Interpretation of

Urinalysis
Gross visual examination

Normal color pale light yellow to dark amber color

High concentrated urine has darker yellow appearance (pt. who are volume depleted
Lighter color for diluted urine seen in pt. with Diabetes insipidus
Red urine UTI, nephrolithiasis, hemoglobinuria (rhabdomyolysis), porphyrias (port wine
urine)
Orange urine rifampin, phenazopyridine
Green urine UTI
Blue urine Blue diaper syndrome (tryptophan malabsorption)
Purple urine Bacteriuria in pt with urinary catheters (purple bag syndrome)
Brown urine gilbert syndrome, tyrosinemia, hepatobillary dse
Black urine Alkaptonuria, malignant melanoma
White urine chyluria, pyuria, phosphate crystals
Urine turbidity or clarity
Determined by substances in urine such as amount of cellular debris, casts, crystals, bacteria or
significant proteinuria.
 Chemical examination via urine dipstick
Urine pH useful in evaluation of stones, infection, and renal tubular acidosis
Alkaline urine calcium oxalate/ calcium phosphate, magnesium ammonium
phosphate and staghorn calculi
Acidic urine uric acid and cystine calculi

Specific gravity measurement of urine concentration and representative of

kidneys ability to concentrate urine. It is the comparison of the amount of
solutes in urine as compared with pure water
Low values may be seen due to glucose,urea, or alkaline urate and high
values may be due to significant amounts of protein or ketoacids

Glucosuria, ketonuria, bilirubinuria, nitrite in urine and leukocyte esterase

(UTI or pyuria)
Proteinuria in dipstick urine testing

Trace proteinuria approx. 10 30mg/dL

1+ approx. 30mg/dL
2+ approx. 100 mg/dL
3+ approx. 300 mg/dL
4+ 1000 mg/dL or more

Sulfosalicylic acid test (SSA) detects all proteins in urine at any amounts, including
albumin, globulin, and bence jones proteins. However contrast can cause false positive
results
0 no turbidity (proteinuria 0 mg/dL)
trace slight turbidity (20 mg/dL)
1+ - print visible through specimen (50mg/dL)
2+ - print visible (200 mg/dL)
3+ - flocculation (500 mg/dL)
4+ - dense precipitate (> 1000 mg/dL)
Proteinuria
Types of Proteinuria

Sustained - >1 2 g/24h, pt. become edematous with

foaming urine
Benign/ transient/ functional nonsustained <1g/24h,
may be caused by fever, stress, obesity, sleep apnea,
exercise, congestive heart failure
Orthostatic in upright position
Selective albumin and mixture of other serumprotein ,
common in adults
Nonselective largely of albumin, common in children
with MCD
Mechanism of proteinuria

Disruption of glomerular barrier

Smaller proteins (<20 kDa) are freely filtered but are readily
reabsorbed by the proximal tubule.
Excessive production of abnormal protein overwhelming the absorption
capacity of proximal tubule

Fusion of glomerular epithelial cell foot processes due to

glomerular diseases (MSD) causes increased pressure across
the capillary basement membrane, resulting in areas with
larger pore sizes (and more severe nonselective proteinuria
Excess excretion of light chains by plasma cell dyscrasia ---
proximal tubule injury,tubule obstruction (cast nephropathy),
and light chain deposition ---- renal failure
Hematuria

2 5 RBCs per high power field & can be

seen in dipstick
Isolated hematuria without proteinuria is
indicative of urinary tract bleeding
A single urinalysis with hematuria is
common and can result from menstruation,
viral illness, allergy, exercise, or mild
trauma.
Persistent or significant hematuria (>3
RBCs/ HPF on three urinalyses, a single
urinalysis with >100 RBCs, or gross
hematuria) is associated with significant
renal or urologic lesions in 9.1% of cases.
Hematuria with dysmorphic RBCs, RBC
casts, and protein excretion >500 mg/d is
virtually diagnostic of glomerulonephritis
Nephrotic Syndrome
Definition of Nephrotic Syndrome

Presents with heavy proteinuria (> 3.5 g/24 h) , minimal hematuria,

hypoalbuminemia 3g/dL, hypercholesterolemia,lipiduria, edema and
hypertension
PRIMARY NEPHROTIC SYNDROME: Minimal change disease, focal
segmental glomerulosclerosis, membranous glomerulonephritis,
SECONDARY NEPHROTIC SYNDROME: Lupus, hepatitis,HIV, CMV,
Diabetes, Lymphoma, Amyloidosis, Heart failure and medications
The higher the 24h urine protein excretion, the more rapid is the
decline in GFR
Untreated leads to renal failure
With increase risk of infection, thrombotic and thromboembolic
complications
Pathophysiology

Nephrotic syndrome is caused by a derangement in

glomerular capillary walls resulting in increased
permeability to plasma proteins.
The generalized edema is a direct consequence of
decreased intravascular colloid osmotic pressure.
There is also sodium and water retention, which
aggravates the edema
Edema is characteristically soft and pitting, and is most
marked in the periorbital regions and dependent
portions of the body. If severe, it may also lead to
pleural effusions and ascites.
Minimal Change Disease

nil lesion, causes 7090% of nephrotic syndrome in childhood but only 1015% of
nephrotic syndrome in adults
characterized by diffuse effacement of foot processes of visceral epithelial cells
(podocytes), detectable only by electron microscopy, in glomeruli that appear
virtually normal by light microscopy
can be associated with several other conditions, including Hodgkins disease,
allergies, or use of nonsteroidal anti-inflammatory agents
The pathophysiology of this lesion is uncertain. Most agree there is a circulating
cytokine, perhaps related to a T cell response that alters capillary charge and
podocyte integrity
presents clinically with the abrupt onset of edema and nephrotic syndrome
accompanied by acellular urinary sediment.
Average urine protein excretion reported in 24 h is 10 g with severe
hypoalbuminemia. characteristic feature is its usually dramatic response to
corticosteroid therapy
Focal Segmental Glomerulosclerosis

pattern of renal injury characterized by segmental glomerular scars that

involve some but not all glomeruli; the clinical findings of FSGS largely
manifest as proteinuria.
The pathogenesis of FSGS is probably multifactorial. Possible mechanisms
include a T cellmediated circulating permeability factor, increased
soluble urokinase receptor levels, TGF-mediated cellular proliferation
and matrix synthesis, and podocyte abnormalities associated with genetic
mutations.
The pathologic changes of FSGS are most prominent in glomeruli located
at the corticomedullary junction
present with hematuria, hypertension, any level of proteinuria, or renal
insufficiency
Membranous
Glomerulonephritis/nephropathy

Most common cause of nephrotic syndrome in elderly

Can be associated with rheumatologic disorders like lupus
or rarely rheumatoid arthritis. The presence of
subendothelial deposits or the presence of tubuloreticular
inclusions strongly points to a diagnosis of membranous
lupus nephritis, which may precede the extrarenal
manifestations of lupus.
Membranous nephropathy is characterized by diffuse
thickening of the glomerular capillary wall due to the
accumulation of deposits containing Ig along the
subepithelial side of the basement membrane.
Diabetic Nephropathy

Within 12 years after the onset of clinical diabetes,

morphologic changes appear in the kidney. Thickening of the
GBM is a sensitive indicator for the presence of diabetes but
correlates poorly with the presence or absence of clinically
significant nephropathy.
GBM is altered notably with a loss of heparin sulfate moieties
that form the negatively charged filtration barrier. This
change results in increased filtration of serum proteins into
the urine, predominately negatively charged albumin.
Earliest manifestation microalbumunuria 30300 mg/24 h 5
10 yrs after onset of diabetes
Expansion of mesangium due to accumulation of
 Glomerular deposition diseases

Plasma cell dyscrasias producing excess light chain

immunoglobulin sometimes lead to the formation of glomerular
and tubular deposits that cause heavy proteinuria and renal
failure; the same is true for the accumulation of serum amyloid A
protein fragments seen in several inflammatory diseases.
Light chain depositon disease (kappa light chains do not form
amyloid fibrils)
Renal Amyloidosis ( immunoglobulin light chains amyloid L or
serum amyloid A)
Fibrillary-immunotactoid glomerulopathy (nonamyloid
nonbranching randomly arranged fibrils)