THE MAIN SYMPTOMS AND SYNDROMES IN KIDNEY DISEASES. SYMPTOMS OF ACUTE AND CHRONIC...

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THE MAIN SYMPTOMS AND SYNDROMES IN KIDNEY DISEASES. SYMPTOMS OF ACUTE AND CHRONIC GLOMERULOENPHRITIS AND PYELONEPHRITIS.

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THE MAIN SYMPTOMS AND SYNDROMES IN KIDNEY DISEASES. SYMPTOMS OF ACUTE AND CHRONIC GLOMERULOENPHRITIS AND PYELONEPHRITIS. - PowerPoint PPT Presentation

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THE MAIN SYMPTOMS AND SYNDROMES IN KIDNEY DISEASES. SYMPTOMS OF ACUTE AND CHRONIC

GLOMERULOENPHRITIS AND PYELONEPHRITIS.

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•What do the kidneys do?What do the kidneys do?

1.1. remove toxic waste remove toxic waste products products 2. remove excess water 2. remove excess water and salts and salts 3. 3. taketake part in controlling part in controlling your blood pressure your blood pressure 4. produce erythropoietin 4. produce erythropoietin ((epoepo for short) which stimulates red cell for short) which stimulates red cell production from the bone marrow - you production from the bone marrow - you get anaemic without this get anaemic without this 5. help to keep calcium and phosphate in 5. help to keep calcium and phosphate in balance for healthy bones balance for healthy bones 6. maintain the blood in a neutral (non-6. maintain the blood in a neutral (non-acid) stateacid) state

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Signs, which point on kidney Signs, which point on kidney affectionaffection

• main

• pain in lumbar region, • urination disoders, • change of urine,• oedema.

• secondary• chills, • headache, • dizziness, • vision deranged,• heart pain, • skin itching, • loss of appetite, • nausea, • vomiting , • fever.

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Pain in lumbar regionPain in lumbar regionPain is caused by: stretching of kidney capsule, spasm of urethers, inflammation of peryrenal cellular tissue, kidneys infarction.

Intensity of the pain feelings can be different

– from dull, boring pain (at acute and exacerbation of chronic pyelonephritis) to sharp, very severe pain with an irradiation along ureters, in a groin, in genitals, in the front surface of thigh (nephrocolic which arises up as a result of ureter corking with a stone, at his bend, at the trauma of kidneys, kidneys infarction).

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Urination disoders

Oliguriya (decreasing of urine excretion of less than 500 ml per day).Anurya (complete stop of urine excretion - symptom of acute kidney

insufficiency, mechanical obstacles of urine passage (stone, tumour). Nycturia (advantage of nightly diuresis above daily ( normaly 1:2);

Dysuriya – (painful urination) Polakiuriya – (frequent urination, which combines with polyuria at

chronic nephritis, cystitis).

Isosthenuria (At disorders of dilution and concentration function of

kidneys specific gravity is 1010-1011)

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OedemaOedema are one among the main symptoms of renal pathology.

Often oedema is the first sign of such diseases.

Renal oedema can suddenly develop as well as disappear.

As a rule they are located on the face especially on eyeleads

(where the subcutaneous fat tissue is more loose ).

Sometimes oedema is equally distributed all over the body (anasarka).

Oedema have mild consistency, deep elevation of skin is present even in slight pressing on it.

Oedema can spread on internal organs and cavities (profound oedema) with accumulation of transsudate in serous cavities — pleural, abdominal and pericardial cavities.

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Uric syndrome.Uric syndrome.• moderate proteinuria (from 100 mg up to 3,5 g moderate proteinuria (from 100 mg up to 3,5 g

a day), a day), • red blood cells in the urine more than 1red blood cells in the urine more than 1106/L 106/L

perper day day ((erythrocyturiaerythrocyturia)),, • leukocyturia - more than 1leukocyturia - more than 1106/l 106/l perper day), day), • custs in urine, custs in urine, • bacteriuria, bacteriuria, • ddischargingischarging of salts and their cristals with urineof salts and their cristals with urine• cells of renal and transitionalcells of renal and transitional — — epithelium epithelium

and other elements of pathological both and other elements of pathological both organized and non- organized renal sedimentsorganized and non- organized renal sediments,,

• The leading symptom The leading symptom inin uric syndrome is uric syndrome is proteinuria (albuminuria).proteinuria (albuminuria).

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Nephrotic syndrome.• A massive leak of protein (albumin) into the

urine (proteinuria) (more than 3,5 gr per day).• A low blood level of albumin due to the large

amounts lost in the urine (hypoproteinemia mostly because of hypoalbuminemia).

• An increased level of cholesterol in the blood (hyperlipidemia).

• Retention of fluid in the body (edema) causing swelling.

• Hypercoagulation.

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Renal arterial hypertension.Renal arterial hypertension.This is symptomatic hypertension caused by affectionThis is symptomatic hypertension caused by affectionof kidneys or renal vessels with following disorders of of kidneys or renal vessels with following disorders of blood pressure regulatioblood pressure regulationn. .

Elevation of blood pressure is caused by 3 mechanismsElevation of blood pressure is caused by 3 mechanisms: :

1.1.sodium and water retention, sodium and water retention, 2.2.activation of pressor systemactivation of pressor system,, 3.3.inhibition of depressory mechanisms.inhibition of depressory mechanisms.

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Acute nephritic syndromeAcute nephritic syndrome..

It is characterized by the abrupt onset (days)It is characterized by the abrupt onset (days)of haematuria with red blood cellsof haematuria with red blood cells,, casts or casts ordysmorphic red blood cells appeardysmorphic red blood cells appearinging in inthe urine, proteinuria, renal impairementthe urine, proteinuria, renal impairement(oliguria, uremia, raised urea and creatitine), (oliguria, uremia, raised urea and creatitine), hypertension due to water and salt hypertension due to water and salt retention, edema (usually periodical).retention, edema (usually periodical).

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What is What is glomerulonephritis?glomerulonephritis?

• Diffuse glomerulonephritisDiffuse glomerulonephritis is the general is the general infectious-allergic disease with prevalent and infectious-allergic disease with prevalent and primary envolvement of nephrone glomerular primary envolvement of nephrone glomerular apparatus into the pathological process.apparatus into the pathological process.

• Glomerulonephritis is a type of glomerular kidney disease in which the kidneys' filters become inflamed and scarred, and slowly lose their ability to remove wastes and excess fluid from the blood to make urine.

• Types of glomerulonephritis include kidney• disease of diabetes, IgA nephropathy, and• lupus nephritis.

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Classification Classification (by L. Pyrih)(by L. Pyrih)

• The following forms of glomerulonephrites are determinedThe following forms of glomerulonephrites are determined• I. I. Acute diffuse glomerulonephritis :Acute diffuse glomerulonephritis :• uric syndrome;uric syndrome;• nephrotic syndrome (mostly haematuria, hypertension and nephrotic syndrome (mostly haematuria, hypertension and

edema are present).edema are present).• II. II. Subacute fulminant glomerulonephritis.Subacute fulminant glomerulonephritis.• III. III. Quickly progressing glomerulonephritis.Quickly progressing glomerulonephritis.• IV. IV. Chronic glomerulonephriis:Chronic glomerulonephriis:• 1st type1st type: : pprimary chronicrimary chronic, secondary chronic, secondary chronic..• 2. 2. syndromes:syndromes: uricuric, , nephrotic.nephrotic.• 3. 3. stages:stages:• non-hypertensivenon-hypertensive, , hypertensive;hypertensive;• chronic renal failure;chronic renal failure;• 4. 4. phase:phase: exacerbationexacerbation, remission, remission..

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Acute glomerulonephritisAcute glomerulonephritis (AG, lat. - (AG, lat. - glomerulonephritis glomerulonephritis ааcutcutа).а).

• This is acute immune inflammatory lesion This is acute immune inflammatory lesion of kidneys parenchima with primary of kidneys parenchima with primary damage of glomerules and following damage of glomerules and following involvement of all renal structures into involvement of all renal structures into the pathological process. the pathological process.

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• Ethiology and pathogenesisEthiology and pathogenesis• • AG develops 2-3 weeks after acureAG develops 2-3 weeks after acure • infectious disease (tonsillitisinfectious disease (tonsillitis pharyngitispharyngitis skarlet feverskarlet fever more more rarely —etysipelasrarely —etysipelas etc.)etc.) caused by caused by -haemolytic-haemolytic streptococcus, group Astreptococcus, group A

or by otheror by other bacteriological agents bacteriological agents (pneumococus, (pneumococus, staphylococcus, staphylococcus, viruses).viruses).

• TThe process develops as a hyperergic reaction of sensebilized organism. he process develops as a hyperergic reaction of sensebilized organism. • Administration of serum preparations, other medical preparations, Administration of serum preparations, other medical preparations,

vaccination, penetration of toxic substances into the organism, deranged vaccination, penetration of toxic substances into the organism, deranged venous outflow from kidneys may be the causes of AGvenous outflow from kidneys may be the causes of AG..

• Provoking factors are overooling, dump weather, traumas. Provoking factors are overooling, dump weather, traumas.

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Pathological anatomy

1. Enlarged and hyperaemic glomeruli;

2.Ischaemia of the glomeruli;

3. Fibrinoid swelling of the capillary walls, proliferation of their endothelium;

4. Accumulation of coagulated proteinous exudates in the space between the capillary loops and the glomerular capsule, blood stasis, thrombosis of the capillary loops, and hemorrhages.

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This symptoms are combined in following syndromes: hypertension, uric syndrom, edema

• Uric syndromeUric syndrome isis presence of protein in the urinepresence of protein in the urine,, blood blood formed elements, casts. formed elements, casts.

• Even at the beginning of the disease urine colour is changed Even at the beginning of the disease urine colour is changed because of blood admixtures. because of blood admixtures. UUrine has the colour of “meet rine has the colour of “meet wastes”. Erythrocytes quantity at the peak of the disease is wastes”. Erythrocytes quantity at the peak of the disease is about 100—200 in a vision fieldabout 100—200 in a vision field. .

• Hypertension occurs due to activation of renin-angiotensin-aldosterone and sympathoadrenal systems as well as water and salt retenstion in the organism and inhibition of depressor systems.

• Blood pressure elevates from insignificant level till 180-200 mm Hg (systolic) and 120 mm Hg (diastolic one).

• Main complaints of these patients are: headache, heaviness in the head, dyspnea, palpitation, nausea and sometimes — periodical imparement of vision.

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Data of general inspectionData of general inspection:: patient’s appearance is quite specific patient’s appearance is quite specific

and it is called “and it is called “facies nephritic a”facies nephritic a”: : skin paleness, skin paleness, swelling of the face and eyeleadsswelling of the face and eyeleads

edema under the eyesedema under the eyes,, Patient’s condition is heavy, his Patient’s condition is heavy, his

posture in bed may be forced — posture in bed may be forced — sitting or semirecumbent.sitting or semirecumbent.

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::

Palpation:Palpation: pulse is full, dull and slow. pulse is full, dull and slow. Apex beat Apex beat isis intensified and displaced intensified and displaced

leftward.leftward. PercussionPercussion:: may reveal fluid in pleural may reveal fluid in pleural

cavity, lung cavity, lung congestion and and displacement of left heart border displacement of left heart border

leftward. leftward. AAuscultationuscultation:: bradicardia, I heart sound bradicardia, I heart sound

is weakenedis weakened,, systolic murmur over heart systolic murmur over heart apexapex,, accentuation of the II heart sound accentuation of the II heart sound

over the aorta.In severe cases over the aorta.In severe cases especially in left ventricular especially in left ventricular

hyperthrophy hallop rhythm occurs. hyperthrophy hallop rhythm occurs. Vesicular breathing is heard over the Vesicular breathing is heard over the

lungs. lungs.

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Laboratory methods of examination: Total blood count: moderate

leukocytosis anaemia accelerated ESR. Вiochemical blood analysis — increased

content of seromucoid, sialic acids fibrinogen, C-reactive protein, antistreptoliase, immune complexes, 2- і -globulines.

In heavy cases oliguria, decreased urine density, nicturia. In resilience of edema (period of recovering) amount of urine increases and ability of kindeys for concentration raises.

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Instrumental methods of examination:

Eye grоunds: narrowing of arterioles, dilatation of veins, sometimes - aedema of ophthalmic nerve, hemorrhage into the retina.

ECG — overloading and hyperthrophy of the left ventricle decreased voltage of Р і R, depression of ST interval, T is low of biphasic.

X-ray examination of the chest: probable presence of fluid in pleural cavity signs of lung congestion, enlargement of the right ventricle.

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Treatment: bed regimen for 1-15 months dry and warm ambient

temterature.

Diet № 7, limitation of salt ( to 05-15 gr a day) liquid. Medicamentous treatment — antibiotics for 7-10 days

(penicillin or semisynthetic penicillins). Hypotensive agents: sedative (valerian mothewort bromine

tranquilizers) antiadrenergic preparations (apressin clonidine metildopum, -bloquers) in combination with saluretics, losartan (angiotensin converting enzyme inhibitor), perypheric vasodilatators.

Diuretics (in edema, heart failure, hypertension). Pathogenetic therapy — immunodepressants glucocorticoids

agents that improve haemosthasis and microcirculation (indometacin tiklopidine, curantyl heparin).

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Chronic Chronic glomerulonephritisglomerulonephritis

((glomerulonephritis chronicaglomerulonephritis chronica, ChG) is , ChG) is inflammatory process in renal glomeruliinflammatory process in renal glomeruli degeneration of canalicular epithelium and degeneration of canalicular epithelium and

progressive development of connective tissue progressive development of connective tissue

that that resulting in secondary shrinked resulting in secondary shrinked

kidney.kidney. Ethiology and pathogenesis.Ethiology and pathogenesis. Often ChG develops after acuteOften ChG develops after acuteglomerulonephritis. If information about AG in glomerulonephritis. If information about AG in patient’s anamnesis is abcent than thay speapatient’s anamnesis is abcent than thay speakkabout primary form of ChGabout primary form of ChG

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Clinical picture.

In unhypertensive stage: general weakness, quick fatigue, dull boring pain in lumbar region, change of urine colour, edema below eyes and on the face, on the legs.

In hypertensive stage: the same plus headache, dizziness, periodical nassal bleeding, dyspnoe, nictural dyspnoe, palpitation.

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Data of inspection: patient’s condition is satisfactory in remission but in exacerbation may be severe. Skin is pale, edema are visible on the face (below the eyes (facies nephritica). Sedimentation of uric acid cristals is possible on the skin. Inspection of precordial region: displacement of apex beat leftward from the left midclavicular line. In dilatation of the left ventricle apex beat becomes diffuse.

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PalpationPalpation:: Apex beat is intensified, diffuse Apex beat is intensified, diffuse and displaced leftwardand displaced leftward. .

PercussionPercussion:: the left border of relative the left border of relative heart dullness is displaced leftward from heart dullness is displaced leftward from

the left midclavicular line in the left midclavicular line in VV interspace. interspace.

PalpationPalpation of organs of abdominal cavity of organs of abdominal cavity:: is is painful in epigastrium and above the large painful in epigastrium and above the large

bowel. In the case of right ventricular bowel. In the case of right ventricular failure the liver is enlarged. failure the liver is enlarged.

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Auscultation:Auscultation: in patients with left ventricular in patients with left ventricular failure moist rales may be heard in lover parts failure moist rales may be heard in lover parts

of the lungs (because of lung congestion). of the lungs (because of lung congestion). Heart soungs are intensified but later become Heart soungs are intensified but later become

weakened, accenttuation of the II sound is weakened, accenttuation of the II sound is heard over the aorta, systolic murmur over the heard over the aorta, systolic murmur over the

apex. In terminal stage pericardial friction apex. In terminal stage pericardial friction sound may be haerd on the hart basis, along sound may be haerd on the hart basis, along the left sternal border and in zone othe left sternal border and in zone off absolute absolute

heart dullness. heart dullness. Blood pressure is elevated up to 200Blood pressure is elevated up to 200//120 mm 120 mm Hg. If heart failure develops systolic pressure Hg. If heart failure develops systolic pressure may decrease but diastolic one is steel high. may decrease but diastolic one is steel high.

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Chronic glomerulonephritis with nephrotic Chronic glomerulonephritis with nephrotic syndrome syndrome is manifested by decreased is manifested by decreased diuresis, edema and changes in the blood diuresis, edema and changes in the blood and urine: hypo- and dysproteinaemia and urine: hypo- and dysproteinaemia (hypergammaglobulinaemia, (hypergammaglobulinaemia, hypoalbuminaemia), hyperlipidaemia, hypoalbuminaemia), hyperlipidaemia, proteinuria more than 3,5 grproteinuria more than 3,5 gr/l/l, casts in , casts in urine (hyaline, granular and rarely - urine (hyaline, granular and rarely - ceraceous (waxy). Respiratory infections ceraceous (waxy). Respiratory infections are frequent because of are frequent because of immunodepression that provoke immunodepression that provoke exacerbation of ChG. exacerbation of ChG.

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Eye grounds:Eye grounds: retinal arteriosclerosis retinal arteriosclerosis hemorrhagias hemorrhagias focci of degeneration and affections of n. focci of degeneration and affections of n. ophthalmicus (neuroretinopathy). ophthalmicus (neuroretinopathy). In the stage of renal failure In the stage of renal failure patient’s condition is patient’s condition is heavy. Forced posture (sitting). Deranged heavy. Forced posture (sitting). Deranged conscioussness, sometimes coma. Main complaints conscioussness, sometimes coma. Main complaints are nausea, vomiting, skin dryness and itching, are nausea, vomiting, skin dryness and itching, deranged vision, oliguria or anuria. deranged vision, oliguria or anuria. Laboratory exLaboratory exaaminationmination. Changes in urine: . Changes in urine: compensatory poliuria, nikturia. Zimnitsky’s test show compensatory poliuria, nikturia. Zimnitsky’s test show hypoisosthenuria, nicturia. Urine density decreases hypoisosthenuria, nicturia. Urine density decreases and become monotonousand become monotonous hypoisosthenuria (1009- hypoisosthenuria (1009-1012). 1012). CCreatinine and urea content in the blood may reatinine and urea content in the blood may be normal. be normal. Proteinuria from insignificant till 3-10 grProteinuria from insignificant till 3-10 gr/l/l. Casts — . Casts — hyalinehyaline granular and ceraceous. granular and ceraceous.

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Laboratory exLaboratory exaaminationmination.. Changes in urine are folowing:Changes in urine are folowing: compensatory compensatory

poliuria, nikturia. Simnitsky’s test show poliuria, nikturia. Simnitsky’s test show hypoisosthenuria, nicturia. Urine density hypoisosthenuria, nicturia. Urine density decreases and become monotonousdecreases and become monotonous hypoisosthenuria (1009-1012). Due to poliuria hypoisosthenuria (1009-1012). Due to poliuria products of nitrogen metabolism is possible to products of nitrogen metabolism is possible to evacuate from the organism that is why kreatinine evacuate from the organism that is why kreatinine and urea content in the blood may be normal. and urea content in the blood may be normal.

Proteinuria develops. Its degree may be from Proteinuria develops. Its degree may be from insignificant till 3-10 grinsignificant till 3-10 gr/l/l. It depends on patient’s . It depends on patient’s diet, physical loading, overcooling etc. On urine diet, physical loading, overcooling etc. On urine sediments there are casts — hyalinesediments there are casts — hyaline granular and granular and ceraceous. ceraceous.

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TrTreatmenteatment is perormed taking is perormed taking into account clinical variant of into account clinical variant of the disease, its phase and the disease, its phase and stage. stage. Patient should avoid Patient should avoid overcoolings, physical overcoolings, physical loadings, psychoemotional loadings, psychoemotional stresses. stresses. In exacerbation long-standing In exacerbation long-standing treatment is indicated. Diet № treatment is indicated. Diet № 7, limitation of salt intake to 7, limitation of salt intake to 10 gr a day10 gr a day in nephrotic in nephrotic variant - 6-8 gr a day.variant - 6-8 gr a day.

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TreatmentTreatment In exacerbation long-standing treatment is indicated. In exacerbation long-standing treatment is indicated. Diet № 7, limitation of salt intake to 10 gr a dayDiet № 7, limitation of salt intake to 10 gr a day in nephrotic in nephrotic

variant - 6-8 gr a day. variant - 6-8 gr a day. Medicamentous treatment:Medicamentous treatment: In unhypertensive stage - In unhypertensive stage -

corticosteroids, cytostatics, aminoquinoline derivatives. In corticosteroids, cytostatics, aminoquinoline derivatives. In hypertension hypotensive drugs also should be prescrobed hypertension hypotensive drugs also should be prescrobed ((-bloquers-bloquers methyldopum, apressin etc.). methyldopum, apressin etc.).

Diuretics (furosemideDiuretics (furosemide ethacrynic acid, hydrochlorothiazide) in ethacrynic acid, hydrochlorothiazide) in edema; edema;

Anticoagulants and antiaAnticoagulants and antiagggregants (heparingregants (heparin curantyl curantyl indometacin) indometacin)

HemosoHemosorrption, plasmapheresis.ption, plasmapheresis. If infection develops than antibiotics are administered. If infection develops than antibiotics are administered. Nephrotic syndrome is indication for administration of Nephrotic syndrome is indication for administration of

prednisolone 30-80 mg a day, azathioprine – 100-150 mg a prednisolone 30-80 mg a day, azathioprine – 100-150 mg a day, heparin – 10000-15000 Un, aspirin – 0,25 gr. day, heparin – 10000-15000 Un, aspirin – 0,25 gr.

In remission stage – sanatorium-resorting treatment is useful In remission stage – sanatorium-resorting treatment is useful with warm and dry climate, mineral waters. with warm and dry climate, mineral waters.

If high risk of renal failure and exaggerated asotaemia are If high risk of renal failure and exaggerated asotaemia are present present it is necessary to perform chronic hemodialisis and it is necessary to perform chronic hemodialisis and transplantation of kidney.transplantation of kidney.

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Prognosis.Prognosis. DurationDuration of patient’s life depends of patient’s life depends on clinical form of ChG and on clinical form of ChG and functional functional conditioncondition of kidneys. of kidneys. In the stage of chronic renal failure In the stage of chronic renal failure patients are disable.patients are disable.ProphylaxisProphylaxis includes in-time includes in-time treatment of acute and chronic focci treatment of acute and chronic focci of infection as well as treatment of of infection as well as treatment of exacerbations, dyspancery exacerbations, dyspancery observationobservation. .

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PyelonephritisPyelonephritis Pyelonephritis is a bacterial infection of Pyelonephritis is a bacterial infection of

one or both kidneys. one or both kidneys. Ethiology:Ethiology: E. Coli, streptococci, E. Coli, streptococci,

staphylococci, proteus and differrent staphylococci, proteus and differrent bacterial assotiations, sometimes it may bacterial assotiations, sometimes it may be caused by virusesbe caused by viruses

Provoking factors:Provoking factors: disorders of urine disorders of urine outflow (congenital anomalias, stones, outflow (congenital anomalias, stones, obstruction, pareses, paralises etc.); obstruction, pareses, paralises etc.); metabolic disorders (diabetes mellitus, metabolic disorders (diabetes mellitus, gout); iatrogenic diseases (catheterization, gout); iatrogenic diseases (catheterization, cystoscopy); immunodepression (chronic cystoscopy); immunodepression (chronic diseases, focci of infection, overcooling).diseases, focci of infection, overcooling).

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Pathogenesis:Pathogenesis: P Penetration of microoenetration of microorrganisms ganisms to calicules and renal interstitium by to calicules and renal interstitium by hematogenic hematogenic oror ascending ways (thrugh ascending ways (thrugh urinary tract).urinary tract).

Classification:Classification: unilateral and bilateral, acute unilateral and bilateral, acute and chronic pyelonephritis, primary and and chronic pyelonephritis, primary and secondary. secondary.

Primary pyelonephritisPrimary pyelonephritis occurs when occurs when morphological changes in urinary tract are morphological changes in urinary tract are abcent. abcent.

Secondary pyelonephritisSecondary pyelonephritis occurs when occurs when anomalias of kidneys and urinary tract are anomalias of kidneys and urinary tract are presentpresent which cause disorders of urine which cause disorders of urine outflow (narrowing of ureters or urethra, outflow (narrowing of ureters or urethra, stonesstones nephroptosis nephroptosis adenoma of prostatic adenoma of prostatic gland etc.). gland etc.).

Acute pyelonephritisAcute pyelonephritis devides on serous and devides on serous and purulent. purulent.

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Clinical pattern.Clinical pattern. Acute pyelonephritis (AP)Acute pyelonephritis (AP) starts from starts from

elevation of body temperature up to 38-elevation of body temperature up to 38-3939СС chills chills headache headache unilateral or bilateral unilateral or bilateral dull pain in lumbar regiondull pain in lumbar region dysuria. Nusea, dysuria. Nusea, vomiting, myalgias and arthralgias are vomiting, myalgias and arthralgias are possible. Patient’s condition is heavy, toxic possible. Patient’s condition is heavy, toxic shock may develop. Respiration is frequent, shock may develop. Respiration is frequent, vesicular. Tachicardia is present. vesicular. Tachicardia is present.

Tongue is dry and coated. Herpes labialis. Tongue is dry and coated. Herpes labialis. Urination is frequentUrination is frequent painful painful sometimes sometimes urinary retention develops. Pasternatsky’s urinary retention develops. Pasternatsky’s symptom is positive on the affected side.symptom is positive on the affected side.

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Urine relative densityUrine relative density is decreased is decreased (1012-1015) Poliuria is possible.(1012-1015) Poliuria is possible.

Urine reaction is acid. Leukocyturia and Urine reaction is acid. Leukocyturia and bacteriuria are typical. Non-significant bacteriuria are typical. Non-significant haematuria and proteinuria (till 1 gr/l), haematuria and proteinuria (till 1 gr/l), casts in urine (hyalinecasts in urine (hyaline granular and granular and epythelial).epythelial).

NecNechhipoiporrenko’s and Addis-Kakovsky’s enko’s and Addis-Kakovsky’s teststests are positive.Sometoimes urine is are positive.Sometoimes urine is of alkaline reaction and of unpleasant of alkaline reaction and of unpleasant smell, becomes cloudy, salt sediments smell, becomes cloudy, salt sediments and purulent flakes are present is it.and purulent flakes are present is it.

Microscopic examination: leukocytes, Microscopic examination: leukocytes, granular custs and erythrocytes on all granular custs and erythrocytes on all fision fields.fision fields.

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TreatmentTreatment:: Вed mode; diet enriched with milk, vegetables Вed mode; diet enriched with milk, vegetables

and fruits. Alkohol, spicy food and fruits. Alkohol, spicy food preserved food preserved food coffee are prohibited. Liquid 3 liters a day (wild coffee are prohibited. Liquid 3 liters a day (wild rose decoction, mineral waterrose decoction, mineral water))..

AntibioticotherapyAntibioticotherapy: а) penicillin, semisynthetic : а) penicillin, semisynthetic penicillicnes, hentamycin, claforan ets., b) penicillicnes, hentamycin, claforan ets., b) nitrofurantoin derivatives: nitrofurantoin (0,1 g nitrofurantoin derivatives: nitrofurantoin (0,1 g 3—4 tablets a day 7-10 days), biseptol-480 (2 3—4 tablets a day 7-10 days), biseptol-480 (2 tablets 2-3 times a day 2-3 weaks). tablets 2-3 times a day 2-3 weaks).

Spasmolithics and diureticsSpasmolithics and diuretics. . In heavy cases catheterization, lawage of In heavy cases catheterization, lawage of

calices and bladder with desinfectant solutions. calices and bladder with desinfectant solutions.

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Chronic pyelonephritisChronic pyelonephritis Chronic pyelonephritisChronic pyelonephritis ( (pyelonephritis chronicapyelonephritis chronica, ,

ChP ) is a chronic non-specific inflammation of renal ChP ) is a chronic non-specific inflammation of renal interstitium and calicular mucosa with following interstitium and calicular mucosa with following affection of renal vessels. affection of renal vessels.

Ethiology and pathogenesisEthiology and pathogenesis. . Chronic pyelonephritis Chronic pyelonephritis may be the result of not effective treatment of acute may be the result of not effective treatment of acute pyelonephritis. Provoking factors of ChP: urine pyelonephritis. Provoking factors of ChP: urine congestion, inflamatory diseases of female sexual congestion, inflamatory diseases of female sexual organs, appendicitis, urolithiasis, diabetes mellitus, organs, appendicitis, urolithiasis, diabetes mellitus, chronic intoxications, inhibition of immune system.chronic intoxications, inhibition of immune system.

The main way of penetration of infectionThe main way of penetration of infection is is ascending in disorders of urine outflow ascending in disorders of urine outflow ((kidney kidney stones, anomalias and strictutes (narrowings) of stones, anomalias and strictutes (narrowings) of urinary tracturinary tract tumors tumors pregnancy etc.). Infection pregnancy etc.). Infection spreads from renal calices to the renal parenchyma.spreads from renal calices to the renal parenchyma.

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Clinical pattern.Clinical pattern. There are latent, recidiving, hypertensive, There are latent, recidiving, hypertensive,

anaemic and asotaemic forms of the anaemic and asotaemic forms of the disease. disease.

Main complaintsMain complaints are elevation of body are elevation of body temperature, chills, pain in the projection temperature, chills, pain in the projection of one or two kidneys, headacheof one or two kidneys, headache general general weaknessweakness fatique fatique dysuria. dysuria.

If the patient develop renal failure, his If the patient develop renal failure, his appetite is lost, nausea, vomiting, thirst appetite is lost, nausea, vomiting, thirst and metheorismus are presentand metheorismus are present. .

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Blood analysis:Blood analysis: anaemia anaemia leukocytosis leukocytosis neutropenia neutropenia and lymphopeniaand lymphopenia thrombocytopenia thrombocytopenia accelerated ESR. accelerated ESR.

UrineUrine:: its density decreases to 1003-1005 its density decreases to 1003-1005 (hypoisosthenuria). Mild proteinuria (to 1 gr(hypoisosthenuria). Mild proteinuria (to 1 gr/l/l), ), leukocyturia. leukocyturia.

Nechiporenko’s and Kakovsky-Addis’ testsNechiporenko’s and Kakovsky-Addis’ tests data: data: leukocyturia prevails before erythrocyturia.leukocyturia prevails before erythrocyturia.

Bacteriologic examination of the urine reveales marked Bacteriologic examination of the urine reveales marked amount of bacteria. amount of bacteria.

Zimnitsky’s testZimnitsky’s test at the beginning of the disease at the beginning of the disease reveales hyposthenuria and later hypoisosthenuria. reveales hyposthenuria and later hypoisosthenuria.

Kreatinine and urea clearance are decreased. The level Kreatinine and urea clearance are decreased. The level of blood kreatinine and urea rise. of blood kreatinine and urea rise.

X-ray, ultrasonic examination and computer X-ray, ultrasonic examination and computer tomographytomography show distension and deformation of renal show distension and deformation of renal calices, asymethry, shrinked kidneys. calices, asymethry, shrinked kidneys.

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TreatmentTreatment:: to avoid overcoolings and viral respiratory to avoid overcoolings and viral respiratory infections; diet № 7 (in exacerbation). In anaemia - food rich infections; diet № 7 (in exacerbation). In anaemia - food rich on iron (strawberrieson iron (strawberries apples); grapes, melon and water- apples); grapes, melon and water-melon. melon.

Antibiotics Antibiotics in 10-12- days courses with breaks for 2-3 in 10-12- days courses with breaks for 2-3 weaks. nalidixic acid derivatives — negramweaks. nalidixic acid derivatives — negram nevigramone; nevigramone; nitrofurantoinsnitrofurantoins biseptol biseptol sulfa-drugs of short action (ethazol sulfa-drugs of short action (ethazol urosulfane). urosulfane).

Vitamins of B groupVitamins of B group, ascorbic acid, ascorbic acid antihistamine antihistamine preparations and spasmolitics. preparations and spasmolitics.

In the case of hypertesion salt intake should be limited tIn the case of hypertesion salt intake should be limited to 4-o 4-66 gr a day gr a day hypotensive drugshypotensive drugs should be prescribed. should be prescribed.

In remission In remission sanatory-resorting treatmentsanatory-resorting treatment is useful . is useful . PrognosisPrognosis is favorable in active treatment and abcense is favorable in active treatment and abcense

of complications. of complications. ProphylaxisProphylaxis of ChP means treatment of chronic infection of ChP means treatment of chronic infection

focci as well as inflammation of urogenital tract, observation focci as well as inflammation of urogenital tract, observation of rules of aseptics and antiseptics during instrumental of rules of aseptics and antiseptics during instrumental examinations (cystoscopy, catheterization etc.).examinations (cystoscopy, catheterization etc.).

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Simple renal cysts demonstrated at MRI The patient had one cyst in each kidney.a) T1-weighted image.b) T2-weighted image. MRI clearly delineates renal cysts. On T1-weighted images the content is signal poor often with a clearly delineated wall, whereas on T2weighted images it is signal intensive, sometimes with edge enhancement

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Figure 32.Adult autosomal dominantpolycystic kidney disease demonstrated at intravenous urography. Both kidneys are enlarged with irregular contours. The pyelocalyceal systems are splayed and deformed.

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Fibromuscular dysplasia. Arteriogram demonstrating several narrowings in the right renal artery of a young woman.