- sudden onset of symptoms indicating
glomerular damages such as:
RENAL DISEASE
- Edema ( swelling)
1. Glomerular disease - Fever and fatigue
a. Affected the glomerulus - Hypertension ( high blood pressure)
2. Tubular Additional lab findings
a. Affected is the tubular - Increased BUN ( blood urea nitrogen)
3. Tubulointerstitial - Elevated ASO ( antistreptolysin O) titer
a. Affected is the lower urinary tract such Urinalysis findings:
as: - Gross hematuria ( visible blood in urine)
i. Urinary bladder - Proteinuria ( protein in urine )
ii. Urethra - RBC casts and dysmorphic RBCs ( indicating
iii. Ureter glomerular bleeding)
- Hyaline and granular casts
GLOMERULAR DISEASE - WBCs ( white blood cells in urine)
● Acute post streptococcal glomerulonephritis
● Rapidly progressive/ crescentic Rapidly progressive/ crescentic ( crescent )
glomerulonephritis glomerulonephritis
● Goodpasteur syndrome - A severe form of acute glomerular disease
● Wegener’s granulomatosis characterized by rapid loss of kidney function
● Henoch- schonlein purpura - Deposition of immune complexes associated
● Membranous glomerulonephritis with systemic immune disorder ( eg.
● Membranoproliferative glomerulonephritis Goodpasture syndrome, systemic lupus
● Chronic glomerulonephritis erythematosus)
● IgA nephropathy/ Berger’s disease - Damaged glomeruli
● Nephrotic syndrome - Crescent formation
● Alport syndrome Urinalysis findings
● Minimal change disease - Gross hematuria ( visible blood in urine)
● Focal segmental glomerulosclerosis - Proteinuria ( protein in urine )
● Diabetic nephropathy/ kimmelstiel - wilson - RBC casts and dysmorphic RBCs ( indicating
glomerular bleeding)
Tubular disease - Hyaline and granular casts
- WBCs ( white blood cells in urine)
● Acute tubular necrosis
● Fanconi’s syndrome
● Nephrogenic diabetes insipidus Goodpasteur syndrome
- (+) anti glomerular basement membrane
Tubulointerstitial disease - May lead to chronic glomerulonephritis and end
● Urinary tract infection - stage renal disease
● Acute interstitial nephritis - Signs and symptoms
- Hemoptysis and dyspnea
- Urinalysis:
OTHER RENAL DISORDERS - Hematuria, proteinuria, RBC casts
● Renal calculi/ lithiasis Antibody anti glomerular basement membrane are found
● Renal failure in the:
- Glomerular and Alveolar basement membrane
Acute post streptococcal glomerulonephritis
Wegener’s granulomatosis
- Deposition of immune complexes formed in
- Aka granulomatosis with polyangiitis (
response to a Group A streptococcal (
GPA)
Causative agent) infection
Clinical features
- (+) antineutrophil cytoplasmic antibody ( - Extremely dense deposits in GBM
ANCA) tubules
- It will bind to the neutrophil in the - Type 3
vascular walls that damages the small - Both sub endothelial and subendothelial
vessels in the lungs and glomerulus deposits
- Urinalysis
- Hematuria, proteinuria, RBC casts
Chronic glomerulonephritis
- Other lab finding:
- Increased serum BUN and creatinine - Gradual worsening of symptoms leading to loss
CLASSIFICATION of kidney functions
1. P- ANCA - Signs and symptoms
a. perinuclear - Fatigue,
b. Neutrophil fixed with ethanol - Anemia
2. C- ANCA - Hypertension
a. Cytoplasmic - Edema
b. Neutrophil is fixed with formalin - Oliguria
- Urinalysis
- Hematuria
Henoch- schonlein purpura
- Proteinuria
- Common in children following viral infections
- Glucosuria
- Allergic purpura that causes decrease int he - Isosthenuria
number of platelet and affects vascular integrity - Many casts
- Signs and symptoms - Other lab finding:
- Red skin patches, blood in sputum and - Increased BUN and creatinine,
stool electrolyte imbalance
- Urinalysis - Expected casts
- Proteinuria - Waxy casts
- Hematuria - Broad casts
- RBC casts
IgA nephropathy/ Berger’s disease
Membranous glomerulonephritis
- IgA deposition on the glomerular membrane
- Involves IgG depositions on the glomerular leading to thickening
membrane leading to pronounced thickening - Most common cause of glomerulonephritis
- Seen in SLE, Sjogren’s syndrome, secondary
syphilis and hepatitis B infection
Nephrotic syndrome
Urinalysis
- Hematuria - Acute onset may occur as a result of circulatory
- Proteinuria disruption causing systemic shock and decrease
in blood pressure
- Loss of albumin (-) causes decrease in capillary
Membranoproliferative glomerulonephritis
oncotic pressure and edema
- Cellular proliferation affecting capillary walls or - Urinalysis
the glomerular basement membrane - Massive proteinuria ( >3.5 g/ day)
- Urinalysis - Lipiduria ( fat droplet, oval fat bodies,
- Hematuria fatty, and waxy casts)
- Proteinuria - Hematuria
- Other lab findings: - Other lab findings:
- Decreased serum complement - Decrease serum albumin
- Type1 - Increase serum lipids
- Increase cellularity in the sub- = there is a disruption of electrical charges
endothelium
- Type 2
Alport syndrome damaging renal Other casts
tubular cells
- Inherited disease that affects the glomerular >2 RTE/ HPF:
basement membrane ( lamellated appearance tubular injury
with areas of thinning)
- Urinalysis: hematuria Odor: odorless
Minimal change disease
- Aka Nill disease/ lipoid disease TUBULOINTERSTITIAL DISEASE
- Disruptions of podocytes occurring primarily in
children following allergic reactions and
immunization Tubulointerstiti cause Urinalysis
al disease findings
Focal segmental glomerulosclerosis Urinary tract Bacterial - WBC
- Similar to minimal change ( childrens) infection ( UTI) infection of the - bacteria
lower or upper - mild
- Disruptions of the podocytes in certain areas of urinary tract proteinuria
- microscopic
the glomerulus
hematuria
- Associated with heroin and analgesic abused - increased pH
and AIDS
Cystitis Lower urinary WBC
No casts tract infection ( - bacteria
Diabetic nephropathy/ kimmelstiel - wilson bladder) - mild
- Most common cause of end- stage renal disease proteinuria
- Glomerular damage may be due capillary - microscopic
hematuria
thickening, increase proliferation of the
- increased pH
mesangial cells, increase deposition of cellular
and non- cellular materials Pyelonephritis Infection (not specified,
= there is a deposition of glycosylated proteins 1. Acute affecting renal but includes
= (+) micral tests microalbuminuria pyelonephritis:re tubules and WBC, bacteria,
nal tubule and interstitium casts)
interstitium
2. chronic Upper UTI
TUBULAR DISEASE pyelonephritis:
recurrent
infections of
Tubular causes Urinalysis your renal
disease findings tubules and
interstitium
Nephrogenic Inherited defect - dilute urine
diabetes of tubular - low specific Can be seen in
insipidus response to gravity broad and waxy
ADH ( water) or casts
acquired from
medications Acute Allergic (not specified,
interstitial inflammations but includes
Fanconi’s Failure of tubular - glycosuria nephritis due to WBC,
syndrome reabsorption in - possible mild medications eosinophils ,
PCT ( glucose, proteinuria >1% eosinophil mild proteinuria
amino acids, )
electrolytes) No bacteria
Acute tubular Ischemia or - hematuria
necrosis nephrotoxic - RTE cells
agents - RTE casts
OTHER RENAL DISORDERS
Renal disorder Cause characteristics OTHER RENAL DISEASE
Renal calculi/ Formation of Stones may
lithiasis stones in the pass in urine or
RENAL FAILURE
renal calyces, obstruct the
(kidney stones) pelvis, ureters urinary tract
TYPE CHARACTERI URINALYSIS
or bladders
STICS FINDINGS
Primary calculi
acute / Decline in Isosthenuric Urine (
constituents
chronic kidney specific gravity:
function, may 1.010)
Calcium Metabolic 75% of renal
progress to - Proteinuria
oxalate/ disorders or stones
end- stage - Renal glycosuria
phosphates diets
disease - Telescope
sediments ( variety
Magnesium UTI with urea- Common in
of casts seen in the
ammonium splitting bacteria infection -
same specimen)
phosphates related stones
End stage renal disease (irrevesible)
(triple
phosphate)
Chronic GFR< 25 ml/ Same as renal
min, failure with
Uric acid High purine Seen in
worsening severity
intake conditions like
rising
gout
azotemia (
increases BUN
cystine Hereditary Rare,
and creatinine)
cysteine associated with
Metabolism genetic
electrolyte
disorder disorders
imbalance
Waste to eliminate kidney stones:
Lithotripsy
- Uses high energy shocks waves to break kidney
stones into pieces.
Condition favoring the formation of kidney stones
1. pH
2. Chemical concentration
3. Urinary stasis
Primary findings
- Hematuria
Calcium oxalate
- Very hard, dark and rough surface
Uric acid
- Yellowish
Cysteine
- Yellow- brown - greasy
Phosphate
- Pale and friable
Magnesium ammonium phosphates
- Splitting bacteria such as proteus vulgaris
- Appearance: staghorn, branching
