Kidney stone pathophysiology

Jump to navigation Jump to search
https://https://www.youtube.com/watch?v=uloDkeBOxGQ%7C350}}

Kidney stone Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Kidney stone from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Ultrasonography

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Kidney stone pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Kidney stone pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

National Guidelines Clearinghouse

NICE Guidance

FDA on Kidney stone pathophysiology

CDC on Kidney stone pathophysiology

Kidney stone pathophysiology in the news

Blogs onKidney stone pathophysiology

Directions to Hospitals Treating Kidney stone

Risk calculators and risk factors for Kidney stone pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Pathogenesis

  • It is understood that nephrolithiasis is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
  • [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
  • Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
  • [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
  • The progression to [disease name] usually involves the [molecular pathway].
  • The pathophysiology of [disease/malignancy] depends on the histological subtype.
Type of stone Cause Pathophysiology Stone composition Labs
All stones Low urine volume (raises production of solutes) Reduced intake or increased loss of water Renal water conservation All stones
  • Urine volume <1 L per day
  • Osmolarity >600 mOsm/kg
Calcium stones Hypercalciuria (raises saturation of calcium salts) Absorptive hypercalciuria Increased absorption in gut Calcium oxalate or phosphate Urine calcium concentrations >6 mmol/L (240 mg) per day
Hyperparathyroidism Increased absorption in gut and bone release High concentrations of parathyroid hormone
Immobilisation Bone resorption High concentrations of vitamin D
Excess of sodium in the diet Sodium-induced physiological renal calcium leak. Possible component of gut hyperabsorption Urine sodium concentrations >200 mmol/L per day
Excess of protein or acid in diet Protein-induced bone loss and renal leak.
  • Urine ammonium iron concentrations high
  • Urine sulfate concentrations high
  • Urine pH low
  • Urine citrate concentrations <1·7 mmol/L per day
Range of monogenic disorders Bone loss, gut hyperabsorption, and renal leak in various combinations
Hypocitraturia (raises levels of ionised calcium and reduces inhibitor activity against calcium salts) Renal tubular acidosis (distal type) Renal defence of acid-base balance Calcium phosphate
  • Urine citrate concentrations <1·7 mmol/L per day
  • Urine pH high
High acid load (absence of detectable acidemia) Physiological hypocitraturia Calcium oxalate or phosphate
  • Urine citrate concentrations <1·7 mmol/L per day
  • Urine pH low
Hyperoxaluria (raises saturation of calcium oxalate) Excess of oxalate in diet Increased delivery of luminal oxalate Calcium oxalate Urine oxalate concentrations >70·7 mmol/L per day
Bowel pathology Reduced formation of luminal calcium and calcium-oxalate complex
Increased production of endogenous oxalate Primary hyperoxaluria (type 1 and type 2)
Hyperuricosuria (sodium urate precipitation causes crystallisation of calcium salts) High purine intake Raised production and urinary excretion of sodium and urate
  • Urine uric acid concentrations >600 mg per day
  • Hyperuricaemia
Myeloproliferative diseases
Enzymatic defects Urine uric acid concentrations >600 mg per day
Uricosuric drugs Hypouricaemia
Genetic primary renal leak Increased excretion of uric acid
Uric acid stones Low urine pH or hyperuricosuria
  • High acid load
  • Metabolic syndrome
Titrates urate to poorly soluble uric acid Uric acid Urine pH <5·5
Cystine stones Cystinuria Congenital mutations of dibasic aminoacid transporter subunits rBAT and b0+AT Renal leak of basic aminoacids Cystine Urine concentrations of cystine high (>150 μmol/mmol creatinine)
Infection stones Urinary tract infection Urea-splitting organisms Production of ammonium and bicarbonate from urea
  • Magnesium ammonium phosphate
  • Carbonate apatite

Genetics

Associated Conditions

Gross Pathology

  • On gross pathology, the characteristic findings of nephrolithiasis are:
    • Location = 80% unilateral, usually in calyces, pelvis or bladder
    • Size=variable, 2-3 mm usually
    • All stones contain an organic matrix of mucoprotein
    • Shape:
      • Struvite stone= staghorn calculus

Microscopic Pathology

  • On microscopic histopathological analysis, the characteristic findings of nephrolithiasis are:
    • Shapes of different stones/crystals are different:
      • Cysteine= hexagonal
      • Struvite= coffin lid shape
      • Calcium oxalate= pyramid shape
      • Calcium oxalate= dumbbell shape
      • Uric acid= rectangular/rhomboidal
    • Oxalate crystals are highlighted by polarized light
    • Foreign body giant cells and macrophages are seen with the stones

References

  1. By Amadalvarez - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=46706235
  2. By H. Zell [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], from Wikimedia Commons
  3. By Jakupica - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=45324355
  4. By RJHall - Own work, Public Domain, https://commons.wikimedia.org/w/index.php?curid=4070842
  5. Han H, Segal AM, Seifter JL, Dwyer JT (July 2015). "Nutritional Management of Kidney Stones (Nephrolithiasis)". Clin Nutr Res. 4 (3): 137–52. doi:10.7762/cnr.2015.4.3.137. PMC 4525130. PMID 26251832.
  6. http://kidneypathology.com/Imagenes/Diabetes/Oxalato.4.w.jpg
  7. http://www.kidneypathology.com/English_version/Diabetes_and_others.html
  8. By Kempf EK - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18036112
  9. By Sergio Bertazzo - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=45316797

Template:WH Template:WS