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Table of contents :
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,
which causes local supersaturation and crystallization of calcium and magnesium
phosphates as carbonate apatite (Ca10(PO4)6
.
CO3)
and struvite (MgNH4PO4
.
6H2O),
respectively. This effect may also be enhanced by bacterial LPS : macromolecules
of such kind contain negatively charged residues that are able to bind
Ca2+ and Mg2+, leading to the accumulation of these
ions around bacterial cells, either enhancing or inhibiting the crystallization
of struvite and apatite, depending on its chemical structure and ability
to bind cations
associated with high urinary pH.
Patients with struvite stones may present with acute flank pain or remain
completely asymptomatic.
if ureteral catheter obstruction or percutaneous nephrostomy
(useless in ureteral lithiasis unless ureter is dilated)
for terminal ureter
(location, size, morphology, and parenchymal cavities) : if patient has
renal
failure replace with ascending
(urethrocystouretero)pyelography
and urease-inhibitors (acetohydroxamic acid and fluorofamide) in urinary
infection stones
(risk of perirenal hematomas),
local pain, and tenderness on pressure
),
and intracranial
aneurysm.
It occurs in 2 unrelated forms :.
In older children cystic and fibrotic disease of the liver may be associated.
CDK
inhibitor
roscovitine is effective in murine modelsref
after adolescence
or necropsy, located in the cortex, solitary or multiple, with number
increasing with age; no malignant transformation; when very large they
may break or cause compression atrophy
in disseminated
intravascular coagulation
causes acute cortical necrosis (whole renal cortex is involved)
due to or associated with renal disease with a factor of parenchymal ischemiaref
is positive only when the homolateral kidney is analyzed in 2 separate
regions
confirms severe stenosis in the upper branch of the homolateral renal artery
due to insertion/deletion polymorphism in intron 16)
in the first third (most) or ostium (30%) of renal artery (55-70%, > 90%
in elderlies), bilateral in 33%),
coronary
arterial disease (CAD),
and sometimes systemic
arterial hypertension
experimentally induced with clamping that causes a Goldblatt kidney). The
ischemic kidney incretes more renin => hyperreninemic
hyperaldosteronism
=> systemic vasoconstriction => systemic
arterial hypertension.
The contralateral kidney has renin incretion suppressed and pressure
natriuresis.
reduces filtration in the unaffected kidney => hypercreatininemia
(sensitivity = 80-85%, usually diagnosed as >/< 60%; specificity = 90-95%)
detects dimensional asymmetry of kidneys with conserved normal
shape (differential diagnosis with tubulointerstitial
nephropathies where scars deformate renal parenchyma)
(not nephrotoxic contrast enhancement agent : can't assess distal segments
of renal artery => reduced sensitivity in fibrodysplasia, poor visualization
of small accessory renal arteries, artifacts in presence of stents)
(pay attention to contrast enhancement media chosen !)
(nephrotoxic contrast enhancement agent; preferred to MRA in patients with
stents)
or AT1a antagonists
don't prevent nephrosclerosis and may cause ARF in patients with bilateral
stenosis or single kidney with stenotic renal artery => diuretics
+ b1-blockers
or a1/b1-blockers
OR CCBs
(PTRAS) (efficacy similar to classical surgery) in ostial atherosclerotic
stenoses or in restenosis after PTRA.
Onset occurs a few weeks (differential diagnosis with ATN
!) after angiography
(2% : aortography, arteriography), angioplasty, or vascular surgery and
maybe spontaneous or after antiplatelet
or thrombolytic
therapy due to inference in plaque healing.
,
eosinophils in urine sediment.
(decrease foreign body reaction ?) allow improvement (differential diagnosis
with ATN which is self-limiting
within 3 days and leads to full recovery within 1 week)
,
pallor
(defined a posteriori as cured or improved by tratment of renovascular
disease)
(sensitivity = 83-95%; specificity = 81-100%).
Cyclosporine, cyclophosphamide, plasmapheresis, protein A immunoabsorption,
and mycophenolate mofetil have been variably effectiveref1,
ref2
: recurs in about 30% of patients who undergo for this condition and leads
to the nephrotic syndrome and accelerated
graft lossrefref
in individuals with VEGF
I allele (-2549 promoter SNP) and Z+2 5'aldose-reductase-like
(ALDRL2) allele in which there is glomerular mesangial expansion
with either,
systemic
arterial hypertension,
chronic
renal failure, and retinopathy
,
microangiopathies, and scleroderma
common in old age
(hypertensive nephrosclerosis),
with insidious onset, cylindruria, edema,
hypertrophy of the heart, degeneration of the renal tubules, and glomerulonephritis,
resulting in chronic renal failure,
congestive
heart failure (CHF),
and cerebral hemorrhage.
2 types are distinguished;
in younger persons, it may occur in patients with diabetes
mellitus
with a predisposition to arteriosclerosis and in those with systemic
arterial hypertension
resulting from an apparent underlying disease such as pheochromocytoma.
and hyperplastic
arteriolosclerosis.
It may occur without previous hypertension or superimposed on benign hypertension
or primary renal disease, especially glomerulonephritis,
benign
arteriolar nephrosclerosis, or pyelonephritis
alone or in combination with an ACEI
or an angiotensin receptor blocker (ARB), are more effective than dihydropyridine
calcium antagonists (DCA) in treatment of hypertensive nephropathyrefwith
reduction
of differential blood pressure => further renal damage via both ischemia
and glomerular hypertension => tubular hypertension => interstitial hypertension
=> activation of fibroblasts => fibrosis)
: decreased CO => systemic
arterial hypotension
=> increased RAA system activation => cardiogenous edema
:
in late stages
(Löhlein-Baehr
lesion : necrosis and hyalinization)
(linear IIF pattern),
lung
cancers
and melanoma,
secondary
syphilis,
congenital
syphilis,
Plasmodium
spp.,
HBV,
HCV)
+ LRPAP1)
derived from tubule brush borders, which causes an autoimmune reaction
by the native tubules)ref.
Megalin is a large (approximately 600 kD) glycoprotein belonging to the
LDL receptor gene familyref,
located at the clathrin-coated pits, internalizing the ligands into the
endocytic compartments, and recycled to the cell surfaceref1,
ref2.
It is expressed abundantly at the apical membranes of proximal tubule cells
(PTC) that normally reabsorb and metabolize low–molecular weight proteins
(LMWP) filtered by glomeruliref.
Megalin is known to serve as a major receptor for endocytosis of multiple
LMWP, including transcobalamin-B12ref,
vitamin D-binding proteinref,
retinol-binding proteinref,
parathyroid hormoneref,
insulin, b2-microglobulin (b2-m),
epidermal growth factor, prolactin, lysozyme, cytochrome cref,
a1-microglobulin,
PAP-1, odorant-binding proteinref,
transthyretinref,
and advanced glycation end products (AGE)ref.
In renal failure, LMWP accumulate in serum and tissues; some of them, such
as b2-m causing dialysis-related
amyloidosis (DRA)ref,
act as uremic toxin proteins associated with complications in patients.
Parathyroid hormone is also recognized as a uremic toxinref.
Megalin thus appears to be a useful therapeutic molecular tool to remove
such uremic toxin proteins in uremia, and a novel cell therapy model has
been recently developed by subcutaneous implantation of megalin-expressing
cells to metabolize b2-m in renal
failureref.,
ssRNA via TLR7ref)
with chills
=> nephrotic syndrome
(detected also with IF)
(urinary schistosomiasis)
(usually type II),
Henoch-Schonlein
purpura)
,
but few, if any, immune deposits
: amyloid deposits within mesangium and below glomerular endothelium =>
crosslinked glycated proteins entrap nonglycated proteins (e.g. albumin)
and increase capillary permeability => stimulation of fibroblast proliferation
=> increased ECM synthesis
(ALA).
The morphological findings have been classified into 6 subgroups by the
WHO in 1992 (15 glomeruli / biopsy) :
and cyclophosphamide.
and cyclophosphamide,
hemodialysis..
endocarditis
infection of mesangial cells
(urinary schistosomiasis)
(DIC => GFR decreases more than renal blood flow, leading to a 25% decrease
in FF : as FF is normally increased by 35-50% in pregnancy, creatininemia
may still be < 0.8 mg/dL, while hyperuricemia,
hypocalciuria
and hyponatriuria occur),
pleural
effusion,
and/or pericardial
effusion)
and hypertriglyceridemia)
=> lipiduria (foamy urines)
(not practiced in babies, in adults only to assess primary glomerulopathies)
=> IIF and TEM; amyloidosis is diagnosed with abdominal subcutaneous
fat pad aspiration (ASFA))
=> hypercoagulability
=> thrombosis (expecially renal
vein thrombosisref)
=> thromboembolism
is reported to induce remission of proteinuria in patients with steroid-sensitiveref1,
ref2,
ref3
and steroid-resistantref
nephrotic syndrome
and seem to contribute to the formation of intrarenal lymphoid follicle-like
structuresref
,
thiazides,
triamterene)
(captopril)
rejection,
hyperkalemia,
metabolic
acidosis,
non-nephrotic proteinuria, and abnormal urine sediment. It usually has
a chronic course with progressive renal atrophy and loss of function; an
acute form occurs particularly after bacterial infection.,
occurring usually as a complication of pneumonia or empyema.
complicated with acute nephritis.
(icterohemorrhagic leptospirosis)
=> autoimmunity => generalized
distal / type 4 renal tubular acidosis (RTA),
ADH-resistance
,
especially phenacetin
: PGE2 decreases significantly only in patients with hypovolemia
(congestive
heart failure (CHF),
liver
cirrhosis,
nephrotic
syndrome, anaesthesia, shock,
hemorrhages,
water depletion, Na+ depletion)
=> acute renal failure (ARF) reversible
within 1-2 months, otherwise evolving to chronic
renal failure (strip fibrosis, tubular atrophy, obliterative arteriolopathy)
=> thrombotic microangiopathy
(also hypomagnesemia,
hypocalcemia,
and hypokalemia)
(saturnine nephritis)
(it binds metallothionein in lysosomes of proximal tubular cells),
poisoning by grains containing the mycotoxins citrinin
and ochratoxin A (OTA)
(a widespread contaminant of food and feedstuffs), or other factors. Some
proposed it is caused by wheat contamination with Aristolochia clematis,
also known as birthwort, similar to the disastrous mix-up in which thousands
of healthy Belgium women developed severe kidney failure requiring transplants
after accidentally receiving the Chinese herbal drug guang fang ji instead
of the similar-sounding han fang ji. Aristolochic acid induces p53 mutation.
100 000 people are at risk of nephropathy in the Balkans as a result of
inadvertently eating birthwort. birthwort has been used as an herbal remedy,
being given to mothers following birth because it reputedly helped to expel
the placentaref1,
ref2.
Aristolochia means "excellent birth" and refers to the traditional use
of the fresh juice to induce labor. (Ingestion would be toxic, so it is
likely used externally as some type of rub or poultice.) The Indian Root
(possibly another name for the plant) was used mainly in childbirth. In
England, it was known as birthwort and used for this purpose (assisting
in birth, expelling the child or the afterbirth). Theophrastus (c. 372-286
BCE) records that the plant was used to treat disorders of the uterus,
reptile bites, and sores to the head. (The reference does not tell us what
disorders of the uterus.) Of the 350 or so species of _Aristolochia_, several
carry the common name of snakeroot because many of the species were used
by Native Americans to treat snake bites. They also employed the plants
to treat stomachaches, toothaches, and fevers. In the 16th century, when
Francisco Hernandez was cataloging the flora of "New Spain," he came across
a plant that looked the same as the herb he knew back in Europe. The Mexican
species, however, can
=> nephrocalcinosis
: urate
nephropathy / uric acid nephropathy,
chronic acidosis, polyuria, and dehydration, all
resulting from proximal renal tubular dysfunction, and by corneal opacities,
growth failure, uremia, and death before age 10,
including microangiopathy with capillary obstruction, dilated or obliterated
vasa recta, enlarged glomeruli, interstitial fibrosis, and an increased
GFR
nephritis,
nephrocalcinosis,
rickets,
and progressive renal failure.
acidosis :)
thanks to hypovolemia,
less tendency to edema
;
cavities are found in the kidney, filled with puslike, cheesy masses and
tubercle bacilli. Usually associated with ureteritis (and eventually cystitis
and contralateral ureteritis) and fibrosis => stenosis/failure
from a donor whose blood is incompatible with that of the recipient.
characterized by dilatation of the renal pelvis and the ureters; some degree
of ureteric obstruction may be caused by the gravid uterus as the head
of the fetus pulls against the right iliac wing > left iliac wing, causing
acute
tubulo-interstitial nephritis and decreased ability to concentrate
urine. Pyuria leads to pyelonephritis
or immunodepression
(interstitial nephritis)
(36%)
(16%)
(16%)
(10%)
(6%)
(2%)
(4%)
(3%).
(4%)
(2%)
(1%),
in which gas produced by lactose-fermenting bacteria collects within the
parenchyma of the kidney, resulting in necrosis.
with shaking chills during bacteremia, pain in the costovertebral region
or flanks, and symptoms of cystitis.
detects septic hot-spots within renal cortex => pyonephrosis and hypodense
necrotic areas
with infection of the renal parenchyma, a condition closely resembling
xanthogranulomatous
pyelonephritis. It is an unusual form of chronic tubulointerstitial
nephritis with a predilection for patients with recurrent urinary tract
infections and an immunocompromised state; more common in women (female
to male ratio 3:1), in whom the lesions develop in a younger age group
(third to fifth decade) than in men (over 50 years). Enlarged kidneys in
the presence of persistent urinary infection should lead to the consideration
of this entity. (coexistence of extensive invasion into the liver and duodenum
is extremely rareref)
and antibiogram
(all papillae at the same stage)
or albuminuria.
or other endocrine disturbance.
(sometimes steroid-dependent or steroid-resistant)
.
,
IGF-2
(deleted in BWS), and PDGF-A.
IGF2
loss of imprinting (LOI) and associated precancerous lesions occur at a
lower frequency in children of east-Asian origin (in which WT develop at
younger ages and predominantly in males) and a high frequency in Caucasian
children, indicating that tumorigenesis is occurring by 2 distinct mechanismsref.
,
fever,
weight loss, systemic
arterial hypertension,
hematuria,
eventually peritonitis due to rupture; 10% has associated genitourinary
malformations or hemihypertrophies
,
CT,
chest
X-rays
,
liver
metastases,
or bone metastases,
or to lymph nodes far away from the kidneys
(ranging from heminephrectomy in localized cancer to partial nephrectomy
in bilateral cancer) + ablation of perirenal fat + ureterectomy
+ eventual adrenalectomy +
+ vincristine)
for 6 months
+ chemotherapy for 6 months
+ chemotherapy
.
have improved the 6 year survival rate to 63%, versus 25% without doxorubicin.
However, late recurrence remains a problem with these tumors; 30% of relapses
occur after 2 years, and prolonged follow up is required.
occurring in the midline of the posterior or middle cranial fossa has been
reported in approximately 15% of cases.
due to ectopic PTH incretion. It often metastasizes to the brain (?)
and alternating courses of ICE
and VDC
results in constitutive activation of wild-type NTRK3, which activates
the Ras-MAPK and the PI(3)K pathways for mitogenesis and cancer survival),
a mutations seen also in congenital fibrosarcoma (limb dysproportion;
good prognosis) and juvenile secretory
breast carcinoma (SBC)
,
hyperreninism, hypercalcemia
due to PGE2 production, usually asymptomatic, but with more
infiltration of surrounding tissue than in classic Wilms' tumor)
(hyperechogenic), spiral CT
(low attenuation)
=> secondary
systemic arterial hypertension
(RR = 2). Bilateral RCCs are common in von
Hippel-Lindau syndrome (VHL),
tuberous
sclerosis,
and chronic hemodialysis;
however, bilateral RCCs occur in only approximately 2% of sporadic cases
of RCC. RCCs are multicentric in as many as 25% of patients. Jade-1
is a short-lived, kidney-enriched transcription factor that is stabilized
by direct interaction with pVHL.
Loss of Jade-1 stabilization by pVHL correlates with renal cancer risk,
making the relationship between Jade-1 and renal cancer compelling. Jade-1
expression was barely detectable in all tested RCC lines, regardless of
VHL status. Strikingly, proteasome inhibitor treatment increased endogenous
Jade-1 expression up to 10-fold. Jade-1 inhibited RCC growth, colony formation,
and tumor formation in nude mice. Intriguingly, Jade-1 also affected the
pattern of cell growth in monolayer culture and 3D culture. Jade-1 increased
apoptosis by 40-50% and decreased levels of antiapoptotic Bcl-2. Antisense
Jade-1-expressing cells confirmed these results. Therefore, Jade-1 may
suppress renal cancer cell growth in part by increasing apoptosis. Jade-1
may represent a proapoptotic barrier to proliferation that must be overcome
generally in renal cancer, perhaps initially by pVHL inactivation and subsequently
by increased proteasomal activity. Therefore, Jade-1 may be a renal tumor
suppressorref.
Less aggressive tumours were more likely to be found in patients who were
considered to be overweight (having a BMI of 25-29), or obese (having a
BMI > 30), compared with patients who were underweight or normal weight.
The 5-year survival rate from kidney cancer was 82% for obese patients,
77% for overweight patients and 62% for normal-weight patients. It was
found that compared with normal-weight patients the risk of death from
clear cell renal cell carcinoma was reduced by 52% for obese patients and
by 36% for overweight patients. However, BMI adds little in the way of
prognostic information beyond that afforded by available methods.
(del3p)
(up to 90% after 8 years of hemodialysis)
due to infiltration of left renal vein (which enters cava vein by a right
angle, while the right one enters diagonally)
(3% : due to increased Epo incretion or renal hypoxia), hypercalcemia
(5% : due to osteolytic bone
metastases
or incretion of PTH-like molecules), systemic
arterial hypertension
(20% : increased renin incretion or renal parenchymal ischemia), biochemical
hepatic abnormalities without hepatic metastasis of the tumor (15% : Stauffer
syndrome), neuromyopathy (3%)
(5%)
(sensitivity = 98%) : cancers are iso- or hyperechogenic, while
renal cysts are anechogenic with refrangent walls
for staging
for differential diagnosis with hematomafor
patients with single kidney
(evaluation of vascular infiltration)
(bone metastases
evaluation)
(including adrenalectomy, ureterectomy
and ablation of perirenal fat) and eventually regional lymphadenectomy.
Survival after 10 years :
(tumor enucleation, polar amputation) in patients with bilateral cancers,
single kidney, chronic renal failure,
exophytic or T1a cancers < 2-3 cm (50% are accidentaliomas)
in patients with metastases
with or without IFN-g
6-10 mIU for 3 times a week for 1 year : 15-20% undergoes improvement
: high-dose bolus IL-2 produces significantly more responses (21%
vs. 13%) of apparent better quality (and a borderline significant difference
in the number of patients who were progression-free at 3 years) relative
to low-dose subcutaneous outpatient IL-2 and IFN-aref.
However, not all patients can tolerate high-dose IL-2
(side effect : anasarca)ref.
+ IL-2
in well-selected patients improve outcome, induce long-term survival and,
in a minority of patients, even produce long-lasting complete remissions
for lung metastases
given locally by inhalation achieves long-term progression-free survival
and long-term overall survival similar to high-dose systemic IL-2 but without
the toxicity associated with it.
to elicit graft-versus-tumor
(GvT) response
(0.2-0.3 mg/kg/week; objective response in 5-20%)
or capecitabine
(objective response in 15%)
for continuous or cirdadian chronotherapy (catabolyzing DPD is maximally
expressed at hours 3-9 p.m.) (objective response in 20%)
is poorly effective (radioresistant tumor) => practiced only for pain palliaton
in unresectable tumor (50-55 Gy in 5-6 weeks; effective in 50-60%) and
over metastases. Conventional radiotherapy has been an effective palliative
treatment for most sites of metastatic renal-cell carcinoma, including
lung, bone, and soft tissuesref.
In particular, stereotactic radiosurgery has been reported to have local
control rates for brain metastases of > 85%ref.
Recently, stereotactic radiosurgery for spinal metastases has demonstrated
high efficacy in pain relief with minimal toxic effects from radiationref.
In addition, stereotactic body-radiation therapy — which allows for more
conformal, high-dose extracranial radiation delivery — may expand the role
of radiation in treating both metastatic and nonoperative primary casesref
and hormonotherapy with PR
antagonists and ER
antagonists is palliative
: 6 intradermal injections at 4-week intervals, can be considered in patients
undergoing radical nephrectomy due to organ-confined RCC > 2.5 cm in diameter.
> 700 patients treated to date, minimal toxicity. Now in phase III clinical
trial comparing nephrectomy followed by Oncophage after 4-8 weeks to nephrectomy
followed by observation, please call 866.805.8994 (toll-free), or e-mail
Antigenics Clinical Affairs.
(short-lasting objective responses in 2-8%)
is active, RCC patients are three times as likely to die from their cancer
as RCC patients whose tumors don't express B7-H4. nearly 82% of RCC tumors
have active B7-H4 on the blood vessels that nourish tumors, compared to
only 6.5% of nearby normal renal tissues showing B7-H4ref
in the kidney, usually in the capsule; it occurs more often in women.-like
carcinoma of the renal pelvis
on the contrary of other LELCs
tumor of the kidney
=> cardiogenic shocknephritis
rejection=> lower
nephron nephrosis / crush kidney : ATN in the lower nephron (if after
crushing injury to muscles it is a.k.a. crush syndrome),
acute
interstitial nephritis due to drug sensitization)|
|
|
|
| urine density |
|
|
| urine osmolality
(mOsm/kg) |
|
|
| natriuria
(mmol/L) |
|
|
| BUN/creatininemia |
|
|
| creatininuria/creatininemia |
|
|
| Na+ excretion
fraction
(%) |
|
|
| sediment |
hyalinous cylinders |
tubular cells |
and hyperCPK => rhabdomyolysis
(> 15 mg/dL) and hyperLDH => acute urate
nephropathy
is a biomarker for acute renal injury after cardiac surgery in children
with initially normal renal functionref1,
ref2
(50-90%)
avoid the need for dialysis in > 80% of adults in the hospital with ARF
is needed, up to 90% in MOFs. 75% from opportunistic infections, 25% from
cardiac arrhythmias
(28-33.2%)
(22-24%)| Grading |
(mg/dL) |
(mL/min) |
| mild CRF |
|
|
| intermediate CRF |
|
|
| severe CRF |
|
|
| end-stage renal diseases (ESRD) |
|
|
(80% of total excreted nitrogen) => anorexia, malaise, nausea
and vomiting,
headache
=> dimethylguanidine and sarcosine,
insulin,
LH,
PRL,
and glucagon)
=> Kussmaul's
breathing
or Cheyne-Stokes'
breathing
=> edema (including subacute pulmonary edema)
and arrhythmias
(including hemorrhagic
gastritis)
=> hypersplenism
=> leukopenia
with lymphopenia
in mild CRF)
in mild CRF reduce hyperfiltration
(furosemide 125-500 mg/die) to prevent sodium retention
with gastrointestinal pharmacokinetics to prevent conversion of urea into
ammonium
to treat hyperphosphatemia
to treat uremic pruritus
(calcium carbonate)
or hemofiltration
(3 times a week) : peritoneal
dialysis
in diabetic nephropathy as it allows insulin clearance
: anemia is common among patients with chronic kidney diseaseref.
In such patients, treatment with erythropoietin has been shown to enhance
the quality of liferef1,
ref2,
ref3,
ref4.
However, evidence suggesting that the correction of anemia improves cardiovascular
outcomes has largely been derived from observational studies and small
interventional trials associating a high level of hemoglobin (>12.0 g/dl)
with a lower rate of complications and death from cardiovascular causesref1,
ref2,
ref3.
Other evidence has also indicated that cardiovascular complications, such
as left ventricular hypertrophy, might be improved through the use of a
high hemoglobin level as a targetref.
However, in a randomized, controlled study comparing a hematocrit target
of 42% with that of 30% among patients with heart disease who were undergoing
hemodialysis, the former group had higher rates of nonfatal myocardial
infarction and death, but not significantly soref.
In 2000, a panel of the Kidney Disease Outcomes Quality Initiative of the
National Kidney Foundation recommended that the target level of hemoglobin
should be 11.0-12.0 g/dl in patients with chronic kidney disease, whether
or not they were receiving dialysisref.
A recent update of guidelines regarding anemia in such patients expanded
the target range to 11.0 to 13.0 g/dlref,
with the increase in the upper limit of the target range justified on the
basis of a potential improvement in the patients' quality of life. Several
studies have demonstrated that the correction of anemia in patients with
chronic kidney disease improves the quality of life and exercise tolerance
while reducing the need for transfusionref1,
ref2.
However, there remains much uncertainty about the validity of various assessments
of the quality of life in published studiesref.
Data on the effects of the correction of anemia on cardiovascular outcomes
and survival have been both discordant and controversial. Recent large,
controlled studies involving patients with pre–end-stage or end-stage renal
disease have shown either an increase in adverse events or no benefit from
the normalization of hemoglobin levelsref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7.
Furthermore, in several studies, complete correction of anemia, as compared
with partial correction, did not improve left ventricular hypertrophyref1,
ref2,
ref3,
ref4,
ref5.
In the Correction of Hemogloblin and Outcomes in Renal Insufficiency (CHOIR)
trial, the use of a target hemoglobin level of 13.5 g/dl (as compared with
11.3 g/dl) with epoetin a was associated with
increased risk and no incremental improvement in the quality of liferef.
This results, coupled with the results of other recent interventional trials
involving patients with chronic kidney diseaseref1,
ref2,
reinforce the differences between observational and clinical trial data,
which appear particularly notable in the setting of anemia therapyref.
In the Cardiovascular Risk Reduction by Early Anemia Treatment with Epoetin
Beta (CREATE) trial, the hypothesis that complete correction of anemia
in patients with stage 3 or 4 chronic kidney disease improves cardiovascular
outcomes as compared with partial correction of anemia was tested : during
the 3-year study, early complete correction of anemia (target : 13.0-15.0
g/dl) with s.c. epoetin b did not affect the
likelihood of a first cardiovascular eventref.
(+ 0.5-1 mEq/L/die) (no metabolic
acidosis
until GFR < 10 mL/min thanks to compensatory hypertrophy) => left congestive
heart failure
=> complete
intraventricular block or ventricular asystolia (cardiac standstill)
=> circulatory
standstill
=> cardiac death
(due to both precipitation by phosphate and reduced renal synthesis of
1a,25-(OH)2-vitamin
D3:
in the latter case replacement therapy would worsen hyperphosphoremia)
and hyperphosphatemia
=> secondary
hyperparathyroidism
=> hyponatremia
are directly related to the risk of death in patients with ESRD.ref
of the ureterref
and curves round this vessel to regain its anterior position as it descends
to the bladder
(cobra-headed ectasia)
and a small, split phallus or a split
clitoris,
a bifid uterus, and a duplicate or exstrophic vagina.involving
the bladder
+ M3 antagonists
ref
in babies
in babies
in HSCT
recipients (7-68%)
and cyclophosphamide
,
a1d-AR
and IL-4genes
with bladder dyscharge for exocrine secretions
cystitis associated with immunosuppressionref
is better than co-amoxiclavref
from the bladder)
of the bladder and ureters, resulting from infection
and use of permanent hair dye contribute substantially to current arylamine
exposure. Low levels of 4-ABP exposure have been associated with non–smoking-related
bladder cancer. Other arylamine compounds coming from as yet unidentified
environmental sources may also be human bladder carcinogens. Levels of
all arylamine–hemoglobin adducts in peripheral blood (2,3-dimethylaniline
(2,3-DMA), 2,4-DMA, 2,5-DMA, 2,6-DMA, 3,4-DMA, 3,5-DMA, 2-ethylaniline
(2-EA), 3-EA, 4-EA), with the exception of 2,6-dimethylaniline (2,6-DMA),
are higher in smokers than in nonsmokers, and levels of all arylamine–hemoglobin
adducts are higher in case subjects than in control subjects. Arylamine–hemoglobin
adducts of 2,6-DMA, 3,5-DMA, and 3-EA are all independently, statistically
significantly (all P<.001) associated with bladder cancer risk
after adjusting for cigarette smoking at the time of blood collection,
lifetime smoking history, and other potential risk factors. These adducts
are also independently associated with bladder cancer risk when only nonsmokers
at time of blood draw were considered (highest quartile versus lowest quartile:
2,6-DMA, relative risk [RR] of bladder cancer = 8.1, 95% confidence interval
[CI] = 3.6 to 18.0; 3,5-DMA, RR = 2.7, 95% CI = 1.2 to 6.0; 3-EA, RR =
4.3, 95% CI = 1.6 to 11.6). Diverse arylamine exposures are strongly associated
with bladder cancer risk among nonsmokers. Because arylamines may account
for a substantial proportion of bladder cancers among the general population,
identification of environmental sources of these compounds is neededref
-containing
analgesics for upper urinary tract carcinomas|
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| grades | 1 | 1 | low grade | low grade | PNLMP |
| 2a | 2a | high grade | high grade | LGPUC | |
| 2b | 2b | HGPUC | |||
| 3 | 3 | ||||
| 4 | |||||
| grading criteria | |||||
| cellular atypia | + | + | + | + | + |
| cellular polarity | + | + | + | + | + |
| mitoses | + | + | |||
| epithelial thickness | + | + | + | + | |
(20%)
(incidences are particularly high in the Nile River Valley, Egypt) (schistosomal
bladder cancer)
(0.5-2%)
of the bladder-like
carcinoma of the bladder (LELCB) (0.4%-1.3%), first reported by Zukerberg
et al in 1991, is an undifferentiated epithelial tumor with a dense inflammatory
infiltrate that resembles the lymphoepithelioma of the nasopharinx occurring
in other sites. The mean age at diagnosis is 69 years. Of the patient population
69% are men.
on the contrary of other LELCs
of the bladder developing from endometriosis
vesicae / bladder endosalpingiosis (mullerianosis) : tubulocystic and
papillary glands lined by glycogen-rich, cubical or hobnail cells with
clear to eosinophilic cytoplasm. Finding of CA125 expression in bladder
tumors of apparent urothelial origin contrasts with some studies that have
regarded CA125 expression as evidence for a mullerian origin. The frequency
of gland differentiation in transitional cell carcinomas and the rarity
of vesical endometriosis could be taken to suggest that these tumors are
mostly of urothelial derivation, but the strong preponderance in the urethras
of women argues for a mullerian origin, and this is almost certain in those
cases with benign mullerian components. In the absence of endometriosis
or conventional foci of transitional cell carcinoma, it may be impossible
to determine whether a tumor with the morphology of clear cell carcinoma
is of mullerian or transitional (urothelial) cell lineage, and at this
time immunochemistry does not solve this problem. Despite high stage at
diagnosis, most patients have been alive with no evidence of disease when
reported, a prognosis that seems to apply regardless of length of follow-up.
of the urinary bladder
+ intravesical BCG
(complete and durable response rates in > 70% of patients)
+ endovesical chemotherapy (mitomycin
C,
thiotepa,
or doxorubicin)
or intravesical BCG
(75 mg for 6 weeks)
(in very selected patients)
(radiosensitive : 55-65 Gy in 5-8 weeks) for unresectable patients
for multicentric tumors,
M-VAC,
CMV,
CISCA(15-35%
has complete response but long-time survival is just 20%)
and gemcitabine
and reimplantation| pathologic stage | 5-yr OS | 10-yr OS |
| T2, N0 | 89% | 87% |
| T3a, N0 | 78% | 76% |
| T3b, N0 | 62% | 61% |
| T4, N0 | 50% | 45% |
| any T, N1 | 35% | 34% |
tumor of the urinary bladder
(unless patient is obese or bladder is empty; accuracy = 60% as anterior
wall and cupule are masked)
(ureteroscopy and infusional
urography
or ascending
(urethrocystouretero)pyelography
for upper urinary tract neoplasms)
in early stages (to detect neoangiogenesis) and late stages (tumor appears
as a noncalcium stone) (overstaging but allows study of bladder wall and
lymph nodes sized > 1 cm with accuracy : 69-72%)
(less defined lymph nodal study)
(after air insufflation (air is otherwise seen in bladder only in patients
with fistulae or catheters) or MRI
=> mapping in narcosis to search carcinoma in situ (cupule, lateral
walls and trigonus)
for staging and therapy,
CYFRA
21-1;
NMP22 proteomic test (BladderChek®; source : Matritech
Inc.) is a more dependable, less expensive tool to help detect bladder
cancer earlier (sensitivity, 55.7%), whereas cytology test results has
sensitivity = 15.8%. The specificity of the NMP22 assay was 85.7% compared
with 99.2% for cytology. The proteomic marker detected 4 cancers that were
not visualized during initial endoscopy, including 3 that were muscle invasive
and 1 carcinoma in situref,
chemotherapy
and tabes dorsalis.
(25-50%)
(15-40%)
(25-50%)
(15-25%)
(cystophthisis)
(false membrane : croupous cystitis / diphtheritic cystitis)(13.5%)
(29.3%)
(17.7%)
(7.8%)
(7%)
(6.1%)
(6.2%),
cystoscopy,urolithiasis,
urinary tract neoplasms, urethral and ureteral catheters, vesicoureteric
reflux (30-50% in childhood UTIs)
,
prulifloxacin,
cephalexin
in pregnancy
,
hydrogel, and silver
regularly may make urine more acidic and less hospitable to bacteria, but
there is no evidence that it prevents UTIs.
in infant males : although there is some controversy over whether circumcision
helps prevent UTIs in boys, a 2000 analysis of nearly 15,000 male infants
born in 1996 reported that the uncircumcised boys younger than one year
had 9 times the risk for UTIs as circumcised boys, but this risk is still
very low
(resorption of cardiogenic edema at clinostasis))
fistulaeand
obesity
(tabetic bladder) and pernicious
anemia,
but may be seen in association with other diseases,
hiccup,
laugh, weight lifting, or sneeze) in patients with rupture during dystocic
delivery
or congenital malacia of pubourethral ligaments => dislocation of proximal
urethra out of pelvis, so that increase in intrabdominal pressure act on
urinary bladder but not on urethra
is thought to increase urethral-sphincter muscle contraction, which may
help prevent urinary leakage => continence surgery,
diabetic neuropathy, and postmenopause (due to hypoestrogenism that thins
urethral mucosal epithelium and reduces blood blow to urethral submucosal
venous plexuses) (often part of overactive bladder (OAB) syndrome
: urinary urgency with or without urge incontinence, often with urinary
frequency > 8 times a day and nocturia. The condition is believed to occur
in 17% of the U.S. population and three to 42% of people in Europe)
caused by nonneurological problems such as bladder outlet obstruction
(oxybutynin,
tolterodine)
),
but the urine dribbles away drop by drop from mere pressure (ischuria
paradoxa) => urinary retention => slow ureterohydronephrosis
=> sepsis,
p.o. oxybutinin chloride or imipramine.|
|
|
| I | only cough and sneeze |
| II | also change of posture, fast movements and/or stair lifting |
| III | also with minimal efforts in orthostatism |
|
|
|
|
| cause of loss | laugh, sneeze, weight lifting, running | walking, stair lifting, during sexual intercourses |
| frequency of loss | weekly | daily |
| quantity of loss | < 1 pad/day | > 2 pad/day |
to monitorate post-urinary residue
with CO2 or H2O up to V = 300 mL)
: introduce a cotton-fioc in urethra and measure with a goniometer the
angle between the urethra and the vertical of the bladder during both rest
and Valsalva's maneuver (dislocations should normally be < 20-30°)
infiltrationsref1,
ref2
(7% of all patients; phenothiazines induce throat dryness)
leading to constitutive deficiency
mutations
mutations
block sodium reabsorption in distal convoluted tubule => contraction of
extracellular volume => increased ADH-independent salt and water reabsorption
in proximal tubule
(Gilbert's sign)ref
urinary tract infection,
methylene blue, zaleplonref,
metoclopramideref,
amitriptyline,
indometacin,
food colouring (e.g. Food Dye and Color Blue Number 1 (FD&C Blue No.
1)ref),
herbicides (mefenacet and imazosulfuronref))ref
due to extrarenal causes
(instead loop diuretics
reduce medullar osmolality and hence capacity to concentrate urine)
.
It may be seen in
abuse
derivatives
inhibitors
-induced
polyuria)
inherited as an X-linked dominant trait; the bone disease is due to defects
in the resorption of phosphate by the proximal renal tubule and in the
regulation of renal 25-hydroxyvitamin D activation, and to decreased intestinal
absorption of calcium with secondary hyperparathyroidism
>
2g/die
(inhibits post-secretory reabsorption)
(including preeclampsia
/ gestosis)
in the urine
in the urine.)
or urethra
: asymptomatic bacteriuria exists
(gold standard : freely filterable, not secreted, not reabsorbed, not metabolized)
= ([inulin]urine . Vurine) / [inulin]plasma
= 125 mL/min in young males (in females value = 85-90% of males). This
value is hard to determine as to keep [inulin]plasma value constant
for some hours, inulin has to be infused i.v. and Vurine determination
needs urinary catheterization.
: it has 2-3 days of latency in acute renal
failure, and its value is independent of age but directly relates with
lean body mass, body weight, body cell mass, height, diseases (diabetic
ketoacidosis, severe hyperbilirubinemia, and abundant meaty diet). Anyway
32% of Clcreatinine depends on its secretion. Clcreatinine
= [ml/min/1,73m²] :
: its value directly relates to introduction of exogenous proteins, H2O,
liver failure and hyperacatabolic conditions (malnutrition,
fever,
...). Urea is filtered and passively reabsorbed]plasma
is not sensitive to body weight, height, fat-free mass, or body cell mass]plasma]plasma
with 99mTc-diethylentriaminopentaacetic acid (DTPA).
CV = 8%.
administered by intravascular injection
(anterior or posterior approach if patient has meteorism) detects parenchymal
renal alterations. The dyshomogenous renal cortex appears hyperechogenic,
while the renal homogeneous renal medulla appears hypoechogenic. It ..
detects renal blood vessels until arciform arteries
is used in functioning kidneys (ureters - imaged after 15-20' -
are rarely completely seen due to peristalsis)
is used to assess morphology of nonfunctioning kidneys
detects vesicoureteral reflux (sometimes
bladder is partially masked by prolapsed uterus)detects
alterations of renal parenchyma (e.g. pyonephrosis)
and surrounding tissues. It is used for renal traumas.
detects malformations
is used to assess morphology of nonfunctioning kidneys)
:
Copyright © 2001-2009 Daniele Focosi.
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