5. GLOMERULOPATHIES
•Glomerular diseases may be primary or
secondary to systemic disorders. It may present
with isolated haematuria, or proteinuria.
• The presentation may be in the form of
nephritic or nephrotic syndrome.
• Renal biopsy often provides useful diagnostic,
therapeutic, and prognostic information
6. There are many causes of glomerular
damage, including immunological injury,
inherited diseases such as Alport’s
syndrome
Metabolic diseases such as diabetes
mellitus and deposition of abnormal
proteins such as amyloid in the glomeruli
12. NEPHROTIC SYNDROME
•Nephrotic syndrome is a condition in which the
kidneys leak large amounts of protein (albumin)
into the urine
•Is urinary excretion of more than 3 grams of protein
per day due to a glomerular disorder
13. •This is characterised by albuminuria (> 3.5 gm/1.73
m2/day)
Hypoalbuminaemia (< 3 gm/100 ml) and accompanied
by oedema, hyperlipidaemia (cholesterol> 300 mg/dl),
and lipiduria
14. •It is common among children and has both primary
and secondary causes
•Diagnosis is by determination of urine protein
/creatinine ratio in a random urine sample or
measurement of urinary protein in a 24 hour urine
collection
•Cause is diagnosed based on history physical
examination ,serological testing and renal biopsy
•Prognosis and treatment vary with by the cause
15. Epidemiology
•Peak incidence: 2 – 5 years
•Sex: boys > girls
•More common in families with history of
allergies.
•Prevalence varies with the causes
17. AETIOLOGY
Occurs at any age but is more prevalent in children mostly
between ages one and half year and 4 years
The most common primary causes are the following
•Minimal-change nephropathy
•Focal glomerulosclerosis
•Membranous nephropathy
•
•Hereditary nephropathies
18.
19. The Secondary causes accounts for less than 10% of the
childhood but more than 50% of adult cases . The most
commonly are
• Diabetes nephropathy
• Systemic Lupus erythematosus
• Amyloidosis and paraproteinemias
• Viral infections (Hepatitis B, Hepatitis C, HIV nephropathy
• Preeclampsia
20. Pathophysiology
Proteinuria occurs because of changes to capillary endothelial
cells of the glomerular basement membrane or podocytes
which normally filter serum protein selectively by size and
charge
Evidence suggests that T cells may up regulate a circulating
permeability factor or down regulate an inhibitor of
permeability factor in response to un identified immunogens
and cytokines
21. Activation of complement leading to damage of the
glomerular epithelial cells and loss of the negatively charged
groups attached to proteins of the GBM and glomerular
epithelial cells
•The disorder results in urinary loss of macromolecular
proteins primary albumin but also opsonins ,
immunoglobulins , erythropoietin, trans ferritin , hormone –
binding globulins and vitamin D binding protein and anti-
thrombin III
22. SYMPTOMS AND SIGNS
•Primary symptoms include anorexia , malaise and frothy
urine (caused by high concentrations of protein)
•Fluid retention may cause dysponea (pleural effusion or
laryngeal oedema ) hydrathrosis )
•Abdominal pain (ascites or in children mesentery
oedema )
•Peripheral odema and ascites
•Oedema may obscure signs of muscles wasting and
cause parallel whites lines in fingernails beds
(muehrck’s lines)
27. CAUSATIVE DISORDER
Prompt treatment of infection (e.g staphylococcal endocarditis ,
malaria , syphilis , schistosomiasis
Allergic disentization e,g for poison oak or IVY and insect antigen
exposures
Stopping drugs (e.g gold , penicillamine NSAIDS
PROTEINURIA angiotensin converting enzymes inhibitors or
angiotensin II receptors blockers ) to reduce systemic and
intraglomerular blood pressure and proteinuria
These drugs may cause or exacerbate hyperkalemia in patient with
moderate to severe renal insufficiency
28. A protein restriction is no longer recommended
because of demonstrated effect on progression
OEDEMA sodium restriction (less than 2 grams or
about 100mmol/day ) is recommended for patient
with symptomatic oedema
Loop diuretics are usually required to control oedema
but may worsen pre-existing renal insufficiency and
hypovolemia , hyper viscosity and hypercoagulability
and thus should be used only if sodium restriction is
ineffective
29. HYPERLIPIDEMIA statins are indicated for
hyperlipidaemia and limitation of saturated fat and
cholesterol intake is recommended to help control
hyperlipidaemia
HYPERCOAGULABILITY
Anticoagulants are indicated for treatment of
thromboembolism
INFECTION RISKS
All patients should receive pneumonococal
vaccination
30. • NEPHRECTOMY
Is necessary in severe nephrotic syndrome because of persistent
hypoalbuminaemia or renal replacement therapy is used as necessary
31. DIABETES NEPHROPATHY
Is glomerular sclerosis and fibrosis caused by the metabolic
and hemodynamic changes of diabetes mellitus .
It manifests as slowing progressive Albuminuria with
worsening hypertension and renal insufficiency
Diagnosis is based on history , physical examination ,
urinalysis and urine albumin /creative ratio
Treatment is strict glucose control and Angiotensin inhibition
(ACE inhibitors or angiotensin II Receptor blockers ) and
control of blood pressure and control of lipids
32. • Diabetes Nephropathy is the most common cause of nephrotic
syndrome in adults and of end stage renal disease
• Renal failure usually takes more than 10 year after the onset of
nephropathy to develop however because type 2 diabetes is
often present for several years before being recognized
• Nephropathy often develops less than 10 years after diabetes is
diagnosed
• PATHOPHSIOLOGY
• Glycosylation of protein , hormonally influenced cytokine
release (for example transforming growth factor B ) deposition
of mesangial matrix and alteration of glomerular
hemodynamic – hyper filtration
• Hyperglycemia causes glycosylation of glomerular proteins
which may be responsible for mesangial cell proliferation and
matrix expansion and vascular endothelial damage
33. The central features are activation of the renin–angiotensin
system,leading to both intrarenal and systemic effects, as well
as direct toxic effects of prolonged hyperglycaemia, leading to
renal inflammation and fibrosis
Pathologically, the first changes coincide with the onset
of microalbuminuria and include thickening of the glomerular
basement membrane and accumulation of matrix material in
the mesangium
Subsequently, nodular deposits are characteristic, and
glomerulosclerosis worsens as heavy proteinuria develops,
until glomeruli are progressively lost and renal function
deteriorates.
34. • The glomerular basement membrane classically become thickened
• Diabetes Nephropathy begins as glomerular hyper filtration (increased
Glomerular Filtration Rate )
• Micro albuminuria progresses to protein more than 3grams at a variable
course usually over years
• SYMPTOMS AND SIGNS
• Sustained micro albuminuria is the earliest warning signs
• Hypertension and dependent edema eventually develop in most
untreated patients
• Symptoms and signs of ureamia (e.g vomiting anorexia )
DIAGNOSIS
Screening of all patients with diabetes and random urine albumin
/creation ratio
35. •Urinalysis for signs of other renal disorders e.g hematuria ,
RBCS casts
•Renal biopsy can confirm the diagnosis but rarely necessary
TREATMENT
Maintenance of glycosylated Hemoglobin (HbA1c) less than
7.0
Aggressive blood pressure control beginning with
angiotensin inhibitors
Primary treatment is strict glucose control to maintenance
hemoglobin A1c less than 7.0
The ACE inhibitors or angiotensin II receptors blockers are
the antihypertensive of choices , they reduce blood pressure
and proteinuria and slow the progression of DN
Diuretics are required by most patients in addition to
angiotensin inhibition to reach the target blood pressure
levels
36. •Non dihydropyidine calcium channel blockers
diltiazem and verapamil are also antiprotein urine and
Reno protective and can be used if proteinuria does
not meaning fully decrease
•Dietary protein restrictions should be due only with
close dietary monitoring to ensure a balanced supply
of amino acids
•Kidney transplantation with or without simultaneous
or subsequent
37.
38. FOCAL SEGMENTAL GLOMERULOSCLEROSIS
• It is scattered mesangial sclerosis in some but not all glomeruli
• It is most often idiopathic but may be secondary to use of Heroin or
other drugs
• HIV infection , obesity , sickle cell disease, athero-embolic disease
• It manifests mainly in adolescents but also in young and middle aged
adults
• Patients have insidious onset of proteinuria ,Mild hematuria ,
hypertension and azotemia
39. AETIOLOGY
•It is idiopathic but may associated with drugs use (heroin ,
interferon alfa, pamironate , cyclosporine or acetaminophen
or NSAIDS causing analgesic nephropathy
•Atheroembolic diseases affecting the kidneys obesity , HIV
infection
•
SYMPTOMS AND SIGNS
Present with heavy proteinuria , hypertension renal
dysfunction edema
Microscopic hematuria is occasionally present
40. DIAGNOSIS
•Renal biopsy when possible with immunostaining
and electron microscopy
•Urinalysis is done and BUN serum creatinine and 24
hours urinary protein excretion are measured
•Biopsy shows focal and segmental hyalinization of
the glomeruli
•Immunostaining showing IgM and complement (C3)
deposit
41.
42. TREATMENT
•Angiotensin inhibitor
•Corticosteroid and sometimes cytotoxic drugs ,
prednisone 1mg/kg po once/day or 2mg/kg every
other day for 2months
•For recurrent, cyclosporine (1.5 to 2mg/kg po bd for
6 months mycophenolate mofetil (750 to 1000mg )
po bd for 6months
43. HIV-ASSOCIATED NEPHROPATHY
•characterized by clinical finding similar to those of
focal segmental glomerusclerosis and often biopsy
features of collapsing glomerulopathies
•DIAGNOSIS
•Renal biopsy and light microscopy shows capillary
collapse
•TREATMENT
•Antiretroviral and ACE inhibitors and sometimes
dialysis
46. MEMBRANOUS NEPHROPATHY
•It is deposition of immune complexes on the GBM with
GBM thickening
•AETIOLOGY
•It is usually idiopathic but may be secondary to any of the
following
•Drugs (e,g hepatitis B Virus infection syphilis
•Autoimmune disorders e.g SLE
•Thyroiditis
•Cancer (lung cancer , cancer colon , cancer stomach
47. SYMPTOMS AND SIGNS
•Present with oedema nephrotic range proteinuria and
occasionally microscopic hematuria
•Hypertension
•Symptoms and signs of a disorders causing MN e.g cancer
may be present initially
DIAGNOSIS
Renal biopsy (immune complexes are seen as dense deposits
on electron microscopy
TREATMENT
Treatment of secondary causes and of nephrotic syndrome as
indicated (ACE ,AR II inhibitors
Immunosuppressive therapy for patients at high risk of
progression
48.
49.
50. •Methyl prednisolone 1g intravenous for 3 days
•Prednisone 0.5mg/kg po once /day
•Chlorambucil 0.1 to 0.2mg /kg po once /days
•Cyclosporine 4 to 6mg/kg po once /day for 4 months
MINIMAL CHANGE DISEASES (LIPOID
DISEASE NIL DISEASE)
Causes abrupt onset of edema and heavy proteinuria ,
mostly in children and renal function is typically
normal
51. AETIOLOGY
• The causes is almost always unknown , although rare causes may occur
secondary to drug use especially NSAIDS ) and hematologic cancers
especially HODGKIN lymphoma )
SYMPTOMS
Proteinuria and microscopic hematuria occurs in about 20% of patients
Azotemias can occur in secondary causes and in patients more than 60%
DIAGNOSIS
Biopsy in adults with idiopathic nephrotic syndrome syndrome
TREATMENT
Corticosteriods (prednisolone 60mg /m2 po once/day or cytotoxic drugs
Sometimes cyclophosphamide or cyclosporine
Cyclosphosphamide 2 to 3mg/kg once for 12 weeks
Chlorambucil 0.15mg/kg for week and cyclosporine 3mg/kg po bid
52. NEPHROTIC-NEPHRITIC SYNDROMES
• Several glomerular disorders typically manifest with features of both nephritic
and nephrotic syndromes
• They include fibrillary and immunotactoid glomerulopathies , membrano-
proliferative glomerulonephritis, GN, lupus nephritic
• FIBRILLARY AND IMMUNOTACTOID GLOMERULOPATHIES
• It is defined pathologically by organized deposition of non amyloid microfibrillar
or micro tubular structures within the renal mesangium and basement
membrane
• AETIOLOGY
• Deposition of immunoglobulin , particularly IgG light chains and complement
(C3) suggest immune system dysfunction
53.
54. • Patients may have accompanying paraproteinemia , cryoglobulinemia
,plasma cell dysuria
• Hepatitis C infection or SLE
SYMPTOMS AND SIGNS
All patients have proteinuria more than 60% in the nephrotic range
Microscopic hematuria is present in about 60% , hypertension in about
70%
Renal insufficiency at presentation
DIAGNOSIS
Renal biopsy and immunostainings reveals IgG and C3 and sometimes k
light chain in the area of the deposits
In light microscopy shows glomerular depositions of microfibrils or
microtubules
55. TREATMENT
• Immunosuppressant have been used based on Anecdotal evidence,
success may be greater complement is decreased
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
It is a heterogenous group of disorders that share mixed nephritic and
nephrotic features and microscopic fundus
A group of immune immediated disorder changes , there are 3 types
Type 1 (mesangial proliferation with immune-deposits, it could occur
secondary to the following SLE cryoglobulinemia , sjrogens syndromes
Chronic infection (bacterial endocarditis HIV infection hepatitis B and C
infection
56. •Cancer (e.g chronic lymphocytic leukemia lymphomas ,
melanoma
•Type II (less mesangial proliferation and with GBM dense
deposits
•An IgG auto antibodies (c3 nephritic factors binds c3
convertase rendering C3 resistant to inactivation
•Type III , It is related to immune complex (IgG, C3)
deposition
•SYMPTOMS AND SIGNS
•Proteinuria , hematuria and hypertension
•DIAGNOSIS
•Renal biopsy as a confirmatory tests
•Serum complement profile low C3 level ,cryoglobulinuria
57. TREATMENT
•Corticosteroid for children with nephrotic range
proteinuria (prednisolone 2.5mg/kg po od
•Dipyridamole and aspirin for adults , dipyridamole
225mg po once /day
•Asprin 975mg po once /day
58. LUPUS NEPHRITIS
• It is caused by SLE , clinical finding include hematuria nephrotic range
proteinuria and in advanced stages , Azotemia
• PATHOPHYSIOLOGY
• It involves immune complex deposition with development of GN
• The immune complexes consists of nuclear antigens especially DNA
• SYMPTOMS AND SIGNS
• Oedema , proteinuria (foaming urine ), hypertension
• DIAGNOSIS
• Urinalysis and serum creatinine
• Renal biopsy
59. NEPHRITIC SYNDROMES
•Classically present with hypertension , hematuria , red
blood cells casts , pyuria and mild to moderate proteinuria
•Extensive inflammatory damage to glomeruli causes a fall in
GFR and eventually produces uremic symptoms with salts
and water retention
Defined by hematuria and the red blood and red blood casts
on microscopic examination of urinary sediment
Often more than of the following elements are present
Mild to moderate proteinuria edema , hypertension , elevated
serum creatinine and oliguria
60.
61. It has both primary and secondary causes
Nephritic syndrome is a manifestation of acute and
chronic and primary (idiopathic ) or secondary
Diagnosis is based on history , physical examination
and sometime renal biopsy
Post infections GlomeruNephritis is the prototype of
acute GN
Other cause can be connective diseases and
hematologic dyscrasias for example IgA
Nephropathy and hereditary nephritis
62. HEREDITARY NEPHRITIS (ALPORTS
SYNDROMES)
A genetically heterogeneous disorders x-terized by
hematuria, impaired renal function sensor neural
deafness and ocular abnormalities
AETIOLOGY
It cause is a gene mutation affecting type IV collagen ,
mutation in the COL4A5 gene that encodes the alpha
chain of the type IV collagen strands
63. •The causes of a glomerular disorders may results from
thickening and thinning of the glomerular and tubular
basement membranes occur which could result from
glomerular scaring and interstitial fibrosis
•Most commonly inherited in x-linked fashion , although
autosomal recessive varieties exist
•Two forms (a juvenile form with onset of renal insufficiency
between ages 20 and 30 years
•Adult forms with onset of renal insufficiency after age 30
•Mutation in COL4A3 and COL4A4 are less common and
causes autosomal recessive diseases
64. SYMPTOMS AND SIGNS
•Microscopic hematuria and eventually gross hematuria
•Progressive to renal failure
•Sensor neural deafness
•Opthalmology abnormalities cataracts
•Anterior lenticonus (a regular conical protrusion on the
anterior aspect of the lens due to thinning of the lens
capsules
•Spherophakia (spherical lens deformation that can
predispose to lens subluxations
•Nystagmus and retinitis pigmentosa
•Blindness also occurs but less frequently than deafness
•Other non renal manifestation include polyneuropathy and
thrombocytopenia
65. DIAGNOSIS
•Clinical findings and urinalysis
•Renal biopsy with immunostaining for the sub types
of the IV collagen
•Characteristics disorganization of the lamina densa of
the glomerular capillary seen using electron
microscopy
•Skin biopsy with immunostaining for the type IV
collagen subtypes in a patient with a positive family
history
•A combination of immunostaining and electron
microscopy is often needed to distinguish hereditary
nephritis from some forms of thin basement
66. TREATMENT
•ACE inhibitors or ANGIOTENSIN II receptors
blockers may slow the progression of renal diseases
•Transplantation has been successful,
Genetic counselling is indicated
67. IMMUNOGLOBULIN A NEPHROPATHY
•Deposition of IgA immune complexes in glomeruli,
manifesting as slowly progressive hematuria ,
proteinuria and often renal insufficiency
•It is a common form of GN world wide
•It occurs in all ages with a peak onset in the teens
and 20s
•It affects men 2 to 6 times more frequently than
worms
•More common in whites and Asians than blacks
•Prevalence estimates for IgA kidney deposits are 5%
in the US 10 to 20% in southern Europe and
Australia and 30% to 40% in asian
68. AETIOLOGY
•Several mechanisms, increased IgA , production ,
defective IgA glycosylation causing increased
binding to mesangial cells
•Decrease clearance , defective mucosal
immunosystem and over production of cytokines
stimulating mesangial cell proliferation
•Familial clustering with genetics factors
•SYMPTOMS AND SIGNS
•Persistent or recurrent macroscopic hematuria or
asymptomatic microscopic hematuria with mild
proteinuria in later feature
69.
70. •Sometimes febrile illness (minor respiratory infection
•Hypertension is also very common
•DIAGNOSIS
•It can be through clinical findings and urinalysis or
sometimes renal biopsy but it is confirm by biopsy
•Urinalysis (microscopic hematuria dysmorphic RBCS
and RBC casts
•Mild proteinuria (1g/day)
•RENAL BIOPSY shows granular deposition of IgA
and complement (C3) on immunoflourescent staining
in an expanded mesangium
•Foci of segmental proliferation or necrotizing
71. TREATMENT
•ACE inhibitors /AR II receptors blockers lisinopril
10mg/day
•Corticosteriods and immunosuppressants
•Methylprednisolone 1g IV once /day for 3 days plus
prednisone o.5mg/kg po for every other day for 6
month
•Combination of corticosteroid , cyclosphosphamide
and Azathiopurine are also used
•PROGNOSIS
•It has a good prognosis (15-20%) of patient develop
hypertension and end stage renal diseases within 10
years
72. POSTINFECTION GLOMERULONEPHRITIS
•Occurs after infection usually with a nephritogenic strain of
group A , B hemolytic streptococcus
•It is the most common cause of a glomerular disorder in
children between 5 and 15 years rare in under 2 years
•AETIOLOGY
•Are cause by nephritogenic strain of A beta streptococci,
most notably type 12 which causes pharyngitis and type 49
which causes impetigo
•Less common cause pathogens are non streptococcal bacteria
,virus ,parasites, rickettsia and fungi
•A microbial antigens are thought to bind to the glomerular
basement membrane and activate complement pathway
73.
74. SYMPTOMS AND SIGNS
•Asymptomatic hematuria and mild proteinuria to full blown
nephritis with microscopic or gross hematuria and renal
insufficiency
•DIAGNOSIS
•Suggested by history of pharyngitis or impetigo
•Antistreptysin O, anti hyalurindase , anti deoxyribonuclase
(anti DNASE ) are commonly measured
•Serum creatinine and complement levels C3 and total
haemolytic complement activity are usually measured
•Biopsy confirms the diagnosis but is rarely necessary
•Demonstration of hypo complementation is essentially
confirmatory
•Urinalysis shows proteinuria (0.5 to 2g/m2/day
75. TREATMENT
•Support care ,restriction of dietary protein Na and
fluid and in more severe cases or treatment of
oedema and hypertension
•Dialysis is occasionally necessary
•Antimcrobial therapy is preventive only when given
within 36 hours of infection
76. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS
•It is extension glomerular crescent formation (which can be
seen on biopsy specimen) that if untreated progresses to end
–stage renal diseases over weeks or months . It is relatively
uncommon affecting 10 to 15% of patients with GN and
occurs predominantly in patients 20 to 50 years
•Types and causes are classified by findings using
immunofluorescence microscopy
•Anti glomerular basement membrane (BGM ) antibody
disease (type 1 RPGN) is autoimmune GN and accounts for
up to 10% of RPGN cases
•It may arises when respiratory exposures (e,g cigarette smoke
, viral upper respiratory infection
77.
78. •Some other stimulus exposes alveolar capillary
collagen triggering anticollagen anti collagen
antibodies
•The anti collagen antibodies cross react with GBM
fixing complement and triggering a cell mediated
inflammatory response in the kidneys and usually the
lungs
•The term good pastures syndrome usually refers to a
combination of GN and alveolar hemorrhage in the
pressure of anti GBM antibodies
•Renal biopsy demonstrates linear IgG deposit
79.
80. IMMUNE COMPLEX RPGN (TYPE 2 RPGN)
•Complicates numerous and connective tissue
disorder
•Immunoflourescent staining demonstrates non
specific granular immune deposits , it accounts for
40%
•PAUCI IMMUNE RPGN (TYPE 3 RPGN)
•Is distinguished by the absence of immune complex
or complement deposition on immunoflourescent
staining
•All patients have elevated anti neutrophil
cytoplasmic antibodies usually myeloperoxidase
(ANCA and systemic vasculitis )
81. DOUBLE ANTIBODY DISEASES (TYPE 4 RPGN)
•It has features of types 1 and 3 within presence of
anti GBM and ANCA antibodies
•SYMPTOMS AND SIGNS
•Are usually insidious with weakness , fatigue, fever ,
nausea and vomiting ,anorexia , arthralgia and
abdominal pain
• abrupt onset hematuria and oedema in fifty percent
, history of an acute influenza –like illness within 4
weeks of onset renal failure
•Severe oliguria
•Nephrotic syndrome is present in 10 to 30%
•Pulmonary hemorrhage in anti GBM anti body
82. DIAGNOSIS
•It is suggested by acute renal failure in patients with
hematuria and RBC casts
•Serum creatinine is almost always elevated
•On CBC anemia is always present and leukocytosis is
common
•Serologic testing should include anti GBM
antibodies (anti GBM antibody disease )
•Antistreptolysin O antibodies
•Anti DNA anti bodies or cryoglobulins
83. •Complement measurement may be useful in suspected
immune complex RPGN because hypocomplementemia is
common
•Early renal biopsy is essential
•TREATMENT
•Corticosteriods , cyclosphosphamid
•Plasmapheresis for anti GBM RPGN
•FOR ANTI-GBM ANTIBODY DISEASES
•Plasmapheresis (daily 3 to 4 exchanges for 14 days is
recommended . It rapidly for 14 days is recommended .It
rapidly removes free antibody intact immune complexes and
mediators of inflammation (e.g fibrinogen complement )
•Prednisone and cyclophosphamide are typically started and
continued to minimize new antibody formation
84. FOR IMMUNE COMPLEX AND PAUCI IMMUNE
RPGN
•Corticosteroids (methyl prednisolone 1g IV once /day
for over 30 min for 3 to 5 days followed prednisone
1mg/kg po once /day
•Delay dialysis for more than 3years in 50% of
patients
•Cyclosphosphamide 1.5 to 2mg /kg po once/day
•Lymphocytapheres, a technigue to remove peripheral
lymphocytes from circulation
•Renal transplantations is effective for all types
85. THIN BASEMENT MEMBRANE DISEASE
BENIGN FAMILIAL HEMATURIA
•This disease is diffuse thinning of the glomerular
basement membrane from a width of 300 to 400nm
in normal subjects to 150 225nm usually transmitted
autosomal dorminant fashion .there is a mutation in
the type IV collagen alpha 4 gene
•Most patients are asymptomatic with microscopic
hematuria on routine urinalysis
•Mild proteinuria and gross hematuria are
occasionally present but renal function is typically
normal
86. •Diagnosis is based on family history and findings of
hematuria without other symptoms or pathology
•Renal biopsy often due as part of a hematuria
evaluation
•Patients may benefits from ACE inhibitors or
angiotensin receptor II blocker
