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Glomerular diseases

Last updated: February 2, 2021

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Renal glomeruli excrete urinary substances and excess water as an ultrafiltrate into the urine by selectively filtering the blood. Any damage to the glomeruli disrupts the filtration process and results in the appearance of blood components (proteins and red blood cells) in the urine. Glomerular damage is commonly caused by immune-mediated processes, which often lead to glomerulonephritis. Non-inflammatory causes, such as metabolic disease (e.g., diabetes, amyloidosis), can also result in significant damage to the glomeruli. The pathophysiology of glomerular diseases is complex; most patients present with either nephritic syndrome (low-level proteinuria, microhematuria, oliguria, and hypertension) or nephrotic syndrome (high-level proteinuria and generalized edema). All glomerular diseases can progress to acute or chronic renal failure. Thus, quick diagnosis and immediate initiation of therapy are required to prevent irreversible kidney damage.

Terminology of glomerular diseases

Nephrotic vs. nephritic syndrome [1][2]

  • Nephritic syndrome and nephrotic syndrome are both common clinical manifestations of glomerular diseases.
  • Both syndromes are composed of characteristic clinical (e.g., edema, hypertension) and laboratory findings (e.g., glomerular hematuria, massive proteinuria), which result from damage to the glomeruli.
  • Glomerular diseases are usually categorized by the syndrome they cause, which is either nephritic or nephrotic.
  • Some diseases that manifest with nephritic syndrome can simultaneously cause nephrotic-range proteinuria (> 3.5 g/day), the main feature of nephrotic syndrome. When the criteria for both syndromes are fulfilled, the findings are referred to as mixed nephritic-nephrotic syndrome.
  • Classifying the patient's presentation as nephritic, nephrotic, or mixed nephritic-nephrotic can help narrow down the list of likely differential diagnoses.

Nephritic syndrome

Nephrotic syndrome


All glomerular diseases can lead to acute and chronic kidney failure.

  1. Goldman L, Schafer AI. Goldman-Cecil Medicine, 25th Edition. Elsevier ; 2016
  2. Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J. Harrisons's Principles of Internal Medicine, 18th Edition, 2011. McGraw-Hill Medical ; 2011
  3. Goljan EF. Rapid Review Pathology. Elsevier Saunders ; 2013