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Glomerulonefritis Akut Paska Streptokokus

Muhammad Sjaifullah Noer, Ninik Soemyarso

BATASAN

Glomerulonefritis akut paska-streptokokus (GNAPS) adalah suatu proses radang non-supuratifyang mengenai glomeruli, sebagai akibat infeksi kuman streptokokus beta hemolitikus grup A,

tipe nefritogenik di tempat lain. Penyakit ini sering mengenai anak-anak.

ETIOLOGISebagian besar (75%) glomerulonefritis akut paska streptokokus timbul setelah infeksi saluran

pernapasan bagian atas, yang disebabkan oleh kuman Streptokokus beta hemolitikus grup A tipe1, 3, 4, 12, 18, 25, 49. Sedang tipe 2, 49, 55, 56, 57 dan 60 menyebabkan infeksi kulit 8-14 hari

setelah infeksi streptokokus, timbul gejala-gejala klinis. Infeksi kuman streptokokus beta

hemolitikus ini mempunyai resiko terjadinya glomerulonefritis akut paska streptokokus berkisar

10-15%.

PATOFISIOLOGI

Patogenesis yang mendasari terjadinya GNAPS masih belum diketahui dengan pasti. Berdasarkanpemeriksaan imunofluorosensi ginjal, jelas kiranya bahwa GNAPS adalah suatu glomerulonefritis yangbermediakan imunologis. Pembentukan kompleks-imun in situ diduga sebagai mekanisme patogenesis

glomerulonefritis pascastreptokokus. Hipotesis lain yang sering disebut adalah neuraminidaseyangdihasilkan oleh streptokokus, merubah IgG menjadi autoantigenic.Akibatnya, terbentuk autoantiboditerhadap IgG yang telah berubah tersebut. Selanjutnya terbentuk komplek imun dalam sirkulasi darahyang kemudian mengendap di ginjal.Streptokinase yang merupakan sekret protein, diduga juga berperan pada terjadinya GNAPS.

Sreptokinase mempunyai kemampuan merubah plaminogen menjadi plasmin. Plasmin ini diduga dapatmengaktifkan sistem komplemen sehingga terjadi cascade dari sistem komplemen. Pada pemeriksaanimunofluoresen dapat ditemukan endapan dari C3 pada glomerulus, sedang protein M yang terdapat pada

permukaan molekul, dapat menahan terjadinya proses fagosistosis dan meningkatkan

virulensi kuman. Protein M terikat pada antigen yang terdapat pada basal

membran dan IgG antibodi yang terdapat dalam sirkulasi.Pada GNAPS, sistim imunitas humoral diduga berperan dengan ditemukannya endapan C3 dan IgG pada

subepitelial basal membran. Rendahnya komplemen C3 dan C5, serta normalnya

komplemen pada jalur klasik merupakan indikator bahwa aktifasi

komplemen melalui jalur alternatif.Komplemen C3 yang aktif akan

menarik danmengaktifkan monosit dan neutrofil, dan menghasilkan infiltrat akibat adanya proses

inflamasi dan selanjutnya terbentuk eksudat. Pada prosesinflamasi ini juga dihasilkan sitokin oleh selglomerulus yang mengalami injuri dan proliferasi dari sel mesangial.GNAPS dapat terjadi pada semua kelompok umur, namun tersering pada golongan umur 5-15

tahun, dan jarang terjadi pada bayi. Penyakit ini dapat terjadi pada laki laki dan perempuan,

namun laki laki dua kali lebih sering dari pada perempuan. Diduga ada faktor resiko yangberhubungan dengan umur dan jenis kelamin.

GEJALA KLINIS Sembab preorbita pada pagi hari (75%)


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Malaise, sakit kepala, muntah, panas dan anoreksia

Asites (kadang-kadang)

Takikardia, takipnea, rales pada paru, dan cairan dalam rongga pleura Hipertensi (tekanan darah > 95 persentil menurut umur) pada > 50% penderita

Air kemih merah seperti air daging, oliguria, kadang-kadang anuria

Pada pemeriksaan radiologik didapatkan tanda bendungan pembuluh darah paru, cairan dalam

rongga pleura, dan kardiomegali

LABORATORIUM- Air kemih :

Proteinuria ringan (pemeriksaan urine rebus)

Hematuria makroskopis/mikroskopis

Torak granular, torak eritrosit

- Darah

BUN naik pada fase akut, lalu normal kembali

ASTO >100 Kesatuan Todd

Komplemen C3 < 50 mg/dl pada 4 minggu pertama

Hipergamaglobulinemia, terutama IgG

Anti DNA-ase beta dan properdin meningkat

DIAGNOSISDiagnosis GNAPS dibuat berdasarkan :

- Gejala klinis

- Laboratorium :

Air kemih : harus lengkap

Darah : - ASTO > 100 Kesatuan Todd

- C3 < 50 mg/dl

DIAGNOSIS BANDING- Hematuria berulang dengan glomerulonefritis fokal (IgA nefropati)

Hematuria berulang yang asimtomatis, tanpa penurunan fungsi ginjal

Timbunan IgA di glomeruli- Hematuria berulang ringan- Purpura Henoch-Schonlein

- Glomerulonefritis progresif

PENATALAKSANAAN

1. TerapiMedikamentosa

Golongan penisilin dapat diberikan untuk eradikasi kuman, dengan amoksisilin 50 mg/kg BB

dibagi 3 dosis selama 10 hari. Jika alergi terhadap golongan penisilin, diganti denganeritromisin 30 mg/kg BB/hari dibagi 3 dosis.

Diuretik diberikan untuk mengatasi retensi cairan dan hipertensi. Jika terdapat hipertensi,

berikan obat antihipertensi, tergantung pada berat ringannya hipertensi.Bedah

Tidak diperlukan tindakan bedah.

Suportif


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Pengobaan GNAPS umumnya bersifat suportif. Tirah baring umumnya diperlukan jika

pasien tampak sakit misalnya kesadaran menurun, hipertensi, edema. Diet nefritis diberikan

terutama pada keadaan dengan retensi cairan dan penurunan fungsi ginjal. Jika terdapatkomplikasi seperti gagal ginjal, hipertensi ensefalopati, gagal jantung, edema paru, maka

tatalaksananya disesuaikan dengan komplikasi yang terjadi.

Lain-lain (rujukan subspesialis, rujukan spesialisasi lainnya dll)Rujuk ke dokter nefrologi anak bila terdapat komplikasi gagal ginjal, ensefalopati hipertensi,gagal jantung.

2. PemantauanTerapi

Meskipun umumnya pengobatan bersifat suportif, tetapi pemantauan pengobatan dilakukan

terhadap komplikasi yang terjadi karena komplikasi tersebut dapat mengakibatkan

kematian. Pada kasus yang berat, pemantauan tanda vital secara berkala diperlukan untuk

memantau kemajuan pengobatan.Tumbuh Kembang

Penyakit ini tidak mempunyai pengaruh terhadap tumbuh kembang anak, kecuali jika

terdapat komplikasi yang menimbulkan sekuele.

KOMPLIKASI- Hipertensi ringan sampai berat (enselopati hipertensif)- Payah jantung karena hipertensi dan hipervolemia (volume overload)

- Gagal ginjal

DAFTAR PUSTAKA1. Arant Jr BS, Roy III S, Stapleton BF, 1983. Poststreptococal acute glomerulonephritis. In

: Kelley VC, ed. Practice of Pediatrics. Volume VIII. New York : harper and Row Publ., 7 :

1.2. Cole BR, Madrigal LS, 1999. Acute Proliferative Glomerulonephritis. In Barratt TM, Avner

ED, Harmon WE. 4th

ED. Baltimor, Maryland USA : Lippincott William & Wilkins, 669-689.

3. Jordan CS, Lemire MJ, 1982. Acute Glomerulonephritis : Diagnosis and Treatment. Pediatr

Clin N Am , 29 : 857.4. Kempe CH, Silver HK, OBrien D, 1980.Current Pediatric Diagnosis and

Treatment. 6th

ed. Singapore : Maruzen Co./Lange Medical Publ., 508.

5. Noer MS . Glomerulonefritis, 2002. In Alatas H, Tambunan T, Trihono PP, PardedeSO. Buku Ajar Nefrologi Anak. 2

nd.Ed. Jakarta : Fakultas Kedokteran Universitas Indonesia,

323-361.

6. Smith JM, Faizan MK, Eddy AA, 2003. The child with acute nephritic syndrome. In Webb

NJA, Postlethwaite RJ ed, Clinical Paediatric Nephrology3rd ED. Great Britain : OxfordUniversity Press, 197-225.


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PathophysiologyMost forms of acute poststreptococcal glomerulonephritis (APSGN) are mediated by an immunologic process. Cellular andhumoral immunity is important in the pathogenesis of this disease, and humoral immunity in APSGN. Nonetheless, the exactmechanism by which APSGN occurs remains to be determined. The 2 most widely proposed theories include (1) glomerulartrapping of circulating immune complexes and (2) in situ immune antigen-antibody complex formation resulting fromantibodies reacting with either streptococcal components deposited in the glomerulus or with components of the glomerulusitself, which has been termed molecular mimicry.

Additional evidence has also been presented to support the anti-immunoglobulin activity or glomerular plasmin-bindingactivity of streptococcal antigens. The cross-reactivity of streptococci and mammalian tissue implicating molecular mimicry inacute rheumatic fever led to evidence of a similar mechanism involved in APSGN. However, the similar cross-reactivitypatterns of rheumatogenic and nephritogenic strains of streptococci argue against molecular mimicry involving M proteins.

Immune complex-mediated mechanisms

An immune complexmediated mechanism is the most widely proposed mechanism leading to the development of APSGN.Nephritogenic streptococci produce proteins with unique antigenic determinants. These antigenic determinants have aparticular affinity for sites within the normal glomerulus. Following release into the circulation, the antigens bind to thesesites within the glomerulus. Once bound to the glomerulus, they activate complement directly by interaction with properdin.

Glomerular-bound streptococcal antibodies also serve as fixed antigens and bind to circulating antistreptococcal antibodies,forming immune complexes. Complement fixation via the classic pathway leads to the generation of additional inflammatorymediators and recruitment of inflammatory cells.

Zymogen (NSAP) and NAPlr

Two major antigens have presently been identified as the potential cause(s) of APSGN: A zymogen precursor of exotoxin B(SPEB [streptococcal pyrogenic toxin B]) or nephritis strainassociated protein (NSAP), and nephritis-associated plasminreceptor (NAPlr), a glycolytic enzyme, which has glyceraldehydes-3-phosphate dehydrogenase (GAPDH) activity[8, 9, 10, 11, 12]

NSAP is a 46- to 47-kd protein that is unique to the extracellular products of nephritogenic streptococci. NSAP wasdemonstrated in glomerular deposits of 14 of 21 patients with APSGN, but none in control biopsy samples from 5 patientswith acute kidney injury and 11 with nonstreptococcal glomerulonephritis. NSAP was also detected in serum from 96% ofAPSGN patients compared with 15-20% of patients with either acute kidney injury or impetigo.[13] NSAP has antigenic,biochemical, and structural similarities to streptokinase from group C streptococcal organisms, binds to plasmin, and is aplasminogen activator. However, streptokinase cannot be demonstrated in glomerular deposits for patients with APSGN,and serum levels of purified group A streptokinase were similar in patients with APSGN and those with acute kidney injury.Thus, although NSAP and streptokinase have similarities, they appear to be 2 distinct proteins. [13]

Yoshizawa et all isolated a 43-kd protein called preabsorbing antigen (PA-Ag) that is putatively identical to endostreptosin.[14,15] PA-Ag has the ability to preabsorb the antibody in convalescent sera from patients with APSGN and thus prevent itsdeposition in glomeruli. PA-Ag activates the alternative pathway.[15] This 43-kd protein was later identified by Yamakami et alas NAPlr.[16] These researchers noted that NAPlr was present in 100% of the early biopsy samples from in glomeruli ofpatients with APSGN.[17] The glomerular distribution of NAPlr deposition and plasmin activity determined by in situzymography are identical.

The fact that NAPlr did not co-localize with C3 in glomerular deposits suggests that (1) complement was activated by NAPlrin the circulation rather than in situ, and (2) NAPlr induced APSGN independently of complement activation by binding to theglomerular basement membrane (GBM) and mesangial matrix via its adhesive character, subsequently trapping andactivating plasmin and causing in situ glomerular damage by degrading the GBM or activating latent matrixmetalloproteases.[17, 18]

A proposed mechanism for acute poststreptococcal glomerulonephritis is that soluble, released NAPlr binds to glomeruli andprovide a mechanism to capture plasmin activated by streptokinase. The activated plasmin bound to NAPlr associates withthe GBM and mesangium. Both NAPlr and NSAP are capable of inducing chemotactic (monocyte chemoattractant protein 1)and interleukin (IL)6 moieties in mesangial cells, promoting enhanced expression of adhesion molecules. Peripheral bloodleukocytes also release other cytokines such as tumor necrosis factor-alpha, IL-8, and transforming growth factor-beta,which react with NSAP. These findings highlight the inflammatory potential of these nephritogenic antigens. [19, 20, 21, 22]

Bound plasmin can cause tissue destruction by direct action on the glomerular basement membrane or by indirect activationof procollagenases and other matrix metalloproteinases (MMPs). NAPlr can also activate the alternate complementpathway, leading to accumulation of polymorphonuclear cells and macrophages and local inflammation. In addition, the insituformed and circulating immune complexes can readily pass through the altered glomerular basement membrane andaccumulate on the subepithelial space as humps.

Complement activation from both serum profiles and immunofluorescence patterns for glomerular deposits indicates that C3activation in APSGN is predominantly via the alternative pathway.[23, 24, 25] The immune deposits consist of immunoglobulin G


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(IgG), C3, properdin, and C5.[25] These deposits rarely contain C1q or C4, both components of the classic complementpathway. A recent study also showed evidence for activation of the lectin-binding pathway from deposition of membrane-bound lipoprotein in some patients with APSGN.[26]

During the early phase of the diseases (first 2 wk), evidence of classical pathway activation is seen, as demonstrated bytransient depression of serum C1q, C2, and/or C4 concentrations. [27, 28, 29] and the presence of circulating C1-inhibitor-C1r-C1scomplexes or C4d fragments. It is proposed that the circulating immune complexes in the acute stage of the disease due toclassic complement pathway activation is distinct from that seen in the glomerular immune deposits. APSGN with typical

findings on histopathology may occur in patients with no evidence of complement activation, as manifested by depression ofserum C3 concentrations.[30, 31]

Hypocomplementemic patients differ from normocomplementemic patients by virtue of the presence of factor B in theglomerular deposits and the absence of factor H, which is a regulatory protein of the alternative pathway. [25] These findingssuggest that the glomerular immune deposits of C3bBb convertase may be due to ongoing complement activation in siturather than systemic activation. Crescentic APSGN may have an increased association with normocomplementemia. Thereason for this possible association of normocomplementemia with crescent formation in APSGN is not clear.

Serum IgG levels are elevated in about 44% of patients with APSGN.[32] Less than 50% of patients with elevated serum IgGlevels, however, have glomerular deposits of IgG. Elevated IgG levels were more likely to be found in patients withantistreptolysin O titers of greater than or equal to 833 Todd units (P< .001). However, elevated serum IgG concentrationsdo not correlate with severity of disease, age of the patient, or serum albumin or C3 levels. It would appear that failure toform antibody to a glomerular-bound protein produced by nephritogenicStreptococcus,is thought to be the origin of the IgGin glomerular deposits, is in some way significantly associated with elevated serum levels of IgG and antibody to streptolysinO.[32]

A mechanism for acute poststreptococcal glomerulonephritis proposed by Yoshizawa et al is shown in the image below.

A schematic representation of the proposed mechanism for acute poststreptococcalglomerulonephritis (APSGN). C = Activated complement; Pl = Plasmin; NAPlr = Nephritis-associated plasmin receptor; SK = Streptokinase; CIC =Circulating immune complex.

There is considerable evidence both for and against most putative nephritogenic antigens. Genomic sequencing ofnephritogenic strains of streptococci may lead to the discovery of new nephritogenic antigen candidates in conserved anddiffering regions of the streptococcal genome. This will lead to improved understanding of the pathogenetic mechanism(s)leading to the development of APSGN.

Nonimmune complex-mediated mechanisms

Other nonimmune complex mediated mechanisms have been proposed for the development of APSGN, such as delayed-type hypersensitivity, superantigens, and autoimmune phenomena.

A role for delayed-type hypersensitivity has been implicated in the pathogenesis of this disease. Early in the course ofAPSGN, resident endothelial and mesangial cells are predominantly proliferated, and this is accompanied by infiltration withpolymorphonuclear leukocytes and monocytes. Macrophages are effector cells that cause resident cellular proliferation. Theinfiltration of macrophages in the glomeruli is mediated by complement-induced chemotaxis and, most likely, by an antigen-specific event related to delayed-type hypersensitivity mediated by helper/inducer T cells.

Streptococcal M proteins and pyrogenic exotoxins can act as superantigens. These cause a marked expansion of T cells

expressing specific T-cell receptor B-chain variable gene segments. Massive T-cell activation occurs, with release of T-cellderived lymphokines such as IL-1 and IL-6.

Autologous IgG in APSGN becomes antigenic and elicits an anti-IgG rheumatoid factor response, leading to formation ofcryoglobulins. Cryoglobulins, rheumatoid factors, and other autoimmune phenomena occur in APSGN and are thought toplay a role in the pathogenesis of the disease together with streptococcal superantigens.

Prognosis
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The course and prognosis for acute poststreptococcal glomerulonephritis (APSGN) is well

known and almost always favorable in children, but this is not so with nonstreptococcal forms of

the condition. In addition, for unknown reasons, the prognosis for individuals with APSGN is notas good for adults (particularly elderly persons) as it appears to be for children. In elderly

patients with debilitating conditions (eg, malnutrition, alcoholism, diabetes, chronic illness), the

incidences of azotemia (60%), congestive heart failure (40%), and nephrotic-range proteinuria(20%) are high. Death may occur in 20-25% of these patients.[37, 38] Prolonged follow-upobservation appears to be indicated. The ultimate prognosis in individuals with APSGN largely

depends on the severity of the initial insult.

Epidemic poststreptococcal acute glomerulonephritis appears to end in virtually complete

resolution and healing in all patients, and the prognosis is favorable for 95% of children with

acute sporadic poststreptococcal glomerulonephritis. The prognosis for persons with acuteglomerulonephritis secondary to other causes is less certain.

Edema usually resolves within 5-10 days, and the blood pressure usually returns to normal after2-3 weeks, even though persistence of elevated pressures for as many as 6 weeks is compatible

with complete resolution.

Urinary abnormalities resolve at various times after onset. Proteinuria may disappear within the

first 2-3 months or may slowly decrease over 6 months. Intermittent or postural proteinuria has

been noted for 1-2 years after onset.

Gross hematuria usually disappears within 1-3 weeks but may be exacerbated by physicalactivity. C3 concentration returns to normal in more than 95% of patients by the end of 8-10

weeks. Microscopic hematuria usually disappears after 6 months, but its presence for as long as 1

year should not cause undue concern, and even more prolonged hematuria (1-3 y) has been

observed in some patients who ultimately have demonstrated complete resolution of their renaldisease. Strongly consider the possibility of chronic renal disease when both hematuria and

proteinuria persist longer than 12 months.

In a few hospitalized patients, the initial injury is so severe that either persistent renal failure or

progressive renal failure ensues. However, histologic regression of the disease in most patients is

predictable, and the ultimate prognosis is good.

Although clinical resolution occurs in most patients, several authors report time-related reduction

in precise measurements of renal function, as well as diminished renal functional reserve. Thesestudies further support the thesis that any significant loss of nephrons leads to hyperfiltration of

the remaining units. Studies that have followed up children with APSGN for 10-20 years have

shown that approximately 20% of the patients have abnormal urine analyses, with less than 1%

having azotemia.[39]

Clinical manifestations of the disease rarely recur after the first 3 months, and second episodes ofacute glomerulonephritis are rare.

Complications

The most common acute complication is hypertension with or without central nervous system

(CNS) manifestations.


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Anemia is common early in the disease and is primarily due to dilution, although in 2 instances,

autoimmune hemolytic anaemia was documented in the early stages of APSGN.[40, 41] Anemia

tends to resolve with diuresis. A few patients may have diminished erythropoiesis in the recoveryphase and have some persisting anemia.

An occasional patient develops pulmonary edema because of the marked increase in vascular

volume that is present in the early phase of the disease.

Congestive heart failure is rare but has been reported. Definite myocarditis has also beendocumented.

In most patients with moderate to severe APSGN, a measurable reduction in volume of

glomerular filtrate (GF) is present, and the capacity to excrete salt and water is usually

diminished, leading to expansion of the extracellular fluid (ECF) volume. The expanded ECF

volume is responsible for edema and, in part, for hypertension, anemia, circulatory congestion,and encephalopathy. Persistence or worsening of azotemia is always troubling and may suggest

acute kidney injury. The presence of acute kidney injury may suggest an alternate diagnosis (eg,

membranoproliferative glomerulonephritis [MPGN], Henoch-Schnlein purpura [HSP], systemiclupus erythematosus [SLE]) or a severe or worsening APSGN, such as observed in those with

crescentic glomerulonephritis or rapidly progressive glomerulonephritis.[42]

Previous

Diagnostic ConsiderationsIn the evaluation of a patient with acute glomerulonephritis, if evidence of a previous streptococcal infection is missing orinconclusive, then a search for another infectious cause appears appropriate.

See alsoAcute GlomerulonephritisandEmergent Management of Acute Glomerulonephritis.

Bacterial and viral infections

The syndrome of acute glomerulonephritis has been reported following many other bacterial illnesses (eg,Streptococcuspneumoniae, Staphylococcus aureusand S epidermidis, Rickettsia rickettsiae,Mycoplasmaspecies, Meningococcusspecies, Leptospiraspecies). In addition, certain viral illnesses have preceded theonset of fairly typical acute glomerulonephritis; among the most common are varicella-zoster virus (VZV), cytomegalovirus(CMV), and the Epstein-Barr virus (EBV).

IgA-associated glomerulonephritis

Immunoglobulin A (IgA)associated glomerulonephritis may be confused with acute poststreptococcal glomerulonephritis.[4,18, 42, 54] In the form of IgA nephropathy associated with a typical anaphylactoid purpura (ie, Henoch-Schnlein purpuranephritis), the characteristic rash and the associated symptoms of either abdominal pain or arthritis and/or arthralgia help inthe differentiation; however, in atypical cases, marked similarity may be present.

All of the clinical manifestations of APSGN have been reported in persons with Henoch-Schnlein purpura nephritis,although significant hypertension and edema are found less commonly in individuals with Henoch-Schnlein purpura than inthose with APSGN. In addition, evidence of a previous streptococcal illness is usually lacking in individuals with Henoch-

Schnlein purpura nephritis, and complement values (C3 and/or C4) are usually normal.

Urticarial or purpuric rashes, abdominal complaints, and arthritis and/or arthralgia are found almost exclusively in personswith Henoch-Schnlein purpura.

Berger disease or IgA nephropathy usually presents as an episode of gross hematuria occurring during the early stages of arespiratory illness; no latent period occurs, and hypertension or edema is uncommon.

Recurrent episodes of gross hematuria, associated with respiratory illnesses, followed by persistent microscopic hematuria,are highly suggestive of IgA nephropathy. In contrast, acute poststreptococcal glomerulonephritis usually does not recur,and second episodes are rare.
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MPGN

Mesangiocapillary or membranoproliferative glomerulonephritis (MPGN) may have a presentation that is virtually identical tothat of poststreptococcal acute glomerulonephritis. The initial manifestations are often more serious in persons with MPGNthan in those with IgA nephropathy; the renal function is reduced markedly (ie, large elevation of serum creatinine).

Evidence of preexisting streptococcal infection is absent, although cases of MPGN have been reported in which clearevidence of such an infection is present. In most cases, C3 levels are depressed persistently, longer than 6 weeks.

Urinary abnormalities persist past the time of expected resolution for acute poststreptococcal glomerulonephritis.

Crescentic glomerulonephritis

Crescentic glomerulonephritis is the term used to describe a histologic picture of severe proliferative glomerulonephritis. Inpersons with crescentic glomerulonephritis, in addition to inflammatory changes within the glomerular tuft, extensiveproliferation exists within the Bowman space, leading to the formation of synechiae between the glomerular tuft andBowman capsule.[42]

The clinical picture is generally referred to as rapidly progressive glomerulonephritis and may be secondary to numerouscauses, including an immune-complex mediated poststreptococcal nephritis. The initial clinical picture is generally severe,and resolution appears delayed.

Other types of glomerulonephritis

Other forms of glomerulonephritis (eg, systemic lupus erythematosus nephritis, familial nephritis, chronic glomerulonephritis)

may occasionally be confused with acute poststreptococcal glomerulonephritis when an acute exacerbation of the previouslypresent nephropathy is present. In addition to the lack of expected complete resolution, other features suggest a conditionother than acute poststreptococcal glomerulonephritis.

See Hemolytic Complement under Workup for the differential diagnosis of acute glomerulonephritis according to C3 levels.

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