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The role of a doctor-dentist in early diagnostics and
prophylaxis.
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
What do the kidneys do?1. remove toxic wasteproducts2. remove
excess waterand salts3. take part in controllingyour blood
pressure4. produce erythropoietin(epo for short) which stimulates
red cell production from the bone marrow - you get anaemic without
this5. help to keep calcium and phosphate in balance for healthy
bones6. maintain the blood in a neutral (non-acid) state Signs,
which point on kidney affection
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. 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 astone, at his bend, at the trauma of kidneys, kidneys
infarction). Urination disoders Oliguriya (decreasing ofurine
excretion of less than 500 ml per day). Anurya (complete stop
ofurine 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 ) Oedema Often oedema is the first sign of such
diseases.
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 rulethey 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 inslight 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 1106/L per day
(erythrocyturia), leukocyturia - more than 1106/l per day), custs
in urine, bacteriuria, discharging of salts and their cristals with
urine cells of renal andtransitional epithelium and other elements
of pathological both organized and non- organized 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 (hypoproteinemiamostly 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. 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 thepathological 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, andlupus nephritis. Classification (by
L. Pyrih)
The following forms of glomerulonephrites are determined I. Acute
diffuseglomerulonephritis : uric syndrome; nephrotic syndrome
(mostlyhaematuria, hypertension and edema are present). II.
Subacute fulminant glomerulonephritis. III. Quickly progressing
glomerulonephritis. IV. Chronic glomerulonephriis: 1sttype: 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 cut).
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 morerarely etysipelas etc.) caused by
-haemolytic streptococcus, group A or by otherbacteriological
agents(pneumococus,staphylococcus, viruses). The process develops
asa 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. 2.Ischaemia of the
glomeruli;
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
Uric syndrome is presence of proteinin 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
about100200 in a vision field. Hypertension occurs due to
activation of renin-angiotensin-aldosterone and
sympathoadrenalsystems as well as water and salt retenstion in the
organism and inhibition of depressor systems. Blood pressure
elevates from insignificant level till 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:
patients appearance is quite specific and it is called facies
nephritic a: skin paleness, swelling of the face and eyeleads edema
under the eyes, Patients condition is heavy, his posture in bed may
be forced sitting or semirecumbent. Palpation: pulse is full, dull
and slow
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.
iochemical blood analysis increased content of seromucoid, sialic
acids fibrinogen, C-reactive protein, antistreptoliase, immune
complexes,2- -globulines. Instrumental methods of
examination:
Eye grunds: 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 R, depression of ST interval, T is low of biphasic.
X-ray examinationof the chest: probable presence of fluid in
pleural cavity signs of lung congestion, enlargement of the right
ventricle. 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 mothewortbromine tranquilizers) antiadrenergic
preparations (apressin clonidine metildopum, -bloquers) in
combination withsaluretics, 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 thatresulting in secondary
shrinked kidney. Ethiology and pathogenesis. Often ChG develops
after acute glomerulonephritis. If information about AG in patients
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: patients 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 ventricleapex beat
becomes diffuse. Palpation: Apex beat is intensified, diffuse and
displaced leftward
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 inV 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. Chronic glomerulonephritis with nephrotic syndromeis
manifested by decreased diuresis,edema and changes in the blood and
urine: hypo- and dysproteinaemia (hypergammaglobulinaemia,
hypoalbuminaemia), hyperlipidaemia, proteinuria more than3,5 gr/l,
casts in urine (hyaline, granular andrarely - ceraceous (waxy).
Respiratory infections are frequent because of immunodepression
thatprovoke exacerbation of ChG. Eye grounds: retinal
arteriosclerosis hemorrhagias focci of degeneration andaffections
of n. ophthalmicus(neuroretinopathy). In the stage of renal failure
patients 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. Zimnitskys test show hypoisosthenuria, nicturia. Urine
density decreases and become monotonous hypoisosthenuria ( ).
Creatinine and urea content in the blood may be normal.
Proteinuriafrom insignificant till 3-10 gr/l. Casts hyaline
granular and ceraceous. Laboratory examination.
Changes in urine are folowing: compensatory poliuria, nikturia.
Simnitskys test show hypoisosthenuria, nicturia. Urine density
decreases and become monotonous hypoisosthenuria ( ). 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 patients 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.
Simnitskys test show hypoisosthenuria, nicturia. Urine density
decreases and become monotonous hypoisosthenuria ( ). 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 patients 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 to10 gr a day in
nephrotic variant gr a day. Treatment In exacerbation long-standing
treatment is indicated.
Diet 7, limitation of salt intake to10 gr a day in nephrotic
variant gr a day. Medicamentous treatment: In unhypertensive stage
- corticosteroids, cytostatics, aminoquinoline derivatives. In
hypertensionhypotensive 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 mg a day, azathioprine mg a day, heparin Un,
aspirin 0,25 gr. In remission stage sanatorium-resorting treatment
is useful with warm and dry climate, mineral waters. Ifhigh risk of
renal failure and exaggerated asotaemia are presentit is necessary
to perform chronic hemodialisis and transplantation of kidney.
Prognosis.Duration of patients 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 byhematogenic or
ascending ways (thrugh urinary tract). Classification: unilateral
and bilateral, acute and chronic pyelonephritis, primary and
secondary. Primary pyelonephritisoccurs when morphological changes
in urinary tract are abcent. Secondary pyelonephritisoccurs
whenanomalias 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 chills headache unilateral or bilateral dull pain in lumbar
region dysuria. Nusea, vomiting, myalgias and arthralgias are
possible. Patients 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. Pasternatskys 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). Nechiporenkos and
Addis-Kakovskys tests are positive.Sometoimesurine 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: ed mode; diet enriched with milk,
vegetables and fruits. Alkohol, spicy food preserved food coffee
are prohibited. Liquid3 liters a day (wild rose decoction, mineral
water). Antibioticotherapy:) penicillin, semisynthetic
penicillicnes, hentamycin, claforan ets., b) nitrofurantoin
derivatives: nitrofurantoin (0,1 g 34 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
andbladder 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 pyelonephritismay be the result of not effective treatment
of acute pyelonephritis The main wayof penetration of infection
isascending indisorders of urine outflow (kidney stones, anomalias
and strictutes (narrowings) ofurinary 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, hisappetite is lost, nausea,
vomiting, thirst and metheorismus are present. Blood analysis:
anaemia leukocytosis neutropenia and lymphopenia thrombocytopenia
accelerated ESR. Urine: its density decreases to
(hypoisosthenuria). Mild proteinuria (to 1 gr/l),leukocyturia.
Nechiporenkos and Kakovsky-Addis tests data: leukocyturia prevails
before erythrocyturia. Bacteriologic examination of the urine
reveales marked amount of bacteria. Zimnitskys 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 days courses
with breaks for2-3 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: 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:
Severe pain or aching in the back on one or both sides 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 Bloody, cloudy,
orange or smelly urine Burning sensation during urination Chronic
urinary tract infections Depression Disorientation and fatigue Dull
pain in low back (often for days) Feeling or being sick Fever and
chills Frequent urge to urinate (polakyuria) Loss of appetite
Nausea with possible vomiting (like having the flu) Pain in
stomach, back or groin (sometimes severe agony compared to the
pangs of natural childbirth which responds only to some severe pain
medication) 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 cant 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 imageswhile other stone are
translucent (radio-opaque 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 stoneseventually pass on their own
within 48 hours 1,4 . TREATMENT OF RENAL STONES BY EXTRACORPOREAL
SHOCK-WAVE LITHOTRIPSY For kidney stones that do not pass on their
own, a shock waveprocedure called lithotripsy is often used to
break up a large stone into smaller pieces to pass. laser
lithotripsyA 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 available in most hospitals in the world.
PERCUTANEOUS STONE REMOVAL
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
anti-hepatitis 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 wild 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. THANK
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