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They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are one which are intrinsic to the [[kidney]], whilst secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), [[drug]]s, systemic disorders ([[SLE]], [[vasculitis]]) or [[cancers]].  
They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are one which are intrinsic to the [[kidney]], whilst secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), [[drug]]s, systemic disorders ([[SLE]], [[vasculitis]]) or [[cancers]].  
==Proliferative Glomerulonephritis==
This type is characterised by increased number of cells in the glomerulus (hypercellular). Usually present as a nephritic syndrome and usually progress to end-stage renal failure (ESRF) over weeks to years (depending on type).
===1. IgA disease (Berger's nephropathy)===
This is the most common type of [[glomerulonephritis]] in adults world-wide. It usually presents as macroscopic [[haematuria]] (visibly bloody urine). It occasionally presents as a [[nephrotic syndrome]]. It often affects young males after an upper respiratory tract infection. Microscopic examination of biopsy specimens shows increased number of mesangial cells with increased matrix (the 'cement' which holds everything together). Immuno-staining is positive for [[immunoglobulin A]] deposits within the matrix. Prognosis is variable, 20% progress to ESRF. Steroids and immunosuppression are not effective treatments for this disease; [[ACE inhibitor]]s are the mainstay of treatment.
===2. Post-infectious Glomerulonephritis===
Post-infectious glomerulonephritis occurs after Streptococcal infection - usually of the skin, after a latency of 10 days. This condition is essentially defined as an inflammation of the kidneys.  Light microscopy shows diffuse hypercellularity due to proliferation of endothelial and mesangial cells, inflammatory infiltrate with neutrophils and with monocytes. The Bowman space is reduced (compressed), in severe cases might see cresent formation [see later]. However, biopsy is seldom done because the disease usually regresses. Patients present with a nephritic syndrome. Diagnosis is suggested by positive streptococcal titers in the blood (ASOT). Treatment is supportive, and the disease resolves (as a rule) in 2 weeks.
===3. Mesangiocapillary Glomerulonephritis===
This is primary, or secondary to [[SLE]], [[viral hepatitis]], hypocomplementemia. One sees 'hypercellular and hyperlobular' glomeruli due to proliferation of both cells and the matrix within the mesangium. Presents usually with as a [[nephrotic syndrome]] but can be nephritic, with inevitable progression to ESRF.
===4. Rapidly progressive Glomerulonephritis (Crescentic GN)===
As the name suggests, this type has a poor prognosis, with rapid progression to [[kidney failure]] over weeks. Any of the above types of GN can be rapidly progressive. Additionally two further causes present as solely RPGN.
One is [[Goodpasture's syndrome]]. This is an autoimmune disease whereby antibodies are directed against antigens found in the [[kidney]] and [[lung]]s. As well as [[kidney failure]], patient have hemoptysis (cough up blood). High dose immunosupression is required (intravenous methylprednisone) and [[cyclophosphamide]], plus plasmapharesis.
Immunohistochemistry staining of tissue specimens shows linear [[IgG]] deposits.
The second cause is vasculitic disorders such as Wegener's and [[polyarteritis]]. There is a lack of immune deposits on staining, but blood tests are positive for ANCA antibody.


=====Histopathology=====  
=====Histopathology=====  

Revision as of 14:19, 31 August 2012

Glomerulonephritis
Acute Glomerulonephritis: Micro H&E high mag; an excellent example of acute exudative glomerulonephritis.
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology
ICD-10 N00, N01, N03, N18
ICD-9 580-582
DiseasesDB 5245
MeSH D005921

Glomerulonephritis Main page

Glomerulonephritis patient information

Overview

Classification

[[]]
[[]]
[[]]

Pathophysiology

Differential Diagnosis

Screening

Diagnosis

Prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: GN; glomerular nephritis

Overview

Glomerulonephritis, also known as glomerular nephritis and abbreviated GN', is a primary or secondary immune-mediated renal disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys. It may present with isolated hematuria and/or proteinuria (blood resp. protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute renal failure, or chronic renal failure.

They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are one which are intrinsic to the kidney, whilst secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis) or cancers.

Histopathology

The majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space which leads to renal failure within weeks or months.

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • Glomerulonephritis: Micro H&E med mag; an excellent example of AGN with many neutrophils

    Glomerulonephritis: Micro H&E med mag; an excellent example of AGN with many neutrophils

  • Acute Glomerulonephritis: Micro H&E high mag; an excellent example of acute exudative glomerulonephritis.

    Acute Glomerulonephritis: Micro H&E high mag; an excellent example of acute exudative glomerulonephritis.


Glomerulonephritis Videos

Rapidly progressive glomerulonephritis

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Chronic glomerulonephritis

{{#ev:youtube|eA1vYarRAWo}}

Pathological Findings: A Case Example

Clinical Summary

A 17-year-old white male had end-stage renal disease requiring hemodialysis for 10 years. For the previous four years he had hypertension which slowly increased to about 180/120 mm Hg. Laboratory findings included a greatly elevated BUN and creatinine. He was admitted for bilateral nephrectomy and discharged in satisfactory condition on the 10th postoperative day. He was to be contacted in the future for transplantation.

Autopsy Findings

The left (97 grams) and right (88 grams) kidneys were of similar appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • This is a low-power photomicrograph of a saggital section of end stage chronic glomerulonephritis (GN). Note the marked thinning of the cortex (arrow).

    This is a low-power photomicrograph of a saggital section of end stage chronic glomerulonephritis (GN). Note the marked thinning of the cortex (arrow).

  • This is a higher-power photomicrograph of hyalinized glomeruli (arrows) and glomeruli with thick basement membranes.

    This is a higher-power photomicrograph of hyalinized glomeruli (arrows) and glomeruli with thick basement membranes.


  • This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).

    This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).

  • This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.

    This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.


  • This is an immunofluorescent photomicrograph of granular membranous immunofluorescence (immune complex disease). The antibody used for these studies was specific for IgG.

    This is an immunofluorescent photomicrograph of granular membranous immunofluorescence (immune complex disease). The antibody used for these studies was specific for IgG.

  • This is an electron micrograph of subepithelial granular electron dense deposits (arrows) which correspond to the granular immunofluorescence seen in the previous image.

    This is an electron micrograph of subepithelial granular electron dense deposits (arrows) which correspond to the granular immunofluorescence seen in the previous image.


  • This is a photomicrograph of a glomerulus from another case with acute poststreptococcal glomerulonephritis. In this case the immune complex glomerular disease is ongoing with necrosis and accumulation of neutrophils in the glomerulus.

    This is a photomicrograph of a glomerulus from another case with acute poststreptococcal glomerulonephritis. In this case the immune complex glomerular disease is ongoing with necrosis and accumulation of neutrophils in the glomerulus.

  • This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.

    This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.


  • This electron micrograph demonstrates scattered subepithelial dense deposits (arrows) and a polymorphonuclear leukocyte in the lumen.

    This electron micrograph demonstrates scattered subepithelial dense deposits (arrows) and a polymorphonuclear leukocyte in the lumen.

  • For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.

    For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.

Related chapters

Resources

Images:

HDCN

  • HDCN Nephritis Channel - Collection of lectures and links pertaining to glomerulonephritis on the HDCN (Hypertension, Dialysis, and Clinical Nephrology) on-line journal.

References

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