Rapidly progressive glomerulonephritis (RPGN) is defined as any glomerular disease characterized by extensive crescents (usually >50%) as the principal histologic finding and by a rapid loss of renal function (usually a 50% decline in the glomerular filtration rate [GFR] within 3 mo) as the clinical correlate.
The image shown below depicts the histologic findings observed in patients with severe types of RPGN.
View Image
Glomerulonephritis, crescentic. Light microscopy (200x hematoxylin and eosin stain): The normal renal architecture is lost. The glomerulus (*) is soli....
Transient azotemia with oliguria is common in patients with acute glomerulonephritis.
Some patients have acute glomerulonephritis and present with rapidly progressive renal failure that develops within weeks to months and displays little tendency for spontaneous or complete recovery. Glomerular crescents can complicate any glomerulopathy, even noninflammatory glomerulopathy. In patients with noninflammatory glomerulopathies, the crescents tend to be fibrotic rather than cellular. Cellular crescents are a manifestation of a severe inflammatory process.
Classification
Idiopathic or primary crescentic glomerulonephritis is classified into the following types:
Type I with linear deposits of immunoglobulin G (IgG) (anti–glomerular basement membrane [GBM] disease)
Type II with granular deposits of immunoglobulin (immune-complex mediated)
Type III with few or no immune deposits (pauci-immune) - Antineutrophil cytoplasmic antibody (ANCA–associated is related to small vessel vasculitis (SVV) and may be renal-limited or part of a systemic disease, like granulomatosis with polyangiitis (GPA), previously known as Wegener granulomatosis or microscopic polyangiitis (MPA)
Type IV combinations of types I and III
Type V ANCA-negative pauci-immune renal vasculitis (5-10%)
RPGN can develop in any of the following clinical settings:
Complication of acute or subacute infectious process
Renal complication of multisystem disease: Secondary forms comprise more than 40% of cases.
In association with use of certain drugs: A review of published data on an association between hydrocarbon exposure and anti-GBM antibody-mediated disease suggests the possibility of a casual relationship.
Primary glomerular disease in which the kidney is the sole organ involved and in which extrarenal manifestations are caused by renal function disturbances
Acute RPGN is mediated by antibody or cellular immunity or by interaction of the two arms of the immune system. Deposition of antibody along the basement membrane and/or glomerular deposition of preformed soluble immune complexes can result in glomerulonephritis. Lymphocytes and macrophages, along with deposited antibody, are important in the production of proliferation and proteinuria. The involved lymphocytes are identified as T cells; most are helper T cells with some suppressor T cells. Antibody- and cell-mediated immunity are together responsible for many lesions observed in patients with acute RPGN, and cell-mediated immunity without antibody may produce crescentic glomerulonephritis.
Crescents are defined as the presence of 2 or more layers of cells in the Bowman space. The presence of crescents in glomeruli is a marker of severe injury, and this may be seen with any form of severe glomerular injury.
The initiating event is the development of a physical disruption in the GBM. The lesions are mediated by processes involving macrophages and cell-mediated immunity. Following disruption of the glomerular capillary, circulating cells, inflammatory mediators, and plasma proteins pass through the capillary wall into the Bowman space. Cells and mediators from the interstitium enter the Bowman space with disruption of the Bowman capsule, which leads to development of crescents.
The major participants in crescent formation are coagulation proteins, macrophages, T cells, fibroblasts, and parietal epithelial cells. Activated macrophages contribute to the crescents by proliferating and releasing procoagulant tissue factor, interleukin-1 (IL-1) and tumor necrosis factor (TNF). T cells are not prominent components, but they play an important role in glomerular injury by antigen recognition and macrophage recruitment.
The crescents may be circumferential or noncircumferential, and the presence of circumferential crescents in over 80% of glomeruli portends a poor prognosis and often manifests as advanced kidney disease.
The reversibility of crescents correlates with relative predominance of cellular components. Whether crescents progress or resolve may depend upon the integrity of the Bowman capsule and resulting cellular composition of the crescent. Progression to fibrous crescents is more common when capsular rupture occurs and fibroblasts along with macrophages are prominent in the Bowman space. The presence of fibrous crescents usually correlates with glomerular sclerosis or irreversibility.
Idiopathic crescentic glomerulonephritis accounts for fewer than 10% of all patients presenting with primary glomerulopathy. RPGN type III is more common than RPGN types I or II. More than 50% of patients with crescentic glomerulonephritis present with acute nephritic syndrome and rapidly deteriorating renal function; however, other modes do occur (eg, asymptomatic, 15%; nephrotic, 10%; chronic renal failure, 15%).
International
Peak incidence of anti-GBM disease occurs in spring and early summer. No seasonal predilection is observed in patients with non–anti-GBM disease.
Mortality/Morbidity
Renal failure at presentation carries an increased risk for end-stage renal disease and death despite immunosuppressive therapy.[1] Death or dialysis occurs in 73% of patients who are treated with conventional therapy and in 88% of patients if they are oligoanuric at time of presentation.
Race
No racial predilection exists.
Sex
For RPGN types I and III, a predilection for males exists.
Age
RPGN has a broad age distribution, as follows:
RPGN type I generally occurs in young adults.
RPGN types II and III generally occur in older adults; the peak incidence occurs in the fourth to sixth decades of life.
Clinical and laboratory presentations of all types of acute RPGN are quite similar.[2]
Some patients present with signs and symptoms of renal disease, for example, anemia, hematuria, fluid retention, oliguria, or even uremia.
Symptoms of weakness, nausea, and vomiting (indicative of azotemia) usually dominate the clinical picture.
Other patients present with signs and symptoms of their primary etiology (eg, Goodpasture syndrome, Wegener granulomatosis, systemic lupus erythematosus [SLE]).
Still others give a history of a flulike or viral prodrome. Vague aches and pains or frank arthritis, sinusitis, otitis, episcleritis, skin rash, neuritis, or encephalopathy are uncommon and are more common with a multisystem disease (suggesting secondary form).
Oliguria, abdominal or flank pain, and hemoptysis may occur (eg, Goodpasture syndrome).
Erythrocyte sedimentation rate (ESR) is usually elevated.
Blood urea nitrogen (BUN) and serum creatinine levels are usually elevated.
Electrolytes, especially the serum potassium level, are consistent with the degree of renal failure.
Urinalysis shows modest proteinuria (1-4 g/d), microscopic hematuria, RBCs, and RBC and WBC casts.
Proteinuria could be quantified by timed (24-h collection) or spot urine protein/creatinine ratio.
Rarely, urine findings may be minimal.
An absence of active urine sediment does not exclude a diagnosis of RPGN.
Complement levels (C3 and C4) are within reference ranges in patients with RPGN types I and III and may be decreased in patients with RPGN type II.
Circulating anti-GBM antibodies are detected in plasma of patients with RPGN type I, but this finding is neither 100% sensitive nor 100% specific for type I.
ANCAs: Typically, myeloperoxidase (MPO)–ANCA (previously known as perinuclear ANCA [p-ANCA]) is observed in 80-90% of patients with RPGN type III pauci-immune, but neither MPO-ANCA nor PR3-ANCA is 100% specific for type III.
Antinuclear antibody findings are usually negative (unless lupus related).
Serum cryoglobulin levels may be elevated in cryoglobulinemias and may be falsely negative.
Type I (anti-GBM disease with or without lung hemorrhage) - Linear deposits of IgG (5-20%)
Type II (immune complex-mediated disease) - Granular deposits of immunoglobulins by immunofluorescence and electron-dense deposits by electron microscopy (15-30%)
Type III (pauci-immune glomerulonephritis) - Little or no deposits observed by immunofluorescence or electron microscopy (55%)
The normal renal architecture is lost, and the glomerulus is solid, hypercellular, and surrounded by severe interstitial mononuclear cell infiltrate (see the first image below) is observed in patients with severe types. The glomerular tuft is distorted by proliferation of epithelial cells crescents that occupy most of the Bowman space as shown in the second, third, and fourth images below.
View Image
Glomerulonephritis, crescentic. Light microscopy (200x hematoxylin and eosin stain): The normal renal architecture is lost. The glomerulus (*) is soli....
View Image
Glomerulonephritis, crescentic. Light microscopy (25x hematoxylin and eosin stain): Compression of the glomerular tuft with a circumferential cellular....
View Image
Glomerulonephritis, crescentic. Light microscopy (200x periodic acid-Schiff stain): Bowman capsule (arrow) surrounds each glomerulus. The glomerular t....
View Image
Glomerulonephritis, crescentic. Light microscopy (400x trichrome stain): The remnant of the glomerular tuft (*) is surrounded by the cellular crescent....
Anti-GBM disease is characterized by linear IgG deposits as depicted below. Endocapillary proliferation, if prominent, suggests the presence of infection. Segmental or diffuse endocapillary necrosis suggests underlying vasculitis.
View Image
Glomerulonephritis, crescentic. Immunofluorescence (25x): Anti–glomerular basement membrane characterized by the presence of linear immunoglobulin G d....
A nephrologist should be involved early in the disease course. Rheumatologist consultation may be considered and may require hematologist involvement if plasma exchange is required.
Renal diet: Provide a low-salt, low-protein (0.8 g/kg/d) diet, if renal dysfunction is present. Restrict potassium if the patient has hyperkalemia. Avoid malnutrition.
Principles of therapy include supportive and specific therapies. Supportive therapy involves control of infection (especially Pneumocystis jiroveci (PCP) infection with trimethoprim-sulfamethoxazole or Atovaquone), control of volume status (providing dialysis if required), and smoking cessation.
Goals of specific therapy
Induction of remission
The initial therapy is to induce remission and typically consists of glucocorticoids and cyclophosphamide, and this induces remission in 85-90% of patients in 2-6 months, with about 75% achieving complete remission. Recently, rituximab in RAVE[4, 5] and RITUXIVAS[6] trials was shown to be not inferior to cyclophosphamide and may be used in patients who cannot take or refuse to take cyclophosphamide. Methotrexate is an option in patients with mild disease, but the relapse rate was significantly higher with methotrexate compared with cyclophosphamide (70% vs 47%, respectively).[7] Etanercept in the WGET (Wegener's Granulomatosis Etanercept Trial) achieved remission in just over 90% of patients but had about a 50% relapse rate at 27 months.[8]
At present, the mainstay of therapy remains cyclophosphamide and steroids for induction of remission, with an option to consider rituximab in select patients.
Plasma exchange, although still controversial in patients with granulomatosis with polyangiitis, microscopic polyangiitis, or renal limited necrotizing glomerulonephritis, is useful in patients with advanced renal failure (serum creatinine >500 µmol/L or requiring dialysis),[1] in patients with severe pulmonary hemorrhage, and when associated with antiglomerular basement membrane antibody disease. Although short-term results with plasma exchange are encouraging, the long-term benefits remain unclear,[9] and the PEXIVAS (Plasma Exchange in VASculitis) trial is currently ongoing to better define the role of plasma exchange.[10]
Maintenance of remission to prevent relapse
As relapses are common, especially in granulomatosis with polyangiitis and microscopic polyangiitis, it is important to continue with immunosuppressive therapy, using less toxic agents, to maintain remission and prevent relapse. Most often, either azathioprine or methotrexate is used for maintenance therapy to reduce risk of relapse. Other agents that have been used for maintenance therapy include etanercept in WGET[8] and mycophenolate.[11]
In a recent pilot study, rituximab maintenance therapy was well tolerated but did not completely prevent relapses and persistent "grumbling" disease[12] ; however, in the interim analysis of an ongoing trial, rituximab at 500 mg every 6-months by the French Vasculitis Study Group in the MAINRISTAN trial show a remarkable reduction in relapse rate with rituximab versus azathioprine, at 28 months (5% vs 25%)[43] .
Clinical Context:
Potent anti-inflammatory steroid with greater anti-inflammatory potency and fewer tendencies to induce retention of salt and water than prednisolone.
Clinical Context:
Decreases inflammation through multiple mechanisms. Reduced to its pharmacologically active form prednisolone. When used on a long-term basis, alternate-day therapy may elicit fewer adverse effects than daily therapy.
Pulses of intravenous methylprednisolone (5-20 mg/kg) followed by high-dose oral prednisone (2 mg/kg) daily or on alternate days for 2-3 months have shown improved 1-year renal survival rates of 40-70%.
Clinical Context:
Activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in an all-or-none–type reaction.
Clinical Context:
Mechanism by which azathioprine affects autoimmune diseases is unknown. Slow acting, and its effects may persist after discontinuation.
Clinical Context:
Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy- chain variable region sequences and human constant region sequences.
Addition of cytotoxic agents to corticosteroids has yielded varying success in treating patients with crescentic glomerulonephritis. Although pulse cyclophosphamide is often preferred in lupus nephritis, oral cyclophosphamide appears to have an advantage in Wegener granulomatosis.
Oral versus intravenous: Recently completed, prospectively randomized Cyclophosphamide daily oral versus PulSed (CYCLOPS) trial has shown very little difference in time to remission and time to relapse between daily oral or intermittent intravenous cyclophosphamide for induction therapy.
Cyclophosphamide 3 mg/kg/d for 12 weeks is a common recommendation, but the duration of therapy may be longer (4-6 mo) in patients with pauci-immune glomerulonephritis. This therapy should be followed by the administration of azathioprine (1.5-2 mg/kg/d) or methotrexate (5-20 mg qwk as a single dose) until the patient is in remission for at least 6-12 months. The duration of azathioprine therapy to prevent further relapses is unknown, but it should be at least for 2 years.
Continuing cyclophosphamide for longer than 6 months is not necessary, as recently shown by Cyclophosphamide versus Azathioprine during Remission (CYCAZAREM) trial, where the time to relapse was identical whether the patient was given cyclophosphamide for less than 6 months or more than 6 months.
Mycophenolate mofetil at 0.75-1 g twice daily versus azathioprine was compared for maintenance of remission in an open-label, randomized, controlled trial.[11] Both agents were withdrawn after 42 months and at a median follow-up of 39 months, but relapses were significantly higher in mycophenolate-treated group than in the azathioprine group (55% vs 38%).
Clinical Context:
Long-term treatment with TMP (160 mg) and SMX (800 mg) bid has been reported in a prospective, controlled, double-blind trial to sustain remission of Wegener granulomatosis. The mechanism of this effect is not clear. Eradication of Staphylococcus aureus in the anterior nares of patients with Wegener granulomatosis has recently been reported to sustain remission of Wegener granulomatosis. TMP-SMX is also helpful as Pneumocystis carinii pneumonia (PCP) prophylaxis in patients who are on corticosteroids and other immunosuppressive agents.
After induction of remission with oral cyclophosphamide and steroids, conversion to oral azathioprine (2 mg/kg/d) at 3 months appears to be safe and effective compared to continuation of cyclophosphamide for 1 year (if clinical signs of activity are minimal and preferably ANCA is negative) (CYCAZAREM). The duration of maintenance therapy with azathioprine to prevent further relapses is unknown but should be at least for 2 years. Studies of longer periods of azathioprine maintenance (2 y vs 4 y) are in progress.
Monitor BUN, electrolyte, and serum creatinine levels in all patients.
Drug-responsive relapses may occur as late as 2-4 years after remission.
RPGN may recur after renal transplantation. At present, after initiating dialysis, a waiting period of 3-6 months is recommended before considering renal transplantation.
No convincing evidence suggests that a bilateral nephrectomy performed before a renal transplantation reduces the risk of recurrent disease in patients with renal allografts.
For patients who have achieved remission, evaluation at 2-month intervals is usually sufficient. The following testing is recommended:
Urinalysis with special emphasis on the presence of cellular casts: BUN, electrolyte, and serum creatinine levels should be evaluated in all patients.
C-reactive protein or ESR (whichever correlates better with disease activity in a given patient)
ANCA (in ANCA-positive patients at 6- to 9-mo intervals): An increasing ANCA titer is often evidence of an impending relapse. A 4-fold or higher rise in ANCA titer may herald a relapse and require preemptive intervention.
Intensive plasma exchange: Plasmapheresis (2-4 L of plasma qd or 3 times/wk), combined with glucocorticoids and cytotoxic agents, is beneficial in anti–GBM-mediated disease, provided therapy is initiated before renal failure has progressed to require dialysis support. Plasma exchange is also valuable as an adjunctive measure in patients with positive ANCA results who present with life-threatening pulmonary hemorrhage (ie, MEthylprednisolone versus Plasma EXchange [MEPEX]) or advanced renal failure.[13, 1]
Plasma exchange increased the rate of renal recovery in ANCA-associated systemic vasculitis that presented with renal failure when compared with intravenous methylprednisolone; however, patient survival and adverse event rates were similar in both groups.[1]
In the absence of any response within 3-5 weeks, acceptance of a diagnosis of end-stage renal disease is preferable to death secondary to iatrogenic causes.
High-dose intravenous immunoglobulin has been reported to be successful in suppressing the activity of pauci-immune ANCA-positive vasculitis. The mechanism is not clear, but pooled normal immunoglobulin contains antibodies that neutralize ANCA and suppress complement activation through a nonspecific effect of the immunoglobulin heavy chains.
Intravenous immunoglobulin may have a role in the temporary management of severe pauci-immune vasculitis when severe infection is present in patients in whom it is desirable to withhold cytotoxic agents and high-dose corticosteroids until the infection is controlled.
In difficult to treat cases of ANCA-associated vasculitis, humanized monoclonal anti-CD52 antibodies (alemtuzumab, CAMPATH-1H) that selectively deplete lymphocytes may be considered. In a recent study by Walsh et al, CAMPATH-1H induced remission in such a group of patients, but relapse and adverse events were common.[14] Further study of CAMPATH-1H as an induction agent is warranted.
Administer oral cyclophosphamide for 4-6 months, followed by azathioprine or methotrexate until the patient is in remission for 6 months to 1 year.
Administer prednisone as a low-dose alternative for 6-9 months.
Administer trimethoprim-sulfamethoxazole 160/800 mg bid (for Wegener granulomatosis) if renal function normal. Decrease the dose as guided by renal function. A lower dosage as PCP prophylaxis may be considered.
Because patients with pauci-immune vasculitis typically have a prodrome lasting for weeks to months—during which time they experience 1 or more vague symptoms (eg, intermittent fever, weight loss, anorexia, arthralgias, shortness of breath, hemoptysis, middle ear effusions, conjunctivitis, episcleritis, nasal septal perforation, saddle nose deformity)—a high index of clinical awareness, early diagnosis, and treatment may prevent significant morbidity and mortality associated with this condition.
In general, the prognosis is poor and aggressive therapy is warranted. The chance of renal recovery exceeds the chance of dying in most cases. Intravenous methylprednisolone as an adjunctive therapy plus less than 18% normal glomeruli and severe tubular atrophy increased the chance of therapy-related death over the chance of dialysis independence. Plasma exchange treatment plus severe tubular atrophy and less than 2% normal glomeruli increased the chance of therapy-related death over that of dialysis independence.[15]
Fifty percent of patients require maintenance dialysis within 6 months of disease onset.
Spontaneous remission is uncommon, except among patients with infection as the basis for formation of antigen-antibody complexes, in whom removal of the antigen can take place.
Poor prognostic factors are as follows:
Large crescents in more than 80% of glomeruli (especially circumferential fibrocellular or fibrous/acellular crescents)
Initial serum creatinine level of more than 500 µmol/L or GFR of less than 5 mL/min at presentation
Patients receiving immunosuppressive therapy should be educated about early signs of infection and advised to see their physician or health care worker at the early signs of infection in order to monitor WBC count.
Patients on a high dose of prednisone should be monitored for the development of diabetes and peptic ulcer disease and receive therapy to prevent steroid-induced osteoporosis.
Malvinder S Parmar, MBBS, MS, FRCPC, FACP, FASN, Professor of Medicine, Northern Ontario School of Medicine; Assistant Professor, Department of Medicine, University of Ottawa Faculty of Medicine; Consulting Physician, Timmins and District Hospital, Ontario, Canada
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Ajay K Singh, MB, MRCP, MBA, Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital
Disclosure: Nothing to disclose.
Chief Editor
Vecihi Batuman, MD, FASN, Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Disclosure: Nothing to disclose.
Additional Contributors
James H Sondheimer, MD, FACP, FASN, Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)
European Vasculitis Study Group. Clinical trial protocol: REMAIN. Randomised trial or prolonged remission-maintenance therapy in systemic vasculitis. June 2003.
Jayne DRW, Gaskin G, (EUVAS). Randomized trial of cyclophosphamide versus azathioprine during remission in ANCA-associated vasculitis (CYCAZAREM). J Am Soc Nephrol. 1999. 10:105A.
Glomerulonephritis, crescentic. Light microscopy (200x hematoxylin and eosin stain): The normal renal architecture is lost. The glomerulus (*) is solid and hypercellular and surrounded by severe interstitial inflammatory infiltrate. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Light microscopy (200x hematoxylin and eosin stain): The normal renal architecture is lost. The glomerulus (*) is solid and hypercellular and surrounded by severe interstitial inflammatory infiltrate. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Light microscopy (25x hematoxylin and eosin stain): Compression of the glomerular tuft with a circumferential cellular crescent that occupies most of the Bowman space. Image courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Glomerulonephritis, crescentic. Light microscopy (200x periodic acid-Schiff stain): Bowman capsule (arrow) surrounds each glomerulus. The glomerular tuft (*) is distorted by a proliferation of epithelial cells (crescent), which replaces the urinary space. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Light microscopy (400x trichrome stain): The remnant of the glomerular tuft (*) is surrounded by the cellular crescent with abundant fibrin–red on trichrome stain. Interstitial edema separates the tubules, and scarce inflammatory cells are present. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Immunofluorescence (25x): Anti–glomerular basement membrane characterized by the presence of linear immunoglobulin G deposit along the glomerular basement membrane. Image courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Glomerulonephritis, crescentic. Light microscopy (25x hematoxylin and eosin stain): Compression of the glomerular tuft with a circumferential cellular crescent that occupies most of the Bowman space. Image courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Glomerulonephritis, crescentic. Light microscopy (200x hematoxylin and eosin stain): The normal renal architecture is lost. The glomerulus (*) is solid and hypercellular and surrounded by severe interstitial inflammatory infiltrate. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Light microscopy (200x periodic acid-Schiff stain): Bowman capsule (arrow) surrounds each glomerulus. The glomerular tuft (*) is distorted by a proliferation of epithelial cells (crescent), which replaces the urinary space. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Light microscopy (400x trichrome stain): The remnant of the glomerular tuft (*) is surrounded by the cellular crescent with abundant fibrin–red on trichrome stain. Interstitial edema separates the tubules, and scarce inflammatory cells are present. Image courtesy of Suzanne Meleg-Smith, MD, Department of Pathology, Tulane University School of Medicine, New Orleans.
Glomerulonephritis, crescentic. Immunofluorescence (25x): Anti–glomerular basement membrane characterized by the presence of linear immunoglobulin G deposit along the glomerular basement membrane. Image courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
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