Glomerular Disease - Evaluation and Differential Diagnosis in Adults - UpToDate

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Glomerular disease: Evaluation and differential diagnosis in adults

Author: Jai Radhakrishnan, MD, MS
Section Editors: Richard J Glassock, MD, MACP, Brad H Rovin, MD
Deputy Editor: Albert Q Lam, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2020. | This topic last updated: Apr 16, 2020.
INTRODUCTION
Glomerular disease can result from many inherited or acquired disorders and can manifest in a variety of ways, ranging in severity from
asymptomatic urinary abnormalities to acute kidney injury (AKI) or end-stage kidney disease.
A kidney biopsy is often required to diagnose the underlying pathology in patients with suspected glomerular disease, particularly in those with
nephrotic syndrome or suspected glomerulonephritis. Rarely, a biopsy cannot be performed or is not needed to secure a diagnosis. As examples:
● A biopsy may be deferred if the procedural risk is prohibitive or if the patient is uncooperative or unwilling. In such cases, a presumptive
diagnosis can sometimes be made without a biopsy to facilitate the initiation of therapy. However, a biopsy should often be performed at a
later date if it becomes feasible (eg, after delivery in a pregnant patient with suspected glomerular disease). (See "The kidney biopsy".)
● A biopsy may not be required if a definitive diagnosis can be made by serology (eg, patients with nephrotic syndrome due to membranous
nephropathy associated with anti-phospholipase A2 receptor [anti-PLA2R] autoantibodies). (See "Membranous nephropathy: Epidemiology,
pathogenesis, and etiology".)
More than one glomerular disease can be present in the same individual (eg, underlying diabetic nephropathy with superimposed
glomerulonephritis).
An overview of the differential diagnosis and evaluation of glomerular disease is presented in this topic. Certain clinical syndromes of glomerular
disease are presented in other topics:
● Isolated hematuria (see "Isolated and persistent glomerular hematuria in adults")

● Isolated non-nephrotic proteinuria (see "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in
adults")
● Nephrotic syndrome (see "Overview of heavy proteinuria and the nephrotic syndrome")
● Rapidly progressive glomerulonephritis (see "Overview of the classification and treatment of rapidly progressive (crescentic)
glomerulonephritis")
Detailed discussions of specific glomerular disorders are found elsewhere. (See appropriate topic reviews.)
GLOMERULAR ANATOMY AND TERMINOLOGY
The glomerulus is the basic filtering unit of the kidney ( figure 1). Each glomerulus is essentially a tuft of capillaries formed by the branching of
the afferent arteriole and supported by a structural matrix called the mesangium, which is maintained by specialized mesangial cells. The
glomerular basement membrane (GBM) provides both a size- and charge-selective barrier to the passage of circulating macromolecules from the
plasma ( picture 1). On the urinary side of the GBM is a lining composed of a layer of podocytes, which are specialized epithelial cells
possessing a specialized intercellular junction, the slit diaphragm. The slit diaphragm provides another barrier to the filtration of plasma
macromolecules. The glomerular capillary tufts are surrounded by the Bowman's capsule, a single layer of parietal epithelial cells forming a cup-
like sac that is continuous with the renal tubule, and into which the filtrate from the glomerular capillaries is collected and passed to the renal
tubule [1,2].
On a pathological basis, glomerular lesions can be diffuse (all glomeruli are involved) or focal (only some glomeruli are involved [typically less
than 50 percent]). At the level of the individual glomerulus, a process is global if the whole glomerular tuft is involved or segmental if only a
portion is involved (less than 50 percent). Histologic descriptions include the terms "proliferative" (an increase in the number of cells in the
glomerulus), "sclerosing" (presence of scarring), and "necrotizing" (areas of cell death). Proliferation may occur predominantly in the mesangium
(mesangial proliferative glomerulonephritis), within the capillary wall (endocapillary hypercellularity), and in an extracapillary location.
Extracapillary proliferation (also known as crescents) are lesions associated with accumulations of macrophages, fibroblasts, proliferating
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epithelial cells, and fibrin within Bowman's space and represent rupture of the glomerular membrane, signifying severe injury to the glomerular
capillary wall. Some examples of how this terminology is used include "focal and segmental necrotizing glomerulonephritis" and "diffuse global
proliferative glomerulonephritis" ( picture 2). Lastly, interstitial fibrosis, which accompanies uncontrolled glomerular disease, is a poor
prognostic sign [3].
Several mechanisms lead to glomerular dysfunction [2]. Podocyte dysfunction can occur in genetic disease, affecting key basement membrane
proteins such as collagen IV mutations in Alport syndrome. In diseases such as minimal change disease and focal segmental glomerulosclerosis
(FSGS), putative circulating factors are thought to directly affect podocyte function and lead to proteinuria [4]. In diabetes mellitus and
amyloidosis, there is mechanical disruption of the glomerulus due to accumulation of normal or abnormal protein both in the capillary loops of
the glomerulus and the mesangium. Immune mechanisms include in situ formation of immune complexes in membranous glomerulopathy [5] or
the localized effects of anti-GBM antibodies in Goodpasture's disease; in conditions such as systemic lupus erythematosus, immune-mediated
kidney injury is caused by deposition of circulating immune complexes [6]. Lastly, activated neutrophils and macrophages could directly injure the
glomerulus in diseases such as antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis [2]. (See "Mechanisms of immune injury of the
glomerulus" and "Mechanisms of glomerular crescent formation".)
CLINICAL MANIFESTATIONS OF GLOMERULAR DISEASE
Clinical manifestations associated with glomerular disease include the following:
● Hematuria and/or proteinuria – Glomerular disease should be suspected when hematuria and/or proteinuria are seen on urinalysis.
Glomerular hematuria is established by the presence of urinary red blood cell (RBC) casts (of any number) or hematuria in which a substantial
proportion of RBCs are acanthocytes ( picture 3).
Although interstitial and vascular disorders of the kidney may also cause these abnormalities (and therefore mimic glomerular disease), the
findings of dysmorphic RBCs and RBC casts in the urine sediment and/or nephrotic-range proteinuria (ie, more than 3 to 3.5 g/day of
proteinuria) are more specific for a glomerular origin. (See "Urinalysis in the diagnosis of kidney disease".)
● Renal insufficiency – Patients with acute onset of nephrotic syndrome do not typically present with acute kidney injury (AKI). However, AKI
may be seen at the time of presentation in patients with podocytopathies such as minimal change disease or primary focal segmental
glomerulosclerosis (FSGS). (See "Acute kidney injury (AKI) in minimal change disease and other forms of nephrotic syndrome".)
However, renal impairment (acute or chronic) is commonly seen in patients with glomerulonephritis:
• AKI may occur with acute glomerulonephritis, especially in patients who have crescentic glomerulonephritis, which is often due to
antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis or anti-glomerular basement membrane (GBM) disease. (See
"Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis".)
• Patients with chronic glomerular diseases may develop a progressive decline in glomerular filtration rate and chronic kidney disease.
● Hypertension – Acute onset of hypertension in someone with previously normal blood pressure or acute worsening of hypertension in
someone with preexisting, controlled hypertension should raise suspicion for glomerular disease, particularly if other manifestations (eg,
hematuria, edema) are also present.
● Edema – The presence of peripheral and/or periorbital edema in patients with hematuria or proteinuria may be a sign of primary renal
sodium retention as a result of glomerular disease.
● Hypercoagulability – Some types of glomerular disease, in particular membranous nephropathy or, less commonly, other causes of
nephrotic syndrome, may produce a hypercoagulable state. Thus, thrombotic events, such as pulmonary embolism, may be a manifestation
of glomerular disease.
● Systemic findings – Glomerular disease may be limited primarily to the kidney or may be associated with systemic conditions such as
infections, autoimmune disorders, malignancy, and drug reactions. Thus, in patients with suspected glomerular disease, the history,
examination, and initial laboratory studies should include evaluation for a systemic disorder, as examples:
• Constitutional – Fevers, chills, weight loss, night sweats, fatigue

• Eye – Retinitis or uveitis
• Ear, nose, and throat – Epistaxis, sinusitis, oral ulcers
• Cardiovascular – Murmurs, pain (pericarditis), or heart failure
• Lungs – Hemoptysis, infiltrates, or nodules
• Abdomen – Enteritis, colitis, or pancreatitis
• Nervous system – Seizures or peripheral neuropathy

• Extremities – Digital ischemia or infarction
• Skin – Purpura or rash
• Musculoskeletal – Arthritis, arthralgias, myalgias
• Infections – Particularly evidence of Staphylococcus, Streptococcus, hepatitis virus, or HIV, syphilis
EVALUATION AND DIFFERENTIAL DIAGNOSIS OF MAJOR GLOMERULAR PRESENTATIONS
Glomerular disease syndromes are typically classified based upon the pattern of urinary abnormalities, the existence of systemic features, and
the degree of kidney dysfunction ( algorithm 1).
The nephrotic syndrome and glomerulonephritis are the prototypical presentations of glomerular disease. In the nephrotic syndrome, leakage of
plasma proteins without inflammation is the primary pathogenic mechanism. Conversely, in glomerulonephritis, inflammation within the
glomerulus leads not only to the passage of plasma proteins but also of inflammatory cells (leukocytes) and RBCs into the renal tubule. These
classifications, however, are not exclusive, as some conditions may present with both patterns, and some disorders (eg, lupus nephritis) may
progress from one pattern to the other. In addition, patients may present with mild manifestations such as isolated proteinuria or isolated
hematuria.
Proteinuria — Proteinuria may be caused by glomerular disease (in which there is albuminuria) or other disorders ( table 1) (see "Assessment
of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Types of proteinuria'):
● Proteinuria due to glomerular disease (in which there is albuminuria) is identified on a urine dipstick or with a quantitative measurement of
urine albumin excretion.
● Proteinuria that is not due to glomerular disease may be due to one of three mechanisms:
• Tubular proteinuria, in which low-molecular-weight proteins that are filtered across the glomerulus are incompletely reabsorbed by the
renal tubule
• Overflow proteinuria, in which overproduction of low-molecular-weight proteins (eg, light chains in the patients with multiple myeloma)
leads to an increase in filtration and excretion
• Postrenal proteinuria, which is typically associated with a urinary tract infection and leukocyturia
Proteinuria discovered by a semiquantitative urine dipstick typically reflects glomerular proteinuria because the dipstick is insensitive to
nonalbumin proteins. However, if proteinuria is discovered by a quantitative test for urinary protein (ie, a 24-hour urine collection or a random
urine protein-to-creatinine ratio), the origin of the proteinuria can be determined with a dipstick, a quantification of urine albumin excretion (ie, a
24-hour urine collection or a random urine albumin-to-creatinine ratio), or with a urine protein electrophoresis and immunofixation. (See
"Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Types of proteinuria'.)
The evaluation and differential diagnosis of patients with glomerular proteinuria depends, in part, upon whether or not the patient has nephrotic
syndrome.
Nephrotic syndrome (heavy proteinuria and hypoalbuminemia) — The nephrotic syndrome is characterized by the following (see
"Overview of heavy proteinuria and the nephrotic syndrome"):
● A urine protein excretion of greater than 3500 mg per 24 hours or, if a random urine protein-to-creatinine ratio is measured, a ratio greater
than 3000 mg/g in an adult
● Hypoalbuminemia, usually less than 3.5 g/dL, depending on the method of measurement
Other common findings in patients with nephrotic syndrome include edema (peripheral or periorbital, occasionally ascites or pleural effusions),
hyperlipidemia, and lipiduria. Lipiduria is identified by the presence of fat droplets, which may be free within sloughed tubular cells (oval fat
bodies) or inside fatty casts ( picture 4). Fat droplets have a characteristic "Maltese cross" appearance under polarized light ( picture 5).
The evaluation and differential diagnosis of nephrotic syndrome are displayed in the algorithm ( algorithm 1) and also discussed below.
Evaluation of nephrotic syndrome — Most adults with nephrotic syndrome should be evaluated by a nephrologist and undergo a kidney
biopsy to obtain a definitive diagnosis. However, a kidney biopsy may be deferred in certain patients:
● If there is an obvious etiology (eg, longstanding diabetes mellitus with progressive proteinuria) (see "Diabetic kidney disease: Pathogenesis
and epidemiology")
● If amyloidosis is suspected in a patient with a monoclonal gammopathy (in which case a fat pad biopsy may secure the diagnosis) (see
"Clinical presentation, laboratory manifestations, and diagnosis of immunoglobulin light chain (AL) amyloidosis")
● If the patient with nephrotic syndrome has a positive anti-phospholipase A2 receptor (anti-PLA2R) autoantibody (see "Membranous
nephropathy: Epidemiology, pathogenesis, and etiology")
● If a biopsy cannot be performed or is refused (eg, a patient in the later stages of pregnancy) (see "The kidney biopsy")
In addition to a kidney biopsy, certain laboratory tests, which are often performed in nephrotic patients, include:
● Glycated hemoglobin (HbA1C, to diagnose diabetes)
● Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody
● Anti-PLA2R autoantibody
● In patients older than 50 years – Serum free light chains and serum protein immunofixation
● Tests for hepatitis B and C viruses and HIV (see "Hepatitis B virus: Screening and diagnosis", section on 'Diagnostic algorithms' and
"Screening and diagnosis of chronic hepatitis C virus infection", section on 'Initial testing' and "Screening and diagnostic testing for HIV
infection", section on 'Testing algorithm')
● Serum C3 and C4 complement levels
Other serologic, microbiological, and genetic tests are sometimes performed in patients once a specific histologic diagnosis is established.
Differential diagnosis of nephrotic syndrome — The nephrotic syndrome may be primary ( table 2) or secondary to a systemic disease (
table 3). Secondary nephrotic syndrome due, for example, to diabetes, infection, or autoimmune disease, is more common than primary
nephrotic syndrome. Overall, diabetic nephropathy is the most common cause of nephrotic syndrome. (See "Overview of heavy proteinuria and
the nephrotic syndrome", section on 'Etiology' and "Diabetic kidney disease: Pathogenesis and epidemiology".)
Although minimal change disease is the most common cause of primary nephrotic syndrome in children, membranous nephropathy and focal
segmental glomerulosclerosis (FSGS) are the most common causes of primary nephrotic syndrome in adults. In adults, membranous
nephropathy predominates in white patients and FSGS in black persons. (See "Membranous nephropathy: Epidemiology, pathogenesis, and
etiology" and "Focal segmental glomerulosclerosis: Epidemiology, classification, clinical features, and diagnosis" and "Etiology, clinical features,
and diagnosis of minimal change disease in adults".)
Some disorders (eg, C3 glomerulonephritis or other causes of a membranoproliferative pattern of injury) can present as nephrotic syndrome,
glomerulonephritis, or both. (See "Overview of heavy proteinuria and the nephrotic syndrome".)
Proteinuria without nephrotic syndrome — Glomerular proteinuria without nephrotic syndrome can range in severity from several hundred
mg per day to the nephrotic range (ie, more than 3000 to 3500 mg per day). Such patients may also have variable degrees of renal insufficiency,
hypertension, and hematuria. Glomerular proteinuria is said to be isolated when it occurs in the absence of systemic disease, hypertension,
hematuria, or azotemia.
The evaluation and differential diagnosis of proteinuria without nephrotic syndrome are presented below ( algorithm 1).
Evaluation of proteinuria without nephrotic syndrome — The evaluation of proteinuria in patients without nephrotic syndrome depends
upon whether or not the proteinuria is isolated (ie, proteinuria in the absence of systemic disease, hypertension, hematuria, or azotemia).
● Isolated proteinuria – Patients with isolated proteinuria who are asymptomatic and have no obvious etiology should be evaluated for
transient proteinuria and, if the patient is younger than 30 years, orthostatic proteinuria (see "Assessment of urinary protein excretion and
evaluation of isolated non-nephrotic proteinuria in adults"):
• Transient proteinuria is common, especially in young individuals. Transient proteinuria is diagnosed if a repeat qualitative test is no
longer positive for proteinuria. These patients need no further evaluation and should be reassured that they do not have kidney disease.
(See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Rule out
transient proteinuria'.)
• Orthostatic (also referred to as postural) proteinuria is characterized by an elevated protein excretion while in the upright position and
normal protein excretion in a supine or recumbent position. It is the most frequent cause of isolated proteinuria in children, especially
adolescents, and can be diagnosed by performing a split urine collection ( table 4). Orthostatic proteinuria is discussed in detail
elsewhere. (See "Orthostatic (postural) proteinuria" and "Assessment of urinary protein excretion and evaluation of isolated non-
nephrotic proteinuria in adults", section on 'Rule out orthostatic proteinuria'.)
Patients who have isolated proteinuria that is persistent (ie, not transient and not orthostatic) should undergo kidney ultrasound to evaluate
for structural disorders (eg, reflux nephropathy) and measurement of serum free light chains and a urine protein electrophoresis with
immunofixation to evaluate for a monoclonal gammopathy.
A kidney biopsy is seldom indicated for low levels of urinary protein (eg, less than 1 g per day). However, a biopsy may be helpful in patients
with higher amounts of proteinuria. As an example, kidney biopsies in pediatric patients with proteinuria below the nephrotic range (ie, less
than 3000 to 3500 mg per day) have shown membranous nephropathy, FSGS, infection-related glomerulonephritis, focal global sclerosis,
mesangial proliferative glomerulonephritis, and normal kidneys [7]. Rarely, a biopsy in subnephrotic patients may show findings suggestive
of systemic disease (eg, amyloidosis, Fabry disease), which, if found, could lead to specific therapy. (See "Assessment of urinary protein
excretion and evaluation of isolated non-nephrotic proteinuria in adults" and "Evaluation of proteinuria in children".)
A kidney biopsy is usually indicated if a monoclonal gammopathy is present, if proteinuria is greater than 3000 to 3500 mg per day, or if the
patient subsequently develops hematuria, azotemia, or a progressive increase in proteinuria. (See "Diagnosis and treatment of monoclonal
gammopathy of renal significance", section on 'Diagnosis of MGRS' and "Assessment of urinary protein excretion and evaluation of isolated
non-nephrotic proteinuria in adults", section on 'Persistent isolated proteinuria'.)
● Proteinuria that is not isolated – Patients who have proteinuria that is accompanied by hematuria or reduced kidney function should be
evaluated by a nephrologist and possibly undergo kidney biopsy. A kidney biopsy is often deferred if the etiology of the proteinuria is obvious
(eg, diabetic nephropathy) or if the kidney function is chronically reduced, the kidneys appear atrophic by renal imaging, and a biopsy is not
likely to impact management. In addition, if amyloidosis is suspected in a patient with monoclonal gammopathy, a subcutaneous fat pad
biopsy may secure the diagnosis noninvasively. (See "Renal amyloidosis".)
Differential diagnosis of proteinuria without nephrotic syndrome — The differential diagnosis of proteinuria in the absence of
nephrotic syndrome or glomerulonephritis is broad. Most commonly, such patients have secondary FSGS due, for example, to diabetes, to
reduced nephron mass, or to a prior inflammatory or other form of injury that resulted in fibrosis. (See "Focal segmental glomerulosclerosis:
Pathogenesis", section on 'Pathogenesis of secondary FSGS'.)
Less common causes of glomerular proteinuria without nephrotic syndrome include early or mild membranous nephropathy, a mild form of
glomerulonephritis (which may occasionally present without hematuria), or deposition disorders such as Fabry disease or amyloidosis. (See
"Membranous nephropathy: Epidemiology, pathogenesis, and etiology" and "Fabry disease: Clinical features and diagnosis".)
In addition, patients with no structural glomerular lesions but who have cardiovascular disease (or who are at high risk for cardiovascular
disease) may excrete abnormal amounts of albuminuria (usually less than 300 mg per day), which possibly results from endothelial dysfunction.
(See "Moderately increased albuminuria (microalbuminuria) and cardiovascular disease", section on 'Possible mechanisms'.)
Glomerular hematuria — The hallmark of glomerular hematuria is the presence of dysmorphic RBCs ( picture 3), with or without RBC casts.
Glomerular hematuria may be associated with other manifestations, such as proteinuria, hypertension, a decreased glomerular filtration rate, or
systemic features noted above (see 'Clinical manifestations of glomerular disease' above). By contrast, glomerular hematuria may occur in
isolation without any of these other abnormalities.
Glomerulonephritis (hematuria with proteinuria, renal insufficiency, or other manifestations) — The nephritic syndrome (ie,
glomerulonephritis) is caused by glomerular inflammation that results in hematuria, variable degrees of proteinuria (which can sometimes be in
the nephrotic range), and leukocyturia in the absence of urinary tract infection. Such patients may also have hypertension, renal insufficiency,
and, if the inflammation is not limited to the kidney, findings that suggest involvement of other organ systems (eg, pulmonary hemorrhage,
palpable purpura, arthritis). Glomerular inflammation is typically due to one of three major mechanisms ( figure 2). (See 'Clinical manifestations
of glomerular disease' above and "Mechanisms of immune injury of the glomerulus".)
Glomerulonephritis can present in a variety of ways, including a smoldering course characterized by a chronic, slowly progressive rise in serum
creatinine and proteinuria (eventually leading to advanced chronic kidney disease and end-stage kidney disease), an acute, self-limited course,
and a fulminant course with acute, progressive deterioration of kidney function. This last pattern is referred to as "rapidly progressive
glomerulonephritis" and is typically associated with extensive crescents on the kidney biopsy. (See "Overview of the classification and treatment
of rapidly progressive (crescentic) glomerulonephritis".)
The evaluation and differential diagnosis of suspected glomerulonephritis are presented below ( algorithm 1).
Evaluation of glomerulonephritis — All patients with glomerulonephritis should be evaluated by a nephrologist and many should
undergo a kidney biopsy to obtain a definitive diagnosis. A kidney biopsy may be deferred in patients with advanced renal insufficiency who have
small (likely fibrotic) kidneys by imaging since the diagnostic information gained is unlikely to have substantial benefit that outweighs the risks
associated with kidney biopsy. Similarly, patients with normal kidney function, normal serological tests, and hematuria with low-grade proteinuria
(<500 mg/day) may be observed without a biopsy since, even with a definitive diagnosis, it is unlikely that specific treatment will be instituted.
(See "The kidney biopsy".)
In addition to a kidney biopsy, certain laboratory tests should be obtained in patients with suspected glomerulonephritis, including:
● Serum C3 and C4 complement levels

● Antineutrophil cytoplasmic autoantibodies (ANCA; using enzyme-linked immunosorbent assays [ELISAs] specific for proteinase-3 and
myeloperoxidase)

● Anti-glomerular basement membrane (GBM) autoantibodies
● Antinuclear antibodies
● Anti-dsDNA antibodies
● Serology for hepatitis C virus, hepatitis B virus, and HIV
● Serum free light chains and serum immunofixation
In addition, some laboratory tests are indicated by the clinical context or biopsy findings. As examples:
● A cryocrit should be measured in patients with clinical features of cryoglobulinemia or a known history of hepatitis C virus infection.
● Blood cultures should be obtained in patients with persistent fever or other signs of chronic infection.
Differential diagnosis of glomerulonephritis — Serum complement levels may be useful in differentiating the underlying etiology of
glomerulonephritis; complement levels are typically normal in anti-GBM disease and pauci-immune glomerulonephritis but low in immune
complex-mediated glomerulonephritis (with the exception of immunoglobulin A [IgA] nephropathy). However, in practice, a kidney biopsy is
almost always required to secure the diagnosis.
In patients with an acute presentation of microangiopathic hemolytic anemia, thrombocytopenia, and kidney failure, the diagnosis of thrombotic
microangiopathy (TMA) is a clinical one, and such patients typically do not need a kidney biopsy to secure the diagnosis. However, patients with
subacute and chronic TMA may exhibit minimal or no hematological or systemic abnormalities but present with progressive kidney failure with or
without proteinuria and hematuria (eg, in drug-induced TMA) [8,9]. Such patients do need to be biopsied to secure the diagnosis. (See "Approach
to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".)
Certain clinical findings suggest specific etiologies of glomerulonephritis:
● Gross hematuria may sometimes accompany glomerulonephritis and be associated with upper respiratory infection. The time elapsed
between the respiratory infection and the appearance of hematuria may sometimes be helpful: If a latent period of 7 to 10 days occurs
between the onset of infection and gross hematuria, poststreptococcal glomerulonephritis (especially in children) is the usual culprit.
Hematuria occurring concurrently with the onset of infection (ie, "synpharyngitic glomerulonephritis") is typical of IgA nephropathy.
● The presence of palpable purpura or a petechial rash suggest an underlying vasculitis (eg, ANCA-associated vasculitis, IgA vasculitis [Henoch-
Schönlein purpura], or cryoglobulinemia). Rarely, lupus nephritis may be associated with vasculitis. (See "Overview of cutaneous small vessel
vasculitis".)
● The presence of pulmonary hemorrhage ("pulmonary renal syndrome") also suggests an underlying vasculitis. (See "The diffuse alveolar
hemorrhage syndromes".)
Isolated glomerular hematuria — Persistent glomerular hematuria is distinguished from transient hematuria by repeating the urinalysis
over a period of weeks to months. Transient hematuria is a relatively common finding over time in adults and may be induced by factors such as
exercise or infection. (See "Isolated and persistent glomerular hematuria in adults" and "Etiology and evaluation of hematuria in adults" and
"Exercise-induced hematuria".)
Persistent glomerular hematuria is isolated if the patient is asymptomatic (ie, the systemic findings mentioned above are all absent) and has a
normal urine albumin excretion rate, a normal glomerular filtration rate, normal blood pressure, and if the laboratory tests that are typically
obtained to evaluate glomerulonephritis are all negative. (See 'Evaluation of glomerulonephritis' above.)
The evaluation and differential diagnosis of isolated, persistent glomerular hematuria are discussed below ( algorithm 1).
Evaluation of isolated glomerular hematuria — In such patients, a careful workup for extrarenal etiologies should be undertaken, which
may include imaging of the upper and lower urinary tract, cystoscopy, and evaluation for sickle cell disease or trait in appropriate patients (see
"Etiology and evaluation of hematuria in adults" and "Diagnosis of sickle cell disorders"). A kidney biopsy is usually not performed in the absence
of proteinuria and/or reduced kidney function, especially if there is a strong family history of hematuria or kidney disease. (See "Clinical
manifestations, diagnosis, and treatment of Alport syndrome (hereditary nephritis)" and "Thin basement membrane nephropathy (benign familial
hematuria)".)
Differential diagnosis of isolated glomerular hematuria — Generally, patients with isolated glomerular hematuria are likely to have mild
IgA nephropathy, a disorder associated with membranoproliferative glomerulonephritis, a genetic mutation in type IV collagen associated with
Alport syndrome, or thin basement membrane nephropathy. (See "Isolated and persistent glomerular hematuria in adults" and "Clinical
presentation and diagnosis of IgA nephropathy" and "Genetics, pathogenesis, and pathology of Alport syndrome (hereditary nephritis)" and
"Clinical manifestations, diagnosis, and treatment of Alport syndrome (hereditary nephritis)" and "Thin basement membrane nephropathy
(benign familial hematuria)".)

SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See
"Society guideline links: Glomerular disease in adults".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written
in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics
patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and
are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can
also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Beyond the Basics topics (see "Patient education: Glomerular disease (Beyond the Basics)" and "Patient education: The nephrotic syndrome
(Beyond the Basics)")
SUMMARY
● Glomerular disease can result from many inherited or acquired disorders and can manifest in a variety of ways, ranging in severity from
asymptomatic urinary abnormalities to acute kidney injury (AKI) or end-stage kidney disease. Occasionally, more than one glomerular
disease is present in the same individual. (See 'Introduction' above.)
● Clinical manifestations associated with glomerular disease include the following (see 'Clinical manifestations of glomerular disease' above):
• Hematuria and/or proteinuria – Glomerular disease should be suspected when hematuria and/or proteinuria are seen on urinalysis.
Glomerular hematuria is established by the presence of urinary erythrocyte casts (of any number) or hematuria in which a substantial
proportion of erythrocytes are acanthocytes ( picture 3).
• Renal insufficiency – Renal impairment (acute or chronic) is commonly seen in patients with glomerular disease. AKI may occur with
acute glomerulonephritis, especially in patients who have crescentic glomerulonephritis, or, rarely, in patients with acute onset of
nephrotic syndrome. Patients with chronic glomerular diseases may develop a progressive decline in glomerular filtration rate and
chronic kidney disease.
• Other manifestations – Hypertension, edema, hypercoagulability, and systemic findings.
● Glomerular disease syndromes are typically classified based upon the pattern of urinary abnormalities, the existence of systemic features,
and the degree of kidney insufficiency ( algorithm 1). (See 'Evaluation and differential diagnosis of major glomerular presentations' above.)
• Proteinuria – Proteinuria may be caused by glomerular disease (in which there is albuminuria) or other disorders ( table 1). Proteinuria
due to glomerular disease (in which there is albuminuria) is identified on a urine dipstick or with a quantitative measurement of urine
albumin excretion. The evaluation and differential diagnosis of patients with glomerular proteinuria depend, in part, upon whether or
not the patient has nephrotic syndrome (ie, proteinuria greater than 3500 mg per 24 hours and hypoalbuminemia):
- Adults with nephrotic syndrome should be evaluated by a nephrologist and most should undergo a kidney biopsy to obtain a
definitive diagnosis ( table 2 and table 3). (See 'Nephrotic syndrome (heavy proteinuria and hypoalbuminemia)' above.)
- The evaluation of proteinuria in patients without nephrotic syndrome depends upon whether or not features of glomerulonephritis
are present (eg, systemic disease, hypertension, hematuria, or renal insufficiency). The differential diagnosis of proteinuria in the
absence of nephrotic syndrome or glomerulonephritis is broad. Most commonly, such patients have secondary focal segmental
glomerulosclerosis (FSGS) due, for example, to diabetes, to reduced nephron mass, or to a prior inflammatory or other form of injury
that resulted in fibrosis. (See 'Proteinuria without nephrotic syndrome' above.)
• Glomerular hematuria – Glomerular hematuria may be associated with other manifestations, such as proteinuria, hypertension, a
decreased glomerular filtration rate, or systemic features (glomerulonephritis). By contrast, glomerular hematuria may occur in isolation
without any of these other abnormalities (isolated glomerular hematuria).

- All patients with glomerulonephritis should be evaluated by a nephrologist and many should undergo a kidney biopsy to obtain a
definitive diagnosis ( figure 2). (See 'Glomerulonephritis (hematuria with proteinuria, renal insufficiency, or other manifestations)'
above.)
- A kidney biopsy is usually not performed in patients with isolated glomerular hematuria. Generally, patients with isolated
glomerular hematuria are likely to have mild immunoglobulin A (IgA) nephropathy, a disorder associated with
membranoproliferative glomerulonephritis, a genetic mutation in type IV collagen associated with Alport syndrome, or thin
basement membrane nephropathy. (See 'Isolated glomerular hematuria' above.)
ACKNOWLEDGMENTS
The editorial staff at UpToDate would like to acknowledge Lee A Hebert, MD, and Samir V Parikh, MD, who contributed to an earlier version of this
topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Ellis EN, Mauer SM, Sutherland DE, Steffes MW. Glomerular capillary morphology in normal humans. Lab Invest 1989; 60:231.
2. Dickinson BL. Unraveling the immunopathogenesis of glomerular disease. Clin Immunol 2016; 169:89.
3. http://www.ajkd.org/content/atlasofrenalpathologyii (Accessed on November 25, 2016).
4. Nagata M. Podocyte injury and its consequences. Kidney Int 2016; 89:1221.
5. Ronco P, Debiec H. Membranous nephropathy: A fairy tale for immunopathologists, nephrologists and patients. Mol Immunol 2015; 68:57.
6. Vinen CS, Oliveira DB. Acute glomerulonephritis. Postgrad Med J 2003; 79:206.
7. Trachtman H, Bergwerk A, Gauthier B. Isolated proteinuria in children. Natural history and indications for renal biopsy. Clin Pediatr (Phila)
1994; 33:468.
8. Raife TJ, Lager DJ. Chronic thrombotic microangiopathy associated with antineoplastic therapy with minimal hematologic effects. Mayo Clin
Proc 2002; 77:323.
9. George JN, Nester CM. Syndromes of thrombotic microangiopathy. N Engl J Med 2014; 371:654.
Topic 3041 Version 32.0

GRAPHICS
Diagram of glomerular anatomy
The glomerular basement membrane (GBM; shown in green) is a thin sheet of extracellular matrix protein that surrounds the capillary and
provides support and a barrier.
(A) Renal corpuscle and juxtaglomerular apparatus.
(B) Peripheral portion of a glomerular lobule.
Reproduced from: Kriz W, Elger M. Renal Anatomy. In: Comprehensive Clinical Nephrology, 5th ed, Johnson RJ, Feehally J, Floege J (Eds), Elsevier 2014.
Illustrations used with the permission of Elsevier Inc. All rights reserved.
Graphic 113970 Version 1.0

Electron micrograph of a normal glomerulus
Electron micrograph of a normal glomerular capillary loop showing the fenestrated

endothelial cell (Endo), the glomerular basement membrane (GBM), and the epithelial
cells with its interdigitating foot processes (arrow). The GBM is thin, and no electron-
dense deposits are present. Two normal platelets are seen in the capillary lumen.
Courtesy of Helmut G Rennke, MD.
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Postinfectious glomerulonephritis
Low-power light micrograph showing diffuse, proliferative glomerulonephritis, as may

be seen in postinfectious glomerulonephritis. The glomeruli are so hypercellular
(arrows) that open capillary lumens cannot be seen, and the glomeruli may be hard to
distinguish from the surrounding interstitium.
Courtesy of Helmut Rennke, MD.

Phase-contrast micrograph showing dysmorphic red cells in

urine sediment
Phase-contrast microscopy showing dysmorphic red cells in a patient with glomerular

bleeding. Acanthocytes can be recognized as ring forms with vesicle-shaped
protrusions (arrows).
Courtesy of Hans Köhler, MD.

Overview of the evaluation and differential diagnosis of glomerular disease


Kidney biopsy specimens should always be analyzed with light microscopy and immunofluorescence. In some cases, electron microscopy is also necessary. Because electron microscopy is not available at
with electron microscopy capabilities) if the clinical scenario, light microscopy, and/or immunofluorescence suggest that the following disorders may be present:
Minimal change disease.
FSGS.
C3 glomerulopathy (C3 glomerulonephritis or dense deposit disease).
Thin basement membrane nephropathy.
Alport syndrome.
Fabry disease.
Fibrillary glomerulonephritis.
Immunotactoid glomerulonephritis.
Monoclonal immunoglobulin deposition disease.
Amyloidosis.
C3: complement component 3; C4: complement component 4; ANA: antinuclear antibody; anti-dsDNA: anti-double-stranded DNA; ANCA: antineutrophil cytoplasmic antibody; ELISA: enzyme-linked immunoassay; PR3:
virus; HBV: hepatitis B virus; HCV: hepatitis C virus; IgA: immunoglobulin A; HbA1c: hemoglobin A1C; NSAIDs: nonsteroidal antiinflammatory drugs; anti-PLA2R: anti-phospholipase-A2-receptor; FSGS: focal segmental g
immunotactoid GN: immunotactoid glomerulopathy; APOL1: apolipoprotein L1; eGFR: estimated glomerular filtration rate; RBC: red blood cell.
* Glomerular hematuria and proteinuria are defined as follows:
Glomerular hematuria is established by the presence of urinary RBC casts (of any number) or hematuria in which more than 5% of RBCs are acanthocytes or dysmorphic.
Proteinuria is typically defined as a 24-hour urine protein excretion of ≥150 mg (or a corresponding value using the spot urine protein, spot urine creatinine, and the protein excretion rate equation).
Albuminuria (albumin is a component of urinary protein, is the major component in glomerular disease, and is the protein that is detected by the urine dipstick) is typically defined as a 24-hour urine albumin exc
excretion rate equation).
¶ A systemic disorder that also involves the kidney should be suspected if there is evidence for inflammation of other organ systems, such as the skin (eg, purpura, rash), joints (eg, arthritis), eye (eg, retinitis, uveitis),
neuropathy), extremities (eg, digital ischemia or infarction), or abdomen (eg, enteritis, colitis), or if there is an infection (particularly with Staphylococcus, Streptococcus, hepatitis virus, or HIV).
Δ Orthostatic proteinuria is characterized by increased protein excretion while in the upright posture but normal protein excretion when recumbent; it is typically found in adolescents and young adults but not in olde
either with an overnight urine collection or a first-morning voided urine specimen.
◊ Some patients with FSGS will have a genetic mutation that results in a defect of podocyte or slit diaphragm function; the most commonly involved genes include nephrin, podocin, alpha-actinin-4, TRPC6, INF2, and M

Classification and characterization of proteinuria types
Classification of proteinuria Clinical setting Typical level of proteinuria in adults
Transient proteinuria Fever, heavy exercise, vasopressor infusion, albumin infusion <1 g/day
Persistent proteinuria – orthostatic proteinuria Uncommon over age 30 years, may occur in 2 to 5 percent of <1 to 2 g/day
adolescents
Persistent proteinuria – overflow proteinuria Myeloma (monoclonal light chains), Hemolysis (hemoglobinuria), Variable, could be nephrotic range
Rhabdomyolysis (myoglobinuria)
Persistent proteinuria – glomerular proteinuria Primary glomerular diseases, secondary glomerular diseases, Variable, often nephrotic range
diabetic nephropathy, hypertensive nephrosclerosis
Persistent proteinuria – tubulointerstitial proteinuria Heavy metal intoxications, autoimmune or allergic interstitial <3 g/day
inflammation, medication-induced interstitial injury
Post-renal proteinuria Urinary tract infections, nephrolithiasis, genitourinary tumor <1 g/day

Fatty cast
Urine sediment showing a fatty cast. The fat droplets (or globules) can be
distinguished from red cells (which also have a round appearance) by their variable
size (from much smaller to much larger than a red cell), dark outline, and "Maltese
cross" appearance under polzarized light.
Courtesy of Frances Andrus, BA, Victoria Hospital, London, Ontario.

Fatty cast
Urine sediment showing fatty cast under polarized light. The fat droplets have a
characteristic "Maltese cross" appearance (arrow).
Courtesy of Harvard Medical School.

Renal pathology in primary nephrotic syndrome
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis: C3 glomerulonephritis, dense deposit disease, and "idiopathic" immune complex-mediated membranoproliferative glomerulonephritis*
RBC: red blood cell.

* Indicates those disorders that could also present as a nephritic-nephrotic syndrome (RBC, RBC casts with nephrotic-range proteinuria).
Courtesy of Jai Radhakrishnan, MD, MS.

Renal pathology in nephrotic syndrome associated with genetic and systemic disorders (secondary nephrotic syndrome)
Podocytopathies: Minimal change or FSGS pattern
Infections: HIV, macrophage activation syndrome, polyomavirus, cytomegalovirus
Drugs: Interferon, pamidronate, NSAIDs, lithium, vaccines, venoms, stings
Malignancies: Thymoma, Hodgkin lymphoma (formerly called Hodgkin disease)
Genetic disorders of podocyte proteins (eg, nephrin, podocin, Alport syndrome, etc.)
Other: Sickle cell, myelodysplastic syndromes, hepatitis C, von Gierke disease, Fabry disease, dysautonomia, obesity
Membranous nephropathy pattern
Autoimmune disease: Lupus
Infections: Hepatitis B, malaria, syphilis
Malignancies: Solid organ tumors, leukemia
Drugs: Gold, mercury, heavy metals, captopril, penicillamine, NSAIDs
Other: Sarcoidosis, Sjögren's syndrome, graft-versus-host disease
Membranoproliferative pattern*
Autoimmune disease: Connective tissue diseases including lupus
Infection: Chronic bacterial infections (eg, endocarditis, VA shunts), hepatitis C
Chronic thrombotic microangiopathy
Malignancy: Monoclonal gammopathy, cryoglobulinemia
Other: POEMS syndrome
Transplant glomerulopathy
Glomerular deposition diseases
Amyloidosis: AL, AA, hereditary amyloidosis, and others
Other monoclonal deposition diseases*: Immunoglobulin deposition disease, immunotactoid glomerulopathy
Hereditary disorders
Alport syndrome*
Fabry disease*
Nail-patella syndrome
Partial lipodystrophy*
APOL1-associated nephropathy
Other
Diabetes mellitus
Idiopathic nodular glomerulosclerosis
Fibrillary glomerulonephritis*
Pregnancy related (includes preeclampsia)
FSGS: focal segmental glomerulosclerosis; HIV: human immunodeficiency virus; NSAIDs: nonsteroidal antiinflammatory drugs; VA: ventriculoatrial; POEMS: Polyneuropathy, Organomegaly, Endocrinopathy,
Monoclonal protein, Skin changes; APOL1: apolipoprotein L1; RBC: red blood cell.
* Indicates those disorders that could also present as a nephritic-nephrotic syndrome (RBC, RBC casts with nephrotic-range proteinuria).
Courtesy of Jai Radhakrishnan, MD, MS.

Patient instructions for performing a split urine collection
Introduction
A "split urine test" is a method to determine whether the protein discovered in your urine is due to a condition called orthostatic proteinuria. This is a harmless condition that is not uncommon in young
people. For reasons that are not well understood, some people leak protein into the urine when they are standing or sitting but not while they are lying down. The split urine test is a simple way to
determine if this condition is present.
Equipment
The test requires that you collect all of your urine for 24 hours. Pick a day when this would be convenient for you. Males might want to buy an inexpensive urinal for easy collection; females should buy an
inexpensive basin urinal.
You also need two jugs and a funnel. One-half gallon plastic jugs, thoroughly rinsed, are adequate if jugs are not provided. Label the two jugs: (1) Daytime urine and (2) Nighttime urine, respectively.
Procedure
Perform the following steps on the day that you are going to make the split urine collections.
When you first get up, discard the first morning urine.
For the rest of the day, collect all of the urine each time you void. Put this urine into the Daytime urine jug. You should be as active as you normally are during the day.
In the evening, lie down for two hours before you go to sleep. Just before sleeping, void for the last time during the day and add this urine to the Daytime jug. Lying down for two hours before the
nighttime collection avoids contamination of the nighttime collection with urine formed during the day when you were upright.
The following morning (approximately eight hours after you went to sleep), collect the first-morning urine and put in the Nighttime urine jug.
Take the two jugs to the laboratory.
We will notify you when we get the results.

Histologic appearance and clinical associations of the three major pathogenic types of
glomerulonephritis
GN: glomerulonephritis; GBM: glomerular basement membrane; ANCA: antineutrophil cytoplasmic autoantibody; SLE: systemic lupus
erythematosus; MPGN: membranoproliferative glomerulonephritis; IgA: immunoglobulin A.
Courtesy of Jai Radhakrishnan, MD, MS. Images courtesy of M. Barry Stokes, MD.

Contributor Disclosures
Jai Radhakrishnan, MD, MS Nothing to disclose Richard J Glassock, MD, MACP Speaker's Bureau: Genentech [Vasculitis (Rituximab)]. Consultant/Advisory
Boards: Bristol-Myers Squibb [Lupus Nephritis, Focal Segmental Glomerulosclerosis (Abatacept)]; ChemoCentryx [Vasculitis, C3 Glomerulopathy, Focal Segmental
Glomerulosclerosis (CCX-168, CCX-140)]; Retrophin [Focal Segmental Glomerulosclerosis, IgA Nephropathy (Sparsentan)]; Omeros [IgA Nephropathy]; Ionis [C3
Glomerulopathy]; Apellis [Complement Inhibition on Glomerular Disease]; Achillion [Complement inhibition]; Horizon [Glomerular disease]. Employment: Karger
Publishers [American Journal of Nephrology]. Equity Ownership/Stock Options: Reata [Alport Syndrome, Pulmonary Hypertension, Diabetic Nephropathy
(Bardoxolone)]. Brad H Rovin, MD Grant/Research/Clinical Trial Support: AstraZeneca/MedImmune [Lupus nephritis]; Aurinia Pharmaceuticals [Lupus nephritis,
focal segmental glomerulosclerosis]; Biogen Idec [Lupus nephritis]; Bristol-Myers Squibb [Focal segmental glomerulosclerosis, minimal change disease]; Calliditis
Therapeutics [IgA nephropathy]; ChemoCentryx [Lupus nephritis, ANCA vasculitis, C3 glomerulopathy]; EMD Serono [IgA nephropathy]; Genentech/Hoffmann-La
Roche [Lupus nephritis, ANCA vasculitis]; Human Genome Sciences [Lupus nephritis]; Lupus Clinical Investigation Network [Lupus nephritis]; National Institutes of
Health [Glomerular diseases/molecular interrogation of kidney biopsies, precision medicine/biomarkers]; Omeros [IgA nephropathy]; Retrophin [IgA
nephropathy]; Rigel Pharmaceuticals [IgA nephropathy]. Consultant/Advisory Boards: Admirx [Complement]; AstraZeneca/MedImmune [Lupus nephritis]; Aurinia
Pharmaceuticals [Lupus nephritis, focal segmental glomerulosclerosis]; Biogen Idec [Lupus nephritis]; Bristol-Myers Squibb [Focal segmental glomerulosclerosis,
minimal change disease]; Calliditis Therapeutics [IgA nephropathy]; EMD Serono [IgA nephropathy]; Genentech/Hoffmann-La Roche [Lupus nephritis, ANCA
vasculitis]; Jassen [Lupus nephritis]; Lupus Foundation of America [Lupus nephritis, health care disparities, clinical trial design]; MorphoSys [Membranous
nephropathy]; Novartis [IgA nephropathy]; Omeros [IgA nephropathy]; Retrophin [IgA nephropathy]; Pfizer [Systemic lupus erythematosus and lupus nephritis];
Alexion Pharmaceuticals [Lupus nephritis]; BioMarin Pharmaceuticals [Hereditary disorders of metabolic disorders]; Chugai Pharmaceuticals [Lupus nephritis];
Mallinckrodt [Lupus nephritis, focal segmental glomerulosclerosis]; Ra Pharmaceuticals [Lupus nephritis, other renal indications]; Rigel Pharmaceuticals [IgA
nephropathy]; RILITE Foundation [Lupus nephritis]. Albert Q Lam, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review
process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Glomerular disease: Evaluation and differential diagnosis in adults

● Isolated hematuria (see "Isolated and persistent glomerular hematuria in adults")

GLOMERULAR ANATOMY AND TERMINOLOGY

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CLINICAL MANIFESTATIONS OF GLOMERULAR DISEASE

Clinical manifestations associated with glomerular disease include the following:

• Constitutional – Fevers, chills, weight loss, night sweats, fatigue

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EVALUATION AND DIFFERENTIAL DIAGNOSIS OF MAJOR GLOMERULAR PRESENTATIONS

● Glycated hemoglobin (HbA1C, to diagnose diabetes)

● Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody

● Serum C3 and C4 complement levels

● Serum C3 and C4 complement levels

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Certain clinical findings suggest specific etiologies of glomerulonephritis:

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SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

• Other manifestations – Hypertension, edema, hypercoagulability, and systemic findings.

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Use of UpToDate is subject to the Subscription and License Agreement.

3. http://www.ajkd.org/content/atlasofrenalpathologyii (Accessed on November 25, 2016).

Topic 3041 Version 32.0

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Diagram of glomerular anatomy

Graphic 113970 Version 1.0

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Electron micrograph of a normal glomerulus

Electron micrograph of a normal glomerular capillary loop showing the fenestrated

Courtesy of Helmut G Rennke, MD.

Graphic 50018 Version 7.0

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Low-power light micrograph showing diffuse, proliferative glomerulonephritis, as may

Courtesy of Helmut Rennke, MD.

Graphic 80304 Version 3.0

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Phase-contrast micrograph showing dysmorphic red cells in

Phase-contrast microscopy showing dysmorphic red cells in a patient with glomerular

Courtesy of Hans Köhler, MD.

Graphic 79440 Version 4.0

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Overview of the evaluation and differential diagnosis of glomerular disease

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Graphic 113287 Version 4.0

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Classification and characterization of proteinuria types

Classification of proteinuria Clinical setting Typical level of proteinuria in adults

Graphic 85791 Version 4.0

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Courtesy of Frances Andrus, BA, Victoria Hospital, London, Ontario.

Graphic 69603 Version 1.0

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Courtesy of Harvard Medical School.

Graphic 79604 Version 1.0

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Renal pathology in primary nephrotic syndrome

Minimal change disease

Focal segmental glomerulosclerosis

RBC: red blood cell.

Courtesy of Jai Radhakrishnan, MD, MS.