Tubulointerstitial diseases
This presentation is the property of its rightful owner.
Sponsored Links
1 / 48

Tubulointerstitial Diseases PowerPoint PPT Presentation


  • 44 Views
  • Uploaded on
  • Presentation posted in: General

Tubulointerstitial Diseases. Dr. Raid Jastania. Objectives. By the end of this session the student should be able to Describe the types of Acute tubular necrosis and its clinical importance Know the features of Acute and Chronic pyelonephritis, and the risk factors

Download Presentation

Tubulointerstitial Diseases

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Tubulointerstitial diseases

Tubulointerstitial Diseases

Dr. Raid Jastania


Objectives

Objectives

  • By the end of this session the student should be able to

  • Describe the types of Acute tubular necrosis and its clinical importance

  • Know the features of Acute and Chronic pyelonephritis, and the risk factors

  • Understand the special issues in Drug-induced interstitial nephritis


Tubulointerstitial diseases1

Tubulointerstitial Diseases

  • Acute tubular necrosis

  • Acute pyelonephritis

  • Chronic Pyelonephritis

  • Drug-induced interstitial nephritis


Acute tubular necrosis

Acute Tubular Necrosis

  • The most common cause of acute renal failure

  • Clinicopathological entity

  • Reversible lesion

  • Destruction of tubular epithelium

  • Acute suppression of renal function (urine >400ml/day)


Causes of acute renal failure

Causes of acute renal failure

  • Pre renal, renal, post renal

  • Acute tubular necrosis

  • Glomerular disease. RPGN

  • Vascular disease. Polyarteritis nodosa

  • Acute papillary necrosis

  • Diffuse cortical necrosis


Types of acute tubular necrosis

Types of Acute Tubular Necrosis

  • 1. Ischemic

  • 2. Nephrotoxic


Types of acute tubular necrosis1

Types of Acute Tubular Necrosis

  • 1. Ischemic

    • State of hypoperfusion

    • Eg. Trauma, septicemia, acute pancreatitis, hypotension, shock


Types of acute tubular necrosis2

Types of Acute Tubular Necrosis

  • 2. Nephrotoxic:

    • Heavy metals: mercury

    • CaCl4

    • Antibiotics. Gentamicin


Pathogenesis

Pathogenesis

  • 1. Tubular injury

  • 2. Blood flow disturbance (persistent, severe), (Endothelial cell injury)


Pathogenesis1

Pathogenesis

  • 1. Tubular injury

    • Sensitive to ischemia and toxins

    • Injury

    • Functional defect: increase Na delivery to distal tubules – vasoconstriction

    • Cytokines – vasoconstriction

    • Tubular debris – block urine outflow – increase the pressure

    • Fluid leak in interstitium – collapse of tubules


Pathogenesis2

Pathogenesis

  • 1. Tubular injury

  • 2. Blood flow disturbance (persistent, severe), (Endothelial cell injury)


Pathogenesis3

Pathogenesis

  • 2. Blood flow disturbance (persistent, severe), (Endothelial cell injury)

    • Vasoconstriction

    • Endothelial injury: release of endothelin, decrease in nitric oxide

    • Others: renin-angiotensin, norepinephrine)


Pathogenesis4

Pathogenesis


Morphology

Morphology

  • Subtle findings, similar in ischemic and toxic

  • Interstitium- edema, mild acute inflammation

  • Proximal tubules

  • Necrosis

  • Rupture of basement membrane

  • Proteinaceous cast in distal and collecting tubules

  • Tamm-Horsfall protein

  • Epithelial regeneration


Clinical course

Clinical course

  • 1. Initiating phase: 36 hours

    • Hypotension, decrease urine output, rising urea

  • 2. Maintenance phase: 2-6 days

    • Low urine output 50-400 ml/day

    • Ureamia, fluid overload

  • 3. Recovery

    • Increase urine output (upto 3L/day)

    • Electrolyte imbalance

    • Risk of infections


Tubulointerstitial nephritis

Tubulointerstitial nephritis

  • Causes

    • Infectious: Bacterial, viral, fungal, parasitic

    • Non-infectious: Physical (radiation) Chemical (toxins, drugs), metabolic, Ischemic, Immune

    • Acute pyelonephritis

    • Chronic pylelonephritis


Acute pyelonephritis

Acute Pyelonephritis

  • UTI

  • Commonly bacterial

    • Gram negative: E.coli, Proteus, Klebsiella, Pseudomonas, Enterobacter

  • Risk factors

    • Anomalies, Instrumentation,

    • Obstruction, bladder dysfunction, reflux

    • Pregnancy

    • DM. Immunosuppression


Acute pyelonephritis1

Acute Pyelonephritis

  • Routes of infections

    • Hematogenous

    • Ascending infection:

      • Adhesion to mucosa – colonization of urethra – ascending of infection

      • Female>male


Acute pyelonephritis2

Acute Pyelonephritis

  • Morphology:

    • One or both kidneys

    • Sharp yellow abscess on the surface

    • Necrosis, pus (neutrophils)

    • WBC casts

    • Pyonephrosis

    • Papillary necrosis (DM, obstruction, Analgesic)

      • Sharp yellow necrosis at the apex of the pyramid

    • Cystitis: hypertrophy, trabeculation


Acute pyelonephritis3

Acute Pyelonephritis

  • Symptoms

    • Pain at the costovertebral angle, fever, chills, malaise

    • Urine: pyuria, bacteria

    • Dysuria, frequencey, urgency

  • Natural history

    • Self-limiting

    • Recurrent

    • chronic


Chronic pyelonephritis

Chronic Pyelonephritis

  • Interstitial inflammation and scarring with deformity of the pelvicalyceal system

  • 1. Chronic obstructive pyelonephritis

    • Recurrent infections

  • 2. Reflux nephropathy

    • Vesico-ureteral reflux

    • infections


Chronic pyelonephritis1

Chronic Pyelonephritis

  • Morphology:

    • One or both kidneys

    • Uneven scarring/inflammation (lymphocytes, plasma cells)

    • Papillary blunting and calyceal deformities

    • Dilation/atrophy of tubules, colloid casts (thyoidization)

    • Vascular changes

    • Secondary focal segmental glomerulosclerosis


Chronic pyelonephritis2

Chronic Pyelonephritis

  • Clinical

    • Late presentation: renal insufficiency, hypertension

    • Contracted kidneys

    • Tubular dysfunction: polyruia/nocturia


Drug induced interstitial nephritis

Drug-induced interstitial nephritis

  • Acute drug-induced interstitial nephritis:

    • Antibiotics

    • NSAIDs

    • Diuretics

    • Begin 15 days after exposure

    • Fever, eosinophilia, rash

    • acute renal failure, hematuria, proteinuria


Drug induced interstitial nephritis1

Drug-induced interstitial nephritis

  • Acute drug-induced interstitial nephritis:

    • Pathogenesis

      • Immune mechanism, hypersensitivity

      • Drug is trapped in the kidney during secretion

      • Results in injury

      • ? Type I, high IgE

      • ? Type IV, granuloma


Drug induced interstitial nephritis2

Drug-induced interstitial nephritis

  • Acute drug-induced interstitial nephritis:

    • Morphology:

      • Edema

      • Inflammatory infiltrate: lymphocytes, macrophages, eosinophils

      • Sometimes: granulomas

      • NSAIDs may cause minimal change disease


Drug induced interstitial nephritis3

Drug-induced interstitial nephritis

  • Analgesic Nephropathy:

    • Chronic users

    • Chronic interstitial nephritis

    • Renal papillary necrosis

    • Aspirin, acetaminophen, caffeine, codeine


Drug induced interstitial nephritis4

Drug-induced interstitial nephritis

  • Analgesic Nephropathy:

    • Pathogenesis

      • Unclear, papillary necrosis, inflammation

      • Oxidative damage

      • Aspirin inhibits prostaglandin synthesis (vasoconstriction)


Drug induced interstitial nephritis5

Drug-induced interstitial nephritis

  • Analgesic Nephropathy:

    • Morphology:

      • Papillae: yellow brown, lipofuscin pigment

      • inflammation

      • Coagulative necrosis

      • Clacification

      • Scarring

      • Vessels: basement membrane thickening (analgesic microangiopathy)


Drug induced interstitial nephritis6

Drug-induced interstitial nephritis

  • Analgesic Nephropathy:

    • Clinical

      • Chronic renal failure

      • Hypertension

      • Anemia

      • Increase risk of transitional cell carcinoma


Case presentation

Case presentation


Tubulointerstitial diseases

  • A twelve-year-old boy presents to his family physician with a history of a sore throat and fever. The sore throat began about 3 days previously; a fever of 39°C developed in the last day. Physical examination reveals a well-developed, well-nourished boy of appropriate size for age in mild distress. His temperature is 39.5°C, pulse 90 (nl 60-100/min), blood pressure 100/75, and respirations 20 (nl 8-16/min). Examination of the oropharynx reveals a red, inflamed throat and tonsils with exudate. Otherwise, the exam is unremarkable.


Tubulointerstitial diseases

  • A swab from his throat is used to test for the presence of streptococcal antigens (streptozyme test), and it is positive. When the physician suggests an injection of penicillin, the child throws a wall-eyed fit, and the physician relents, prescribing a ten-day course of ampicillin.


Tubulointerstitial diseases

  • After two or three days of treatment, the boy begins to feel better, and has less throat pain. However, his mother notes a red, macular rash over his chest and back, and the boy complains of itching. Calamine lotion is applied for a day or two without relief, and the fever recurs, this time with the complaint of joint aches. When the child becomes listless and loses his appetite, his mother returns him to the doctor, who performs further lab tests


Tubulointerstitial diseases

  • Urinalysis:

  • pH 7, yellow-brown

  • protein - 2+

  • blood - 1+

  • glucose - neg

  • leukocyte esterase - 3+


Tubulointerstitial diseases

  • Micro:

  • 5-10 RBCs/HPF

  • 10-20 WBCs/HPF

  • no bacteria

  • few hyaline casts

  • (nl 0-2 RBCs or WBCs/HPF)


Tubulointerstitial diseases

  • WBC

  • 12,000/mm3

  • 52% neutrophils

  • 5% bands

  • 28% lymphocytes

  • 15% eosinophils


Tubulointerstitial diseases

  • Creatinine: 2.1 mg/dL

  • BUN: 40 mg/dL

  • ASO: 350 U/mL

  • Liver function tests: normal

  • 24-hour urine protein: 500 mg/24 hr


Tubulointerstitial diseases

  • The child is hospitalized, and a renal biopsy is performed. The ampicillin is discontinued, a course of tapering steroids is begun, and the patient is discharged.


Objectives1

Objectives

  • By the end of this session the student should be able to

  • Describe the types of Acute tubular necrosis and its clinical importance

  • Know the features of Acute and Chronic pyelonephritis, and the risk factors

  • Understand the special issues in Drug-induced interstitial nephritis


  • Login