Denielle

Genesis B. Camato

VI. RENAL DISEASE

ANALYSIS O F URINALYSIS AND BODY FLUIDS | REVIEWER

GLOMERULAR

{
{

v
v
v
v
v
v

IMMUNOLOGIC DISORDERS:
R
Immune complexes (IgA)
R
Complement
R
Neutrophils
R
Lymphocytes
R
Cytokines
NON-IMMUNOLOGIC DISORDERS
R
Exposure to chemicals and toxins
SYSTEMIC DISORDERS
R
Nephrotic syndrome
R
Deposition of amyloid material from systemic
disorders that may involve chronic inflammation &
acute-phase reactants
R
The basement membrane thickening associated
with diabetic nephropathy

{
{

VASCULITIS

HENOCH-SCHONLEIN purpura (latin word, purple) red or purple

discolorations: Bleeding under the skin

Viral respiratory infection

HIV
Hepatitis
Syphilis
LE
Strep Grp A infection
INSTERTITIAL
VASCULAR

GLOMERULONEPHRITIS

Sterile inflammatory process affects the glomerulus

May find blood, protein, casts in urine

v
Acute glomerular nepehritis (AGN)
v
Chronic glomerular nephritis (CGN)
v
Renal failure
ACUTE STREPTOCOCCAL GLOMERULONEPHRITIS

Symptoms usually occur in children and young adults

ffg respiratory infection

Elevated BUN

Usually with Group A strep infection ; EDEMA most

noticeably around the eyes

ASO titer ; provides evidence that the disease is of

streptococcal origin

RAPIDLY PROGRESSIVE (CRESCENTIC)

GLOMERULONEPHRITIS RPGN

Most serious form of acute glomerular disease

Poor prognosis [renal failure

Deposition of immune complexes in the glomerulus;

accompanied by other immune systemic disorder (SLE)

Elevated protein levels and low glomerular filtration

rate

Increased fibrin degradation products, cryoglobulins,

deposition of IgA immune complexes

WEGENERS GRANULOMATOSIS

Granuloma-producing inflammation of the small blood

vessels

Diagnosis: ANTINEUTROPHILIC CYTOPLASMIC

ANTIBODY (ANCA) in patients serum

Binding these autoantibodies to the neutrophils located

in the vascular walls may initiate the immune response
& the resulting granuloma formation; elevated BUN &
CREATININE
HENOCH-SCHONLEIN PURPURA

Occurring primarily in children following upper

respiratory infections

Raised, red patches on skin

Respiratory and gastrointestinal symptoms; Blood in

sputum and in stools

Proteinuria & hematuria with RBC casts; complete

recovery is seen in more than 50% patients
IMMUNOGLOBULIN A NEPHROPATHY

Also known as the Bergers disease, IgA nephropathy;

IgA complexes are deposited on the glomerular
membrane most common cause of
glomerulonephritis

Patients have increased serum levels of IgA; may

result to mucosal infection

Seen in young children & young adults

Macroscopic hematuria; patient may remain

asymptomatic for 20 years or more

Gradual progression to chronic glomerulonephritis and

ESRD
MEMBRANOUS GLOMERULONEPHRITIS

Thickening of the glomerular basement membrane

resulting from the deposition of immunoglobulin G
immune complexes.

Frequent development of nephrotic syndrome;

tendency towards thrombosis

GOOD PASTURES SYNDROME

Appearance of cytotoxic autoantibody against the

glomerular and alveolar basement membranes
(antiglomerular basement membrane antibody);
can be detected in patient serum

Morphologic changes to the glomeruli resembling the

RGPN

Initial pulmonary complaints:

HEMOPTYSIS and DYSPNEA [ development of hematuria

Sjorens syndrome
Secondary syphilis, Hepa B, Gold & Mercury
treatments; Microscopic hematuria, elevated
urine protein

MEMBRANOPROLIFATIVE GLOMERULONEPHRITIS (MPGN)

TYPE 1 Displays increased cellularity in the

subendothelial cells of the mesangium (interstitial area
of the Bowmans capsule) causing thickening of the
capillary walls [ nephrotic syndrome

WEGENERs Granulomatosis

TYPE 2 Displays extremely dense deposits in the

glomerular basement membrane [ chronic
glomerulonephritis

Denielle Genesis B. Camato

VI. RENAL DISEASE

ANALYSIS O F URINALYSIS AND BODY FLUIDS | REVIEWER

CHRONIC GLOMERULONEPHRITIS

Gradually worsening symptoms [ fatigue, anema,

hypertension, edema, oliguria

Hematuria, gulcosuria (tubular dysfunction), varieties of

cast including BROAD CASTS.

Increased BUN, CREATININE, electrolyte imbalance

NEPHROTIC SYNDROME

Marked by massive proteinuria (greater than 3.5g/dL),

low levels of serum albumin, high levels of serum lipids,
and pronounce edema.

Acute onset of the disorder [ systemic shock;

decreases blood pressure (hypotension) and flow of
blood in the kidney

Ensuing hypoalbuminemia appears to stimulate the

increased production of lipids by the liver

Lower oncotic pressure in the capillaries resulting from

the depletion of plasma albumin increases of the loss
of fluid in the interstitial spaces which is accompanied
by sodium retention thus producing edema

Urinalysis: proteinuria, fat droplets, oval fat bodies, RTE

cells, fatty & waxy cats, microscopic hematuria.

MINIMAL CHANGE DISEASE

Also known as LIPID NEPHROSIS

PODOCYTES appear to be less tightly fitting allowing for

the increased filtration of protein

Allergic reactions, recent immunization & possession of

the HUMAN LEUKOCYTE ANTIGEN B-12 (HLA -12) have
been associated

Prognosis is good, disease respond to corticosteroids

FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)

Affects only certain areas of glomeruli & others

remain normal

Often seen in association with abuse of heroin &

analgesics
TUBULAR DISORDERS

Actual damage to the tubules; hereditary disorder that

affects intricate functions of the tubules

ACUTE TUBULAR NECROSIS (ATN)

Primary disorder to the tubule; causes ischemia; lack of

oxygen presentation to the tubules

SHOCK= Cardiac failure, sepsis involving toxigenic

bacteria, anaphylaxis, massive hemorrhage, contact
with high voltage electricity

Proteinuria, microscopic hematuria, RTE cells, granular

cast, waxy, broad cast

HEREDITARY & METABOLIC TUBULAR DISORDER

FANCONIS SYNDROME- frequently associated with

tubular dysfunction; failure of tubular reabsorption in
the proximal convoluted tubule.

PCT glucose, amino acids, phosphorus, sodium,

potassium, HCO3, H20

May be inherited in association in cystinosis & HARTNUP

DISEASE

Exposure to toxic agents; complication of multiple

myeloma & renal transplant

INTERSITIAL DISORDER

TUBULOINTERSTITIAL DISEASE; close proximity

between renal tubules & renal instertitium.

UTI most common renal disease; may involve the lower

urinary tract (URETHRA & BLADDER) or the upper
urinary tract (RENAL PELVIC, TUBULES, &
INSTERTITIUM); reveals presence of numerous WBCs &
bacteria often accompanied by mild proteinuria &
hematuria & an increased in pH

CYSTITIS- infection of the bladder is most common

encountered.

ACUTE PYELONEPHRITIS

Infection of the upper urinary tract including both the

tubules & instertitium is termed as pyelonephritis and
can occur both in acute & chronic form

Bacteria ascending from a lower UTI into the renal

tubules and instertitum

Obstructions renal calculi (stones)

visicouretral reflux - reflux of the urine from the

bladder back into the ureters

Appropriate antibiotic therapy

CHRONIC PYELONEPHRITIS

Recurrent infection; more serious disorder can result in

permanent damage to the tubules & possible
progression to chronic renal failure

CONGENITAL URINARY STRUCTURAL defects producing

REFLUX NEPHROPATHY are the most frequent cause

Often diagnosed in children

ACUTE INSTERTITIAL NEPHRITIS (AIN)

Inflammation of the renal instertitium followed by

inflammation of the tubules.

Fever & skin rash are frequent initial symptoms

AIN is primarily associated with an allergic reaction to

medications that occurs within the renal instertitium;
possible binding of the medication to instertitial protein

Penicillin, methicillin, ampicillin, cephalosporin,

sulphonamides, thiazide diuretics

URINALYSIS: hematuria, proteinuria, numerous WBCs,

WBC casts

LEUKOCYTE STAINING for the presence of increased

Eosinophils maybe useful to confirm diagnosis

Treatment: corticosteroids

VASCULAR DISORDERS

Disorders include autoimmune disorders, vasculitis, and

diabetes mellitus that affects integrity of the renal
blood vessels.

Denielle Genesis B. Camato

VI. RENAL DISEASE

ANALYSIS O F URINALYSIS AND BODY FLUIDS | REVIEWER

RENAL FAILURE

Maybe in acute or chronic form; gradual progression

to chronic renal failure or ESR

ESRD decrease in glomerular filtration rate;

steadily rising of BUN & CREA (azotemia), electrolyte
imbalance, lack of concentrating ability producing an
isosthenuric urine, proteinuria, glycosuria, granular,
waxy, broad cast

Lithotripsy

ACUTE RENAL FAILURE (ARF)

exhibits sudden loss of renal function & is frequently

reversible

Magnesium ammonium phosphate (STUVITE),

uric acid, and cysteine are the other primary
calculi constituents.

PRE-RENAL

sudden decrease in renal blood flow to the kidney

(haemorrhage, burns, surgery, septicemia)
RENAL

acute glomerular and tubular disease, acute

pyelonephritis, acute instertitial nephritis

POST RENAL

renal calculi, tumors, obstructions, crystallization of

ingested substance

RENAL LITHIASIS

stones may form in the CALYCES and PELVIS of the

kidney, ureter, and bladder. Small stone may pass by in
urine thereby causing severe pain but larger stones
cannot

procedure using high energy shock waves that can be

used to break stones located in the upper urinary
tract into pieces that can be passed in the urine;
SURGICAL removal can also be employed
approximately 75% of stones are composed of CAOX
or PHOSPHATE.