Clinical presentation of
renal diseases
The presence of renal disease in a
patient may be detected because of:
1. presentation with a symptom or clinical sign
that indicates an underlying renal disorder;
2. the presence of a systemic disease known to
involve the kidneys;
3. a family history of inherited renal disease;
4. the finding of asymptomatic urinary
abnormalities or disordered renal function
tests.
Asymptomatic urinary abnormalities
• Asymptomatic proteinuria
• Microalbuminuria
• Microscopic haematuria
Asymptomatic proteinuria
• Urinary protein excretion can amount to 150 mg daily
in normal persons, consisting of albumin, Tamm–
Horsfall protein and secretory IgA.
• An accurate 24-h urine collection is difficult to obtain,
particularly in outpatients, and therefore it is
frequently more convenient to estimate the urinary
protein/creatinine ratio on a mid-morning sample of
urine, a normal value would be less than 130 (as this is
a ratio it is without units). Approximately half consists
of low molecular weight proteins or protein fragments,
with the rest being albumin.
• The most common method of detecting
proteinuria is by using dipstix. These paper
strips are impregnated with tetrabromophenol
blue which changes colour from yellow-green
to blue-green in the presence of protein.
• This test is very observer-dependent and it
should be remembered that Bence-Jones
protein will not be detected and that falsepositive results can occur both in alkaline
urine and in urine contaminated with
antiseptics
• Urinary protein excretion can increase during
pyrexial illnesses, with strenuous exercise,
congestive cardiac failure and hypertension.
• In such patients the proteinuria is commonly mild
(generally less than 1.5 g daily) and resolves with
remission of the underlying cause.
• If proteinuria is detected in these circumstances
the test should be repeated once the potential
cause has resolved.
• If persistent proteinuria is detected then further
investigation to determine the nature of the
underlying disease is indicated.
Microalbuminuria
• 'Microalbuminuria' is the term used for urinary protein
excretion greater than normal but still less than that
detectable by dipstix testing.
• The excretion of more than 30 μg/min of albumin in an
overnight collection or 70 μg/min in a 24-h collection
in a patient with diabetes mellitus is indicative of early
diabetic nephropathy.
• It is, however, not specific for diabetes:
microalbuminuria may also be present in hypertension,
obesity, systemic lupus erythematosus, and following
exercise.
• Specifically designed stix tests are now available for
screening purposes, but these remain only
semiquantitative.
Microscopic haematuria
• There is no agreed definition of microscopic
haematuria as all urine samples contain some red
blood cells.
• The Scottish Intercollegiate Guideline Network (SIGN)
has suggested the presence of a positive result on
dipstix testing and/or the presence of more than five
red blood cells per high-power field on urine
microscopy.
• Asymptomatic microscopic haematuria is occult
haematuria, however detected and excludes
haematuria visible to the naked eye or associated with
urinary tract pain, infection or other symptom.
• The further investigation of a patient found to have
asymptomatic haematuria depends on a number of
factors.
• As haematuria can arise from any part of the urinary
tract from the glomerulus to the urethra, the first issue
is to determine whether further investigations should
be urological or nephrological.
• In men, particularly those over the age of 50 years, it is
most likely that urological investigations will be
required because of the increasing incidence of
prostatic problems and urothelial malignancy and in
such patients clinical examination must include a rectal
examination to determine whether any prostatic
abnormality can be detected.
• By contrast, the presence of significant proteinuria,
clinical evidence of renal disease and/or impaired renal
function indicate the need for nephrological
investigation.
• Urine microscopy can be of value if performed on
a fresh sample. Red cell casts are diagnostic of
glomerular bleeding and do not arise from
bleeding anywhere else in the renal tract.
• Consideration of the morphology of red cells in
the urine can also be useful: dysmorphic red cells,
in particular those appearing as a ring form with
bubbles, are probably the consequence of
glomerular bleeding, whereas red cells of normal
appearance are more likely to arise from a site in
the lower urinary tract.
• However, discrimination is not always
straightforward, considerable interobserver
variability is reported and the technique is not
robust enough to be routinely applied in most
centres.
Symptomatic presentations
• Acute nephritic syndrome
(haematoproteinuria syndrome)
• Nephrotic syndrome
• Disorders of micturition
• Pain
• Disorders of renal function
Disorders of micturition
•
•
•
•
•
Polakiuria
Nocturia
Dysuria
Polyuria
Olyguria and anuria
Polakiuria
• Is the term applied when the bladder is emptied more
often than normal, hence in obtaining a history it is
therefore necessary to determine how often the
patient passes urine.
• This may be associated with a normal or increased 24hour urine volume.
• It is important to distinguish between these two
situations as frequency in the presence of a normal
output indicates a bladder (lower urinary tract)
problem, whereas an increase in output is indicative of
a disorder of urinary concentration or excessive fluid
intake
Nocturia
• Nocturia may arise from the many conditions that cause
frequency.
• On lying down there is an increase in renal perfusion
resulting in increased urine flow, but ADH is secreted during
sleep, thereby increasing urinary concentration and
meaning that urine volume diminishes during sleep. In
patients with sleep disturbance there is less ADH
production and thus urine concentration is reduced, with
increased urine volume such that nocturia may occur.
• Enquiry should be made regarding sleep patterns in
patients presenting with nocturia, in addition to
considering those conditions that cause polyuria and
frequenc
Dysuria
• Dysuria is pain or discomfort on micturition and one of the most
frequent symptoms, accounting for about 2% of consultations in
primary care.
• It is more common in women and is usually described as a burning,
scalding or tingling sensation in the urethra or at the urethral
meatus occurring during or immediately after micturition.
• Most commonly it is due to urinary infection, but it may also be
caused by chemical irritation such as rarely occurs with
cyclophosphamide. If associated with frequency and urgency of
micturition it indicates bladder irritation such as cystitis. In young
women this is usually associated with sexual activity, but in older
persons it may indicate a lesion in the bladder or prostate.
• Prostatic inflammation usually gives rise to perineal or rectal pain.
• Very young children will be unable to complain of dysuria but
urethral irritation may be inferred if the child cries during
micturition.
Polyuria
• Polyuria is an increase in the daily volume of urine and may arise
from a number of different conditions. The normal daily urine
volume varies considerably depending on fluid intake and insensible
loss, but is normally in the range of 1 to 2 litres.
• An increase in solute load, most commonly due to hyperglycaemia,
reduces tubular reabsorption and increases urine production.
Inadequate ADH secretion, such as following a head injury or
associated with tumours or infection, result in an impaired urinary
concentration and increased output (central diabetes insipidus).
• Conditions that impair the tubular response to ADH, such as
potassium depletion, lithium toxicity and some rare inherited
diseases, also increase urine volume (nephrogenic diabetes
insipidus), as do renal disorders that impair medullary
concentration, such as analgesic nephropathy, papillary necrosis,
medullary cystic disease and nephrocalcinosis.
Olyguria and anuria
• Oliguria is a reduction in urine volume to such an
extent that there is inability to excrete the residues of
normal daily metabolic functions.
• This normally means to a volume of less than 500 ml
daily in an adult, usually indicating acute renal failure
of whatever cause.
• Anuria is the lack of any urine output and is indicative
of obstruction, although it may occur in some forms of
severe acute renal failure.
• If anuria is present it is essential to perform a rectal
examination to determine if there is any pelvic
malignancy, such as a rectal or cervical carcinoma, to
account for the obstruction.
Renal pain
• Stretching of the capsule of the kidney causes
renal pain that is felt in the loin ('renal angle').
• It can be produced by any condition that distends
the kidney, such as inflammation, mass lesions or
an obstruction.
• The last is the most common cause, particularly
obstruction of the pelviureteric junction, when
the patient may give a history that anything that
causes an acute increase in urine volume (for
example, drinking a large quantity of water, beer,
or lager or taking a diuretic) precipitates the pain.
Renal pain
• Inflammatory pain, such as in pyelonephritis and
(uncommonly) in glomerulonephritis, develops
gradually, is usually constant in nature and is variable in
severity.
• A perirenal abscess, which may not always be
associated with fever or tenderness, can give rise to
symptoms and signs of diaphragmatic irritation and/or
psoas irritation.
• In the latter case, the patient usually prefers to rest
with the hips flexed and reports that extension of the
hips is accompanied by an increase in pain.
Renal pain
• It can be difficult to distinguish renal pain from
musculoskeletal pain, hence the history should enquire
specifically about the relationship of pain to movement or
position, neither of which greatly affects renal pain.
• Clinical examination of the back and spine should
determine any limitation of movement or localized point
tenderness, which would suggest a musculoskeletal
problem.
• Some patients with polycystic renal disease complain of a
constant dull loin ache. They may also suffer from the
sudden onset of renal pain if there is bleeding into a cyst,
or from pain of a more gradual onset if there is cyst
infection.
Ureteric colic
• Pain arising from an acute obstruction is frequently sudden
in onset, severe, colicky and may radiate to the groin,
scrotum, labia or upper thigh.
• Many describe it as 'the worst pain that they have ever
had' and the patient with ureteric colic typically thrashes
about, unable to find comfort, looks pale and sweaty and
often vomits, which can lead to diagnostic confusion.
• The pain is due to acute distention of the pelvis of the
kidney and the upper ureter and the associated increased
peristalsis. If the obstruction is ureteric the pain resolves
rapidly once the cause is extruded into the bladder,
although when in the bladder it may result in bladder
irritation with strangury or further obstruction if it becomes
impacted at the urethral orifice.
Renal colic
•
•
•
•
•
•
Sudden onset
Very intense
Antalgic position
Unilateral
Lasts for minutes, hours, days (rare)
Precipitated by phisical effort, trepidations,
wattery diet, heat
• Accompanied by urinary , digestive, circulatory
symptoms
Phisical exam
• Anxiety
• Agitated
• Antalgic position
• + Giordano
Causes
•
•
•
•
•
Nephrolithyasis
Cancer
Renal tuberculosis
Renal trauma
Sulphamide and cytostatics intake
Ureteric colic
• The most common differential diagnoses of rightsided renal colic are biliary colic and appendicitis:
diagnostic difficulty is less likely on the left side,
although colonic pain requires consideration.
• Chronic obstruction may be surprisingly
asymptomatic. Retroperitoneal fibrosis is
accompanied by a dull-aching back discomfort
but is not associated with colic in spite of an
obstruction.
Non-colicative lumbar pain
(renal origin)
• Acute – without irradiation, without disorders
of micturition : APN, AGN
• Chronic – lower intensity: CGN, renal
tuberculosis
• Differential diagnosis: muscular back pain
(lumbago), hernia, spondilitis, spondilosis
Endogenous creatinine clearance
NEPHRITIC SYNDROME
Definition
• This clinical syndrome typically presents with
clinical findings of hematuria, proteinuria and
dysmorphic red blood cells and/or red blood
cell casts.
• The proteinuria can range from 200 mg per
day to heavy proteinuria (greater than 10
grams per day). <3.5 g/day
• Clinically, it is accompanied by hypertension
and edema.
Assessment
• In cases in which the nephritic syndrome is the
predominant clinical presentation, a search for
systemic diseases is warranted.
• The history and physical exam should particularly
focus on the assessment of rashes, lung disease,
neurologic abnormalities, evidence of viral or
bacterial infections, and musculoskeletal and
hematologic abnormalities.
• Laboratory assessment should be tailored to the
clinical findings in the history and physical
examination.
Clinical findings
• Not all four clinical features may be present
simultaneously.
• In some patients there is oedema due to salt and
water retention in the oliguric phase.
• Encephalopathy, particularly in children, may
occur due to hypertension or electrolyte
disorders such as hyponatraemia.
• Hypertension is variable and oliguria depends to
a large extent on the degree of glomerular
involvement.
Urine exam
• The urine typically appears 'smoky' due to the
presence of red blood cell casts and rarely it
will appear frankly red.
• Proteinuria is variable in amount.
Causes
• The 'classical' cause of acute nephritis is poststreptococcal
glomerulonephritis and other infective causes .
• However, these diseases are becoming less common,
particularly in developed countries and it is more usual to
see patients who have proteinuria and haematuria
accompanied by variable hypertension and renal functional
impairment in whom no identifiable preceding infection
can be identified.
• The presence of blood and protein in the urine is a sign of
glomerular inflammation and is not indicative of any
particular glomerular pathology.
• On investigation such patients have a wide variety of
glomerular appearances , hence renal biopsy is essential for
precise diagnosis.
Laboratory
• A complete blood count (CBC), electrolyte
panel, 24-hour urine collection for protein and
creatinine clearance, and liver function tests
should be obtained initially. Serum
complement (C3) levels are often clinically
helpful to assist in the diagnosis of a specific
renal disease (Table 9-5).
Immunology
• Further laboratory assessment may be
performed based on these findings, and may
include an anti-streptolysin (ASO) titer,
antinuclear antibody (ANA), antineutrophil
cytoplasmic antibodies (ANCA), cryoglobulins,
and/or an anti-GBM antibody. These early
assessments may provide a presumptive
diagnosis and should lead the clinician to an
appropriate therapeutic intervention while
awaiting renal biopsy results.
Renal biopsy
• tissue diagnosis confirms the clinical findings
and provides information regarding the acuity
and chronicity of the disease process can a
glomerular disease can be properly managed
Acute glomerulonephritis
• inflammatory process causing renal dysfunction over
days to weeks that may or may not resolve
• If the inflammatory process is severe, the
glomerulonephritis may lead to a greater than 50% loss
of nephron function over the course of just weeks to
months.
• Such a process, called rapidly progressive
glomerulonephritis, can cause permanent damage to
glomeruli if not identified and treated rapidly.
• Prolonged inflammatory changes can result in chronic
glomerulonephritis with persistent renal abnormalities
that progress to ESRD.
Symptoms and Signs
• Edema is first seen in regions of low tissue
pressure such as the periorbital and scrotal
areas.
• Hypertension, if present, is due to volume
overload rather than vasoactive substances
such as angiotensin II, whose levels are low.
Laboratory Findings
• Serum chemistries
• Urinalysis
• Biopsy
Serum chemistries
• There are no serum chemistries characteristic of
nephritic syndrome, but certain special tests are
often performed depending on the history and
the results of the preliminary evaluation.
• These include complement levels, antinuclear
antibodies (ANA), cryoglobulins, hepatitis
serologies, ANCA, anti-GBM antibodies,
antistreptolysin O (ASO) titers and C3 nephritic
factor.
Urinalysis
• The urinalysis shows red blood cells. These may
be misshapen from traversing a damaged
capillary membrane—so-called dysmorphic red
blood cells.
• Red blood cell casts and moderate degrees of
proteinuria are also characteristic of the urinary
sediment.
• Placing the patient in a lordotic position for an
hour increases sensitivity for finding red cell casts
in the next urine specimen.
Biopsy
• Renal biopsy should be considered if there are no
other contraindications to biopsy (eg, bleeding
disorders, thrombocytopenia, uncontrolled
hypertension).
• Rapidly progressive glomerulonephritis is likely
when over 50% of glomeruli contain crescents.
• The type of disease can be categorized according
to the immunofluorescent pattern and
appearance on electron microscopy
Essentials of Diagnosis
• Edema.
• Hypertension.
• Hematuria (with or without dysmorphic red
cells, red blood cell casts).
Nephrotic syndrome
Definition
• Another major cause of edema is nephrotic syndrome,
the clinical hallmarks of which include proteinuria
(>3.5 gm per day), hypoalbuminemia,
hypercholesterolemia and edema.
• The degree of the edema may range from pedal edema
to total body anasarca, including ascites and pleural
effusions.
• The lower the plasma albumin concentration, the more
likely the occurrence of anasarca; the degree of sodium
intake is, however, also a determinant of the degree of
edema.
Causes
• Systemic causes include diabetes mellitus,
lupus erythematosus, drugs (e.g., phenytoin,
heavy metals, NSAIDs), carcinomas and
Hodgkin's disease
• Primary renal diseases such as minimal
change nephropathy, membranous
nephropathy, focal glomerulosclerosis and
membranoproliferative glomerulonephritis.
Pathogenesis
• Traditionally, ECF volume expansion in
nephrotic syndrome was believed to depend
on hypoalbuminemia and underfilling of the
arterial circulation. Several observations have
raised questions about this hypothesis
Pathogenesis
• First, the interstitial oncotic pressure in
normal individuals is higher than previously
appreciated. Transudation of fluid during ECF
volume expansion reduces the interstitial
oncotic pressure, thus minimizing the change
in transcapillary oncotic pressure.
Pathogenesis
• Second, patients recovering from minimal-change
nephropathy frequently begin to excrete sodium
before their serum albumin concentration rises.
• Third, the circulating concentrations of volumeregulatory hormones are not as high in nephrotic
patients as in patients with severe cirrhosis or
congestive heart failure. These and other
observations have suggested a role for primary
renal NaCl retention in the pathogenesis of
nephrotic edema.
Hypoalbuminemia
• is compounded further by increased renal
catabolism and inadequate, albeit usually
increased, hepatic synthesis of albumin
• the greater the proteinuria, the lower the
serum albumin level
Hyperlipidemia
• Is believed to be a consequence of increased hepatic
lipoprotein synthesis that is triggered by reduced
oncotic pressure and may be compounded by
increased urinary loss of proteins that regulate lipid
homeostasis.
• Defective lipid catabolism is also thought to play an
important role. Low-density lipoproteins and
cholesterol are increased in the majority of patients,
whereas very low density lipoproteins and triglycerides
tend to rise in patients with severe disease.
• Although not proven conclusively, hyperlipidemia may
accelerate atherosclerosis and progression of renal
disease.
Hypercoagulability
• Is probably multifactorial in origin and is caused,
at least in part, by increased urinary loss of
antithrombin III, altered levels and/or activity of
proteins C and S, hyperfibrinogenemia due to
increased hepatic synthesis, impaired fibrinolysis
and increased platelet aggregability.
• As a consequence of these perturbations,
patients can develop spontaneous peripheral
arterial or venous thrombosis, renal vein
thrombosis and pulmonary embolism.
Other metabolic complications of
nephrotic syndrome include
• Protein malnutrition and iron-resistant microcytic
hypochromic anemia due to transferrin loss
• Hypocalcemia and secondary hyperparathyroidism
can occur as a consequence of vitamin D deficiency
due to enhanced urinary excretion of cholecalciferolbinding protein, whereas loss of thyroxine-binding
globulin can result in depressed thyroxine levels.
• An increased susceptibility to infection may reflect
low levels of IgG that result from urinary loss and
increased catabolism.
• In addition, patients are prone to unpredictable
changes in the pharmacokinetics of therapeutic agents
that are normally bound to plasma proteins.
Proteinuria
• It should be stressed that the key component of
nephrotic syndrome is proteinuria, which results
from altered permeability of the glomerular
filtration barrier for protein, namely the GBM and
the podocytes and their slit diaphragms.
• The other components of the nephrotic
syndrome and the ensuing metabolic
complications are all secondary to urine protein
loss and can occur with lesser degrees of
proteinuria or may be absent even in patients
with massive proteinuria.
Six entities account for 90% of cases
of nephrotic syndrome in adults
•
•
•
•
minimal change disease (MCD)
focal and segmental glomerulosclerosis (FSGS)
membranous glomerulopathy
membranoproliferative glomerulonephritis
(MPGN)
• diabetic nephropathy
• amyloidosis
Essentials of Diagnosis
• Urine protein excretion > 3.5 g/1.73 m2 per
24 hours.
• Hypoalbuminemia (albumin < 3 g/dL).
• Peripheral edema.
Poststreptococcal acute
glomerulonephritis
• Beta hemolytic group A streptococcus, type
4,12,23,25
• At 7-12 days after streptococcal infection
• Pro-s: - history of infection
- epidemiology
- streptococcus positive cultures
- ↑ASLO
Predisposing factors
•
•
•
•
Age – maximum incidence at 5-10 yrs
Sex – men>women
Cold
Fatigue
Pathogenesis
• Circulating immune complexes accumulated in
glomeruli – inflammatory reaction
Onset
• Sudden (rare) – fever
- chills
- headache
- vomiting
- lumbar pain
- olyguria
• Insidious (frequent) – malaise
- anorexia
- low fever
- lumbar pain
Urinary syndrome
•
•
•
•
•
Olyguria
High urine density
Medium proteinuria (2-3 g/24h)
Hematuria (micro/macroscopic)
Casts
Cardio-vascular syndrome
•
•
•
•
HBP
Bradicardia
Heart failure
Ecg: T wave aplatization, ↓ ST, rithm
disorders
Edema
• White, smooth
• For the beginning – face (eyelids, periorbitary
region)
• Limbs, generalised
Neurological disorders
•
•
•
•
Amaurosis
Vomiting
Headache
Seizures
Chronic glomerulonephritis
• Microscopic hematuria
• Medium proteinuria
• Absence of edema (except when nephrotic
syndrome)
• Signs of renal failure (advanced stages)
Urinary tract infections
Classification
• Acute infections of the urinary tract can be
subdivided into two general anatomic
categories: lower tract infection (urethritis
and cystitis) and upper tract infection (acute
pyelonephritis, prostatitis and intrarenal and
perinephric abscesses).
Cystitis
• Patients with cystitis usually report dysuria,
frequency, urgency, and suprapubic pain.
• The urine often becomes grossly cloudy and
malodorous, and it is bloody in 30% of cases.
Acute pielonephritis
• Symptoms of acute pyelonephritis generally
develop rapidly over a few hours or a day and
include a fever (39-40 C), shaking chills, nausea,
vomiting and diarrhea.
• Symptoms of cystitis may or may not be present.
• Besides fever, tachycardia and generalized muscle
tenderness, physical examination reveals marked
tenderness on deep pressure in one or both
costovertebral angles or on deep abdominal
palpation.
• In some patients, signs and symptoms of gramnegative sepsis predominate.
• Most patients have significant leukocytosis and
bacteria detectable in Gram-stained unspun
urine.
• Piuria and leukocyte casts are present in the
urine of some patients and the detection of these
casts is pathognomonic.
• Hematuria may be demonstrated during the
acute phase of the disease; if it persists after
acute manifestations of infection have subsided,
a stone, a tumor or tuberculosis should be
considered.
Diagnosis
• Blood tests
• Urinalysis
• Renal ultrasound
Urinalysis
• Determination of the number and type of
bacteria in the urine is an extremely important
diagnostic procedure.
• In symptomatic patients, bacteria are usually
present in the urine in large numbers
(100000/mL).
• In asymptomatic patients, two consecutive urine
specimens should be examined bacteriologically
before therapy is instituted and 100000 bacteria
of a single species per milliliter should be
demonstrable in both specimens.
Microscopy of urine
• Microscopic bacteriuria, which is best assessed with
Gram-stained uncentrifuged urine, is found in 90% of
specimens from patients whose infections are
associated with colony counts of at least 100000/mL
and this finding is very specific.
• Bacteria cannot usually be detected microscopically in
infections with lower colony counts (10,000/mL).
• The detection of bacteria by urinary microscopy thus
constitutes firm evidence of infection, but the absence
of microscopically detectable bacteria does not exclude
the diagnosis.
Sterile pyuria
• may indicate infection with unusual bacterial
agents
• C. trachomatis
• U. urealyticum
• Mycobacterium tuberculosis
• Fungi
• may be demonstrated in noninfectious urologic
conditions such as calculi, anatomic abnormality,
nephrocalcinosis, vesicoureteral reflux, interstitial
nephritis or polycystic disease
The surgically removed kidney is swollen and its surface shows whitish zones.
A section shows white suppurative areas (scattered with small abscesses) extending
eccentrically from the medulla to the cortex. There also were sloughed papillae
UROLOGIC EVALUATION
• Urologic evaluation should be performed in selected
instances— namely, in women with relapsing infection,
a history of childhood infections, stones or painless
hematuria or recurrent pyelonephritis.
• Most males with UTI should be considered to have
complicated infection and thus should be evaluated
urologically.
• Men or women presenting with acute infection and
signs or symptoms suggestive of an obstruction or
stones should undergo prompt urologic evaluation,
generally by means of ultrasound.
Prognosis
• Acute uncomplicated pyelonephritis in adults
rarely progresses to renal functional
impairment and chronic renal disease.
• Repeated upper tract infections often
represent relapse rather than reinfection and
a vigorous search for renal calculi or an
underlying urologic abnormality should be
undertaken.
Chronic pielonephritis
• Insidious onset
• Symptoms and signs of acute pielonephritis
General signs
•
•
•
•
Astenia
Fever
Headaches
Nausea and vomiting
Renal signs
•
•
•
•
Lumbar pain
Polakiuria
Disuria
Piuria
Signs of sclerotic lesions
• HBP
• CRF
Urinalysis
•
•
•
•
•
Piuria
Sternhelmer – Malbin cells
Leucocyte casts
Proteinuria
Positive urine cultures
Renal function
• Low urine concentration
• Low PSP retention (less than 30% in 15 min)
• Low creatinine clearence – renal failure
Blood tests
•
•
•
•
•
Leucocytosis
↑ alfa-2 and gammaglobulins
Hyponatremia
Acidosis
↑ureea and creatinine levels (advanced
disease)
Investigations
• Abdominal X-ray: lithiasis, renal asymetry
• IVU: reduced renal mass, unregulated shape,
thiner cortical, lithiasis
• Abdominal ultrasound
• CT
nephrolithiasis
TYPES OF STONES
• Calcium salts, uric acid, cystine and struvite
(MgNH4PO4) are the basic constituents of
most kidney stones in the western
hemisphere.
• Calcium oxalate and calcium phosphate stones
make up 75 to 85% of the total and may be
admixed in the same stone.
Manifestations
• As stones grow on the surfaces of the renal papillae or
within th collecting system, they need not produce
symptoms.
• Asymptomatic stones may be discovered during the
course of radiographic studies undertaken for
unrelated reasons.
• Stones rank, along with benign and malignant
neoplasms, and renal cysts, among the common causes
of isolated hematuria.
• Much of the time, however, stones break loose and
enter the ureter or occlude the ureteropelvic junction,
causing pain and obstruction.
STONE PASSAGE
• A stone can traverse the ureter without
symptoms, but passage usually produces pain
and bleeding. The pain begins gradually,
usually in the flank, but increases over the
next 20 to 60 min to become so severe that
narcotic drugs may be needed for its control.
• The pain may remain in the flank or spread
downward and anteriorly toward the
ipsilateral loin, testis or vulva.
STONE PASSAGE
• Pain that migrates downward indicates that the
stone has passed to the lower third of the ureter,
but if the pain does not migrate, the position of
the stone cannot be predicted.
• A stone in the portion of the ureter within the
bladder wall causes frequency, urgency, and
dysuria that may be confused with urinary tract
infection.
• The vast majority of ureteral stones less than 0.5
cm in diameter will pass spontaneously.
PATHOGENESIS OF STONES
• Urinary stones usually arise because of the
breakdown of a delicate balance. The kidneys
must conserve water, but they must excrete
materials that have a low solubility. These two
opposing requirements must be balanced during
adaptation to diet, climate and activity.
• When the urine becomes supersaturated with
insoluble materials, because excretion rates are
excessive and/or because water conservation is
extreme, crystals form and may grow and
aggregate to form a stone.
Symptoms
• Lumbar pain – renal colic
• Digestive intolerance (nausia, vomiting)
• Hematuria (micro/macroscopic)
Signs
• + Giordano
• Uretral pain
Urinalysis
• Hematuria
• Leucocyturia
• Leucocyte casts
Investigations
•
•
•
•
Echo-litiasis
X-ray-radio-opaque stones
IVU-radio-transparent stones
CT
Evaluation
• Most patients with nephrolithiasis have
remediable metabolic disorders that cause
stones and can be detected by chemical
analyses of serum and urine.
Renal cell carcinoma
Epidemiology
• Renal cell carcinoma represents 2% of all
cancers and 2% of all cancer deaths.
• Worldwide, the mortality from renal cell
carcinoma was estimated to exceed 100,000
per year
Classification
• Renal cell carcinomas have historically been classified
according to cell type (clear, granular, spindle, or oncocytic)
and growth pattern (acinar, papillary, or sarcomatoid).
• This classification has undergone a transformation to more
accurately reflect the morphologic, histochemical, and
molecular basis of differing types of adenocarcinomas .
• Based on these studies, five distinct subtypes have been
identified. These include clear cell (conventional),
chromophilic (papillary), chromophobic, oncocytic, and
collecting duct (Bellini duct) tumors.
• Each of these tumors has a unique growth pattern, cell of
origin, and cytogenetic characteristics.
Clinical manifestations
• The clinical presentation of renal cell carcinoma can be extremely
variable.
• Many tumors are clinically occult for much of their course, thus
delaying diagnosis. Indeed, 25% of individuals have distant
metastases or locally advanced disease at the time of presentation.
By contrast, other patients harboring renal cell carcinoma
experience a wide array of symptoms or have a variety of
laboratory abnormalities, even in the absence of metastatic
disease.
• This propensity of renal cell carcinoma to present itself as a panoply
of diverse and often obscure signs and symptoms has led to its
being labeled the “internist's tumor.”
• The increasing incidental discovery of renal cancer on abdominal
imaging, mentioned previously, has led to the re-characterization of
the disease as the “radiologists tumor.”
Symptoms
•
•
•
•
Lumbar pain
Abdominal or flank mass
Wheight loss
Hematuria
• The classic triad of flank pain, hematuria and
palpable abdominal renal mass occurs in at most
9% of patients and when present it strongly
suggests advanced disease
Metastatic signs
• Most (75%) patients presenting with metastatic
disease have lung involvement. Other common
sites include lymph nodes, bone and liver.
• Patients may present with pathologic fractures,
cough, hemoptysis, dyspnea related to pleural
effusions or palpable nodal masses.
• Clear cell pathology in the metastatic lesion or
the finding of a renal mass on staging CT scan (or
both) usually leads to the proper diagnosis.
• Fever is one of the more common manifestations of
renal cell carcinoma, occurring in up to 20% of
patients.
• It is usually intermittent and is often accompanied by
night sweats, anorexia, weight loss and fatigue.
• Anemia is also common in patients with renal cell
carcinoma and frequently precedes the diagnosis by
several months. Although hematuria, hemolysis or
bone marrow replacement by tumor may be
contributing factors, the anemia is often out of
proportion to these factors. It can be either normocytic
or microcytic and is frequently associated with both
low serum iron titer and low iron-binding capacity that
is typical of the anemia of chronic disease.
• Hepatic dysfunction in the absence of metastatic
disease is noted and labeled “Stauffer's syndrome”.
• A spectrum of paraneoplastic syndromes has
been associated with these malignancies,
including erythrocytosis, hypercalcemia,
nonmetastatic hepatic dysfunction (Stauffer
syndrome) and acquired dysfibrinogenemia.
• Erythrocytosis is noted at presentation in only
about 3% of patients.
• Anemia, a sign of advanced disease, is more
common.
Investigations
• Blood tests - ↑ ESR
- Anemia
- Polyglobulia
• X-ray – enlarged renal shadow
• Echo – tumoral mass
• Selective renal arteriography
Investigations
• The standard evaluation of patients with
suspected renal cell tumors includes:
•
•
•
•
a CTscan of the abdomen and pelvis
a chest radiograph
urine analysis
urine cytology
• For patients with symptoms suggestive of renal cell
carcinoma, numerous radiologic approaches are
available for the evaluation of the kidney.
• With the advent of CT, magnetic resonance imaging
and sophisticated ultrasonography, many of the more
invasive procedures of the past are largely of historical
interest and rarely used in clinical practice.
• Although intravenous pyelography remains useful in
the evaluation of hematuria, CT and ultrasonography
are the mainstays of evaluation of a suspected renal
mass.
• As seen on CT, the typical renal cell carcinoma is
generally greater than 4 cm in diameter, has a
heterogeneous density and enhances with contrast.
MTS evaluation
• A CT of the chest is warranted if metastatic disease is
suspected from the chest radiograph, as it will detect
significantly smaller lesions, and their presence may
influence the approach to the primary tumor.
• MRI is useful in evaluating the inferior vena cava in
cases of suspected tumor involvement or invasion by
thrombus, as well as for patients in whom contrast
cannot be administered owing to either allergy or renal
dysfunction.
• In clinical practice, any solid renal masses should be
considered malignant until proven otherwise; a
definitive diagnosis is required.
Differential diagnosis
• cysts
• benign neoplasms (adenoma, angiomyolipoma,
oncocytoma)
• inflammatory (pyelonephritis or abscesses)
• other primary or metastatic malignant neoplasms
• Other malignancies that may involve the kidney include
transitional cell carcinoma of the renal pelvis,
sarcoma, lymphoma, Wilms’ tumor and metastatic
disease, especially from melanoma.
Staging
Two staging systems used commonly are:
• Robson classification and
• American Joint Committee on Cancer (AJCC)
staging system
The Robson system
• stage I tumors are confined to the kidney;
• stage II tumors extend through the renal
capsule but are confined to Gerota’s fascia;
• stage III tumors involve the renal vein or vena
cava (stage III A) or the hilar lymph nodes
(stage III B);
• stage IV disease includes tumors that are
locally invasive to adjacent organs (excluding
the adrenal gland) or distant metastases.
Prognosis
The rate of 5-year survival varies by stage:
• 66% for stage I
• 64% for stage II
• 42% for stage III
• 11% for stage IV
• The prognosis for patients with stage IIIA lesions
is similar to that of stage II disease; 5-year
survival for patients with stage IIIB disease is only
20%, closer to that of stage IV.
Essentials of Diagnosis
• Gross or microscopic hematuria.
• Flank pain or mass in some patients.
• Systemic symptoms such as fever, weight loss
may be prominent.
• Solid renal mass on imaging.