o Proteinuria
RENAL DISEASES
CLASSIFICATIONOF RENALDISEASES
1. GLOMERULAR DISORDER
disorders associated with the glomerulus
− Immune origins
− Increased production/ circulation of Ig.
(Especially IgA)
o Complement, leukocytes &
cytokines involvement
o Thickening of the glomerular
basement membrane &
complement mediated damage
− Nonimmunologic
o Exposure to chemicals and toxins
o Electrical membrane charges
disruption (nephrotic syndrome)
− Deposition of immune complexes in
glomerular membrane. (e.g., amyloidosis)
GLOMERULAR DISORDER: GLOMERULONEPHRITIS
− Refers to sterile inflammatory processes that
affects the glomerulus and associated with
the finding of blood, protein and casts in
urine.
GLOMERULONEPHRITIS:
Acute Poststreptococcal Glomerulonephritis
− Deposition of immune complexes, formed in
conjunction with group A Streptococcus
infection, on the glomerular membranes
− Sudden onset of symptoms with consistent
damage to the glomerular membrane.
− SYMPTOMS:
o Fever, Hypertension, Edema
o Oliguria
o Fatigue
o Hematuria
− Its is CAUSED by:
o Certain strains on Group A
Streptococcus (Streptococcus
pyogenes)
o Pneumonia
o Endocarditis
o Severe infection
− FINDINGS:
o Hematuria
o Oliguria
o Presence of casts(RBC cast, WBC
casts, Hyaline Casts, Granular Casts)
o Increased BUN Levels
o POSITIVE ASO Titer
GLOMERULONEPHRITIS:
Rapidly Progressive (Crescentic) Glomerulonephritis
− More serious form which can definitely lead
to renal failure.
− Has poor prognosis
− Damage to capillary wall is due to
macrophages that will release cells and
plasma in the Bowman’s space.
− Production of crescentic formations
containing macrophage, fibroblast and
polymerized fibrin.
− Lab Findings:
o Similar to AGN
o Elevated protein evels
o Very low GFR
− Deposition of immune complexes from
systemic immune disorders on the
glomerular membrane
GLOMERULONEPHRITIS:
Good pasture Syndrome
− Due to the cytotoxic antibody
(Antiglomerular Basement membrane)
found attached to the glomerular and
alveolar membranes during viral respiratory
infection.
− Autoantibody attachment and
complement activation causes the
damage to the capillaries. (Antiglomerular
basement membrane antibody)
− Patient’s initial complaints are hemoptysis &
dyspnea followed by the development of
hematuria.
GLOMERULONEPHRITIS:
Vasculitis
− Disorders affecting the systemic vascular
system resulting to the glomerular damage.
− These disorders are immune mediated.
o damage may result of immune
complex deposition
 oauto-antibodies binding to vascular
structures G
A. WEGENER’S GRANULOMATOSIS
» Antineutrophilic cytoplasmic
autoantibody binds to neutrophils in
vascular walls producing damage to
small vessels in the lungs and
glomerulus
» Pulmonary symptoms including
hemoptysis develop first followed by
renal involvement and possible
progression to end-stage failure
B. HENOCH- SCHÖNLEIN PURPURA
» Occurs primarily in children following
viral respiratory infections; a
decrease in platelets disrupts
vascular integrity
» Initial appearance of purpura
followed by blood in sputum and
stools and eventual renal
involvement
» Complete recovery is common, but
may progress to renal failure
GLOMERULONEPHRITIS:
Immunoglobulin A Nephropathy/ Berger’s Disease
− Frequently seen in children and young
adults.
− Immune complexes are deposited on the
glomerular membrane.
− Patient’s serum IgA level is increased which
may result from mucosal infection.
− Patient may remain asymptomatic for 20
years may there is a gradual progression to
chronic glomerulonephritis and end stage
renal disease.
GLOMERULONEPHRITIS:
Membranous Glomerulonephritis
− Thickening of the glomerular membrane
following IgG immune complex deposition
associated with systemic disorders
− DISORDERS ASSOCIATED:
o Systemic Lupus Erythematosus (SLE)
o Sjögren Syndrome
o a chronic progressive inflammatory
autoimmune disorder characterized
by marked excessive drying of
mouth and eyes from exocrine
disorder and B cell
lymphoproliferative disorder.
o Secondary syphilis
o Hepatitis B
o Gold & mercury treatent
o Malignancy
GLOMERULONEPHRITIS:
Membranoproliferative Glomerulonephritis
− Immune mediated disorder mostly affecting
children characterized by cellular
proliferation in capillary walls or glomerular
basement membrane.
O TYPE I
▪ Increased cellularity in the
subendothelial cells of the
interstitial area of the
Bowman’s capsule, causing
thickening of the capillary
walls; progress to nephrotic
syndrome
O TYPE II
▪ Extreme dense deposits in the
glomerular membrane
▪ Experience symptoms of
chronic glomerulonephritis.
GLOMERULONEPHRITIS:
Chronic Glomerulonephritis
− Glomerular damage as a result of renal
disorder leads to marked decreased in renal
functions and eventually to renal failure.
− Lab findings:
o hematuria
o proteinuria
o glucosuria
o Cast ( broad cast)
 o Dec GFR
o Inc BUN, Creatinine level
o Imbalance electrolytes
GLOMERULONEPHRITIS:
Nephrotic Syndrome
− There is increase permeability of the
glomerular membrane due to disruption in
the electrical charges in the basal lamina
and podocytes, producing a less tightly
connected barrier that allows massive loss
of protein and lipids.
− Characterized by the presence of RTE cells,
RTE cell casts, & fatty casts.
− Marked massive proteinuria (> 3.5 g/d)
− Low level of albumin
− PRIMARY URINALYSIS RESULT
o Heavy proteinuria
o Microscopic hematuria
o Renal tubular cells
o Oval fat bodies
o Fat droplets
o Fatty and waxy casts
− OTHER SIGNIFICANT TESTS
o Serum albumin
o Cholesterol
o Triglycerides
GLOMERULONEPHRITIS:
Minimal Change Disease(Lipid Nephrosis)
− Podocytes appear to be less tightly fitting
allowing increase infiltration of protein.
− Seen in children following allergic reaction
and immunization.
o Urinalysis results Heavy proteinuria
Transient hematuria Fat droplets
− Other Significant Tests
o Serum albumin
o Cholesterol
o Triglycerides
GLOMERULONEPHRITIS:
Focal Segmental Glomerulosclerosis
− Only a certain number and areas of the
glomerulus are affected.
− The disease is caused by the disruption of
podocytes associated with analgesic and
heroin abuse and AIDS.
− IgM and C3 are seen in the undamaged
glomerulus.
GLOMERULONEPHRITIS:
Alport Syndrome
− an inherited disorder affecting the
glomerular basement membrane.
− inherited as a sex-linked or autosomal
genetic disorder.
− males are frequently more severely affected
than females.
− glomerular basement membrane has a
lamellated appearance with areas of
thinning.
− prognosis ranges from mild symptoms to
persistent hematuria and renal insufficiency
in later life to the nephrotic syndrome and
end-stage renal disease.
GLOMERULONEPHRITIS:
Diabetic Nephropathy
− also known as Kimmelstiel-Wilson disease
− currently the most common cause of end-
stage renal disease.
− increased proliferation of mesangial cells
and increased deposition of cellular and
noncellular material within the glomerular
matrix resulting in accumulation of solid
substances around the capillary tufts.
− Microalbumin monitoring in DM patients is
important to detect the onset of Diabetic
Nephropathy.
2. TUBULAR DISORDER
− affecting the renal tubules include those in
whichtubular functionis disrupted as a result
of actual damage to thetubules andthosein
which a metabolic or hereditary disorder
affects theintricatefunctions of the tubules.
TUBULAR DISORDER:
Acute Tubular Necrosis
− primary disorder associated with damage to
the renal tubules
− RTE cells are damaged by toxic agents
(aminoglycosides, amphotericin,
cyclosporine, radiographic dyes, ethylene
glycol, mushroom poisoning, heavy metals)
or ischemia (shock, trauma caused by
crushing injuries and surgical procedures.)
TUBULAR DISORDER:
Hereditary and Metabolic Disorder
I. FANCONI’S SYNDROME (HEREDITARY)
» disorder most frequently associated
with tubular dysfunction (failure off
tubular reabsorption in the PCT)
» May be inherited in association with
cystinosis and Hartnup’s Disease.
II. ACQUIRED
» Associated with exposure to toxic
agents.
Renal Glycosuria
> affects only the reabsorption of glucose.
> The disorder is inherited as an autosomal
recessive trait.
> 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
> Patients with renal glycosuria have
increased urine glucose concentrations with
normal blood glucose concentrations.

Uromodulin-Associated Kidney Disease LABORATORY TESTING IN METABOLIC AND

HEREDITARY TUBULAR DISORDERS
> Uromodulin
o is a glycoprotein and is the only PRIMARY OTHER
protein produced by the proximal DISORDER URINALYSIS SIGNIFICANT
and distal convoluted tubules RESULTS TEST
> primarily an inherited disorder caused by an Acute − Microscopic Hemoglobin
tubular hematuria
autosomal mutation in the gene that
necrosis − Proteinuria Hematocrit
produces uromodulin.
− Renal
> in persons developing gout as early as the tubular epithelial
teenage years before the onset of cells Cardiac
detectable renal disease − Renal enzymes
tubular epithelial
Nephrogenic Diabetes Insipidus cell cast
− Hyaline,
> Nephrogenic DI can be inherited as a sex- granular, waxy,
linked recessive gene or acquired from broad casts
medications, including lithium and Fanconi − Glucosuria Serum and urine
amphotericin B. syndrome electrolytes
> It also may be seen as a complication of
− Possible Amino acids
polycystic kidney disease and sickle cell cystine crystals chromatography
anemia Uromodulin-
> nephrogenic diabetes insipidus associated
− Renal
o action of ADH is disrupted either by kidney
tubular epithelial Serum uric acid
the inability of the renal tubules to disease
cells
respond to ADH (early
stages)
> neurogenic DI
Late stage − See chronic
o failure of the hypothalamus to glomerulonephritis
produce ADH Nephrogenic − Low
diabetes specific gravity. ADH testing
insipidus polyuria
Renal
− glucosuria Blood glucose
glucosuria
 CLINICAL INFORMATION ASSOCIATED UTI - common renal disease
WITH METABOLIC AND − infection involve the lower urinary tract
TUBULAR DISORDERS (urethra and bladder)
CLINICAL − the upper urinary tract (renal pelvis,
DISORDER ETIOLOGY tubules, and interstitium).
COURSE
Acute tubular Damage to Acute onset of
Cystitis
necrosis renal tubular renal
cells caused dysfunction − bacterial infection of the bladder
by ischemia or usually − seen more often in women and children
toxic agents resolved when
underlying Acute Pyelonephritis
cause is
corrected − Infection of the upper urinary tract
Fanconi Inherited in Generalized involving the interstitium and tubules due
syndrome association defect in renal to interference of urine flow to the
with cystinosis tubular bladder, reflux of urine from the bladder
and Hartnup reabsorption untreated cystitis
disease or requiring
acquired supportive Chronic Pyelonephritis
through therapy
exposure to − serious disorder that can result in
toxic agents permanent damage to the renal tubules
Uromodulin- Inherited Continual and possible progression to chronic
associated defect in the monitoring of renal failure Acute Interstitial Nephritis
kidney disease production of renal function
− Congenital urinary structural defects
normal for progression
producing reflux nephropathy
uromodulin by to renal failure
the renal and possible
Acute Interstitial Nephritis
tubules and kidney
increases uric transplantation − Inflammation of the renal interstitium
acid causing associated with allergic reaction to
gout
medications.
Nephrogenic Inherited Requires
diabetes defect of supportive
insipidus tubular therapy to CLINICAL INFORMATION ASSOCIATED
response to prevent WITH INTERSTITIAL DISORDERS
ADH or CLINICAL
acquired from DISORDER ETIOLOGY
COURSE
medications
Renal Inherited Benign Cystitis Ascending Acute onset of
glucosuria autosomal disorder bacterial urinary
recessive trait infection of frequency and
the bladder burning
resolved with
antibiotics
Acute Infection of Acute onset of
3. INTERSTITIAL DISORDER
pyelonephritis the renal urinary
− Disorders affecting the renal interstitium tubules and frequency and
which also affects the tubules interstitium burning and
(tubulointerstitial disease) related to lower back
interference of pain resolved
− Involves inflammatory conditions and
urine flow to with antibiotics
infections.
the bladder,
and untreated
cystitis
Chronic Recurrent Frequently RENAL FAILURE
pyelonephritis infection of diagnosed in
the renal children; CHRONIC RF
tubules and requires
− The progression to end-stage renal disease:
interstitium correction of
caused by the underlying o characterized by a marked
structural structural decrease in the glomerular
abnormalities defect filtration rate(less than25mL/min)
affecting the Possible o steadily rising serum BUN and
flow of urine progression to creatinine values (azotemia)
renal failure
o electrolyte imbalance
Acute Allergic Acute onset of
o lack of renal concentrating
interstitial inflammation renal
nephritis of the renal dysfunction ability producing an isosthenuric
interstitium in often urine
response to accompanied o proteinuria
certain by skin rash renal glycosuria
medications Resolves an abundance of granular,
following
waxy, and broad casts, often
discontinuation
of medication referred to as a telescoped urine
and treatment sediment.
with
corticosteroids ACUTE RENAL FAILURE
− exhibits a sudden loss of renal function and
LABORATORY RESULTS IN INTERSTITIAL is frequently reversible.
DISORDERS − CAUSES:
PRIMARY OTHER
DISORDER URINALYSIS SIGNIFICANT PRERENAL CAUSES (DECREASE BLOOD FLOW TO THE
RESULTS TESTS KIDNEY)
cystitis Leukocyturia Urine culture
Bacteriuria > Burns
Microscopic > Hemorrhage
hematuria > Surgery
Mild proteinuria
Increased pH RENAL CAUSES (ACUTE GD AND TD)
Acute Leukocyturia Urine culture
pyelonephritis Bacteriuria > Acute glomerulonephritis
WBC casts > Acute pyelonephritis
Microscopic
hematuria > Acute tubular necrosis
Proteinuria
Chronic Leukocyturia Urine culture POSTRENAL CAUSES (RENAL CALCULI OR TUMOR
pyelonephritis Bacteriuria BUN OBSTRUCTIONS)
WBC casts
Bacterial casts > Tumors
Granular, waxy, Creatinine > Calculi
broad casts > Crystallization of ingested substances
Hematuria
Proteinuria
eGFR
Acute interstitial Hematuria Urine eosinophils
nephritis BUN
Proteinuria Creatinine
Leukocyturia eGFR
WBC casts

RENAL LITHIASIS
− Deposition of renal calculi or kidney stones
in the calyces and pelvis of the kidney,
ureters and urinary bladder.
− 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 2ormore
inches.
− Lithotripsy, a 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.
o Lithotripsy - a procedure using high-
energy shock waves, to break stones
located in the upper urinary tract
into the pieces that can be then
passed in the urine.
− CONDITIONS FAVORING STONE FOMATION:
o pH
o Chemical concentration
o Urinary stasis
− CHEMICAL COMPOSITION OF RENAL
CALCULI:
o Calcium oxalate or phosphate
o Magnesium ammonium phosphate
o Uric acid
o Cystine
− PATIENT MANAGEMENT:
o Maintaining the urine at a pH
incompatible with crystallization of
the particular chemicals
o Maintaining adequate dehydration
to lower chemical concentration
o Dietary restrictions