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Nephritic syndrome


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Yazan Daaboul, Serge Korjian, Dildar Hussain, MBBS [3], Mehrian Jafarizade, M.D [4]

Synonyms and keywords: Acute nephritis syndrome; Acute glomerulunephritis

Overview

Overview

Nephritic syndrome is defined as the inflammation of the renal glomeruli. It is characterized by the presence of glomerular microscopic or gross hematuria with active sedimentation of dysmorphic red blood cells in the urine. Due to renal involvement, the syndrome includes a reduced glomerular filtration rate (GFR), oliguria, azotemia, high blood pressure, and edema. Unlike nephrotic syndrome, proteinuria in nephritic syndrome is not very significant, although frequently present nonetheless. Nephrotic and nephritic syndromes can both still occur concomitantly.

Historical Perspective

Historical Perspective

The symptoms of glomerulonephritis were first described by Richard Bright in 1827 when he discovered that several patients died with generalized edema were found to have renal disease.[1] It was not until 1914 that Volhard and Fahr classified renal diseases in Die Brightsche Nierenkrankheit to 3 main categories: nephroses, nephritis, and arteriosclerotic disease.[2] Acute post-streptococcal glomerulonephritis is thus considered the earliest nephritic syndrome to be described. In 1908, C.F. Wahrer described an epidemic of hemorrhagic nephritis preceded by scarlet fever in 35 patients. Epidemics of nephritis continued in 1915 among British troops during World War I.[3] Clinical and pathological findings from both epidemics were similar. Hemolytic streptococci were isolated from cultures of the oropharynx in many patients.[3]

Classification

Classification

The acute nephritic syndrome can be classified according to the etiology of the underlying disease (renal vs. non-renal etiology). Similarly, acute nephritis may be classified as idiopathic vs. secondary to other conditions. Finally, diseases may be classified according to the proliferative vs. non-proliferative changes seen on pathology.

Renal vs. Non Renal

Renal Diseases[4][5]

Systemic Diseases[4][5]

Primary vs. Secondary

Classification of Glomerular Diseases[6]
Type of Disorder Proliferative Changes No Proliferative Changes
Primary Renal Disorder
Secondary Disorder
Adapted from Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med. 1998;339(13):888-99

Renal vs. Non Renal

Renal Diseases[4][5]

Systemic Diseases[4][5]

Primary vs. Secondary

Classification of Glomerular Diseases[6]
Type of Disorder Proliferative Changes No Proliferative Changes
Primary Renal Disorder
Secondary Disorder
Adapted from Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med. 1998;339(13):888-99
Pathophysiology

Pathophysiology

Role of Antibodies

Immunological mechanisms mediated by antibodies are required in the pathogenesis of glomerulonephritis. Antibodies are thought to bind either intrinsic glomerular components or specific compounds with unique physiochemical features that are present surrounding the glomerulus. Type IV collagen is an intrinsic glomerular component involved in Goodpasture’s syndrome; whereas histone-DNA complexes in systemic lupus erythematosus are not intrinsic compounds to the glomerulus.[6][7][8] However, presence of antibodies alone is not sufficient for glomerular inflammation.[9] Complexes formed by the antibody-antigen complexes must in fact be able to evade clearance by the reticuloendothelial system to effectively deposit at the glomerulus.[6][10]

Role of Neutrophils

When complement pathway is activated, complement-derived neutrophil chemotactic factors facilitate the infiltration of neutrophils.[11] Neutrophils undergo respiratory burst to release toxic oxygen metabolites that are nephritogenic.[12][13] Hydrogen peroxide interacts with myeloperoxidase enzyme derived form the neutrophils leading to a direct injury to the glomerular basement membrane.[13] Damage to the capillary wall and proteinuria have also been shown to be induced by elastase and cathepsin G, both of which are serine proteases derived from neutrophils.[14][15]

Role of Platelets

Platelets play a role in the neutrophil-mediated injury as well. It is believed that platelets exacerbate the injury caused by neutrophils in a mechanism that is yet to be understood.[15]

Role of Macrophages

Macrophages are involved in glomerular injury through the release of oxidants and proteases. These compounds help in the synthesis of tissue factor that leads to deposition of fibrin material on the glomerulus. Subsequently, cytokines and growth factors, such as IL-1 and TGF-B, are released and cause the abnormal production of extracellular matrix.[16][17]

Role of T Cells

T cells are important for inducing glomerular hypercellularity.[18] T cells are present in both proliferative and non-proliferative glomerular diseases.[19] Pro-inflammatory pathways are activated following initial injury to induce further synthesis of cytokines, complement activation, influx of circulating leukocytes, release of proteolytic enzymes, and activation of coagulation pathway.[20][21] These changes make the glomerular cell itself, in addition to the infiltrating glomerular cells, an active component of destruction and subsequent restoration.[21][22][23]

Matrix Remodeling

Matrix remodeling is in part involved in the activation and proliferation of glomerular cells. The resident and the infiltrating cells will both receive unique signals following matrix remodeling that are involved in the activation of pro-inflammatory pathways in these cells.[6] Autocrine activation of platelet-derived growth factors (PDGF) B-chain and B-receptors is believed to cause the proliferation of mesangial cells during glomerular injury.[24] Growth factors ultimately cause the increase in proteinase synthesis and matrix expansion.[25][26]

Adaptive Mechanisms

Due to ongoing injury, adaptive changes take place in order to help in the resolution of glomerulonephritis. Hyperfiltration, intraglomerular hypertension, and irregular intravascular stress and shear are all processes that may on one hand worsen the renal injury, but are also crucial for the remainder of the functioning glomerulus.[21][22][23][27]

Resolution of Disease

Apoptosis, defined as programmed cell death, plays a significant role in defining the resolution of disease and in the renal scarring following glomerulonephritis.[28]

Causes

Causes

  • Causes of nephritic syndrome may vary by age. Causes of nephritic syndrome include post-infectious glomerulonephritis, IgA nephropathy (Berger disease), thin basement membrane disease, and rapidly progressive glomerulonephritis.
  • Age plays an important role in identifying the cause of nephritic syndrome. Nonetheless, age should not be the only factor in defining the etiology of nephritic syndrome.[29]
Common Causes of Nephritic Syndrome by Age
Age (Years) Cause of Nephritic Syndrome
< 15
15-40
> 40
Adapted from Rose BD. Pathophysiology of renal diseases, ed. 2. New York, McGraw-Hill, 1987,p. 167
  • There are a number of different causes of nephritic syndrome such as:[29]
Primary renal diseases Secondary renal diseases Multi-system disease Allergy
Acute allergic tubulointerstitial nephritis
Differential Diagnosis

Differential Diagnosis

The clinical differentiation between nephritic and nephrotic syndromes is crucial to establish the proper differential diagnosis and determine the appropriate management. In addition, the clinical history and prognosis of nephritic syndrome is different from that of nephrotic syndrome.

  • The following table summarizes the key differences between nephrotic syndrome and nephritic syndrome:
Distinguishing Nephritic Syndrome from Nephrotic Syndrome
Clinical Feature Nephritic Syndrome Nephrotic Syndrome
Hematuria Yes Yes / No
Proteinuria < 3.5 g/24 hrs > 3.5 g/24hrs
Red Cell Casts Yes No
Hypoalbuminemia Yes / No Yes
Hypertension Yes Yes / No
Progression Insidious Abrupt

Nephritic syndrome should be differentiate from other causes of glomerular disease. The various types of glomerular diseases may be differentiated from each other based on associations, presence of pitting edema, hemeturia, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features. The following table differentiates between various types of glumerular diseases:

Glomerular diseases Disease History and Symtoms Laboratory Findings Pathology
History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Acute Nephritic Syndromes Poststreptococcal Glomerulonephritis[30][31][32] +/- + +/- +/- +/- +/- +/- +/-
  • Immune complex GN
  • Granular deposit
Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[33][34] +/- + +/- +/- +/- +/- +/- +/-
  • Crescentic GN is the most common pathological features
  • Mesangial deposits,
  • Subendothelial deposits
  • Subepithelial “humps,” in minority of cases
  • Pauci-immune GN
Lupus Nephritis[35]
  • History of SLE features
 +/- + +/- +/- +/- +/- +/- +/-
  • Differs based on the disease classification
  • Differs based on the disease classification
  • Differs based on the disease classification, mostly immune complex GN
  • Granular deposit
Antiglomerular Basement Membrane Disease (Goodpasture’s syndrome)[36][37]
  • Young adults
 + + + + + + – – Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits 
  • Immune complex GN
  • Linear deposit
IgA Nephropathy[38][39] + +/- + +/- + – + –
  • Immune complex deposition
  • Crescent formation
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
ANCA Small-Vessel Vasculitis[40][41] Granulomatosis with Polyangiitis (Wegener’s)[42][43][44]
  • Middle age male
 + + + +/- + – + –
  •  Pauci-immune GN
Microscopic Polyangiitis[45] +/- + + + + + + –
  •  Pauci-immune GN
Churg-Strauss Syndrome[46] +/- + + + + + + –
  •  Pauci-immune GN
Membranoproliferative Glomerulonephritis[47][48] + + + +/- + + – – –
  • Immune complex GN
  • Granular deposite
Henoch-Schönlein purpura [49] + + + +/- + + – – –
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Cryoglobulinemia[50] Patients having cryoglobulinemia may have positive history of: Pulmonary symptoms:
  • Cough

Cutaneous symptoms:

Gastrointestinal symptoms:

  • Abdominal pain

General symptoms:

+/- + +/- + +/- +/- +/- +/- +/-
  • Prominent IgM and C3
Nephrotic Syndrome Minimal Change Disease[51][52] – + – + +/- + – +
  • Normal
 –
Focal Segmental Glomerulosclerosis[53][54][55] – + – + +/- + – + –
Membranous Glomerulonephritis[56][57] – + – + +/- + – + Immune complex deposition Immune complex GN, granular deposite
Diabetic Nephropathy[58][59][60][61][62][63][64][65][66][67] For more information on diabetes click here. – + – + +/- + – +
  • Diffuse mesangial matrix expansion (nodular glomerulosclerosis)
  • Increased mesangial hypercellularity
  • Prominent glomerular basement membranes
  • Thick basement membrane without any deposit
  • Nodular glomerulosclerosis
 –
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
 Glomerular Deposition Diseases  Light Chain Deposition Disease[68]
  • Occurs in the setting of high tumor burden
 – – + – + +/- + – + –
  • Light-chain deposits
  • Granular deposits on electron microscopy
  • Detection of light chain deposits using anti–light chain antibody
Renal Amyloidosis[69][70][71][72] – + – + +/- + – + –
  • Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
  • Nodular deposit
  • AA amyloidosis type: negative for immunoglobulins and complement
  • AL amyloidosis type: Positive for lambda or kappa light chains
Fibrillary-Immunotactoid Glomerulopathy[73] – +/- + +/- +/- +/- + +/- +/- –
  • Diffuse sclerosing glomerulonephritis
  • Diffuse proliferative glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Mesangioproliferative/sclerosing disease
  • Membranous glomerulonephritis
  • Large fibrillar deposits in the mesangium randomly
  • Glomerular capillary walls different from amloidosis
  • No staining with Congo red or thioflavine-T or with antibodies to a specific type
  • Positive for immunoglobulin G (IgG), C3
  • Kappa and lambda (ie, polyclonal) light chains
Fabry’s Disease[74][75][76] – + – + +/- + – + –
  • Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
  • Glycolipid accumulation
  • Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
  • Inclusions, composed of concentric layers (onion skin appearance)
 –
Basement Membrane Syndrome Alport’s Syndrome[77][78][79][80][81][82]
  • Positive family history
 Auditary:

Occular problems:

  • Refractory Error
 – + – + +/- + – + –
  • Early stage: unremarkable
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Thin Basement Membrane Disease[83][84]
  • Positive family history
 – – + -/+ – -/+ – -/+ – – – Diffuse thinning of the glomerular basement membranes (GBM) –
Nail-Patella Syndrome[85][86]
  • Positive family history
  • Poorly developed fingernails, toe nails, and patellae (kneecaps).
  • Elbow deformities
  • Abnormally shaped pelvis bone (hip bone)
  • Knee may be small, deformed or absent
 + + – – – – – – –
  • Mostly unremarkable changes
  • Secondary FSGS
  • Late stages:
    • Global glomerulosclerosis,
    • Tubulointerstitial fibrosis
  • Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
  • Similar collagen fibrils can be seen in mesangial matrix.
  • Podocytes: Segmental effacement of foot processes.
  • Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
 Glomerular-Vascular Syndromes  Hypertensive Nephrosclerosis[87] Chronic hypertension +/- +/- + +/- +/- +/- – +/- –
  • Interstitial fibrosis and atrophy
  • Medial thickening and intimal fibrosis of medium-sized and larger vessels
  • Arteriolar thickening, and hyalinosis
  • Chronic stages:
Cholesterol Emboli[88]
  • Depends on the organ involved
 +/- +/- + +/- +/- +/- – +/- –
  • Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals
  • Acute lesions:
    • Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions
  • Chronic lesions:
    • Cholesterol clefts are surrounded by intimal fibrosis
    • Vessel recanalization of chronic lesions can occur.
  • Global and segmental sclerosis of glomeruli may be present.
  • Extensive foot process effacement can be seen
  • Not specific changes
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Sickle Cell Disease[89]
  • Positive family history
 +/- +/- +/- – – – – – –
  • Glomerular hypertrophy
  • Hemosiderin deposits
  • Focal areas of hemorrhage or necrosis
  • Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts
  • Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
Thrombotic Microangiopathies[90] Click for more information on Thrombotic Microangiopathies. + +/- + +/- +/- +/- – – –
  • Acute stage:
    • Inravasculr fibrin thrombi
  • Chronic stage:
    • Endocapillary hypercellularity.
    • Intimal proliferation of arterioles
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.
Antiphospholipid Antibody Syndrome [91][92][93]
  • Fatigue
  • Fever
  • Weight loss
 + +/- + +/- +/- +/- – – –
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.


Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

Epidemiology and Demographics

Epidemiology and Demographics

Approximately 25% of patients with acute glomerulonephritis present with nephritic syndrome.[94] Acute glomerulonephritis accounts for 10-15% of glomerular diseases in the USA.[95] The reported incidence of glomerulonephritis in adults varies between 0.2 to 2.5/100,000 annually with a male to female ratio reaching 2 to 1.[96] The most common cause of glomerulonephritis worldwide is IgA nephropathy (Berger disease). Approximately 25-30% of patients eventually develop end-stage renal disease (ESRD).[96] The yearly variation of incidence of glomerulonephritis is not validated. While some studies report a decrease in the incidence due to improved healthcare and socioeconomic status, others report an increase in the reported incidence due to increased number of biopsies.[96] Additionally, the true incidence is difficult to predict because the disease might present subclinically.

Natural History, Complications, and Prognosis

Natural History, Complications, and Prognosis

Prognosis, complications, and outcome depend on the underlying etiology. Generally, nephritic syndrome is characterized by an abrupt onset. The course of the disease varies greatly.

Diagnosis

Diagnosis

History and Symptoms

History and Symptoms

Symptoms of nephritic syndrome include change in the urine color, decreased urine output, nocturia, and fatigue. In patients with secondary etiologies of glomerular diseases, the clinical presentation might be consistent with the etiology of the disease. Patients must always be inquired about recent illnesses, symptoms of vasculitides or other organ involvement, and constitutional symptoms. Symptoms of nephritic syndrome include change in the urine color, decreased urine output, nocturia, and fatigue. In patients with secondary etiologies of glomerular diseases, the clinical presentation might be consistent with the etiology of the disease. Patients must always be inquired about recent illnesses, symptoms of vasculitides or other organ involvement, and constitutional symptoms.

Symptoms

Symptoms

Physical Examination

Physical Examination

The physical examination of patients with nephritic syndrome due to a primary glomerular disease is usually not very remarkable. Nonetheless, a few signs on physical exam might still be present such as high blood pressure in a minority of patients and signs of fluid overload (peripheral or periorbital edema, pulmonary edema, ascites, and jugular venous distention). A full physical examination is required when patients present with nephritic syndrome in search for causes of secondary glomerular pathology.

Laboratory Findings

Laboratory Findings

Laboratory work-up must be directed to first identify the exact diagnosis of nephritic syndrome by ruling out common etiologies, and to monitor disease progression and renal function. Work-up might be different from one individual to another based on the patient’s presentation and medical history and physical examination findings.

Initial Work-Up

Blood Work-up

Findings associated with glomerulonephritis include anemia, leukocytosis, and electrolyte disturbances such as hyperkalemia. Creatinine and BUN are required to monitor renal function, calculate eGFR, and possible renal deterioration.

Inflammatory markers, such as CRP and ESR, may or may not be elevated in acute glomerulonephritis. They may be helpful in the diagnosis of systemic illnesses, such as malignancies or vasculitides.

Urinalysis

A urinalysis is always recommended in acute glomerulonephritis, looking for:

Further Work-Up

A more extensive work-up may be necessary for patients who present with symptoms of signs consistent with secondary glomerulonephritis. Work-up includes, but is not limited to:

Renal Biopsy

Renal Biopsy

A renal biopsy may be helpful to differentiate etiologies of renal disease, monitor disease progression, and estimate prognosis. Not all cases of nephritic syndrome require renal biopsy. The procedure itself is invasive and may be associated with its own risks. As such, renal biopsy is only indicated if benefit will outweigh the risks. Renal biopsies for patients with initial presentation of nephritic syndrome may be affected greatly by age, progression of symptoms, clinical suspicion, and response to empirical therapy.

Echocardiography or Ultrasound

Echocardiography or Ultrasound

Renal ultrasound is useful to estimate the kidney size and echogenicity. Decreased renal size (eg. less than 8 cm) is consistent with irreversible renal injury.[97] Echocardiography is indicated when a cardiac murmur is noted on physical examination or when there is a high suspicion of bacterial endocarditis causing renal involvement and nephritic syndrome.

Treatment

Treatment

Medical Therapy

Medical Therapy

Management and therapy vary greatly according to the diagnosis of nephritic syndrome. While most causes of nephritic syndrome are self-resolving and do not require medical intervention, such as post-infectious streptococcal glomerulonephritis, other etiologies require high doses of steroids and immunotherapy, such as rapidly progressing glomerulonephritis. In secondary etiologies of nephritic syndrome, management of the underlying disease is the mainstay of the management.

References

References

  1. ↑ Bright, R (1827–1831). Reports of Medical Cases, Selected with a View of Illustrating the Symptoms and Cure of Diseases by a Reference to Morbid Anatomy, vol. I. London: Longmans.
  2. ↑ Volhard, F (1914). Die Brightsche Nierenkrankheit. Springer.
  3. ↑ 3.0 3.1 RAMMELKAMP CH, WEAVER RS (1953). “Acute glomerulonephritis, the significance of the variations in the incidence of the disease”. J Clin Invest. 32 (4): 345–58. doi:10.1172/JCI102745. PMC 438348. PMID 13052693.
  4. ↑ 4.0 4.1 4.2 4.3 Madaio MP, Harrington JT (1983). “Current concepts. The diagnosis of acute glomerulonephritis”. N Engl J Med. 309 (21): 1299–302. doi:10.1056/NEJM198311243092106. PMID 6355846.
  5. ↑ 5.0 5.1 5.2 5.3 Madaio MP, Harrington JT (2001). “The diagnosis of glomerular diseases: acute glomerulonephritis and the nephrotic syndrome”. Arch Intern Med. 161 (1): 25–34. PMID 11146695.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 Hricik DE, Chung-Park M, Sedor JR (1998). “Glomerulonephritis”. N Engl J Med. 339 (13): 888–99. doi:10.1056/NEJM199809243391306. PMID 9744974.
  7. ↑ Kalluri R, Sun MJ, Hudson BG, Neilson EG (1996). “The Goodpasture autoantigen. Structural delineation of two immunologically privileged epitopes on alpha3(IV) chain of type IV collagen”. J Biol Chem. 271 (15): 9062–8. PMID 8621555.
  8. ↑ Jacob L, Viard JP, Allenet B, Anin MF, Slama FB, Vandekerckhove J; et al. (1989). “A monoclonal anti-double-stranded DNA autoantibody binds to a 94-kDa cell-surface protein on various cell types via nucleosomes or a DNA-histone complex”. Proc Natl Acad Sci U S A. 86 (12): 4669–73. PMC 287332. PMID 2660143.
  9. ↑ Cibrik, DM (1997). Immunopathogenesis of renal disease. In: Breenberg A, ed. Primer on kidney diseases. 2nd ed. San Diego, Calif: Academic Press. pp. 141–9. Unknown parameter |coauthors= ignored (help)
  10. ↑ Wilson, CB (1991). The renal response to immunologic injury. In: Brenner BM, Recror FC Jr, eds. The Kidney. 4th ed. Philadelphia: W.B. Saunders. pp. 1062–181.
  11. ↑ Danoff, TM (1997). The role of chemoattractants in renal disease (Chapter 24). In: Nielson EG, Couser WG, eds Immunologic renal diseases. Philadelphia, PA: Lippincott-Raven Publishers. pp. 495–512. Unknown parameter |coauthors= ignored (help)
  12. ↑ Johnson RJ, Couser WG, Chi EY, Adler S, Klebanoff SJ (1987). “New mechanism for glomerular injury. Myeloperoxidase-hydrogen peroxide-halide system”. J Clin Invest. 79 (5): 1379–87. doi:10.1172/JCI112965. PMC 424393. PMID 3033023.
  13. ↑ 13.0 13.1 Johnson RJ, Klebanoff SJ, Ochi RF, Adler S, Baker P, Sparks L; et al. (1987). “Participation of the myeloperoxidase-H2O2-halide system in immune complex nephritis”. Kidney Int. 32 (3): 342–9. PMID 2822992.
  14. ↑ Johnson, RJ (1997). Neutrophils (Chapter 25). In: Nielson EG, Couser WG, eds Immunologic renal diseases. Philadelphia, PA: Lippincott-Raven Publishers. pp. 512–541. Unknown parameter |coauthors= ignored (help)
  15. ↑ 15.0 15.1 Johnson RJ, Alpers CE, Pritzl P, Schulze M, Baker P, Pruchno C; et al. (1988). “Platelets mediate neutrophil-dependent immune complex nephritis in the rat”. J Clin Invest. 82 (4): 1225–35. doi:10.1172/JCI113720. PMC 442673. PMID 2971672.
  16. ↑ Nikolick-Patterson, DJ (1997). Macrophages (Chapter 28). In: Nielson EG, Couser WG, eds Immunologic renal diseases. Philadelphia, PA: Lippincott-Raven Publishers. pp. 567–586. Unknown parameter |coauthors= ignored (help)
  17. ↑ Floege, J (1997). Growth factors and cytokines (Chapter 20). In: Nielson EG, Couser WG, eds Immunologic renal diseases. Philadelphia, PA: Lippincott-Raven Publishers. pp. 415–452. Unknown parameter |coauthors= ignored (help)
  18. ↑ Bhan AK, Collins AB, Schneeberger EE, McCluskey RT (1979). “A cell-mediated reaction against glomerular-bound immune complexes”. J Exp Med. 150 (6): 1410–20. PMC 2185734. PMID 315992.
  19. ↑ Main IW, Atkins RC (1995). “The role of T-cells in inflammatory kidney disease”. Curr Opin Nephrol Hypertens. 4 (4): 354–8. PMID 7552103.
  20. ↑ Couser WG (1993). “Pathogenesis of glomerulonephritis”. Kidney Int Suppl. 42: S19–26. PMID 8361123.
  21. ↑ 21.0 21.1 21.2 Johnson RJ (1994). “The glomerular response to injury: progression or resolution?”. Kidney Int. 45 (6): 1769–82. PMID 7933825.
  22. ↑ 22.0 22.1 Sedor JR, Konieczkowski M, Huang S, Gronich JH, Nakazato Y, Gordon G; et al. (1993). “Cytokines, mesangial cell activation and glomerular injury”. Kidney Int Suppl. 39: S65–70. PMID 8468928.
  23. ↑ 23.0 23.1 Johnson RJ (1997). “What mediates progressive glomerulosclerosis? The glomerular endothelium comes of age”. Am J Pathol. 151 (5): 1179–81. PMC 1858081. PMID 9358740.
  24. ↑ Johnson RJ, Raines EW, Floege J, Yoshimura A, Pritzl P, Alpers C; et al. (1992). “Inhibition of mesangial cell proliferation and matrix expansion in glomerulonephritis in the rat by antibody to platelet-derived growth factor”. J Exp Med. 175 (5): 1413–6. PMC 2119215. PMID 1569407.
  25. ↑ Lovett DH, Johnson RJ, Marti HP, Martin J, Davies M, Couser WG (1992). “Structural characterization of the mesangial cell type IV collagenase and enhanced expression in a model of immune complex-mediated glomerulonephritis”. Am J Pathol. 141 (1): 85–98. PMC 1886574. PMID 1321565.
  26. ↑ Border WA, Noble NA (1994). “Transforming growth factor beta in tissue fibrosis”. N Engl J Med. 331 (19): 1286–92. doi:10.1056/NEJM199411103311907. PMID 7935686.
  27. ↑ Brenner BM, Lawler EV, Mackenzie HS (1996). “The hyperfiltration theory: a paradigm shift in nephrology”. Kidney Int. 49 (6): 1774–7. PMID 8743495.
  28. ↑ Savill J, Mooney A, Hughes J (1996). “Apoptosis and renal scarring”. Kidney Int Suppl. 54: S14–7. PMID 8731187.
  29. ↑ 29.0 29.1 Pathophysiology of renal diseases, ed. 2. New York, McGraw-Hill, 1987,p. 167
  30. ↑ GERMUTH FG (1953). “A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type”. J Exp Med. 97 (2): 257–82. PMC 2136196. PMID 13022878.
  31. ↑ Germuth FG, Senterfit LB, Dreesman GR (1972). “Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system”. Johns Hopkins Med J. 130 (6): 344–57. PMID 5031005.
  32. ↑ Radhakrishnan J, Cattran DC (2012). “The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines–application to the individual patient”. Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
  33. ↑ Neugarten J, Baldwin DS (August 1984). “Glomerulonephritis in bacterial endocarditis”. Am. J. Med. 77 (2): 297–304. PMID 6380288.
  34. ↑ Arze RS, Rashid H, Morley R, Ward MK, Kerr DN (January 1983). “Shunt nephritis: report of two cases and review of the literature”. Clin. Nephrol. 19 (1): 48–53. PMID 6831779.
  35. ↑ Weening JJ, D’Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M (February 2004). “The classification of glomerulonephritis in systemic lupus erythematosus revisited”. Kidney Int. 65 (2): 521–30. doi:10.1111/j.1523-1755.2004.00443.x. PMID 14717922.
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  84. ↑ Hou P, Chen Y, Ding J, Li G, Zhang H (2007). “A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy”. Am. J. Nephrol. 27 (5): 538–44. doi:10.1159/000107666. PMID 17726307.
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  86. ↑ Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T (1991). “Nail patella syndrome: a review of 44 orthopaedic patients”. J Pediatr Orthop. 11 (6): 737–42. PMID 1960197.
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  89. ↑ Wesson DE (June 2002). “The initiation and progression of sickle cell nephropathy”. Kidney Int. 61 (6): 2277–86. doi:10.1046/j.1523-1755.2002.00363.x. PMID 12028473.
  90. ↑ Lusco MA, Fogo AB, Najafian B, Alpers CE (December 2016). “AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy”. Am. J. Kidney Dis. 68 (6): e33–e34. doi:10.1053/j.ajkd.2016.10.006. PMID 27884283.
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  94. ↑ Chang, A (2009). Glomerulonephritis, Membranopoliferative In: Lang F, ed. Encyclopedia of Molecular Mechanisms of Disease. Springer. pp. 711–6. Unknown parameter |coauthors= ignored (help)
  95. ↑ Chang, A (2009). Glomerulonephritis, Membranopoliferative In: Lang F, ed. Encyclopedia of Molecular Mechanisms of Disease. Springer. pp. 711–6. Unknown parameter |coauthors= ignored (help)
  96. ↑ 96.0 96.1 96.2 McGrogan A, Franssen CF, de Vries CS (2011). “The incidence of primary glomerulonephritis worldwide: a systematic review of the literature”. Nephrol Dial Transplant. 26 (2): 414–30. doi:10.1093/ndt/gfq665. PMID 21068142.
  97. ↑ Beck L, Bomback AS, Choi MJ, Holzman LB, Langford C, Mariani LH; et al. (2013). “KDOQI US commentary on the 2012 KDIGO clinical practice guideline for glomerulonephritis”. Am J Kidney Dis. 62 (3): 403–41. doi:10.1053/j.ajkd.2013.06.002. PMID 23871408.

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