Transcript Document

THE MAIN SYMPTOMS AND SYNDROMES
IN KIDNEY DISEASES.
SYMPTOMS OF ACUTE AND CHRONIC
GLOMERULOENPHRITIS AND PYELONEPHRITIS.
•What do the kidneys do?
1. remove toxic waste
products
2. remove excess water
and salts
3. take part in controlling
your blood pressure
4. produce erythropoietin
(epo for short) which stimulates red cell production
from the bone marrow - you get anaemic without this
5. help to keep calcium and phosphate in balance for
healthy bones
6. maintain the blood in a neutral (non-acid) state
Signs, which point on
kidney affection
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pain in lumbar region,
urination disoders,
change of urine,
oedema.
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• secondary
chills,
headache,
dizziness,
vision deranged,
heart pain,
skin itching,
loss of appetite,
nausea,
vomiting ,
fever.
Pain in lumbar region
Pain 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).
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)
Oedema
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.
Uric syndrome.
• moderate proteinuria (from 100 mg up to 3,5 g
a day),
• red blood cells in the urine more than 1106/L
per day (erythrocyturia),
• leukocyturia - more than 1106/l per day),
• custs in urine,
• bacteriuria,
• discharging of salts and their cristals with urine
• cells of renal and transitional — epithelium
and other elements of pathological both
organized and non- organized renal sediments,
• The leading symptom in uric syndrome is
proteinuria (albuminuria).
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.
Renal arterial hypertension.
This is symptomatic hypertension caused by affection
of kidneys or renal vessels with following disorders of
blood pressure regulation.
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Elevation of blood pressure is caused by 3 mechanisms:
1.sodium and water retention,
2.activation of pressor system,
3.inhibition of depressory mechanisms.
Acute nephritic syndrome.
It is characterized by the abrupt onset (days)
of haematuria with red blood cells, casts or
dysmorphic red blood cells appearing in
the urine, proteinuria, renal impairement
(oliguria, uremia, raised urea and creatitine),
hypertension due to water and salt
retention, edema (usually periodical).
What is glomerulonephritis?
• Diffuse glomerulonephritis is the general
infectious-allergic disease with prevalent and
primary envolvement of nephrone glomerular
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.
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Types of glomerulonephritis include kidney
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disease of diabetes, IgA nephropathy, and
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lupus nephritis.
Classification (by L. Pyrih)
• The following forms of glomerulonephrites are determined
• I. Acute diffuse glomerulonephritis :
• uric syndrome;
• nephrotic syndrome (mostly haematuria, hypertension and
edema are present).
• II. Subacute fulminant glomerulonephritis.
• III. Quickly progressing glomerulonephritis.
• IV. Chronic glomerulonephriis:
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1st type: primary chronic, secondary chronic.
2. syndromes: uric, nephrotic.
3. stages:
non-hypertensive, hypertensive;
chronic renal failure;
4. phase: exacerbation, remission.
Acute glomerulonephritis
(AG, lat. - glomerulonephritis аcutа).
• This is acute immune inflammatory lesion of
kidneys parenchima with primary damage of
glomerules and following involvement of all
renal structures into the pathological
process.
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Ethiology and pathogenesis
AG develops 2-3 weeks after acure
infectious disease (tonsillitis
pharyngitis skarlet fever more
rarely —etysipelas etc.) caused by
-haemolytic streptococcus, group A
or by other bacteriological agents
(pneumococus, staphylococcus,
viruses).
• The process develops as a hyperergic reaction of sensebilized organism.
• Administration of serum preparations, other medical preparations,
vaccination, penetration of toxic substances into the organism, deranged
venous outflow from kidneys may be the causes of AG.
• Provoking factors are overooling, dump weather, traumas.
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.
This symptoms are combined in following
syndromes: hypertension, uric syndrom, edema
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Uric syndrome is presence of protein in the urine, blood
formed elements, casts.
Even at the beginning of the disease urine colour is changed
because of blood admixtures. Urine has the colour of “meet
wastes”. Erythrocytes quantity at the peak of the disease is
about 100—200 in a vision field.
Hypertension occurs due to activation of reninangiotensin-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.
Data of general inspection:
 patient’s
appearance is quite specific
and it is called “facies nephritic a”:
 skin paleness,
 swelling of the face and eyeleads
edema under the eyes,
 Patient’s
condition is heavy, his
posture in bed may be forced —
sitting or semirecumbent.
Palpation: pulse is full, dull and slow. Apex
beat is intensified and displaced leftward.
Percussion: may reveal fluid in pleural
cavity, lung congestion and displacement of
left heart border leftward.
Auscultation: bradicardia, I heart sound is
weakened, systolic murmur over heart apex,
accentuation of the II heart sound over
the aorta.In severe cases especially in left
ventricular hyperthrophy hallop rhythm
occurs. Vesicular breathing is heard over
the lungs.
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.
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.
Treatment:
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bed regimen for 1-15 months dry and warm ambient
temterature.
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Diet № 7, limitation of salt ( to 05-15 gr a day) liquid.
Medicamentous treatment — antibiotics for 7-10 days
(penicillin or semisynthetic penicillins).
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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).
Chronic glomerulonephritis
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(glomerulonephritis chronica, ChG) is
inflammatory process in renal glomeruli
degeneration of canalicular epithelium and
progressive development of connective tissue
that resulting in secondary shrinked kidney.
Ethiology and pathogenesis.
Often ChG develops after acute
glomerulonephritis. If information about AG in
patient’s anamnesis is abcent than thay speak
about primary form of ChG
Clinical picture.
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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.
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.
Palpation: Apex beat is intensified, diffuse and
displaced leftward.
Percussion: the left border of relative heart dullness
is displaced leftward from the left midclavicular line
in V interspace.
Palpation of organs of abdominal cavity: is painful in
epigastrium and above the large bowel. In the case of
right ventricular failure the liver is enlarged.
Auscultation: in patients with left ventricular failure
moist rales may be heard in lover parts of the lungs
(because of lung congestion).
Heart soungs are intensified but later become weakened,
accenttuation of the II sound is heard over the aorta,
systolic murmur over the apex. In terminal stage
pericardial friction sound may be haerd on the hart basis,
along the left sternal border and in zone of absolute heart
dullness.
Blood pressure is elevated up to 200/120 mm Hg. If heart
failure develops systolic pressure may decrease but
diastolic one is steel high.
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Chronic glomerulonephritis with nephrotic
syndrome is manifested by decreased
diuresis, edema and changes in the blood
and urine: hypo- and dysproteinaemia
(hypergammaglobulinaemia,
hypoalbuminaemia), hyperlipidaemia,
proteinuria more than 3,5 gr/l, casts in urine
(hyaline, granular and rarely - ceraceous
(waxy). Respiratory infections are frequent
because of immunodepression that provoke
exacerbation of ChG.
Eye grounds: retinal arteriosclerosis hemorrhagias
focci of degeneration and affections of n.
ophthalmicus (neuroretinopathy).
In the stage of renal failure patient’s condition is
heavy. Forced posture (sitting). Deranged
conscioussness, sometimes coma. Main complaints
are nausea, vomiting, skin dryness and itching,
deranged vision, oliguria or anuria.
Laboratory examination. Changes in urine:
compensatory poliuria, nikturia. Zimnitsky’s test show
hypoisosthenuria, nicturia. Urine density decreases
and become monotonous hypoisosthenuria (10091012). Creatinine and urea content in the blood may
be normal.
Proteinuria from insignificant till 3-10 gr/l. Casts —
hyaline granular and ceraceous.
Laboratory examination.
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Changes in urine are folowing: compensatory poliuria,
nikturia. Simnitsky’s test show hypoisosthenuria,
nicturia. Urine density decreases and become
monotonous hypoisosthenuria (1009-1012). Due to
poliuria products of nitrogen metabolism is possible to
evacuate from the organism that is why kreatinine and
urea content in the blood may be normal.
Proteinuria develops. Its degree may be from
insignificant till 3-10 gr/l. It depends on patient’s diet,
physical loading, overcooling etc. On urine sediments
there are casts — hyaline granular and ceraceous.
Treatment is perormed taking into account
clinical variant of the disease, its phase
and stage.
Patient should avoid overcoolings,
physical loadings, psychoemotional
stresses.
In exacerbation long-standing treatment
is indicated. Diet № 7, limitation of salt
intake to 10 gr a day in nephrotic
variant - 6-8 gr a day.
Treatment
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In exacerbation long-standing treatment is indicated.
Diet № 7, limitation of salt intake to 10 gr a day in nephrotic variant
- 6-8 gr a day.
Medicamentous treatment: In unhypertensive stage - corticosteroids,
cytostatics, aminoquinoline derivatives. In hypertension
hypotensive drugs also should be prescrobed (-bloquers
methyldopum, apressin etc.).
Diuretics (furosemide ethacrynic acid, hydrochlorothiazide) in
edema;
Anticoagulants and antiaggregants (heparin curantyl indometacin)
Hemosorption, plasmapheresis.
If infection develops than antibiotics are administered.
Nephrotic syndrome is indication for administration of prednisolone
30-80 mg a day, azathioprine – 100-150 mg a day, heparin – 1000015000 Un, aspirin – 0,25 gr.
In remission stage – sanatorium-resorting treatment is useful with
warm and dry climate, mineral waters.
If high risk of renal failure and exaggerated asotaemia are present it
is necessary to perform chronic hemodialisis and transplantation of
kidney.
Prognosis.
Duration of patient’s life depends
on clinical form of ChG and
functional condition of kidneys.
In the stage of chronic renal failure
patients
are
disable.
Prophylaxis
includes
in-time
treatment of acute and chronic focci
of infection as well as treatment of
exacerbations,
dyspancery
observation.
Pyelonephritis
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Pyelonephritis is a bacterial infection of one or both
kidneys.
Ethiology: E. Coli, streptococci, staphylococci,
proteus and differrent bacterial assotiations,
sometimes it may be caused by viruses
Provoking factors: disorders of urine outflow
(congenital anomalias, stones, obstruction,
pareses, paralises etc.); metabolic disorders
(diabetes mellitus, gout); iatrogenic diseases
(catheterization, cystoscopy); immunodepression
(chronic diseases, focci of infection, overcooling).
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Pathogenesis: Penetration of microorganisms to
calicules and renal interstitium by hematogenic
or ascending ways (thrugh urinary tract).
Classification: unilateral and bilateral, acute and
chronic pyelonephritis, primary and secondary.
Primary pyelonephritis occurs when
morphological changes in urinary tract are
abcent.
Secondary pyelonephritis occurs when
anomalias of kidneys and urinary tract are
present which cause disorders of urine outflow
(narrowing of ureters or urethra, stones
nephroptosis adenoma of prostatic gland etc.).
Acute pyelonephritis devides on serous and
purulent.
Clinical pattern.
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Acute pyelonephritis (AP) starts from elevation of
body temperature up to 38-39С chills headache
unilateral or bilateral dull pain in lumbar region
dysuria. Nusea, vomiting, myalgias and arthralgias
are possible. Patient’s condition is heavy, toxic
shock may develop. Respiration is frequent,
vesicular. Tachicardia is present.
Tongue is dry and coated. Herpes labialis. Urination
is frequent painful sometimes urinary retention
develops. Pasternatsky’s symptom is positive on
the affected side.
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Urine relative density is decreased (1012-1015)
Poliuria is possible.
Urine reaction is acid. Leukocyturia and
bacteriuria are typical. Non-significant
haematuria and proteinuria (till 1 gr/l), casts in
urine (hyaline granular and epythelial).
Nechiporenko’s and Addis-Kakovsky’s tests are
positive.Sometoimes urine is of alkaline
reaction and of unpleasant smell, becomes
cloudy, salt sediments and purulent flakes are
present is it.
Microscopic examination: leukocytes, granular
custs and erythrocytes on all fision fields.
Treatment:
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Вed mode; diet enriched with milk, vegetables and fruits.
Alkohol, spicy food  preserved food coffee are prohibited.
Liquid 3 liters a day (wild rose decoction, mineral water).
Antibioticotherapy: а) penicillin, semisynthetic
penicillicnes, hentamycin, claforan ets., b) nitrofurantoin
derivatives: nitrofurantoin (0,1 g 3—4 tablets a day 7-10
days), biseptol-480 (2 tablets 2-3 times a day 2-3 weaks).
Spasmolithics and diuretics.
In heavy cases catheterization, lawage of calices and
bladder with desinfectant solutions.
Chronic pyelonephritis
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Chronic pyelonephritis (pyelonephritis chronica, ChP ) is a
chronic non-specific inflammation of renal interstitium and
calicular mucosa with following affection of renal vessels.
Ethiology and pathogenesis. Chronic pyelonephritis may be
the result of not effective treatment of acute
pyelonephritis. Provoking factors of ChP: urine congestion,
inflamatory diseases of female sexual organs, appendicitis,
urolithiasis, diabetes mellitus, chronic intoxications,
inhibition of immune system.
The main way of penetration of infection is ascending in
disorders of urine outflow (kidney stones, anomalias and
strictutes (narrowings) of urinary tract tumors pregnancy
etc.). Infection spreads from renal calices to the renal
parenchyma.
Clinical pattern.
There are latent, recidiving, hypertensive,
anaemic and asotaemic forms of the disease.
Main complaints are elevation of body
temperature, chills, pain in the projection of
one or two kidneys, headache general
weakness fatique dysuria.
If the patient develop renal failure, his appetite
is lost, nausea, vomiting, thirst and
metheorismus are present.
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Blood analysis: anaemia leukocytosis neutropenia and
lymphopenia thrombocytopenia accelerated ESR.
Urine: its density decreases to 1003-1005 (hypoisosthenuria). Mild
proteinuria (to 1 gr/l), leukocyturia.
Nechiporenko’s and Kakovsky-Addis’ tests data: leukocyturia
prevails before erythrocyturia.
Bacteriologic examination of the urine reveales marked amount of
bacteria.
Zimnitsky’s test at the beginning of the disease reveales
hyposthenuria and later hypoisosthenuria.
Kreatinine and urea clearance are decreased. The level of blood
kreatinine and urea rise.
X-ray, ultrasonic examination and computer tomography show
distension and deformation of renal calices, asymethry, shrinked
kidneys.
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Treatment: to avoid overcoolings and viral respiratory infections;
diet № 7 (in exacerbation). In anaemia - food rich on iron
(strawberries apples); grapes, melon and water-melon.
Antibiotics in 10-12- days courses with breaks for 2-3 weaks.
nalidixic acid derivatives — negram nevigramone; nitrofurantoins
biseptol sulfa-drugs of short action (ethazol urosulfane).
Vitamins of B group, ascorbic acid antihistamine preparations and
spasmolitics.
In the case of hypertesion salt intake should be limited to 4-6 gr a
day hypotensive drugs should be prescribed.
In remission sanatory-resorting treatment is useful .
 Prognosis is favorable in active treatment and abcense of
complications.
 Prophylaxis of ChP means treatment of chronic infection focci as
well as inflammation of urogenital tract, observation of rules of
aseptics and antiseptics during instrumental 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
Figure 32.
Adult autosomal dominant
polycystic kidney disease
demonstrated at
intravenous urography.
Both kidneys are enlarged
with irregular contours.
The pyelocalyceal systems
are splayed and deformed.
Intravenous
urography
demonstrating
crossed
renal ectopy.
The "left"
kidney
is located
below
the right
kidney.
Fibromuscular
dysplasia.
Arteriogram
demonstrating
several
narrowings
in the right
renal artery
of a young
woman.
Arteriosclerosis.
Arteriogram
demonstrating
arteriosclerosis in
the lower
abdominal aorta
and a stenosis
(narrow)
of the left renal
artery dose to the
aorta.