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Nephrolithiasis
Eva Jančová
Nephrolithiasis
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Renal and ureteral stones are a common
problem in primary care practice
Primary care physicians need to be alert to
the possibility of nephrolithiasis and its
consequences to decide upon a diagnostic
approach, therapy, and refferal to a
urologist or stone specialist
Diagnosis and acute managment
of suspected nephrolithiasis
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Epidemiology
Etiology
Clinical manifestation
Differential diagnosis
Diagnosis
Acute therapy
Evaluation and subsequent treatment
Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
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Etiology
Clinical manifestation
Differential diagnosis
Diagnosis
Acute therapy
Evaluation and subsequent treatment
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Epidemiology
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The prevalence of renal calculi varies with the population
studied
The rate of nephrolihiasis increases with
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Patients discharged from hospital with diagnosis of stones
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1.8 per 10 000
Incidence of stones in general practice
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age (is higher in men compared to woman)
whites compared to blacks
7 per 10 000
General practice incidence of stones in males aged 45–60
years
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21 per 10 000
Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
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Etiology
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Clinical manifestation
Differential diagnosis
Diagnosis
Acute therapy
Evaluation and subsequent treatment
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Etiology
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85% of pts with n. form calcium stones
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The other main types include
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most of which are composed primary of calcium
oxalate
less often calcium phosphate
Uric acid
Struvite (magnesium ammonium phosphate)
Cystine stone
The same pts may have more than one type of
stone currently
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Calcium and uric acid
Major Risk Factors for Calcium
Stones
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Low urine volume
Hypercalciuria
Hypocitraturia
Hyperuricosuria
Dietary factors
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Low fluid intake
Type of fluid intake-soft drinks, apple or grapefruite juice
High protein intake
Low calcium intake
History of prior calcium stones
Hyperoxaluria (eg, enteric hyperoxaluria)
Meddulary sponge disease
Unexplained association with disorders-hypertension,
vasectomy
Other factors affect the risk of
stone formation
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History of prior calcium nephrolithiasis
Family history of nephrolithiasis
Inhanced of entetric oxalate absorption
Urinary tract infection
Medivations /indinavir, sulfadiazine,…)
Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
Etiology

Clinical manifestation
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Differential diagnosis
Diagnosis
Acute therapy
Evaluation and subsequent treatment
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Clinical presentations of urinary
stones
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Pain
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Ureteric colic
Lumbar ache
On micturition
Haematuria
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Sterile pyuria
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Asymptomatic
proteinuria
Dysuria and increased
urinary frequency
Urinary tract infections
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Acute (single or
recurrent attack)
Chronic
Pyonephrosis
Calculus anuria
Strangury and
interruption of urine
stream
Clinical manifestions
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Patients may occasionally be
diagnosed with asymtomatic
nephrolithiasis
The asymptomatic phase is more
likely persist in those who have
never had a clinical episode of
renal colic
Clinical manifestions-Symptoms
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Patients occasionally present after
already having passed gravel or a
stone
Uric acid stones are more likely
present with gravel but they cal
also produce acute obstruction
Clinical manifestions
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Symptoms are usually produced
when stones pass from the renal
pelvis into the ureter
Pain is the most common
symtom and varies from
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a mild and barely noticeable ache,
to discomfort which is so intense
that it requires hospitalization and
parenteral medications
Clinical manifestions-Pain
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The pain typically waxes and wanes in
severity, and develops in waves or
paroxysms that are related to
movement of the stone in the ureter
and associated ureteral spasm
Pain is thought to occur due to
muscular contraction of the ureter in
response to the stone
Clinical manifestions-Pain
The site of obstruction determines the
locaton of pain
 Upper ureteral or renal pelvic obstruction
lead to flak pain or tenderness
 Lower ureteral obstruction causes pain
that may radiate to the ipsilateral testicle
or labia
 The location of the pain may change as
the stone migrates
Clinical manifestions-Pain
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Variable location of pain can be
misleading and occasionally mimics an
acute abdomen or dissecting
Clinical manifestions-Hematuria
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Gross or microscopic hematuria occur in
the majority of patients presenting with
symptomatic nephrolithiasis
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Unilateral flank pain, hematuria, and a
positivity plain of the abdomen are present
in 90 percent of emergency room patients
with a stone
Absence of hematuria in the setting of
acute flank pain does not exclude the
presence of nephrolithiasis
Clinical manifestions
Other symptoms
Nausea
 Vommiting
 Dysuria
 Urgency
Complicantions
 Persistent renal obstruction
 Sepsis
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Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
Etiology
Clinical manifestation
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Differential diagnosis
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Diagnosis
Acute therapy
Evaluation and subsequent treatment
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Differential diagnosis
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Ectopic pregnancy
Aortic aneurysm
Acute intestinal obstruction
Renal carcinoma (bleeding within the kidney)
Diagnosis and acute managment
of suspected nephrolithiasis
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Epidemiology
Etiology
Clinical manifestation
Differential diagnosis
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Diagnosis
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Acute therapy
Evaluation and subsequent treatment
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Diagnosis
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The diagnosis of nephrolithiasis is initially
suspected by clinical presentation
Confirmatory radiologic tests include
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Abdominal plain film (KUB)
Intravenous pyelography (IVP)
Ultrasonography
CT scan (including spiral CT)
MRI
Abdominal plain film (KUB)
Will identify radiopaque stones
 Calcium-containing stones
 Struvite stones
 Cystine stones
Abdominal plain film (KUB)
Advantages
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Readily available
Inxpensive
Limited radiation
Useful in acute setting
Disadvantages
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Requies skilled
radiologist to interpret
Limited sensitivity and
specificity
Intravenous pyelography (IVP)
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High sensitivity and specificity for detection of
stones and provides data about the degree of
obstruction
Intravenous pyelography (IVP)
Advantages
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Useful in planning
therapy and confirming
diagnosis
Long established history
as gold standard
Disadvantages
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Moderately expensive
Intravenous contrast
required
Moderate x-ray exposure
Ultrasonography
Advantages
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Readily available
Roughly equivalent to
IVP as a diagnostic test
Improved sensitivity with
use of color Doppler
No radiation exposure
Good for hydronephrosis
Disadvantages
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Moderately expensive
Poor performance with
small stones
Requires skilled
technician and radiologist
CT scan (including spiral CT)
Advantages
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Probably new gold
standard
Can distinguish
radiolucent stones from
blood and tumor
Disadvantages
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Expensive
Moderate x-ray exposure
Not uniform available
MRI
Advantages
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Great potential for
localizing sight of stone
in ureter
Disadvantages
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Vera expensive
Largely investigational
so far except in certain
centres
Results of diagnostic imaging in patients
presenting with renal colic
Sites of calcific lesions which may be confused with
radio-opaque urinary stones:
 gallstones, costal cartilages, mesenteric lymph
nodes, adrenals, pancreas, renal and splenic
arteries, pelvic veins.
The radiotranslucent stones
 uric acid, xanthine, oxipurinol, 2,8dihydroxyadenine, orotic acid, and triamterine.
Finely stippled nephrocalcinosis suggests
 long-standing hypercalcaemia
Dense coarse nephrocalcinosis suggests
 primary hyperoxaluria or renal tubular acidosis.
Results of diagnostic imaging in patients
presenting with renal colic
Obstructive uropathy due to:
 Radio-opaque stone
 Radiotranslucent obstructive lesion (stones,
crystals, sloughed papillae, clots, carcinoma)
 Generalized nephrocalcinosis
 Medullary sponge kidney
 Renal papillary necrosis (sloughed papilla)
 Cortical scars due to chronic pyelonephritis
 Renal carcinoma (cause of ‘clot colic’)
 Coincidental calcific lesion (e.g. tuberculosis,
Randall’s plaques)
Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
Etiology
Clinical manifestation
Differential diagnosis
Diagnosis
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Acute therapy
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Evaluation and subsequent treatment
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Acute Therapy
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Pain control
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Nonsteroidal antiinflammatory drugs
(NSAIDs)
Narcotics
Hydration
Urology consultation
Acute Therapy
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Patients can be managed at home if they
are able to take oral medications and fluids
Hospitalization is required for those who
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cannot tolerate oral intake
have very severe pain
Acute Therapy
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Hospitalization is required for those who
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cannot tolerate oral intake
have very severe pain
Urology consultation
Urgent urologic consultation is warranted in patients
with
 Urosepsis
 Acute renal failure
Outpatient urology referral is indicated in patients
 Who fail to pass the stone after a trial of
conservative management (usually two to four
weeks)
 A stone more 5mm in diameter
 Uncontrolled pain
Diagnosis and acute managment
of suspected nephrolithiasis

Epidemiology
Etiology
Clinical manifestation
Differential diagnosis
Diagnosis
Acute therapy
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Evaluation and subsequent treatment
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Evaluation and subsequent treatment
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The patient shoud be evaluated for possible
underlying causes of stone disease
These include:
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Hypercalcemia
Hypercalciuria
Hyperuricosuria
Hypocitraturia
Hyperoxaluria
Evaluation and subsequent
treatment-Calcium stones
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Composed purely or predominantly of calcium
oxalate can occur in many differënt disordes
Calcium phosphate stones are associated with the
same risk factors as calcum oxalate stones. One
exception- calcium phosphate stones are more
typical of complete or incomplete distal renal
acidosis
Calcium stones
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Oxalate crystals
Urinary risk factors for idiopathic
calcium stones
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Low volume, which increased the concentrations
of the lithogenic factors
Hypercalciuria, with or without hypercalcemia
Hyperuricosuria, which in calcium oxalate-stone
formers, is usually due to increased protein intake
and therefore uric acid production
Hypocitraturia, which can be marked in patients
wih chronic metabolic acidosis
Hyperoxaluria, which may be present in up to 40
percent of male and 15 percent of female stone
formers
Defects of macromolecular inhibitors
Urinary risk factors for idiopathic
calcium stones
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Calcium stone formation is most often
idiopathic, but can occur a number of other
disorders.
Underlying systemic or renal
disorders in calcium stone
disease
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Primary hyperparathyroidism
Medullary sponge kidney
Distal renal tubular acidosis (complete or
incomplete)
Sarcoidosis (and other granulomatous diseases)
Hyperoxaluria
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Enteric
Primary
Evaluation and subsequent
treatment-Uric acid stones
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Pure uric acid stones primary occur in patients in
whom a persistently acid urine promotes uric acid
precipitation
In the absence of gout, uric acid stones may be
seen other causes of chronic overproduction of
uric acid or in chronic diarrheal states in which
bicarbonate loss and volume depletion lead to a
concentrated, acid urine
Caused of Secondary due to increased
Purine Biosynthesis and/or Urate
Production
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Inherited enzyme defects leading to purine
overproduction
Clinical disorders leading to purine and/or
overproduction
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Myeloproliferative disorders
Lymfoproliferative disorders
Malignancies
Hemolytic disorders
Psoriasis
Obesity
Tissue hypoxia
Down Syndrome
Glycogen storage diseases (type III,V,VII)
Caused of Secondary due to increased
Purine Biosynthesis and/or Urate
Production-continue
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Drug-,diet, or toxin-induced purine and /or urate
overproduction
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Ethanol
Excessive dietary purine ingestion
Pancreatic extract
Fructose
Vitamin B12 (pts with pernicious anemia)
Nicotinic acid
Cytotoxic drugs
Warfarin
Evaluation and subsequent
treatment-Struvite stones
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Struvite stones only form in pts with a chronic
urinary tract infection due to a urease production
organism such as Proteus or Klebsiella
The stone may grow rapidly over a period of
week to months and, if not, adequately treated,
can develop into a staghorn or branched calculus
involving the entire renal pelvis and calyces
Evaluation and subsequent
treatment-Cystine stones
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Cystine stones developt in pts with
cystinuria due to the insolubility of cystine
in the urine
The diagnosis of cystinuria is made from
the family history, by identification of the
pathognomonic hexagonal cystine crystal
on urinalysis
Cystine stones
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Typical hexagonal
crystals of cystine
under (a) nonpolarized and (b)
polarized light.
Focused History
All pts with a first stone should undergo a focused
history to identify stone risk factors such as a
family history of stone disease and certain dietary
habits
 Low fluid intake (high concetration of lithogenic
factors)
 High animal protein diet (which can lead to
hypercalciuria, hyperuricosuria, hypocitraturia
 High salt diet (which increases urinary calcium
excretion)
 Increased intake of oxalate-containing foods
 Vitamin D supplements
Investigations in a Calcium
Stone-former
Blood tests
 Serum calcium 2-3x
 Serum uric acid
 Serum bicarbonate
 Serum creatinine (electrolytes)
 PTH
Investigations in a Calcium
Stone-former
Urinalysis
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Urine microscopy and culture
Urine pH
24-hour collections (2-3x)
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Volume
pH
creatinine
calcium
oxalate
uric acid
citrate
(sodium)
(urea)
Methods for stone analysis
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Wet chemical analysis (qualitative or
quantitative)
Optical crystallography
X-ray diffraction
Thermogravimetric analysis
Scanning electron microscopy
IR spectroscopy
Evaluation and subsequent treatment
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Subsequent therapy is based upon the type of
stone and the biochemical abnormalities that are
present
Therapy to prevent new stone formation is
required:
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All pts shoud increase fluid intake to above 2L/day,
including drinking at night
Pts with calcium stones can be treated with a
thiazide diuretic and low sodium diet for
hypercalciuria, allopurinol for hyperuricosuria, and
potassium citrate for hypocitraturia
Evaluation and subsequent treatment
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Therapy to prevent new stone formation is
required-continued:
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Pts wit uric acid stones can bez treated with
potassium citrate to alkalinize the urine ao
allopurinol
Pts with cystine stones can be treated with high fluid
intakem urinary alkalinizatin, and drugs such as
penicillamine or captopril
Treatment of struvite stones is difficult
Causes of macroscopic
nephrocalcinosis (cortical x
medullary)
Cortical
 Chronic glomerulonephritis
 Acute cortical necrosis
 Chronic pyelonephritis
 Benign nodular subcapsular
Nephrocalcinosis
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Cortical
nephrocalcinosis
(necropsy specimen)
Causes of macroscopic
nephrocalcinosis (cortical x
medullary)
 Oxalosis
Medullary
 Autonomous
hyperparathyroidis
 Milk alkali syndrome
 Hypervitaminosis D
 Sarcoidosis
 Idiopathic hypercalciuria
 MacGibbon–Lubinsky
syndrome
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Distal renal tubular
acidosis
Acetazolamide
Dent's disease
Hypomagnesaemiahypercalciuria
syndrome
Medullary sponge kidney
Renal papillary necrosis
Others (Williams' and
Bartter's
Nephrocalcinosis
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Medullary
nephrocalcinosis in a
25-year-old man with
familial distal renal
tubular acidosis.
Prognosis for overall renal
function-continue
Best
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Idiopathic hypercalciuria
Medullary sponge kidney
Distal renal tubular acidosis
Autonomous hyperparathyroidism and other
rectifiable hypercalcaemias
Papillary necrosis
Dent’s disease/X-linked recessive nephrolithiasis
Hypomagnesaemia–hypercalciuria (Michelis–Manz)
syndrome
Worst
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Primary hyperoxaluria, type 1
Renal Neoplasms
Renal Cell Carcinoma
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Primary renal neoplasms
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Renal cell carcinoma (80-85%)
Transitionla cell carcinoma (6%)
Oncocytomas
Collecting duct tumors
Rema sarcomas
Nephroblastomas
Secundary renal neoplasms
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Rarelly
Clinical features
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Hematuria
Abdominal or flan mann
Scrotale varicocele
Vena cava involvement (ascies, hepatic
dysfunction, pulmonary emboli)
Systemic or paraneoplastic syndroms
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Fever
Cachexia
Amyloidosis
Anemie
Hepatic dysfunction
Erythrocytosis and thromocytosis
Hypercalcemia
Polymyalgia-like syndrome