Journal of Clinical Nephrology and Therapeutics

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Perspective - Journal of Clinical Nephrology and Therapeutics (2022) Volume 6, Issue 5

Glomerulonephritis: etiology, pathophysiology, treatment and management

Shashi Pathak*

Division of Nephrology, University of British Columbia, Canada

*Corresponding Author:
Shashi Pathak
Division of Nephrology
University of British Columbia, Canada

Received: 22-Aug-2022, Manuscript No. AACNT-22-73327; Editor assigned: 24-Aug-2022, PreQC No. AACNT-22-73327(PQ); Reviewed: 07-Sep-2022, QC No. AACNT-22-73327; Revised: 10-Sep-2022, Manuscript No. AACNT- 22-73327(R); Published: 17-Sep-2022, DOI: 10.35841/aacnt-6.5.123

Citation: Pathak S. Glomerulonephritis: Etiology, pathophysiology, treatment and management. J Clin Nephrol Ther. 2022;6(5):123

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The term "glomerulonephritis" envelops a subset of renal diseases described by immunemediated harm to the basement membrane, mesangium, or capillary endothelium, causing hematuria, proteinuria, and azotemia. Acute types of Glomerulonephritis (GN) can result from either a primary renal reason or an optional disease that causes renal manifestations.


Glomerulonephritis, Chronic kidney disease, Diabetic nephropathy, Proteinuria.


The structural and functional unit of the kidney, the 'nephron,' comprises of a renal corpuscle (glomerulus encompassed by a Bowman capsule) and a renal tubule. Every kidney in an adult human contains around 1 million nephrons. A fenestrated endothelium frames the inward glomerular layer, trailed by a layer made out of different extracellular proteins shaping a meshwork called the Glomerular Basement Membrane (GBM). The external layer has instinctive epithelial cells, podocytes, and mesangial cells. The intricate arrangement plan gives the premise to continuous plasma volume filtration at the glomerular level [1].

Acute types of Glomerulonephritis (GN) can result from either an essential renal reason or a secondary illness that causes renal indications. For example, acute Post-Streptococcal Glomerulonephritis (PSGN) is an illustration of acute glomerulonephritis secondary to a streptococcal infection; correspondingly, Staphylococcus aureus contamination can likewise cause glomerulonephritis. As of late, nonetheless, the frequency of glomerulonephritis related with staphylococcal has increased rather than the decrease of PSGN in the United States and most developed nations.


Etiological characterization of glomerulonephritis can be made in light of clinical presentation, going from severe proteinuria (>3.5 g/day) and edema meeting all requirements for the nephrotic disorder to a nephritic condition where hematuria and hypertension are more noticeable while proteinuria is less articulated [2].

Nephrotic Glomerulonephritis

• Minimal change disease

• Focal segmental glomerulosclerosis

• Membranoproliferative glomerulonephritis

• Membranous nephropathy

• HIV related nephropathy

• Diabetic nephropathy

Nephritic Glomerulonephritis

• IgA nephropathy

• Henoch Schonlein Purpura (HSP)

• Post streptococcal glomerulonephritis.

• Hostile to glomerular basement membreane disease

• Granulomatosis with polyangiitis

• Eosinophilic granulomatosis with polyangiitis

• Polyarteritis nodosa

• Idiopathic crescentic glomerulonephritis

• Goodpasture disorder

• Lupus nephritis

• Hepatitis C disease

• Membranoproliferative glomerulonephritis (regular show is with intense nephritic condition, notwithstanding, some of the time features looking like nephrotic disorder might happen, also).

The study of disease transmission

Glomerulonephritis (GN) is a prominent reason for renal impairment. It leads 10% to 15% of end-stage renal disease cases in the United States. In many occasions, the sickness becomes moderate without ideal mediation, at last prompting grimness. This makes persistent glomerulonephritis the third most normal reason for end-stage renal illness in the United States, following diabetes mellitus and hypertension, representing 10% of patients on dialysis. Glomerulonephritis is 25% to 30% of all end-stage renal illness cases about a fourth of patients present with nephritic condition [2]. Movement, as a rule, is moderately fast, and end-stage renal sickness might result within weeks or months of the start of acute nephritic syndrome.

IgA nephropathy has been viewed as the most widely recognized reason for glomerulonephritis around the world. Nonetheless, the frequency of post-streptococcal glomerulonephritis has declined in most evolved nations. As announced by Japanese analysts, the rate of post infectious glomerulonephritis in their nation peaked during the 1990s. Post-streptococcal glomerulonephritis, which represented virtually all instances of postinfectious GN during the 1970s, has decreased to around 40-half since the 1990s, while the level of Staphylococcus aureus-related nephritis rose to 30%, and hepatitis C infection related glomerulonephritis additionally increased.

The basic pathogenetic component normal to these various varieties of glomerulonephritis is immune-mediated, in which both humoral as well as cell-mediated pathways are active. The subsequent inflammatory reaction, much of the time, prepares for fibrotic events that follow.

One of the objectives is the glomerular basement membrane itself or some antigen caught inside it, as in post-streptococcal disease. Such antigen-antibody reactions can be systemic, with glomerulonephritis occurring as one of the parts of the disease cycle, for example, in Systemic Lupus Erythematosus (SLE) or IgA nephropathy. Then again, in small vessel vasculitis, cell-mediated immune responses are the main culprit rather than antigen-antibody reactions. Here, T lymphocytes and macrophages are flooded in glomeruli with resultant damage [3].

Structural changes: Structurally, cell multiplication causes an increase in the cellularity of the glomerular tuft because of the overabundance of endothelial, mesangial, and epithelial cells. The multiplication might be of two kinds:

• Endocapillary - inside the glomerular capillary tufts

• Extracapillary - in the Bowman space, including the epithelial cells

In extra-capillary multiplication, parietal epithelial cells multiply to cause the development of sickles, characteristic of certain types of rapidly progressive glomerulonephritis.

Functional changes: Functional changes incorporate the accompanying:

• Proteinuria

• Hematuria

• Decrease in creatinine freedom, oliguria, or anuria

• Active urine sediments, for example, RBCs and RBC casts

This leads intravascular volume expansion, edema, and systemic hypertension.


Based on the clinical presentation, differentiation should be drawn between the nephrotic and the nephritic spectrum. This is significant as it assists with reducing the differentials of the underlying glomerular pathology. Additionally, differential conclusions will incorporate essential versus auxiliary causes relying upon the age bunch and clinical picture.

Primary glomerulonephritis presenting as the nephrotic condition in young patients is probably going to be negligible change disease, while in adults, membranous variety is almost certain. In the secondary class, diabetes mellitus must be precluded [4].

At the point when nephritic syndrome is the fundamental presentation in kids, it is reasonably post-irresistible. In adults, however, IgA nephropathy ought to be thought of. At the point when systemic vasculitis includes glomeruli, the cause in the younger age group is Henoch schonlein purpura, while in adults; granulomatosis with polyangiitis ought to be suspected. Lupus nephritis is seen all the mostly seen in young ladies (20 to 30 years).

Following are a few significant differentials to be considered while making the diagnosis of glomerulonephritis [5]:

• Acute kidney injury

• Focal segmental glomerulonephritis

• Central segmental glomerulonephritis

• Glomerulonephritis associated with nonstreptococcal contamination

• Membranoproliferative glomerulonephritis

• Post streptococcal glomerulonephritis

• Rapidly progressive glomerulonephritis

The accompanying renal conditions habitually mirror the beginning phases of intense GN:

• Idiopathic hematuria

• Chronic GN with an acute worsening

• Anaphylactoid purpura with nephritis

• Familial nephritis


  1. Khalighi MA, Al-Rabadi L, Chalasani M, et al. Staphylococcal infection–related glomerulonephritis with cryoglobulinemic features. Kidney Int Rep. 2018;3(5):1128-34.
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  3. Satoskar AA, Parikh SV, Nadasdy T. Epidemiology, pathogenesis, treatment and outcomes of infection-associated glomerulonephritis. Nat Rev Nephrol. 2020;16(1):32-50.
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  5. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis. Clin Nephrol. 2010;73(3):173-9.
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  7. Mosquera J, Pedreanez A. Acute post-streptococcal glomerulonephritis: analysis of the pathogenesis. Int Rev Immunol. 2021;40(6):381-400.
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  9. Alchi B, Jayne D. Membranoproliferative glomerulonephritis. Pediatric Nephrol. 2010;25(8):1409-18.
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