ANALYSIS IN URINE AND BODY FLUIDS
MIDTERMS, 1st SEM 2022
WEEK 8: RENAL DISEASE
Introduction
• Classification of renal disease – based on the
AREA of the kidney that is affected
▪ Glomerular disorders (affected area:
glomerulus)
▪ Tubular disorders (affected area:
tubules)
▪ Interstitial disorders (affected area:
surroundings or spaces that surrounds
the kidney)
• Basic knowledge of these disorders can be
helpful when analyzing the results of a routine
urinalysis.
Glomerular disorder
Causes:
1. Immunologic disorders
• Most glomerular disorders results from
immunologic disorders
• One example of phenomenon that causes
kidney disorders are immune complexes
formed as a result of immunologic
reactions
• IgA circulate into the bloodstream and
deposited on the glomerulus
• Components of immune system
(Complement, neutrophil, lymphocytes ,
monocytes and cytokines) bind to
glomerulus and start an immunologic
reaction that damage the glomerulus.
• Depending on the immune system
mediators involved, damage may consist
of cellular infiltration or proliferation
resulting in thickening of the glomerular
basement membrane, and complement-
mediated damage to the capillaries and
basement membrane.
2. Non-immunologic disorders
• Exposure to toxic chemicals and toxin
• Disruption of electrical membrane
charges
• Deposition of amyloid material that
may involve
• Chronic inflammation and acute
phase reactants basement membrane
thickening associated w/ Diabetic
nephropathy
• Glomerulonephritis
• Membranous glomerulonephritis
• Membranoproliferative glomerulonephritis
• Chronic glomerulonephritis
• Nephrotic syndrome
• Minimal change disease
• Focal segmental glomerulosclerosis
• Alport syndrome
• Diabetic nephropathy
Glomerulonephritis
• Inflammation of the glomerulus
• Positive with blood, protein and cast in the
urine.
• Sterile, inflammatory process that affects the
glomerulus
Ex.
o Acute post-streptococcal
glomerulonephritis.
o Rapidly progressive glomerulonephritis
o Goodpasture syndrome
o Wegener’s granulomatosis
o Henoch-schonlein purpura
ADDED NOTES:
• The term glomerulonephritis refers to a
sterile, inflammatory process.
• may progress from one form to another (i.e.,
rapidly progressive glomerular nephritis to
chronic glomerulonephritis to the nephrotic
syndrome and eventual renal failure).
Acute post-streptococcal glomerulonephritis
• Acute – fast; Post – post infection
• Clinical signs and symptoms:
- Fever
- Edema (most noticeable in the eyes)
- Fatigue
- Oliguria
- Hematuria
• Symptoms occur following in respiratory
infection caused by certain strains of group A
streptococcus
• Confirmatory: ASO titer
ADDES NOTES:
• Edema -abnormal accumulation of fluid in
certain tissues within the body. (most
noticeably around the eyes)
Group A Streptococcus
- Streptococcus pyogenes
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- Contain M protein in their cell wall
Pathophysiology:
- these nephrogenic strains of streptococci
form immune complexes with their
corresponding circulating antibodies and
become deposited on the glomerular
membranes. → affects glomerular function →
Primary urinalysis findings include marked
hematuria, proteinuria, and oliguria,
accompanied by red blood cell (RBC) casts,
dysmorphic RBCs, hyaline and granular casts,
and white blood cells (WBCs).
- Elevated ASO titer indicates post-infection.
Rapidly progressive glomerulonephritis
• A.k.a crescentic glomerulonephritis
• It is a more serious form of acute glomerular
disease.
• Deposition of immune complexes from
systemic immune disorders on the glomerular
membrane
• Poor prognosis (low chance of recovery)
• It can progress to renal failure (low chance of
recovery)
ADDED NOTES:
• Symptoms are initiated by the deposition of
immune complexes in the glomerulus, often as
a complication of another form of
glomerulonephritis or an immune systemic
disorder such as systemic lupus
erythematosus (SLE).
Pathophysiology:
• Damage by macrophages to the capillary walls
releases cells and plasma into Bowman’s space,
and the production of crescentic formations
containing macrophages, fibroblasts, and
polymerized fibrin, causes permanent damage
to the capillary tufts → Initial laboratory results
are similar to acute glomerulonephritis but
become more abnormal as the disease
progresses, including markedly elevated protein
levels and very low glomerular filtration rates.
• Some forms may demonstrate increased fibrin
degradation products, cryoglobulins, and the
deposition of IgA immune complexes in the
glomerulus
• Cryoglobulin - any of a group of abnormal
plasma proteins, typically appearing in certain
hematological, autoimmune, and infectious
diseases, that become insoluble at temperatures
below the core body temperature and may
obstruct blood flow, especially in the skin.
Goodpasture Syndrome
• Autoimmune disorder
• Fight your own body
• A cytotoxic autoantibody can appear against
the glomerular and alveolar basement
membranes after viral respiratory infections
• Initial pulmonary complaints are hemoptysis
(coughing blood) and dyspnea (difficulty in
breathing)
• Progression to chronic glomerulonephritis and
endstage renal failure is common
ADDED NOTES:
Pathophysiology:
- antiglomerular basement membrane
antibody
- Attachment of this autoantibody to the
basement membrane, followed by
complement activation, produces the capillary
destruction.
- Detected in patient serum.
Hemoptysis coughing up of blood.
Dyspnea difficulty in breathing.
Urinalysis results include proteinuria, hematuria, and
the presence of RBC casts.
Wegener’s Granulomatosis
• causes a granuloma-producing inflammation
of the small blood vessels primarily of the
kidney and respiratory system
• Antineutrophilic cytoplasmic antibody
• Patients usually present first with pulmonary
symptoms and later develop renal
involvement.
ADDED NOTES:
Pathophysiology:
• The binding of these autoantibodies to the
neutrophils located in the vascular walls may
initiate the immune response and the resulting
granuloma formation.
• Testing for ANCA includes incubating the
patient’s serum with either ethanol or
formalin/formaldehyde-fixed neutrophils and
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examining the preparation using indirect
immunofixation to detect the serum antibodies
attached to the neutrophils.
• If the neutrophils are fixed in ethanol, the
antibodies form a perinuclear pattern called p-
ANCA.
• fixed with formalin/formaldehyde, the pattern is
granular throughout the cytoplasm called c-
ANCA
Henoch-Schönlein Purpura
• Occurs primarily in children following viral
respiratory infections
• initial symptoms include the appearance of
raised, red patches on the skin.
ADDED NOTES:
Henoch-Schonlein purpura (also known as IgA
vasculitis) is a disorder that causes the small blood
vessels in your skin, joints, intestines, and kidneys to
become inflamed and bleed.
• Respiratory and gastrointestinal symptoms,
including blood in the sputum and stools, may
be present.
• Renal involvement is the most serious
complication of the disorder and may range
from mild to heavy proteinuria and hematuria
with RBC casts.
• Complete recovery with normal renal function is
seen in more than 50% of patients.
Membranous glomerulonephritis
• Thickening of the glomerular
• nephrotic syndrome symptoms frequently
develop. There may also be a tendency toward
thrombosis
• Laboratory findings:
o hematuria and elevated urine protein
excretion that may reach concentrations
similar to those in the nephrotic
syndrome
ADDED NOTES:
• Caused by IgG immune complex deposition
associated with systemic disorders.
• systemic lupus erythematosus
• Sjögren syndrome - autoimmune disorder
characterized by dryness of mouth and eyes.
• secondary syphilis
• hepatitis B
• gold and mercury treatments
• malignancy.
Membranoproliferative glomerulonephritis
• Cellular proliferation affecting the capillary walls
or the glomerular basement membrane, possibly
immune-mediated.
• Type 1 and Type 2
Type 1
- Increase cellularity in subendothelial cells of
mesangium. Interstitial area of the bowmans
capsule
- Thickening of the capillary walls
- Poor prognosis
- Progress to nephrotic syndrome
Type 2
- Dense deposit in the glomerular basement
membrane
- Symptoms is similar to chronic
glomerulonephritis
Chronic glomerulonephritis
• Marked decrease in renal function resulting
from glomerular damage precipitated by other
renal disorders.
• Laboratory findings:
- hematuria, proteinuria, glucosuria as a result
of tubular dysfunction, and many varieties of
casts, including broad casts
• Depending on the amount and duration of the
damage to the glomerulus in the previously
discussed glomerular disorders, progression to
chronic glomerulonephritis and end-stage renal
disease may occur.
• Gradually worsening symptoms include fatigue,
anemia, hypertension, edema, and oliguria.
IMMUNOGLOBULIN A NEPHROPATHY
• “Berger disease”
• PRINCIPLE: Deposition of IgA on the glomerular
membrane resulting from increased levels of
serum IgA (mucosal infection)
• Seen in children and young adults
ADDED NOTES:
• Patients have increased serum levels of IgA,
which may be a result of a mucosal infection.
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• Patients usually present with an episode of
macroscopic hematuria following an infection or
strenuous exercise.
• a patient with the disorder may remain
essentially asymptomatic for 20 years or more;
however, there is a gradual progression to
chronic glomerulonephritis and end-stage renal
disease.
Nephrotic syndrome
• Non-immunologic disorder
• Disruption of the electrical charges that
produce the tightly fitting podocyte barrier
resulting in massive loss of protein and lipids
o If podocyte are no longer tightly fit,
there is no barrier and substances will
pass through
• Massive proteinuria (greater than 3.5 g/day)
o Protein: most of it will exit in the final
urine causing massive proteinuria
• Low levels of serum albumin, increased level
of serum lipids.
• Urinalysis findings: proteinuria, fat droplets,
oval fat bodies, RTE cells, epithelial, fatty and
waxy cast
• >3.5g/day
• Normal <10mg/dL or 100mg/day
ADDED NOTES:
Pathophysiology:
• damage to the shield of negativity and the
podocytes → Increased permeability of the
glomerular membrane; less tightly connected
barrier → facilitates passage of high-
molecular-weight proteins and lipids and
negatively charged albumin into the urine.
• Albumin is the primary protein depleted from
the circulation
→ hypoalbuminemia
→ stimulate increased lipid
production by the liver
→ lower oncotic pressure in the
capillaries → increases fluid loss into the
interstitial spaces, which, accompanied by
sodium retention, produces edema. Depletion of
immunoglobulins and coagulation factors →
increased risk of infection and coagulation
disorders.
• Both tubular and glomerular damage occurs,
and the nephrotic syndrome may progress to
chronic renal failure
Minimal Change Disease
• A.K.A lipid nephrosis
• damage to the podocytes and the shield of
negativity, allowing for increased protein
filtration.
• Clinical findings:
- edema, heavy proteinuria, transient
hematuria, and normal BUN and
creatinine results.
• Responds well to corticosteroids, prognosis is
generally good.
ADDED NOTES:
• Although the etiology is unknown at this time,
allergic reactions, recent immunization, and
possession of the human leukocyte antigen-
B12 (HLA-B12) antigen have been associated
with this disease.
Focal segmental glomerulosclerosis
• Disruption of podocytes in certain areas of
glomeruli associated with heroin and
analgesic abuse and AIDS.
• May resemble nephrotic syndrome or
minimal change disease.
• focal segmental glomerulosclerosis (FSGS)
affects only certain numbers and areas of
glomeruli, and the others remain normal.
• Immune deposits, primarily immunoglobulin
M and C3, are a frequent finding and can be
seen in undamaged glomeruli.
Alport syndrome
• Genetic disorder showing lamellated and
thinning of glomerular basement membrane
• Males are frequently more severely affected
than females.
• Slow progression to nephrotic syndrome and
end-stage renal disease
• an inherited disorder of collagen production
affecting the glomerular basement
membrane. The syndrome can be inherited as
a sex-linked or autosomal genetic disorder.
• No evidence of glomerular antibodies is
present
Diabetic nephropathy
• A.K.A Kimmelstiel - Wilson disease
• most common cause of end-stage renal
disease.
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• Associated with deposition of glycosylated
proteins resulting from poorly controlled
blood glucose levels.
• increased proliferation of mesangial cells and
increased deposition of cellular and
noncellular material within the glomerular
matrix → accumulation of solid substances
around the capillary tufts
Tubular Disorder
• Tubules are affected
o Most common is the reabsorption
process
• Types of tubular disorders:
o Acute tubular necrosis
o Fanconi syndrome
o Nephrogenic diabetes insipidus
o Renal glucosuria
• tubular function is disrupted as a result of
actual damage to the tubules and those in
which a metabolic or hereditary disorder
affects the intricate functions of the tubules
Acute tubular necrosis
• Necrosis – abnormal cellular depth
• damage to the renal tubule caused by
ischemia (restriction in blood flow, causing
lack of oxygen and death of cells) or toxic
agents.
• Disorders causing ischemic ATN: shock,
trauma, and surgical procedures.
• Toxic agents: aminoglycoside antibiotics,
amphotericin B, cyclosporine, radiographic
dye, organic solvents and toxic mushrooms,
filtration of large amounts of hemoglobin and
myoglobin.
• Laboratory findings:
o mild proteinuria, microscopic
hematuria, and, most noticeably, the
presence of RTE cells and RTE cell casts
containing tubular fragments
consisting of three or more cells
ADDED NOTES:
• Ischemia - inadequate blood supply to an
organ or part of the body
• Damage to the RTE cells may be produced by
decreased blood flow that causes a lack of
oxygen presentation to the tubules (ischemia)
or the presence of toxic substances in the
urinary filtrate.
• “Shock”
o is a general term indicating a severe
condition that decreases the flow of blood
throughout the body
o e.g. cardiac failures, sepsis involving
toxigenic bacteria, anaphylaxis, massive
hemorrhage, and contact with high-
voltage electricity
• Exposure to a variety of nephrotoxic agents
can damage and affect the function of the RTE
cells
• As a result of the tubular damage, a variety of
other casts may be present, including hyaline,
granular, waxy, and broad
Fanconi syndrome
• A generalized failure of tubular reabsorption
in the proximal convoluted tubule (PCT –
major reabsorption site).
• Inherited in association with cystinosis and
Hartnup disease or acquired through
exposure to toxic agents including heavy
metals and outdated tetracycline, or seen as a
complication of multiple myeloma and renal
transplant
• Laboratory findings:
o glycosuria with a normal blood glucose
and possible mild proteinuria.
o Urinary pH can be very low due to the
failure to reabsorb bicarbonate.
ADDED NOTES:
• Hereditary and Metabolic Tubular Disorders
o Disorders affecting tubular function may be
caused by systemic conditions that affect or
override the tubular reabsorptive maximum
(Tm) for particular substances normally
reabsorbed by the tubules.
o by failure to inherit a gene or genes required
for tubular reabsorption
Uromodulin-Associated Kidney Disease
• primarily an inherited disorder caused by an
autosomal mutation in the gene that
produces uromodulin
• The mutation also causes an increase in serum
uric acid, resulting in persons developing gout
as early as the teenage years before the onset
of detectable renal disease
ADDED NOTES:
• mutation causes a decrease in the production
of normal uromodulin that is replaced by the
abnormal form → abnormal uromodulin is
still produced by the tubular cells and
accumulates in these cells, resulting in their
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destruction, which leads to the need for renal
monitoring and eventual renal
transplantation.
Nephrogenic Diabetes insipidus
• inherited as a sex-linked recessive gene
• acquired from medications
• It also may be seen as a complication of
polycystic kidney disease and sickle cell
anemia.
• excessive amounts of urine are excreted
• Laboratory findings:
o low specific gravity, pale yellow color, and
possible false-negative results for
chemical tests
ADDED NOTES:
• Nephrogenic DI - inability of the renal tubules
to respond to ADH
• Neurogenic DI - failure of the hypothalamus
to produce ADH
→ excessive amounts of urine are
excreted
• medications including lithium and
amphotericin B.
Renal glycosuria
• renal glucosuria affects the reabsorption of
glucose.
• The disorder is inherited as an autosomal
recessive trait.
ADDED NOTES:
• In inherited renal glucosuria either the
number of glucose transporters in the tubules
is decreased or the affinity of the transporters
for glucose is decreased.
• In contrast to Fanconi syndrome, which
exhibits a generalized failure to reabsorb
substances from the glomerular filtrate, renal
glucosuria affects only the reabsorption of
glucose
• Patients with renal glycosuria have increased
urine glucose concentrations with normal
blood glucose concentrations
Interstitial Disorders
• The majority of these disorders involve
infections and inflammatory conditions.
• Types of interstitial disorders:
o Cystitis (inflammation of the urinary
bladder)
o Acute Pyelonephritis
o Chronic pyelonephritis
o Acute interstitial nephritis
• Pyelonephritis – one or both kidneys are
infected
ADDED NOTES:
• Considering the close proximity between the
renal tubules and the renal interstitium,
disorders affecting the interstitium also affect
the tubules
• “tubulointerstitial disease”
Cystitis
• Ascending bacterial infection of the bladder.
• Cystitis is seen more often in women and
children.
• Inherited as an autosomal recessive trait
Acute pyelonephritis
• Result of ascending movement of bacteria
from a lower UTI into the renal tubules and
interstitium
• Vesicoureteral reflux.
ADDED NOTES:
• Infection of the upper urinary tract, including
both the tubules and interstitium, is termed
pyelonephritis
• enhanced with conditions that interfere with
the downward flow of urine from the ureters
to the bladder or the incomplete emptying of
the bladder during urination.
o obstructions such as renal calculi,
pregnancy, and reflux of urine from the
bladder back into the ureters
(vesicoureteral reflux)
• reflux (pagbalik) of urine from the bladder
back into the ureters (next is the kidney)
Chronic pyelonephritis
• Recurrent infection of the renal tubules and
interstitium caused by structural abnormalities
affecting the flow of urine.
• The structural abnormalities may cause reflux
between the bladder and ureters or within the
renal pelvis, affecting emptying of the
collecting ducts
ADDED NOTES:
• As its name implies, chronic pyelonephritis is a
serious disorder that can result in permanent
damage to the renal tubules and possible
progression to chronic renal failure.
• Congenital urinary structural defects producing
reflux nephropathy are the most frequent
cause of chronic pyelonephritis
• often diagnosed in children
Acute interstitial nephritis
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• Marked by inflammation of the renal
interstitium followed by inflammation of the
renal tubules.
• Primarily associated with an allergic reaction
to medications that occurs within the renal
interstitium, possibly caused by the
medication binding to the interstitial protein
• penicillin, methicillin, ampicillin,
cephalosporins, sulfonamides, NSAIDs, and
thiazide diuretics.
Renal failure
CAUSES OF ACURE RENAL FAILURE
Prerenal
Decrease blood pressure/cardiac output
Hemorrhage
Burns
Surgery
Septicemia
Renal
Acute glomerulonephritis
Acute Tubular Necrosis
Acute Interstitial Nephritis
Postrenal
Renal calculi
Tumors
Crystallization or ingested substance
• exhibits a sudden loss of renal function
• marked decrease in the glomerular filtration
rate (less than 25 mL/min)
• steadily rising serum BUN and creatinine
values
• electrolyte imbalance
• lack of renal concentrating ability producing
an isosthenuric urine
• Proteinuria
• renal glycosuria
• abundance of granular, waxy, and broad casts,
often referred to as a telescoped urine
sediment.
ADDED NOTES:
• AZOTEMIA - abnormally high levels of
nitrogen-containing compounds
• Causes - include a sudden decrease in blood
flow to the kidney (prerenal), acute
glomerular and tubular disease (renal), and
renal calculi or tumor obstructions (postrenal)
RENAL LITHIASIS
• Renal calculi (kidney stones) may form in the
calyces and pelvis of the kidney, ureters, and
bladder.
o Calcium oxalate – (primary component
of the kidney stone)
o Precipitate in the urinary pH (mostly
acidic pH)
• Severe pain radiating from the lower back to
the legs.
• Lithotripsy procedure using high-energy shock
waves can be used to break stones located in
the upper urinary tract into pieces that can
then be passed in the urine. Stones can also
be removed surgically.
ADDED NOTES:
• Renal calculi - “Kidney stones”
• In renal lithiasis, the calculi vary in size →
from barely visible to large, staghorn calculi
resembling the shape of the renal pelvis and
smooth, round bladder stones with diameters
of 2 or more inches.
• Small calculi may be passed in the urine,
subjecting the patient to severe pain radiating
from the lower back to the legs
• Larger stones cannot be passed and may not
be detected until patients develop symptoms
of urinary obstruction
• Conditions favoring the formation of renal
calculi are similar to those favoring the
formation of urinary crystals, including pH,
chemical concentration, and urinary stasis
• The presence of microscopic hematuria
resulting from irritation to the tissues by the
moving calculus is the primary urinalysis
finding.
Stones can be removed surgically
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