Perspective

Staphylococcus-Related Glomerulonephritis and

Poststreptococcal Glomerulonephritis: Why Defining “Post” Is
Important in Understanding and Treating Infection-Related
Glomerulonephritis
Richard J. Glassock, MD,1 Anthony Alvarado, MD,2 Jason Prosek, MD,2
Courtney Hebert, MD,2 Samir Parikh, MD,2 Anjali Satoskar, MD,2 Tibor Nadasdy, MD,2
John Forman, MD,3 Brad Rovin, MD,2 and Lee A. Hebert, MD2

A spate of recent publications describes a newly recognized form of glomerulonephritis associated with
active staphylococcal infection. The key kidney biopsy findings, glomerular immunoglobulin A (IgA) deposits
dominant or codominant with IgG deposits, resemble those of IgA nephritis. Many authors describe this
condition as “postinfectious” and have termed it “poststaphylococcal glomerulonephritis.” However, viewed
through the prism of poststreptococcal glomerulonephritis, the prefix “post” in poststaphylococcal glomerulo-
nephritis is historically incorrect, illogical, and misleading with regard to choosing therapy. There are numerous
reports describing the use of high-dose steroids to treat poststaphylococcal glomerulonephritis. The decision
to use steroid therapy suggests that the treating physician believed that the dominant problem was a post-
infectious glomerulonephritis, not the infection itself. Unfortunately, steroid therapy in staphylococcus-related
glomerulonephritis can precipitate severe staphylococcal sepsis and even death and provides no observable
benefits. Poststreptococcal glomerulonephritis is an authentic postinfectious glomerulonephritis; post-
staphylococcal glomerulonephritis is not. Making this distinction is important from the perspective of history,
pathogenesis, and clinical management.
Am J Kidney Dis. -(-):---. ª 2015 by the National Kidney Foundation, Inc.

INDEX WORDS: Post-staphylococcal glomerulonephritis; post-infectious glomerulonephritis; latent period;

kidney biopsy; renal disease; nosology; nomenclature; medical error; steroid treatment.

The Domain of Postinfectious Glomerulonephritis
We suggest, based on evidence discussed in this
article, that the domain of postinfectious glomerulo-
nephritis should be occupied only by conditions that
manifest all 3 of the following criteria: the glomeru-
lonephritis is preceded by an infection that resolves
with or without antimicrobial therapy; the infection is
followed by a latent period, lasting more than several
days and up to a few weeks, during which the patient
returns to or toward his or her usual state of health;
and the latent period ends with the acute onset of
features of glomerulonephritis (specifically glomer-
ular hematuria and proteinuria) and often some
decrease in kidney function.
If one accepts this criteria-based diagnostic algo-
rithm, poststreptococcal glomerulonephritis is the
poster child for postinfectious glomerulonephritis. The
pathogenesis of this paradigm is that a nephritogenic
strain of b-hemolytic streptococcus causes an infection
that usually is a pharyngitis, less commonly an impe-
tigo or cellulitis. Early in the infection, and before there
is an antibody response to the infection, antigens
derived from the streptococcal organism enter the cir-
culation and deposit in glomeruli. Later, as the anti-
body response to the streptococcal antigens flourishes,
the infection becomes suppressed but the streptococcal
antigens continue to enter the circulation. However,
now the streptococcal antigens combine with circu-
lating antibodies to form immune complexes. When
these circulating immune complexes achieve a certain
molecular size, configuration, or charge, they deposit
in glomeruli. In addition, the circulating antibodies can
bind to the streptococcal antigens previously deposited
in glomeruli. This leads to in situ immune complex
formation. Together, the deposited circulating immune
complexes and those formed in situ gradually accu-
mulate to inflict a clinically significant glomerulone-
phritis days to weeks after the infection has cleared.1-3
Local activation of the alternative complement path-
way by the deposited streptococcal antigens also can be
involved.1
From the 1Geffen School of Medicine at UCLA, Los Angeles,
CA; 2Ohio State University Wexner Medical Center, Columbus,
OH; and 3Renal Division, Brigham and Women’s Hospital,
Boston, MA.
Received July 22, 2014. Accepted in revised form January 9,
2015.
Address correspondence to Lee A. Hebert, MD, Ohio State
University Wexner Medical Center, Division of Nephrology, 395
W 12th Ave, Ground Fl, Columbus, OH 43210. E-mail: lee.
hebert@osumc.edu
 2015 by the National Kidney Foundation, Inc.
0272-6386
http://dx.doi.org/10.1053/j.ajkd.2015.01.023

Am J Kidney Dis. 2015;-(-):--- 1


It is not clear whether streptococci are the only
organisms that can cause a postinfectious glo-
merulonephritis, as discussed later in this article.
However, it is clear that staphylococcus-associated
glomerulonephritis, now widely referred to as “post-
infectious” or “poststaphylococcal” glomerulonephritis,
does not belong in the domain of a postinfectious
glomerulonephritis.
History of the Term Postinfectious Glomerulonephritis
The precise origin of the term postinfectious
glomerulonephritis is shrouded in the mists of history.
However, as described in the excellent review by
Rodriguez-Iturbe and Batsford,1 17th century physi-
cians recognized that “edematous swelling and.
dark and suppressed urine” was a “feared complica-
tion” of the convalescent period of “scarlet
fever.”1(p1,094),4 Further detail of the duration of the
convalescent period, which later was referred to as the
latent period, was provided by Wells5 in 1806 and
Bright4 in 1836. The latent period now generally is
regarded as about 1 to 4 weeks.6-9 Some authors
emphasized that the “preceding” or “prior”10 infection
often was a pharyngitis or impetigo that was so un-
remarkable that its existence had to be extracted by
direct questioning of the patient.8
By the 1920s, multiple lines of evidence emerged
indicating that a streptococcal infection, particularly
as a pharyngitis or impetigo, was the most common
infection type preceding the onset of acute glomeru-
lonephritis.11 However, the term poststreptococcal
glomerulonephritis apparently was not used in pub-
lication until 1959, when David Earle and Robert
Jennings described their concept of the natural history
of “post streptococcal glomerulonephritis.”7 It is clear
that in their use of the prefix “post,” Earl and Jennings
were acknowledging the historically puzzling
circumstance of acute glomerulonephritis developing
many days or weeks after a preceding infection had
resolved. Like their predecessors, Earle and Jennings
described the interval between the infection and the
onset of glomerulonephritis to be “several weeks.”7
Relevant to this discussion, in their landmark publi-
cation, the authors also described a case of glomeru-
lonephritis associated with streptococcal endocarditis.
However, they notably did not describe this condition
as poststreptococcal glomerulonephritis.7
The notion that poststreptococcal glomerulonephritis
generally is the product of a resolved infection is echoed
in recent and authoritative reviews.1,12 Also consistent
with this idea is that antibiotic therapy does not reduce
the occurrence of nephritis, although it reduces the
development of acute rheumatic fever, another sequela
of streptococcal pharyngitis.13,14 Nevertheless, reports
from the preantibiotic era document that streptococcus
can cause acute glomerulonephritis during the course
2 Am J Kidney Dis. 2015;-(-):---
Glassock et al
of a severe subacute streptococcal infection (for
example, case IV in Longcope et al11). So, the
streptococcal infection need not fully resolve in order
for an associated acute glomerulonephritis to emerge.
Even so, the prior resolution of infection is the most
consistent and intriguing feature of poststreptococcal
glomerulonephritis.
History of the Term Poststaphylococcal
Glomerulonephritis
In the past several years, there have been at least
17 publications that have described an unusual
form of glomerulonephritis that develops in people
with a subacute or chronic infection with
Staphylococcus aureus (most commonly methicillin
resistant [MRSA]).15-32 The remarkable feature of this
glomerulonephritis is its resemblance to immuno-
globulin A (IgA) nephritis in that the glomerular
immune deposits usually consist of IgA that is either
dominant or codominant with IgG and often accom-
panied by C3 deposition. In these recent publications,
the rationale for naming this condition “post-
infectious” or “poststaphylococcal” glomerulone-
phritis often was not stated. However, some authors
required that at least 3 of the following criteria be
present to merit the diagnosis of poststaphylococcal
glomerulonephritis: the glomerulonephritis is pre-
ceded by an infection, likely staphylococcal in nature;
serum C3 level is less than normal; kidney biopsy
shows subepithelial humps in glomerular capillaries;
glomerular IgA deposits in the mesangium and
capillary walls are dominant or codominant with IgG;
and a proliferative glomerulonephritis is present.
This definition can be faulted in a number of ways.
First, to describe the glomerulonephritis as post-
infectious because the glomerulonephritis develops
after the infection prompts the question, What other
form of infection-related glomerulonephritis can there
be? Certainly there is no basis for a “preinfectious
glomerulonephritis” (ie, the glomerulonephritis
appears before the infection). Also, if staphylococcus-
associated glomerulonephritis merits the term post-
infectious glomerulonephritis, surely every form of
infection-related glomerulonephritis warrants the use
of “postinfectious.” For example, human immunode-
ficiency virus-associated nephropathy (HIVAN)
would become “post-HIVAN,” endocarditis-related
glomerulonephritis would become “postendocarditis
glomerulonephritis,” and so on. In this context, it
can be seen that the prefix “post” applied to
staphylococcus-related glomerulonephritis is either
illogical (there is no preinfection-related glomeru-
lonephritis) or redundant (all forms of infection-
related glomerulonephritis would need to have the
prefix “post” added).
Infection-Related Glomerulonephritis

Second, if one accepts poststaphylococcal glomer-
ulonephritis as logical nosology, the glomerulone-
phritis associated with streptococcus infection would
need to be termed “post-poststreptococcal glomeru-
lonephritis” to account for the fact that the glomeru-
lonephritis occurs not just after the start of the
infection, but after the infection has resolved.
Third, the requirement of subepithelial humps by
electron microscopy apparently is intended to shore
up the logic for using the term poststaphylococcal
glomerulonephritis because humps are so character-
istic of poststreptococcal glomerulonephritis.3 How-
ever, subepithelial humps also are described in a
variety of glomerular diseases that are not necessarily
infection related, including C3 glomerulonephritis,33
dense deposit disease,34 membranoproliferative
glomerulonephritis type 1 and type III (now referred
to as C3 nephritis),35,36 Henoch-Schönlein purpura
nephritis,37,38 and monoclonal gammopathy–associated
glomerulonephritis.39 Classic humps also are seen in
the rabbit in experimental glomerulonephritis of
serum sickness.40
Taking all these issues into consideration, our
suggestions for the nomenclature for infection-related
glomerulonephritis are shown in Box 1.
Clinical Implications of Naming Staphylococcal-
Associated Glomerulonephritis Poststaphylococcal
Glomerulonephritis
We suggest that there may have been (and may
continue to be) inadvertent but serious conse-
quences of the incorrect use of the prefix “post”
in so-called poststaphylococcal glomerulonephritis.
For example, if clinicians view poststaphylococcal
glomerulonephritis through the prism of post-
streptococcal glomerulonephritis, they might
conclude that the main problem is the immune com-
plex–mediated glomerulonephritis, not the infection
itself, which often is ongoing. Although this may
seem farfetched, there are numerous reports of treat-
ing poststaphylococcal glomerulonephritis with high
doses of steroids and even cyclophosphamide,41 a
therapeutic approach generally reserved for aggres-
sive forms of IgA nephritis. None of these reports
clearly states a rationale for steroid therapy; however,
it may have been used because the glomerulonephritis
was described as being postinfectious. Of course,
because the glomerulonephritis was being caused by
an active staphylococcal infection, unfortunately, the
high-dose steroid therapy allowed the underlying
staphylococcal infection to reassert itself in some
patients despite antibiotic therapy. This resulted in
sepsis3 and even death.41,42 Although most patients
survived the steroid therapy, it did not appear that the
surviving patients were better off than those who did
not receive the steroid therapy.41
Also relevant to understanding the risk of steroid
therapy in patients with serious infection is the
CORTICUS (Corticosteroid Therapy of Septic
Shock) Study.43 In this study, patients with bacterial
sepsis, as well as low blood pressure that did not
respond to intravenous fluid replacements, were
randomly assigned to placebo or moderate-dose ste-
roid therapy (equivalent to w40 mg of prednisone for
5 days, tapered to 0 mg by day 11). All patients were
receiving appropriate antibiotic therapy. Although the
steroid therapy was only moderate dose and short
term, it caused harm by increasing the risk of super-
infection and septic shock.

Box 1. Proposed Nomenclature for Glomerulonephritis Associated With Infection

Postinfectious GN
Criteria
 The GN is preceded by an infection that resolves or is resolving with or without antimicrobial therapy
 A latent period of a few days to 4 weeks follows in which there is no clinical evidence of GN
 The latent period ends with the acute onset of GN
Cause
 Poststreptococcal GN is the only well-documented cause of postinfectious GN (see text)

Infection-Related GN
Criteria
 The infection is mechanistically related to the GN (see Table 1)
 The GN is a manifestation of an ongoing infection (ie, it is not a postinfectious GN)
Cause
 There are many different bacterial, viral, fungal, and parasitic infections that can cause infection-related GN (see text)

Comment: “Poststaphylococcal GN” is not a postinfectious GN. It is the result of an ongoing infection (there is no latent period). It
has been suggested that postinfectious GN means that the infection preceded the GN. That would be logical only if there was a
form of GN that precedes infection (preinfectious GN), which, of course, there is not. See text for additional arguments that
“poststaphylococcal infection” is a misnomer.
Thus, poststaphylococcal GN should be referred to as staphylococcus-related GN.

Abbreviation: GN, glomerulonephritis.

Am J Kidney Dis. 2015;-(-):--- 3


Table 1. Overview of Infection-Related Glomerulonephritis According to Clinical Features and Glomerular Histology
GN Type Duration
IgA nephropathy (acute flare of the Few days
established GN)
C3 nephritis (acute flare of established Few days
GN)
Poststreptococcal GN (de novo GN) 1 to a few weeks
Staphylococcus-related GN (de novo Weeks
GN)
Other forms of de novo GN during Weeks to months
subacute to chronic bacterial, viral,
fungal, or parasitic infection
Note: Most forms of bacterial infection–related GN are proliferative immune complex–mediated GN. However, the GN associated
with chronic viral, fungal or parasitic infection is often a membranous nephropathy. Also, some of the proliferative GNs associated with
subacute infection are pauci immune (no evidence of glomerular antibody or immune complex deposition).60
Abbreviations: GN, glomerulonephritis; IgA, immunoglobulin A.
a
After the onset of infection.
Use of the Term Postinfectious by Disciplines Other
Than Nephrology
To investigate the use of the term postinfectious in
non-nephrology disciplines, we conducted a PubMed
search using the following search parameters: post-
infectious (All Fields) OR post infectious (All Fields)
OR post-infectious (All Fields) AND English (Lan-
guage). This search yielded 1,486 publications, 69 of
which were published in 2000 or later. To assess the
most recent use of the term, only the 200 most current
publications were surveyed.
This search revealed that many clinical disci-
plines use the term postinfectious (or the alternative
forms included in our search). These fields include
neurology, neurosurgery, gastroenterology, ophtha-
lmology, rheumatology, and dermatology. The most
common use was in connection with neurologic
syndromes such as postinfectious encephalomyelitis,
myelopathy, hydrocephalus, and Guillain-Barré. The
second most common use was postinfectious irritable
bowel syndrome. In these articles, the term often was
used to describe any syndrome that starts after a
preceding infection (ie, a latent period between the
infection and the onset of the disease was not
required). However, in articles focusing on neurologic
symptoms, a postinfectious syndrome was defined as
occurring sometime after the original infection had
resolved.44-47 In cardiology, rheumatic fever is
regarded as postinfectious because the latent period
between the streptococcal infection and the onset of
the rheumatic fever typically is 18 days.6
In summary, in many (if not most) of the instances
that we surveyed, the term postinfectious was used
4 Am J Kidney Dis. 2015;-(-):---
Glassock et al
Infection
Type Onset of GNa
Typically viral pharyngitis or upper 1-3 d
respiratory tract infection
Typically viral pharyngitis or upper 1-3 d
respiratory tract infection
b-Hemolytic streptococcus pharyngitis, A few days to 4 wk (after
sinusitis, otitis media, cellulitis, or resolution of infection
other sites and onset of GN)
Cellulitis in an ischemic extremity, Weeks to months
osteomyelitis, endocarditis, and
other sites
Many different sites Weeks to months
in agreement with the historical and current mean-
ing of “post” as exemplified by poststreptococcal
glomerulonephritis.
Are There Infections, Other Than Those Due to Beta
Hemolytic Streptococcus, That Can Cause an
Authentic Postinfectious Glomerulonephritis?
There have been 2 detailed reviews of infection-
related glomerulonephritis.25,48 Almost all the cases
cited describe glomerulonephritis that occurred in the
context of a chronic infection. Therefore, it seems un-
likely that these cases would be authentic forms of
postinfectious glomerulonephritis. However, there are a
few notable exceptions. Most notable is “postinfectious”
pneumococcal glomerulonephritis. Although the
glomerulonephritis in these reports was described as
occurring postinfection, the glomerulonephritis
appeared during the active infection or a day or 2 after the
initiation of antibiotic treatment that resolved an asso-
ciated fever. So there was no latent period.49-51 In
addition, kidney biopsy did not show evidence of con-
spicuous immune complex deposition. Instead, there
were conspicuous C3 deposits, suggesting that the
nephritis associated with acute pneumococcal infection
may be the result of acute dysregulation of the alternative
complement pathway.50 In this regard, there is intriguing
work by Sethi et al52 that suggests that infection-related
glomerulonephritis (including poststreptococcal
glomerulonephritis) can result in a chronic and pro-
gressive glomerulonephritis, due not to continuing im-
mune complex deposition but rather on account of
continuing dysregulation of the alternative complement
pathway similar to that observed in C3 nephritis.
Infection-Related Glomerulonephritis
Hantavirus infection, which often is an acute and
self-limited infection, also has been reported to cause a
“postinfectious glomerulonephritis.”53 In these reports,
there is a latent period of several weeks between the
infection and the onset of the glomerulonephritis.
Kidney biopsy reveals glomerular immunoglobulin
deposits in most cases and a membranoproliferative
pattern. Thus, hantavirus might be an authentic cause of
postinfectious glomerulonephritis. However, if it is, the
risk of glomerulonephritis after hantavirus infection is
very low, so low that the association might be merely
coincidental. For example, in an area in which hanta-
virus infection is endemic, only 12 cases of hantavirus
“postinfectious glomerulonephritis” were observed
over a span exceeding 10 years.53 In contrast, the risk of
acute nephritis after infection with the M49 nephritic
strain of b-hemolytic streptococcus is 5% after phar-
yngitis and 25% after impetigo/cellulitis.13 This high
risk strongly suggests causality and not coincidence.
In summary, it cannot be proved that b-hemolytic
streptococcal infection is the only cause of a post-
infectious glomerulonephritis. However, if it is not the
only cause, it certainly is by far the most common
cause of postinfectious glomerulonephritis.
“Synpharyngitic Nephritis” and IgA Nephropathy
To compound the nosologic confusion further, the
terms “synphayngitic nephritis” and “synpharyngitic
hematuria” have been used to describe the onset of
features of acute nephritis almost concurrently with the
onset of a pharyngeal infection, which more often is
viral than bacterial in nature.54 This acute nephritis
most often is associated with an underlying covert IgA
nephropathy brought to clinical expression by the
infection, but other lesions also can be seen (eg, the
entity of C3 glomerulopathy).55,56 Moreover, clinical
and experimental studies have shown that staphylo-
coccal infections can at times evoke a de novo form of
IgA nephropathy or exacerbate a previously existing
IgA nephropathy that was clinically silent.57,58
Discriminating between the de novo and exacerbation
forms of infection-provoked IgA nephropathy can be
difficult. It is possible that some cases of post-
streptococcal glomerulonephritis reported in the liter-
ature before 1968 (the year IgA nephropathy was
described by Berger and Hinglais59) in reality may have
been covert IgA nephropathy exacerbated by strepto-
coccal infection or other nonspecific viral infections
masquerading as streptococcal pharyngitis. For refer-
ence, Table 1 summarizes the relationship between
infection type and duration, as well as the clinical fea-
tures of infection-related glomerulonephritis.
Conclusion
The term poststaphylococcal glomerulonephritis is
not a logical construct. It blurs the distinction between
Am J Kidney Dis. 2015;-(-):---
an authentic postinfectious glomerulonephritis and a
glomerulonephritis that is the result of ongoing
infection. This improper construct has both patho-
physiologic and clinical implications, as discussed
here. On this basis, we suggest that the diagnostic
term poststaphylococcal glomerulonephritis should
not be perpetuated. Instead, in our view, the preferred
terminology should be staphylococcus-associated or
-related glomerulonephritis. The treatment consists of
completely eradicating the staphylococcal infection
with an appropriate course of wisely selected antibi-
otic, sometimes combined with surgical drainage in
the case of deep-seated infections.
ACKNOWLEDGEMENTS
Support: None.
Financial Disclosure: The authors declare that they have no
relevant financial interests.
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