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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

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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)



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



  • 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.



  • 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


  • Urinalysis: better, and has less throat pain. However, his mother notes a

  • pH 7, yellow-brown

  • protein - 2+

  • blood - 1+

  • glucose - neg

  • leukocyte esterase - 3+


  • Micro: better, and has less throat pain. However, his mother notes a

  • 5-10 RBCs/HPF

  • 10-20 WBCs/HPF

  • no bacteria

  • few hyaline casts

  • (nl 0-2 RBCs or WBCs/HPF)


  • WBC better, and has less throat pain. However, his mother notes a

  • 12,000/mm3

  • 52% neutrophils

  • 5% bands

  • 28% lymphocytes

  • 15% eosinophils


  • Creatinine: better, and has less throat pain. However, his mother notes a 2.1 mg/dL

  • BUN: 40 mg/dL

  • ASO: 350 U/mL

  • Liver function tests: normal

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



Objectives1
Objectives The ampicillin is discontinued, a course of tapering steroids is begun, and the patient is discharged.

  • 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


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