Glomerular Diseases (Glomerulonephritis)

Overview

Glomerular diseases affect the filtering units of the kidney, the glomeruli. They presents with proteinuria, hematuria or both and is usually diagnosed on a renal biopsy. They account for a significant proportion of acute and chronic kidney disease and are the most common cause of end stage renal disease (the exception is minimal change disease which rarely progresses to renal failure). Glomerular diseases are usually associated with the triad of hypertension, edema and hematuria. They usually have moderately low U Na and FE Na < 1% (similar to pre-renal failure).

Most patients are asymptomatic until abnormalities are detected on routine blood or urine samples. They are many causes of glomerular disease: immunological injury, genetic (inherited) disease, metabolic diseases and the deposition of abnormal proteins such as amyloid. Naming of these condition depends on the histological appearance (membranous, membranoproliferative etc.) or the associated systemic condition (diabetic nephropathy, lupus nephropathy etc.)

Treatment usually involves managing the underlying cause, usually with steroids, and managing hypertension.

Classification

Glomerular diseases can be classified according to the clinical patterns. They exist on a spectrum ranging from proteinuria (neprhosis) to hematuria (nephritis). The main syndromes include:

  • Nephrotic syndrome: Proteinuria (frothy urine) + hyperlipidemia + hypoalbuminaemia due to podocyte damage
  • Nephritic syndrome: Hematuria + oliguria + hypertension due to glomerular inflammation
  • Nephritis nephrosis

The distinction depends on which part of the glomerulus is affected and the constellation of signs and symptoms surrounding each.

Proteinuria usually occurs if a glomerulonephritis causes scarring, meaning that it can complicate any glomerulonephritis in the long-term, including those with a classically nephritic picture.

Investigations

  • Complete blood count (anaemia an dleucocytosis if systemic)
  • U/E/C (Azotemia; BUN/Cr ~ 10:1)
  • Liver function test
  • C-reactive protein
  • Immunoglobulins
  • Electrophoresis
  • Complement C3, C4 (low or normal)
  • ANA, ANCA, ant-dsDNA and anti-GBM antibodies
  • Blood culture
  • ASOT
  • Hepatitis serology
  • Urinalysis (hematuria, proteinuria, RBC casts)
  • 24-hour urine protein collection
  • Spot urine A:CR or P:CR
  • Urine microscopy culture and sensitivity
  • Bence jones proteins
  • RBC casts
  • Chest X-ray (pulmonary hemorrhage)
  • Renal ultrasound (for size and anatomy for biopsy)
  • Renal biopsy (for definitive diagnosis)

Tubulointersitial vs. Glomerular Disorders

TubulointerstitialGlomerulonephritis
Urine osmolalityLow or isosthenuriaHigh or normal
Urine sodiumHighLow or variable
DebrisMuddy brown casts (ATN) and Eosinophils (AIN)Red cell casts
HematuriaRareCommon
ProteinuriaRareCommon
CausesConcomitant illness and drugsCongenital and autoimmune causes
DiagnosisUrine sedimentUrine protein, complement levels and renal biopsy
TreatmentSupportive treatment, dialysisSteroids, immunomodulators

Management

Management is similar to that for CKD

  • Blood pressure control and inhibition of RAAS
  • Immunosuppression (based on histology, severity, progression and comorbidities)
Dr. Leila Jelle
Dr. Leila Jelle

Part of the Hyperexcision team. Interested in broken bones and the stories they tell. Find me exploring the structural integrity of the nearest mountain range!

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