Download What is glomerulonephritis?

Glomerulonephritis and pyelonephritis. Urolithiasis.
Etiology, pathogenesis. Diagnostics. Clinical picture.
Complications. Principles of treatment.
The role of a
doctor-dentist in
early diagnostics
and prophylaxis.
As. of prof. Vereshchahina N.Y.
•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 nonorganized renal sediments,
• The leading symptom in uric
syndrome is proteinuria (albuminuria).
(custs
in urine)
(sieges)
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.
Types of glomerulonephritis
include kidney disease of
diabetes, IgA nephropathy, and
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.
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, aedema
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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 renin-angiotensinaldosterone 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.
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
•
(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.
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.
Laboratory examination.
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.
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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 performed 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
• 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).
• 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.
• 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.
• 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:
• 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 pyelonephriti (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
• 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.
• 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.
• 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.).
Urolithiasis
is the condition where
urinary calculi are formed
or located anywhere in
the urinary system, or
the process of forming
stones in the kidney,
bladder, and/or ureters
(urinary tract).
Urinary stones are typically classified by their
location in the kidney (nephrolithiasis), ureter
(ureterolithiasis), or bladder (cystolithiasis)
Predisposing factors for Stone Formation
(Who gets kidney stones?)
 Abnormal urinary pH:
 Allergies:
 Avoid L-Cysteine if you have a genetic
disposition to stones.
 B Vitamin and Magnesium Deficiency:
 Cadmium:
 Calcium Supplements:
 Chemotherapy:
 Cystinuria:
 Dehydration:
 Drug Overdose;
 Diabetes:
 Essential Fatty Acid Deficiencies:
 Excess Sugar:
 Genetic Predisposition in Humans:
 Gout:
 Having very poor mobility;
 Heavy Metal Poisoning:
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Hypercalciuria:
Hyperoxaluria:
Hyperurcosuria:
Medications:
Metabolic disorders like
Overuse of Aspirin;
People who have been
catheterized for long periods of
time;
Previous History of Stones:
Red meat:
Salt Intake:
Some medications;
Too much Alcohol:
Too much caffeine:
Draws minerals from the body
and acts as a diuretic;
Too much Vitamin D:
Symptoms of Kidney and Bladder Stones include:
1. Severe pain or aching in the back on one or both sides
2. Sudden spasms of excruciating pain (renal or uteric colic) usually starting in the
back below the ribs, before radiating around the abdomen, and sometimes to the
groin and genitalia (see diagram for referred pain because referred pain is often
missed
3. Bloody, cloudy, orange or smelly urine
4. Burning sensation during urination
5. Chronic urinary tract infections
6. Depression
7. Disorientation and fatigue
8. Dull pain in low back (often for days)
9. Feeling or being sick
10. Fever and chills
11. Frequent urge to urinate (polakyuria)
12. Loss of appetite
13. Nausea with possible vomiting (like having the flu)
14. Pain in stomach, back or groin (sometimes severe agony compared to the pangs of
natural childbirth which responds only to some severe pain medication)
15. Straining to urinate (we call it stranguria) or difficult urination (dysuria)
Symptoms and signs of a kidney stone include excruciating, cramping pain
in the lower back and/or side, groin, or abdomen as well as blood in the urine.
Diagram showing the
typical location of renal
colic, below the rib cage
to just above the pelvis
Referred pain from kidneys
necessary examinations
Blood tests – to identify excess amounts of certain
chemicals related to the formation of stones .
ECG- Can show heart rate and rhythm abnormalities if the
stones are caused by an increase in certain minerals (but this
choice of diagnostic technique would not be common).
Imaging techniques which involve an injection of a special
dye that shows up the whole urinary system on x-ray images,
revealing stones that can’t usually be seen. Examples are:
Urinalysis - to look for signs of infection, crystal formation,
determine ph (see urinalysis handout.)
necessary examinations
Excretory urography – where a contrast agent is injected into the
blood stream and is then cleared by the kidneys, outlining the kidney,
ureters and urinary bladder.
Renal angiography – where contrast agents are injected into the
renal artery to assess the blood flow to the kidney.
Retrograde urethrocystography – where contrast agent is
injected into the urethra to outline the urethra and urinary bladder.
Taking an x-ray image – stones that contain calcium usually show
up white on x-ray images while other stone are translucent (radioopaque which means you need additional tests).
Ultrasound scan – this uses high frequency sound waves to produce an
image of the internal organs.
CT Scan (Non-contrast helical computerized tomography) – this
produces pictures from a series of x-ray images taken at different
angles – it is sometimes used to diagnose kidney stones, and is thought
to be the most accurate diagnostic test.
Urinary stones are classified by their
chemical composition (calcium-containing,
struvite, uric acid, or other compounds)
The most common types of stone is calcium
oxalate (dihydrate) - spicules, while the
hardest stone is cystine monohydrate.
Other stone compositions include triple
phosphate, ammonium, magnesium, urate
calcium, oxalate, urate, xanthine, etc.
Calcium oxalate stones – the most common type of stone
staghorn stone
Depending on the size, most stones eventually pass on their own within 48 hours
На фото оксалатний камінь
нирки розміром 1,4см
пацієнтки М.
Оксалатний камінь
TREATMENT OF RENAL STONES BY
EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY
For kidney stones that do not pass on their own, a shock wave
procedure called lithotripsy is often used to break up a large stone into
smaller pieces to pass
.
laser lithotripsy A laser
fiber is inserted through the
working channel of the
scope, and laser is directly
emitted to the stone. The
stone is disintegrated and
the remaining pieces are
washed out of the urinary
tract.
This procedure is done
under either local or general
anesthesia and is considered
minimally invasive surgery.
This procedure is widely
PERCUTANEOUS
STONE REMOVAL
Черезшкірна нефролитотрипсії
A nephroscope may
be inserted through a
nephrostomy tract to
remove a stone from
the renal pelvis. An
ultrasound probe
may be used to
fragment a staghorn
calculus.
Conducting
ureteral
catheterization
0.018
hydrophilic
guide photo
Phillantus Niruri (Stone Breacker,quiebra piedra,Chanka
Piedra,Chanca Piedra)
Phyllanthus Niruri
Phyllanthus Niruri Extracts of this herb have shown
promise in treating a wide range of human diseases.
Some of the medicinal properties suggested by
numerous preclinical trials are anti-hepatotoxic,
anti-lithic, anti-hypertensive, anti-HIV and antihepatitis B. However, human trials have yet to show
efficacy against Hepatitis B virus.
The herbal plant has long been used in Brazil and
Peru as an herbal remedy for Kidney stones.
Research among sufferers of Kidney stones has
shown that, while intake of Phyllanthus niruri didn't
lead to a significant difference in either stone
voiding or pain levels, it may reduce urinary calcium,
a contributing factor to stone growth.In addition,
one study conducted on rats showed that an
aqueous solution of Phyllanthus niruri may inhibit
kidney stone growth and formation in animals who
already have stones.
To help prevent kidney stones, drink enough water to keep your urine clear.
Dietary choices can affect kidney stone development.
Weight gain can increase the risk of kidney stones.
bearberry
parsley
watermelon
d carrot
field horsetail
Figure 32.
Adult autosomal dominant
polyeystic 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.
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