) Observed with Ryperglycemia syndrome (in more detail in the chapter "The main symptoms and syndromes of the endocrine system of an adult patient"), Detection of ketone bodies in the urine (Ketonuria). Occurs with hyperglycemic coma (in more detail in the chapter "The main symptoms and syndromes oF the endocrine system of an adult patient"). The appearance of bilirubin in the urine (bilirubinuria). Observed (as indicated above) with cholestasis syndrome Proteinuria (albuminuria). : * - ‘This is the appearance of protein (albumin) in the urine. At the same time, protéinuria (albuminuria) is considered to be more than 30 x / day for pathology. 4 mg / day for patholog Tages Le aneP ‘ Tt is characteristic of many independent kidney diseases, as well as_kidney damage in various diseases of the intemal organs. eh these are micyoproteinuria, Jaw, moderate, dugh’ sod) massive proteinuria; prerenal, renal and postrenal proteinuria; renal and extrarenal pr 7 "— Microproteinuria, aay This content in daily urine is from| Be wae a prot Ae ecu Observed in the initial stages of Kidney _damage im dishetes-mslitis- hypertension. ; Pow proteinuria: b00 mg to 1p ein (albumin) This content in daily urine from BOO. sa at suk diss oe oe It occurs in ric _syndrome\on the gro! and is iti of pregnant women) and, form of fchronic_glomerulonephriti epbyopatty) of eee ius and hypertensi observed in thetlate sta; e of kidney damage; a Moderate proteinuria. -257-. OF | ; perros’ Clone 3 This is the content in daily wsinfom 11035 of pot albumin) Oceurs with urinary syndiente on the background of primary and secondary — Jomerulonephritis and kidney amloidosis) _ 4 mp teart aes High (massive) proteinuriay coe ® Owkloee Prblrene This protein content (albumin) in an amount of more thanl3S gper day) Itis a sign offnephrotic syndrome Posonal proteinuni Tt arises as a result of an increase in the concentration of low molecular weight proteins in the blood, which are easily filtered in the \glomeruli of the kidney This is Sbserved implood diseasesghemolysis, wuultiple Tea jqums, It may also be due to an increase in pressure in the renal veins, which is observed in heart failure (congestive proteinuria), in some women jn the last months of pregnancy, Renal proteinuria, Tt is caused mainly by theydefeat of the glomeruli, less often by the tubules, leading to an increase in the permeability of the glomerular capillarieg for plasma proteins and aydecreass-in thegeabsorption capacity if the proximal tubules, Renal ‘Proteinuria is observed in glomerulonephritis, poisoning with salts of heavy metalsy toxic kidney damage, SoS penal pore dlormnrel wens ot 125305 Ti is associated with inflammatory oryneoplastic processes in the urinary tract and is caused by the release of protein from disintegrating Teukocytes, epithelium and other cells. ‘Renal proteinuria differs from extrarenal by the presence of yaline eylinders m the urine, which is a grote coagulated jn the genal tubules. Pathological changes in the microsco] ric examination of urine. The presence of a large number of transitional epithelium in the urine, Characteristic of cystitis. The presence of a large number of cells of the renal epithelium. Observed with acute and chronic pyelonephritis nits: = Leukocyturia. THis} urinary leukocyte count in the amount of more than, 6-8 in the field of view. P —— The mechanisms of the origin of leukocyturia depend on the nature and Jocation of the infectious inflammatory process. The following ways of leukocyte entry into the urine are distinguished: from the foci of inflammatory infiltration of the interstitial tissue of the kidneys into the lumen of the tubules through their damaged or destroyed walls, from the mucous membrane of the urinary tract affected by the inflammatory process and from the abscess into the cavity of the calyx or pelvis. Leukocyturia occurs in pyelonephritis, inflammation ‘of the renal pelvis — (pyelitis), bladder or urinary tract (cystitis, urethritis), as well as the breakdown of - tumors and kidney tuberculosis. -258-aad Renal and extrarenal leukocyturia are distinguished, in turn, renal leukocyturia is divided into infectious and aseptic. Under extrarenal leukocyturia understand Jeukocyturia from the lower urinary tract -— Pa ss | Extrarenal Renal leukocyturia leukocyturia pra Sere infectious aseptic 6.000 - 10.000 in 1]6000 - 20000]Up to 6000 in I ml | nd more in | ml} ml 10 - 50 20-70 and more | no more 10 eingamer - = nalbin cells 7 Bacteria, squamous | Bacteria, granular |Protein, hyaline epithelium and leukocyte | and waxy cylinders cylinders | Leukocyte Neutrophils (90% | Neutrophils (90% | Lymphocytes | morphology or more) or more) (20% or more) ae 1 st | three glasses | First portion ‘All three servings | All three servings sample Diseases Chronic prostatitis, | Chronic Primary urethritis pyelonephritis _| glomerulonephritis Detection of urine in the urine (pyuria). Observed with the same diseases as Jeukocyturia. During the 3glass test, the predominance of leukocytes in the first portion (the first glass) Characteristic of urethritis and prostatitis. ee During the 3glass test, the predominance of leukocytes in the third portion (in the third glass). This indicates cystitis. ’ Sieaval During the 3glass rest, leukocytes are equally found in all three portions three glasses). e ‘Observed with acute and chronic pyelonephritis. Detection of active leukocytes in the urinary sediment. - Characterized for exacerbation of chronic pyelonephritis. ~259-——— Hematuria, This is the detection of red blood cells in the urine (but in recent years a more correct name is often used - erythrocyturia), The mechanisms of hematuria are increased permeability of the membranes of the glomerular capillaries, gaps in certain sections of the walls of ¢ glomerular capillaries, damage to the mucous membrane of the pelvis, ureter bladder, the destruction of kidney tissue or urinary tract, reducing blood coagulation, Classification of hematuria: micro: and gross hematuria; renal and extrarenal hematuria; initial, terminal and total hematuria. Microhematuria, The color of urine does not change, and the number of red blood cells in general analysis of urine varies from 1 to 100 in the field of view. Macrohematuria The color of the urine becomes dark red (the urine acquires the color of “m slop”), and the red blood cells densely cover the entire field of view and incalculable. Renal hematuria. = The combination of severe hematuria with moderate and high proteinuria (from _ 1 to 3 g per day or more) is characteristic of renal hematuria. 5 hematuria is the same. Renal hematuria occurs in various renal lesions: acute and chronic glomerulonephritis, heart attack, and kidney tumors. Extrarenal hematuria. With extrarenal hematuria, there is a combination of severe hematuria and low proteinuria (less than 1 g per day), the so-called symptom of protein-erythrocyte dissociation. 3 When extrarenal hematuria during the analysis of several daily portions revealed large fluctuations in the intensity of hematuria, The source of extrarenal hematuria is bleeding from the bladder, ureters, and urethra : f a Extrarenal hematuria is observed in the presence of stone in the kidneys, urinary tract and bladder, as well as in cystitis and tumors of the bladder and prostate 5 gland. re Initial hematuria. i, This is the detection of hematuria (erythrocyturia) in 3glass test. It indicates bleeding from the distal part of the urethra. i It is characteristic of urolithiasis with stone localization in the upper parts of the ureter. Terminal hematuria. q the first glass during the the renal pelvis and =260-Itis characterized by the appearance of blood in the las port ri rin; ance of st ae re of blood in the las ion of urine during Tt indicate: Observed w in the bladder. Total hematuria, This is the presence of blood in all Ttindicates kidney bleeding, Observed in acute and chronic glomerulonephritis, Cylindruria. This urinary excretion conglomerates. ; he appearance in the urine of the cylinder indicates a deep lesion of the renal parenchyma Hyaline, granular, waxy, erythrocyte and leukocyte cylinders are distinguished. Hyaline cylinders are cylinders representing coagulated serum protein that was filtered in the glomeruli and was not reabsorbed in the proximal tubules. The level of hyaline cylinders in the urine increases with nephrotic syndrome, pregnantly nephropathy, poisoning and other pathological conditions that simultaneously cause hematuria Granular cylinders are cylinders formed from modified epithelial cells of the proximal tubules and having a granular structure. Their detection indicates the defeat of the tubules and is found in interstitial nephritis. Waxy cylinders are yellowish cylinders that consist of a homogeneous, structureless material similar to wax. These cylinders are formed as a result of dystrophy and atrophy of the tubular epithelium, which is observed in severe acute kidney damage, or in the late stage of chronic renal diseases. Erythrocyte cylinders are detected in the urine with severe hematuria, and leukocyte cylinders - with severe leukocyturia of different origin. The predominance of hematuria (erythrocyturia) over leukocyturia. : Characteristic of the glomerular pathology of the kidney (acute and chronic glomerulonephritis). The predominance of leukocyturia over hematuria (erythrocyturia). It occurs in renal pathology with a lesion of the renal pelvis system (acute and chronic pyelonephritis). i Pathological changes in the bacteriological examination of urine. a Detection of more than 50 thousand microbial cells in 1 ml of w (bacteriuria). 9 ae It indicates the presence of infection inthe urinary tact and is characteristic of cystitis, urethritis and other inflammatory diseases of the _ ane bleeding from the proximal part of the urethra, ith cystitis, bladder cancer and urolithiasis with stone localization Portions of urine during the 3 cups test of cylinders, which are protein or cellular 261-Bacteriuria with more than 100 thousand microbes in 1 ml of urine ¢ uria) This indicates the presence of infection in the kidneys and is observed in and chronic pyelonephrit Pothole al changes in the functional study of the kidneys. rease in the relative density of urine (hypostenuria), ; he prevalence of nocturnal diuresis over daytime (nocturia). Increased levels of (nitrogenous compounds) urea, residual nitrogen and. inine. Increased serum potassium (hyperkalemia). Hypostenuria, nocturia, increased levels of urea, residual nitrogen creatinine in the blood and hyperkalemia are signs of renal failure syndrome, | increased creatinine levels are the most specific symptom of this syndrome. At the same time, hypostenuria and nocturia are considered early symptoms chronic renal failure. Decreased glomerular filtration rate. Tt is a sign of renal failure syndrome. bae ’ During instrumental studies in adult patients with di organs it is possible to identify the following symptoms characteristi the urinary system. Pathological changes during radiological studies of the Kidneys and tract. urogriphy and retro, It is a confirmation of the ee in the Tana tract and bladder. ~ ‘Reduced renal function on the affected side during excretory roars retrograde pyelography. Characteristic of acute pyelonephritis. Local spasms. of the cup-pelvis system during excretory urography retrograde pyelography. Observed with acute and chronic pyelonephritis. Deformation of the cups and renal pelvis during retrograde pyelography. It is the most specific symptom of chronic pyelonephritis. of Detection of kidney tumors, complex abnormal development of the kidneys and renal artery stenosis during renal angiography. [Tis a Confirmation of the above pe Pathological changes during estoscopye Stones and bladder tumors. eh It is a confirmation of these pathologies of the bladder, e2-AL ne iological changes during ultrasound and computed tomography of th kidneys, urinary tract and prostate gland \ fice mn duction of the kidneys. din the late stages of chronic renal failure syndrome, reduction of the | Kidneys, Occurs in hypoplasia of one of the kidneys Symmetric kidney enlargement, ; Itis found in amyloidosis and polycystic kidney di Stones in the kidneys and urinary trac, (is a confirmation of the presence of stone syndrome in the kidneys, urinary tract and bladder. of the bladder. 'S a confirmation of this pathology of the bladder. Tumor (adenoma) of the prost i It is a confirmation of this pathology of the prostate gland. Pathological changes during ‘radioisotope research and biopsy of the kidneys. Deformation of the secretory and excretory segments of renograms.” Characteristic of glomerulonephritis, pyelo is and renal amvloi: Slowing up and lengthening of the secretory segment of the renogram. Observed with renovascular hypertension. Focal filling defects on the renogram. Allows you to diagnose tumors, cysts and tuberculosis of the kidneys and other destructive processes in the kidneys. Tea 3 Signs of amyloidosis, tumors of the kidneys and morphological forms of chronic. glomerulonephritis during a biopsy of the Kidneys: ~ It is a confirmation of the above pathologies of the kidneys. 15.2, Main yndroms of urinary system diseases The main syndromes of diseases of the urinary system are urinary, nephrotic, nephritic, dysuric, renal arterial hypertension, renal failure, urinary tract infection, the presence of a stone in the kidneys and urinary tract and renal eclampsia. 15.2.1. Urinary syndrome Urinary syndrome is a laboratory syndrome that includes only laboratory symptoms. i : 2 Urinary syndrome is the most common, persistent, and sometimes the only sign of urinary system pathology. ; : The characteristic symptoms of urinary syndrome are: 1) proteinnria (from 50 mg to 3.5 gpper day): —— Jaga?Urinary syndrome is observed in acute and chronic glomerulonephriti anvloidosis, imersttial nephritis, acute and chronle-pyelonephetie olveystic and kidney tumors, as well as in the early s ol kidney de reson of longterm diabereshiet iam hypertensive disease. i When the above kidney diseases have their own characteristics of syndrome: 1) wrinary syndrome with a prevalence of proteinuria and characteristic of acute and chronic lomerulonephritis; 2). urinary syne STE ae hema urolithiasis, cancer of the kidneys and bladder, hematurie Variant of acute and ehre glomey CI 7 3) urinary syndrome with a predominance of leukocyturia and. occurs in acute and chronic pyelonephritis; z 4) urinary syndrome in the form of isolated proteinuria is observed it amyloidosis. Ta 5.2.2. Syndrome of renal edema Renal edema syndrome is accompanied by the following : 1) renal edema (occurs first on the face, on the eyelids and under the on the feet and lower legs), 3 2) pulmonary edema (like dough) on palpation; 3) renal edema is loose and easily moved; J 4) renal edema is persistent, develop gradually, sometimes quickly overnight can reach anasarca degree), 4) the progression of the kidney edema spreads to the entire subcul tissue, stretching the skin to form stretch marks; 5) in severe cases, there is accumulation of fluid in the serous cavities (a hydrothorax, hydropericardium) and throughout the body (anasarea); ©) with the development of ascites, bloating, unreasonable diarthea, nausea ant vomiting appear, and with an increase in hydrothorax and hydropericardium, there marked shortness of breath with little exertion, and then at rest. Re. Renal edema is observed in nephrotic and nephritic syndromes, Renal edema in nephrotic syndrome is a classic type of renal edema and referred to as protein-free edema, as Pathagenesis of the occurrence of renal edema in nephrotic syndrome is t following : massive proteinuria (albuminuria) ++ hypoproteinemia (decrease int -264-QUEEN » ANS Ww plood protein to 40 g / 1 or less) or more o blood albumin to 15 g/T or less) > decrease of hydrostatic blood pressure over oncotic —» blood vessel into the surrounding tissue. Renal edema in nephritic ofrenal edema. The causes of renal edema in nephritie s 3 are a decrease in circulating blood es toed {route nepinte esisna) feereace in Water and proteins (due tothe sotivalion ef thereat hypocalcemia and histaminemia), secondary alist nad ee sesretion of antidiuretic hormone. Se ete At the same time, a decrease in circul ; ating blood volume leads to ci of vascular wall receptors and the inclusion of See eee ‘maintaining intravescular volume with their complex hormonal regulation, in particular, enhanced production of aldosterone in the adrenal cortex. Developing secondary aldosteronism leads to a delay in the body of sodium, chloride and water This leads to an increase in the secretion of antidiuretic hormone, which exacerbates water retention by increasing its tubular reabsorption, wndrome (acute nephritic synch 8 a special type (acute nephritic syndrome) isa special 15.2.3. Nepheatic syndrome ‘This is a clinical and laboratory symptomo complex, which includes massive proteinuria, hypoproteinemia, dysproteinemia, hyperlipidemia and renal edema In ease of nephrotic syndrome, proteinuria is primary cause, which is the main condition for the appearance of all the other signs of this syndrome, namely, the above interrelated disorders of protein, lipid and water-electrolyte metabolism. Pathogenesis. Nephrotic syndrome is a second: that occurs in various diseases and pa! influence of chemical and toxic factors. Tmuunocinflammatory damage to the glomerular membranes leads 10 shap increase in protein filtration through the’ basal membranes of the glomerular capillaries and a deorease in protein reabsorption by proximal tubules which causes massive proteinuria. Massive proteinuria leads hypoproteinemia is explained by the excess of the es ral its y atients. over the intensity of its synthesis in the body of pate apc te i teins in Se eae aa cli “Pathe movement of fluid and to reduce the oncotie pressul dl tissues. Thus, Kidney edema occurs, ‘lectrolytes into interstitial fe 1 dey ed secretion of renin, aldesterone De emia sl ¢ r and La etae “Strengthening the secretion of aldesterone delays sodium, -265- ary immune and inflammatory kidney damage thological conditions, as well as under the to hypoproteinemia, At the same tine, fe ite of albumin in the urineand an increase 1n the supply of antidiuretic hormone to the blood ~ water and water enter the tissues and increase swelling, - Sodium Hypoalbuminem! contributes to the formation of lipoproteins, The and phospholipids is constantly overall ly increased, whi + While 1a level of lipids, cholesterol ‘cir level is proportional to hypoproteinemia. Thus, hyperlipider Some i a pidemia in nephrotic syndrome is pathogenetically associated with impaired protein metabolism and inhibition of blood plasma lipolytic activity Laboratory signs. Urine contains a large amoun detected massive proteinuria (albuminuria). Tn addition, a high relative density of urine (1030-1040) is determined; a j a large number of hyaline, granular and waxy cylinders, and renal epithelial in the urine sediment ao a But the presence of a large number of leukocytes and e1 ytes i a oe is not typical for nephrotic syndrome. : heath ___ Inthe urine of patients with nephrotic syndrome, cholesterol ery ea of neutral fat are usually found, which are not found in other nae cisco A characteristic feature of nephrotic syndrome is hypoproteinemic aan Coal as hyperlipidemia (hypercholesterolemia). et ¢ level of total protein in serum i tients wit arse nt pers etic ty » gf ents with nephrotic syndrome is ‘sproteinemia is manifested by severe ul less aswell asaderease in he content of Saal Soe lyperlipidemia with high blood level: holest ipopro! triglycerides and a violation of the ratio of shee ea eae eee substances is characteristic of the In the peripheral blood of pati i i se ‘0m ee a on : pea nephrotic syndrome, an increase in ESR. ‘ical signs. . The main clinical si ign of nephr ; demas first appear on the face, eee sera Petes are peripheral edema. These anasarea with fluid accumulation in the se Eee ee ee ydiotices au ir ae serous cavities in the form of ascites, Aldrich's positive “blistering” test is positi solution injected jaicseuleneouat amt si ony, sn dotonig socio ety so ee 'y (0.2 ml) dissolves in 1-2 minutes, while nommally it Massive edema contribut z ites to th chi we at, pale atrophic areas (stretch marks), ie stretching of the skin with the formation of chest and upper limbs , especially pronounced on the abdomen, thighs: In the period of increasi ; asing edema diuresi: Dhagneste criteria er ess Seereases to 500 mal pe day or plasti 1 of protein (from 3.5. g or more per day) ie -266-Diagnostic (specific) symptoms ( ) of nephrot 1) massive proteinuria (albuminuria) Me syndrome are 2) hypoproteinemia (hypoalbuminemia) 5) hyperlipidemia (hypercholesterolemni), 4) renal edema, . nes of nephrotic syndrome. ‘mary nephrotic syndrome, These are cases of nephrotic s syndrome due to primary i id ; rimary immune: ys and kidney amyloidosis, PY immune-inflammatory Secondary nephrotic syndrome. This is a variant of nephrotic sy ; ephrotic syndrome, occurring on secondary Kidney diseases with infectious and non-infections (one ee ot pathogenetic mechanism, sometimes iatrogenic (1 en autoimmune) nedical) origi Complete nephrotic syndrome. ) origin. This is the presence of all the diagnostic signs of nephrotic syndromé: tassive proteinuria (albuminuria), hypoproteinemia chypoalbumninemie oon (hypercholesterolemia) and renal edema, Ypoaibuminemia), “hyperlipidemia Incomplete nephrotic syndrome This is the absence of one or several diagnostic signs of nephrotic syndrome with the obligatory presence of massive proteinuria (albuminuria) The course of nephrotic syndrome. In the clinical course of nephrotic syndrome, there are three options: 1) episodic, occurring only at the beginning of the underlying disease with an outcome in a Jong remission (1 2) persistent, when nephrotic syndrome persists for 4-8 years without reducing renal function; 3) progressive, with the transition of nephrotic syndrome for 1-2 years in the stage of chronic renal failure. Causes of nephrotic syndrome. 1. Primary kidney disease. fi 11 Nephrotie form of various morphological variants of glomerulonephritis. 1.2. Amyloidosis of the kidneys (primary, secondary). 2, Secondary kidney disease. yi — 2.1. Infectious etiology: chronic suppurative ee ee osteomyelitis, tuberculosis, syphilis), malaria, schistosomiasis, chronic nee i % i iective tissue 2.2. Non-infectious (often autoimmune) EY eats aaieh hie ts diseases (systemic lupus erythematosus, systemic Sales al : clone and others), systemic vasculitis, ulcerative colitis, Soe lymphogranulomatosis), tumors, thrombosis, diabetes.| as a result of the use of drugs with 1) origin, as a res 88 with ne al bismuth, antibiotics (aminoglyeagt roe jonsteroidal anti-inflammatory dey gs. 9.3. Iatrogenic (medica!) "1 Tetrogr mercury, BOCs oes, ), some ‘anti-tuberoulosis drugs, 15.2.4. ACUTE NEPHRITIC SY NDROME This is a clinical and Laboratory SY mptom complex, which is characterize sani got of the classi triad of symptonns (hematuria, renal edema and rep, tne Sal hypertension), as well as proteinuri reduced urine output (oliguria) and gies arteria s signs of acute renal failure. In acute nephritic Jomerulonephritis develops glome For ats nephritic syndrome (unlike nephrotic syndrome), massive proteinur and hypoproteinemic edema are uncharacteristic: Pathogenesis. " The an pathogenetic mechanism of the development of acute nephritic yndrome is acute inflammation of the glomeruli of the kidneys, we Tmmuno-inflammatory lesions of the basement membrane of the glomenilar capillary wall are considered to be the direct cause of acute inflammation of the glomeruli of the kidneys. The causes of renal edema in acute nephritic syndrome are reduced glomerular filtration, high capillary permeability and fluid flow to the interstitium, as well as increased tubular sodium reabsorption, increased aldosterone levels, and sodium and water retention. Clinical and laboratory signs. ‘The classic symptoms of acute nephritic syndrome are hematuria, proteinuria, renal edema, arterial hypertension and acute renal failure. Characterized by the sudden appearance or increase of renal edema with typical puffiness of the face, accompanied by oligouria, proteinuria, hematuria and hypertension, especially diastolic. Macrohematuria appears in some patients (urine of the color of “meat slop"). Arterial hypertension is accompanied by the development of left ventricular hypertrophy followed by the formation of signs of heart failure. ‘Arterial hypertension together with a significant increase in circulating blood volume can cause acute left ventricular failure (pulmonary edema). Acute renal failure is manifested by oligouria (in severe cases of anuria) @ decrease in glomerular filtration rate and signs of azotemia (increased levels of caine urea and residual nitrogen). cute renal failure in acute nephritic i igniticant dere in glomerular fitation pl syndrome occurs due to & signifi lon-permanent symptoms of ‘ae oe anorexi®, ces eee = gente nephritic syndrome are fever, - 268 - action, cephalosporins syndrome, a set of symptoms resembling seuje du bl i a‘The appearance of pain in the lower by ; ack fluid retention in the body. ck and abdomen, weight ain develops In the study of urinalysis, urinaty sedi : Y sediment « cells, white blood cells and cylinders, proce fen Diagnostic criteria, na reaches The specific symptoms of acute nephriti e sy 1) hematuria; yndrome are: 2) renal edema (without massive proteinuria an 3) renal arterial hypertension; 4) low or moderate proteinuria; 5) signs of acute renal failure (oliguria, i ig : . in severe cases wore glomerular filtration rate and signs of azotemia, primarily an imoeneis wee creatinine in the blood HS cia fe aes At the same time, a prerequisite is the suddennes: ie 3 8, rapid rate of occurre these symptoms. tend Te chacoerence at Causes of acute nephritic syndrome. Acute nephritic syndrome is observed in acute glomerulonephritis of various etiologies, and may also develop at the onset of chronic glomerulonephritis and against the background of a long-existing kidney disease. due to Jarge number of red 05-2 g per day. blood 1d hypoproteinerniay, 15.2.5. Dysuric syndrome Under dysuric syndrome understand a violation of the process of urination. The specific symptoms of dysuric syndrome are: 1) urinary retention (ishuria); 2) urinary incontinence; 3) frequent urination (pollakiuria); 4) difficulty urinating (stranguria); 5) frequent and painful urination. Dysuric syndrome occurs in acute and chi pyelonephritis, urolithiasis. onic. cystitis, urethritis and 15.2.6. Syndrome of kidney arterial hypertension - yma This hypertension, pathogetically: renal parenchy ete.), Rent ae 1 _vessels (vasculitis ic renal insuffi -related to the ae 1 ie arteries (atherosclerosis, ¢ al nefroangiosclerosis), loss of (glomerulonephritis, pyelonephritis, ciency, lack kidneys or stenosis of the renal artery), intrarenal $ tenal tissue and the development of chroni developmental abnormalities the kidneys. Pathogenesis.pressure in kidney disea: is due to three main cprretention, activation of the pressor system and q The increase in blood jum and wat the depressor system. mechanisms: sod! : decrease in the functions of U ‘Sodium and water retention. Pet ee Impaired renal function is most often manifested were fi Nha disorder of tubular reabsorption with a decrease in the excretion of Elrond he delay of sodium and water lends to hypervolemia - an increase Srcealating blood volume, as well as an increase in the sodium content in the Vascular wall. The latter contributes to the swelling of the vascular wall and an increase in its sensitivity to the pressor effects of angiotensin and catecholamines, Following sodium retention, calcium accumulates in the vescular wall, which leads to a decrease in vascular relaxation and an increase in total peripheral resistance. This mechanism is of major importance in the development of renal arterial hypertension in acute glomerulonephritis, acute and chronic renal failure, Activation of the pressure system. The second mechanism responsible for the development of arterial hypertension in renal diseases is an increase in the activity of the renin-angiotensin- aldesterone and sympathetic-adrenal systems. One of the endocrine functions of the Kidneys is the production of renin by juxtaglomerular cells, which very subtly respond to changes in the hemodynamics of the kidney through the release of renin into the blood. Renin secretion is stimulated by renal ischemia and a drop in the concentration of sodium ions in the blood. In blood plasma, renin reacts with angiotensinogen (a2 -globulin) produced in the liver, forming a low-active angiotensin I, which, under the influence of angiotensin-converting enzyme, passes into angiotensin II, which is the strongest vasoconstrictor. Angiotensin II causes systemic spasm of arterioles with an increase in total peripheral resistance, stimulates the secretion of aldosterone by the adrenal cortex, increases sodium reabsorption in the tubules of the kidneys. _ Increased renin synthesis and increased activity of angiotensin II plays a large role in the development of renal hypertension in those renal diseases in which their function is preserved, but there is ischemia in the juxtaglomerular apparatus: in renal artery stenosis, chronic renal failure and chronic glomerulonephritis. Through communication with the sympathetic nervous system, it activates the release of catecholamines by the adrenal glands. ___ The involvement of catecholamines in the origin of renal hypertension in renal diseases is also mediated by vasoconstriction, an increase in total peripheral tesistance, and an increase in cardiac output. ee retains sodium in the body, increasing its reabsorption in the ing tubules, and increases the excretion of potassium, The pressure effect of aldosterone is associated with its effect on the cell membrane with an increase in its Permeability to sodium. In addition, following increased sodium reabsorption, waterThe accumulat t ion of sodi sconstrietion, ‘dium in the walls of blood y An increase in the concentration of the osmoreceptors and an ing €ssels also sodiun i ‘ed secretion pituitary gland, which further increases the reab: Sodium retention leads to an increase in the wall to pressor effects. Activation of the sympathetic-adrenal formation is important in the development vo. of renal hy Pertension with pheochromocytoma or impaired renal r F : pheochromocytom exact Decreased function of the depressor system, " Shtonic renal failure), The dep lem, Which oppo: ql prostaglandins aoe ia - the ee pi ce Prostaglandins reduce the tonus of the i casos sistance, ae powerful nares acini a TR Bradykinin and calliidin possess the prono f i getiotualpccuceeste kalleleea, ki eee "asodilting properties, which Damage to the renal parenchyma leads to depressor mechanisms. ical signs. The clinic of renal arterial hypertension syndrome is determined by the degree of increased blood pressure and the severity of secondary lesions of the heart and blood vessels. Patients complain of headache, blurred vision, pain in the heart, shortness of breath. With labile hypertension, patients complain of fatigue, irritability, palpitations, and less often headache. When assessing the severity of the syndrome of renal arterial hypertension, it is more correct to focus on the level of diastolic and not systolic blood Pressure, Malignant renal hypertension is characterized by excessively high and Persistent systolic and especially diastolic pressure, which leads to a significant increase in the heart size, ECG changes, severe retinopathy (with foci of hemorrhage, edema of the optic nerve head, reduced vision and even blindness), hypertensive encephalopathy, and heart failure. Left ventricular hypertrophy, Tenal arterial hypertension, is determined by ny 'mpulses, displacement of relative cardiac dullness to the le Sccond tone on the aorta, as well as characteristic changes on EchocG. Complications of renal arterial | hypertensive crisis, acute cerebrovs failure, severe retinopathy, encephal M ions in the blood causes of the ‘antidiuretic fomene sorption of water Sensitivity of reo by in the distal ete €ptors of the vascular system with increased catecholamine ion of pressure factors, includes a decrease in the activity of renal a f ‘hich is a sign of a long-existing syndrome of hie eased, diffuse, refractory apical ‘and down, accent of the the X-rays, ECG andLAAN SENN NN STATIS failure corresponds to the persistence and Initially, patients develop left ventricular f breath, cyanosi hma attacks, pulmonary edema failure - with shortness of breath, cya cinch pulmo ‘ radiographic and physical signs of venous stagnation the lungs. Subsequently, a sle of blood circulation: stagnation develops and along @ irole " roy perter w crisis is manifested by an acute and significant rise in blood pressure. It can be triggered by an exacerbation of kidney disease, as well ag emotional or phys stress. Clinically, a hypertensive crisis 1s manifested by a Geterioration of cerebral, cardiac or ocular symptoms, including loss of vision, the development of acute left ventricular failure or an acute violation of cerebral circulation ; Baer save encephalopathy, as a* result of ischemia and ‘brain edema, is manifested by weakness, drowsiness, headaches, memory impairment, decreased intelligence, depression. Disturbance of cerebral circulation with paralysis, disorder of sensitivity, dysfunction of the pelvic organs, as well as myocardial infarction can be a frequent consequence of high arterial hypertension. 5 Renal arterial hypertension accelerates the development of chronic renal failure in individuals suffering from kidney disease. The severity of symptoms of heart duration of renal arterial hypertension Diagnostic criteria. 1) from the first days of the disease sharply increased numbers of blood pressure; 2) a more significant increase in diastolic blood pressure than systolic blood pressure: 3) severe arterial hypertension, low efficacy of antihypertensive drugs and the frequent development of complications (primarily from the heart, brain and eyes). Main reasons. The main causes of renal arterial hypertension syndrome are: 1. Primary acute and chronic glomerulonephritis. 2. Secondary glomerulonephritis on the background of systemic diseases of the connective tissue (systemic lupus erythematosus, systemic scleroderma and others), systemic vasculitis (polyarteritis nodosa, Wegener's granulomatosis and others). 3. Pyelonephritis, urolithiasis. 4, Polycystic kidney disease, hydronephrosis. we 5. Metabolic nephropathy (diabetic nephropathy, kidney damage with gout 6. Interstitial nephritis. 7. Congenital renal hypoplasia 8. Renin secreting tumors. 9. Anomalies of the development of kidney vessels.10. Renal artery stenosis fibromuscular hyperplasia, vasculiti Takayasu’s disease), (atherosclerotic lesion of the 'S of the renal arter See ies, nonspecific aortoarteritis or 15.2.7. Syndrome of kidney ie insufficiency The basis of this : yndrome is a viola i i ine development of intoxication (sel poisoning) of the an Hines ith Severe end-stage renal disease is called uremia, There are acute and chronic renal failure. Syndrome of acute renal failure. Acute renal failure (ARF) is an emergency and dev hours or days. elops rapidly over several mptomatology of ARF depends on the stage of this condition. [stage or initial stage. Itlasts from several hours to several days. Symptoms of this stage are signs of diseases against which the acute renal failure develops. Laboratory manifestation of this stage is an increased level of urea, residual nitrogen and creatinine in the serum, reduced glomerular filtration and hyperkalemia. Stage II or stage oligoanuria. This stage is mainly manifested by a decrease in daily diuresis to 500 ml or less (oliguria) until the cessation of urine (anuria) stops. Laboratory symptoms are the same signs as in stage I, but more pronounced. Clinically, this stage is manifested by symptoms of uremia (see CRF clear period). Stage III or stage polyuria. The main clinical manifestation of this stage is an increase in diuresis up to 2 liters or more per day with a parallel improvement in general condition, and a gradual decrease (up to normal figures) in urea levels, residual nitrogen and creatinine, as well as an increase in glomerular filtration, is found in the laboratory. IV stage or stage of recovery. It starts from the moment of normalization of diuresis and indicators of residual s of protein metabolism. ee pia of acute renal failure can develop with acute and subacute glomerulonephritis, poisoning with nephrotoxic poisons, incompatible blood transfusion (transfusion shock), ee shock, etc. Syndrome of chronic renal failure. eae aa failure (CRF) develops gradually over many months and years CKD has a steadily progressive course. This syndrome is characterized by multiple manifestations. il There are hidden and obvious period of | The hidden period of CRE ja In the latent period, ed levels ©! merular only laboratory signs of CRF: 5, nitrogen and creatinine in the a on this case, the most specific Ibo Sign there are f urea, residual filtration. In in serum creatinine level “ of CRE ws perio inst the background of increasing severity of jabop mihi Kidney disease, clinical symptoms ofthis syndrome pen) signs of chronic = “me toms of the apparent period of CRF are: 7 The specific sympt pee ome (hea 1) intoxication syndrome (he , ; 2) uremic odor (smell of ammonia from the mouth’ a : 3) signs of uremic gastr itis (nausea and vomiting), colitis (colonic di corist (pleural friction noise) and dry pericarditis (pericardial friction isa ache, dizziness, weakness), ’ dry ph { 4) painful pruritus, ; 5) pronounced laboratory signs of CRF: / the size of the kidneys on ultrasound, computed 6) symmetrical reduction of tomography and urogram; 7) in the final stage comes uremic coma, ending with the death of the patient. Sindrome of chronic renal failure is observed in the end of many chronic | kidney diseases, such as chronic glomerulonephritis, chronic pyelonephritis, kidney amyloidosis, kidney damage during long-term diabetes mellitus and hypertension, etc. 15.2.8. Urinary tract infection syndrome Urinary tract infection syndrome is an inflammatory process that develops in the urinary organs from the renal pelvis to the urethra. The specific symptoms of urinary tract infection syndrome are: 1) symptoms of intoxication syndrome (fever, pallor of the skin, loss of appetite, dyspeptic disorders), 2) symptoms of dysuric syndrome (see above); 3) pain in the projection of the kidneys, bladder and urinary tract. The syndrome of urinary tract infection is observed in all infectious inflammatory diseases of the urinary system: from pyelonephritis to urethritis. teil Syadrome of stone in kidneys, urinary tract and pladder e basis of this syndrome is the formati es in the pelvis, urinary tract and bladder. ey and pees and urinely i eens of the syndrome of the presence of stones in the kidneys !1) severe paroxysmal pain in the lo urinary tract and bladd patients rush to bed, sor 2) gross hematuria; 3) microhematuria (erythroeyturiay; 4) the detection of stones in the renal Pelvis-renal system, uri wen stem, urinary tract and The syndrome of the presence of stones of stones in the kidneys, uri po bladder is a diagnostic sign of urolithiasis, oe Wer back ("renal " colic’ (at the same time the intensi i ily of pain is ), in the area of the 80 pronounced that 15.2.10, Kidney syndrome Rea ee angie Tepresenting an attack of excruciating back pain or in the late lo vith distinct irr i sodibe imnersunticen Herein) ‘radiation to the groin urethra, genitals, In the pathogenesis of renal colic syndrome, there is a Violation of urodynamics (urine outflow) in the upper urinary tract, Acute disturbance of urodynamics (urine outflow along the urinary tract) is caused by movement or impairment of dense formations (stones, blood clots or mucus) in the lumen of the ureter. The leading role in the development of this syndrome belongs to the spasm of the urinary tract, their ischemia, stretching of the fibrous capsule of the kidney, as well as renal pelvic reflux. The onset of renal colic often develops unexpectedly and is characterized by severe pain in the lumbar region. They attack is provoked by walking, jogging, jolting, lifting weights, but sometimes it can occur at rest, at night. The intensity of pain during renal colic quickly increases. At the time of the attack, the patient is restless, rushing about in bed in search of a comfortable position to ease the pain. Initially, pain is localized in the lumbar region, but then moves down along the ureter, radiating to the groin and genitals. The attack quickly ends or lasts for many hours (until the discharge of calculus with urine), gis norat : ; Patients may experience reflex nausea and vomiting, oliguria, reaching anuria. Dysurie disorders are often noted. : yr & On palpation and tapping in the area of the kidneys, pain is ees oe affected side (positive symptom of Pasternack). Sometimes there is muscle tension the side of the abdomen. 5 wa re During a painful attack, gross hematuria or marked micro hematuria is noted, Which disappears after the cessation of pain. : rs An attack of renal colic may be accompanied by chills, fever, leukocytosis, increased ESR. ’ . Diagnosis of renal colic is to identify ‘Tadiation of pain, increasing with palpation and 5S, tachycardia, the characteristic localization and tapping in the kidney area, as welleristic changes in urine and instrumental methods of as on the basis of char research, ay examinations of the kidneys (review and During ultrasound and tod NB ot > pyelogmaphy), stone and changes in the urinary tract excretory urography, retrograde pyelography), 7 ieee pathological displacement of the kidney and flexure of the ureter can be detected. hydronephrosis, and Renal colic syndrome occurs with urolithiasis, nephroptosis 15.2.14. Syndrome of kidney eclampsia Renal eclampsia is a convulsive seizure that develops most often on the background of glomerulonephritis and nephropathy of pregnant women, Renal eclampsia is characterized by a rapidly developing significant increase in blood pressure in combination with urinary syndrome and brain symptoms in the form of increasing mental retardation, which can result in cerebral coma. Renal eclampsia develops due to hypervolemic cerebral edema and angiospasm. Lingering, drowsiness, and headache may be harbingers of the development of renal eclampsia. Tonic-clonic convulsions occur suddenly. The patient loses consciousness, the face becomes bluish, the neck veins swell, the pupils dilate and do not react to light. During an attack, biting of the tongue is possible, foam appears from the mouth. Blood pressure is sharply increased (from 200/140 to 300/160 mm Hg.). the pulse is tense, rare. During attacks, involuntary defecation and urination are possible. The attack of renal eclampsia lasts a few minutes. After an attack, the patient remains in a stunned state for some time, then comes to the senses. Sometimes, after awakening, amaurosis (blindness of central origin) and aphasia (speech disorder) persist for a short time. Despite the severe clinical picture of eclamptic seizures, they rarely end in the death of patients and pass for the most part without a trace. An attack of renal eclampsia can be interrupted by spinal puncture and removal of a small amount of cerebrospinal fluid 5 Renal eclampsia syndrome may develop in acute glomerulonephritis, in the last months of pregnancy and the first day afier birth. 15.3. Main diseases of urinary system 15.3.1. Acute glomerulonephritis, Definition ‘This is . acute immune-inflammatory disease, often of an infectious nature, : a primary lesion of the glomeruli of the ki and clinically manifested by renal and extrarenal signs i eine ae -276-Etiology 1. Infectious agents. 1.1. Streptococcal _ infection, $s group A 1.2, Other types of bacteria. 1.3. Viruses (adenoviruses, her 2. Vaccines and serums, 3. Systemic disea Classification There are 4 (four) clinical variants hematuric, nephrotie, and unfolded (classical), Symptomatology + onset of the disease, most often after acute str after acute angina); * pain in the lumbar region on both sides; + fever, + gross hematuria; + isolated urinary syndrome with a predominance of proteinuria up to | g per day with a monosymptomatic variant of the disease; * isolated macro- and microhematuria in the hematuric form of the disease: + signs of nephrotic syndrome with nephrotic variant of the disease, + signs of nephrotic syndrome, renal arterial hypertension syndrome. the development of acute left ventricular heart failure and acute renal failure in the advanced version of the disease; + inflammatory blood changes (leukocytosis, accelerated ESR, ete.). General principles of treatment 1. Etiological treatment (general antibiotics). 2. Pathogenetic treatment. 2.1. Glucocorticoids (prednisone and others). 2.2 NSAIDs. 2.3. Anticoagulant and antiplatelet drugs. mptomatic treatment. : : 3.1. Treatment of hypertension (antihypertensive drugs). ates) 3.2. Treatment of renal edema (restriction of water and salt intake, 3.3. Treatment of heart failure. usually the 12th Strain of B-hemolytic "Pes virus, hepatitis B virus), es of the connective ti issue. Of the disease: monosymptomatic, eptococcal infection (usually 18.3.2. Chronic glomerulonephritis Definition This is a group of diseases manifestations, characterized by immi