57
Renal Pathology

6- Renal Pathophysiology

Embed Size (px)

DESCRIPTION

патофизиология почки

Citation preview

  • Renal Pathology

  • Introduction:150gm: each kidney1700 liters of blood filtered 180 L of G. filtrate 1.5 L of urine / day.Kidney is a retro-peritoneal organBlood supply: Renal Artery & VeinOne half of kidney is sufficient reservekidney function: Filtration, Excretion, Secretion, Hormone synthesis.

  • Kidney Location:

  • Kidney Anatomy:

  • Renal Pathology OutlineGlomerular diseases: GlomerulonephritisTubular diseases: Acute tubular necrosis interstitial diseases: PyelonephritisDiseases involving blood vessels: NephrosclerosisCystic diseasesTumors

  • Clinical Syndromes:Nephritic syndrome.Oliguria, Haematuria, Proteinuria, Oedema.Nephrotic syndrome.Gross proteinuria, hyperlipidemia, Acute renal failure Oliguria, loss of Kidney function - within weeksChronic renal failure.Over months and years - Uremia

  • IntroductionFunctions of the kidney:excretion of waste productsregulation of water/saltmaintenance of acid/base balancesecretion of hormonesDiseases of the kidneyglomerulitubulesinterstitiumvessels

  • Azotemia: BUN, creatinine Uremia: azotemia + more problems Acute renal failure: oliguria Chronic renal failure: prolonged uremia

    Abnormal findings

  • Glomerular diseasesNephrotic syndromeMinimal change diseaseFocal segmental glomerulosclerosisMembranous nephropathyNephritic syndromePost-infectious GNIgA (immune) nephropathy

  • Nephrotic SyndromeMassive proteinuriaHypoalbuminemiaEdemaHyperlipidemia

  • Adults: systemic disease (diabetes)Children: minimal change diseaseCharacterized by loss of foot processesGood prognosisCauses

  • Minimal change disease

  • Minimal change diseaseNormal glumerular structure

  • Normal glomerulusMinimal change disease

  • Focal Segmental GlomerulosclerosisPrimary or secondarySome (focal) glomeruli show partial (segmental) hyalinizationUnknown pathogenesisPoor prognosis

  • Focal segmental glomerulosclerosis

  • Membranous GlomerulonephritisAutoimmune reaction against unknown renal antigenImmune complexesThickened GBMSubepithelial deposits

  • Membranous glomerulonephritis

  • Nephritic SyndromeHematuriaOliguria, azotemiaHypertension

  • Post-infectious GN, IgA nephropathyImmunologically-mediatedCharacterized by proliferative changes and inflammationCauses

  • Post-Infectious GlomerulonephritisChild after streptococcal throat infectionImmune complexesHypercellular glomeruliSubepithelial humps

  • Post-infectious glomerulonephritis

  • IgA NephropathyCommon!Child with hematuria after (URI) Upper Respiratory Infection IgA in mesangiumVariable prognosis

  • IgA nephropathy

  • Tubular and interstitial diseasesInflammatory lesionspyelonephritis

  • PyelonephritisInvasive kidney infectionUsually ascends from UTIFever, flank painOrganisms: E. coli, Proteus

  • Women, elderlyPatients with catheters or mal-formationsDysuria, frequencyOrganisms: E. coli, ProteusUrinary Tract Infection

  • Acute pyelonephritis with abscesses

  • Pyelonephritis

  • Cellular cast

  • Chronic pyelonephritis

  • Drug-Induced Interstitial NephritisAntibiotics, NSAIDSIgE and T-cell-mediated immune reactionFever, eosinophilia, hematuriaPatient usually recoversAnalgesic nephritis is different (bad)

  • Drug-induced interstitial nephritis

  • Acute Tubular NecrosisThe most common cause of ARF!Reversible tubular injuryMany causes: ischemic (shock), toxic (drugs)Most patients recover

  • Acute tubular necrosis

  • Benign NephrosclerosisFound in patients with benign hypertensionHyaline thickening of arterial wallsLeads to mild functional impairmentRarely fatal

  • Benign nephrosclerosis

  • Malignant nephrosclerosisArises in malignant hypertensionHyperplastic vesselsIschemia of kidneyMedical emergency

  • 5% of cases of hypertensionSuper-high blood pressure, encephalopathy, heart abnormalitiesFirst sign often headache, scotomasDecreased blood flow to kidney leads to increased renin, which leads to increased BP!5y survival: 50%Malignant Hypertension

  • Malignant hypertension

  • Adult Polycystic Kidney DiseaseAutosomal dominantHuge kidneys full of cystsUsually no symptoms until 30 yearsAssociated with brain aneurysms.

  • Adult polycystic kidney disease

  • Childhood Polycystic Kidney DiseaseAutosomal recessiveNumerous small cortical cystsAssociated with liver cystsPatients often die in infancy

  • Childhood polycystic kidney disease

  • Medullary Cystic Kidney DiseaseChronic renal failure in childrenComplex inheritanceKidneys contracted, with many cystsProgresses to end-stage renal disease

  • TumorsRenal cell carcinomaBladder carcinoma

  • Renal Cell CarcinomaDerived from tubular epitheliumSmoking, hypertension, cadmium exposureHematuria, abdominal mass, flank painIf metastatic, 5y survival = 5%

  • Renal cell carcinoma

  • Bladder CarcinomaDerived from transitional epitheliumPresent with painless hematuriaPrognosis depends on grade and depth of invasionOverall 5y survival = 50%

  • Bladder carcinoma

    *****************************************************