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MS2 Renal > 9/21- Tubular Disorders > Flashcards

9/21- Tubular Disorders Flashcards

1
Q

What is the kidney interstitial space?

A

Space between tubules and glomeruli containing vasculature and connective tissue cells

  • May be damaged by primary disease or secondary process
  • Interstitial space, tubule, and glomerulus function as a unit; damage to one component will affect others
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2
Q

What is seen here?

A

Normal kidney anatomy

  • Glomerulus and Bowman’s capsule
  • Tubules- (columnar epithelium)
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3
Q

What is seen here?

A

Acute changes: edema and cellular infiltrates

  • Many “black dots” and “red jello”
  • Top arrow = black dot with surrounding red = eosinophilia
  • Can see space between tubules; edema and swelling (multicellular infiltrates between tubules)
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4
Q

What is seen here?

A

Chronic renal changes:

  • Tubule dilation and degeneration
  • Fibrosis
  • Interstitial space (space between tubules) but without inflammatoryinfiltrate
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5
Q

What is seen here?

A

Chronic renal changes:

  • Glomerulosclerosis
  • Vascular sclerosis
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6
Q

What are urinary findings and disease examples in damage to:

  • Tubule
  • Interstitial space
  • Urinary obstruction
  • Glomerular disease
  • Renal cystic disease
  • Metabolic disease
A

Tubule

  • Ex: ATN (acute tubular necrosis)
  • Urine: granular casts

Interstitial space

  • Ex: pyelonephritis
  • Urine: WBC (neutrophils), bacteria, culture

Also IS space:

  • Ex: Allergic IN
  • Urine: WBC (eosinophils), (-) culture

Urinary obstruction

  • Ex: BPH
  • Urine: Benign urine

Glomerular disease

  • Ex: Membranous GN
  • Urine: Proteinuria, hematuria

Renal cystic disease

  • Ex: Polycystic kidney disease
  • Urine: Hematuria

Metabolic disease

  • Ex: Cystinuria
  • Urine: Urinary crystals
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7
Q

List of etiologies of interstitial diseases (don’t memorize)?

A
  • Infections: bacterial, fungal, viral, mycobacterial
  • Drugs: NSAIDS, herbals, cisplatinum, lithium, others
  • Hematopoietic Diseases: sickle cell, myeloma and lymphoproliferative disorders
  • Obstruction: VUR, mechanical
  • Heavy Metals: lead, cadmium, etc
  • Hereditary Diseases: PCKD, medullary cystic dis., hereditary nephritis, medullary sponge kidney, juvenile nephronophthisis, etc
  • Metabolic Disorders: diabetes mellitus, hyperuricemia, cystinosis, K+ depletion, oxaluria, hypercalcemia
  • Immunologic Diseases: SLE, Transplanted kidney, cryoglobulinemia, Sjögrens, Goodpasture
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8
Q

What are methods of bacterial kidney infection (spread)?

A
  • Systemic seeding by staph and strep
  • Ascending infections: gram neg organisms, enterococcus (may present as cystitis)
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9
Q

Common infectious agents that may cause kidney infection/tubulo-interstitial inflammation?

A

Bacteria

  • Staph, strep
  • Gram (-) organisms, enterococcus

Viral: CMV, HIV, BK (polyoma), EBV, Hantavirus, herpes

Fungal: typ candida

Mycoplasma

Other: malaria, leptospira

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10
Q

What is seen here?

A

Pyelonephritis on CT scan

  • Striated nephrogram- poorly perfused area
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11
Q

What can cause interstitial inflammation from a urinary reflux/obstruction standpoint?

  • Clinical presentation
  • Treatment
A

Vesico-urethral reflux nephropathy

  • Caused by combo of VUR and infection, beginning in childhood

Clinically:

  • Recurrent UTIs in childhood
  • Slowly progressive loss of kidney function

Treatment

  • Treat UTIs
  • Correct severe VUR in children
  • No benefit of surgery in adults
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12
Q

What is involved in acute drug induced interstitial nephritis and heavy metal toxicity as etiologies for interstitial inflammation? (Basic principles)

A
  • The drugs causing interstitial inflammation are an unrelated group of agents that aren’t dose related and only occur in small number of exposed
  • Overall, it’s a hypersensitivity reaction; recurs (severe) upon re-exposure
  • May involve systemic manifestations
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13
Q

What drugs can cause interstitial inflammation?

A

Antibiotics

  • Penicillins, methicillin, ampicillin
  • Cephalosproins, floroquinolones (cipro)
  • Rifampin

Sulfonamides

NSAIDs (analgesics)

Miscellaneous:

  • Anticoags (Phenindione)
  • Anticonvulsants (Phenytoin)
  • Diuretics (Thiazides, Furosemide)
  • Others: Cimetidine, Allopurinol, Cyclosporine, Omeprazole
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14
Q

Acute physical findings of tubule and interstitial disease?

A
  • Fever, 50-75%
  • Rash, 25-40%
  • Eosinophilia, 40-60%
  • Flank pain, 25-40%
  • Hypertension, 10-20%
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15
Q

What is the association between Aristolochic acid and nephropathy?

A

Aristolochic acid nephropathy (AAN) aka Chinese herbal nephropathy

  • Extensive paucicellular interstitial fibrosis and tubular atrophy typically found in end-stage CHN
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16
Q

Describe NSAID (analgesic) nephropathy:

  • Clinical Presentation
  • Onset
  • Urinalysis
  • Resolution
  • Permanent damage (prevalence)
  • Systemic manifestations
A

- Clinical Presentation: AKD +/- Nephrotic Syndrome

- Onset: 2 wks - 18 mo

- Urinalysis: microhematuria, pyuria

- Resolution: 1 mo - more than 1 yr

- Permanent damage (prevalence): perhaps > 15%

- Systemic manifestations: eosinophilia, fever, rash

17
Q

Clinical Features of NSAID nephropathy?

  • Gender
  • Age
  • Symptoms
A
  • Gender: female > male (60-85%)
  • Age > 30 yrs
  • Personality disorder (Major 35% Minor 40% Introvert, dependent, anxiety, emotional disorder, neurotic, familial instability)
  • Addictive syndrome (Smoking, alcohol, laxatives, sedatives, psychotropics)
  • Cause of analgesic dependency (Headache 40-60%, mood 6-30%, musculoskeletal pain 20-30%)
18
Q

Pathogenesis of NSAID nephropathy?

A

APC tabs or powders

  • Aspirin blocks synthesis of prostaglandin (a vasodilator)
  • Phenacetin (Acetaminophen)* lowers glutathione, which is needed to block intracellular oxidative stress
  • Caffeine increases adenosine, a vasoconstrictor (works in headaches by decreasing CNS edema)

Results in papillary ischemia

*Can take Tylenol rather than Phenacitin/Acetaminophin

19
Q

What is seen here?

A

NSAID nephropathy

  • Dying papilla
  • Dead tissue coming out in urine
20
Q

How can creatinine levels be normal early on?

A
  • Cortical nephron spared
  • Decreased GFR, but early creatinine is normal ?
21
Q

Treatment for NSAID Nephropathy?

A
  • Discontinue analgesics
  • Control blood pressure (ACEIs)
  • Treat urinary infections
  • Expand vascular volume
  • Psychological support and guidance
  • Monitor for uroepithilial neoplasms (5-10% of phenacetin users)
22
Q

What heavy metals can cause nephrotoxicity?

A

Chronic TIN

  • Lead
  • Bismuth, Cadmium, Chromium, Copper, Iron, Mercury, Platinum, Silicon, Uranium

Acute TIN

  • Bismuth
  • Mercury
  • Uranium
  • Arsenic, Cadmium, Chromium, Copper, Gold, Iron, Lead, Silver
23
Q

ATN and cortical necrosis can cause tubulo-interstitial inflammation. What does ATN involve?

A

Acute tubular necrosis involves multiple renal insults

  • Preexisting renal damage
  • Prerenal state: volume depletion, sepsis, heart failure
  • Nephrotoxin exposure or kidney ischemia
24
Q

What is the pathogenesis of ATN?

A
  • Cell death due to toxin or ischemia
  • With reperfusion, damaged cells undergo apoptosis
  • Damaged cells sloughed off and new cells take their place
  • Combination of vasoconstriction (pre renal state), ischemia, and toxin
  • Vacuolization of tubules, loss of transport polarity
  • Sloughing of cells, cast formation
  • Recovery typically 1-3 weeks
  • Clinical objective, keep patient alive till kidneys recover
25
Q

What is seen here?

A

ATN in kidney biopsy

  • Cells sloughing off in collecting tubule and forming cast
26
Q

What nephrotoxins can cause acute tubular necrosis?

A
  • IV iodinated radiographic contrast
  • Heme pigments (myoglobin and hemoglobin)
  • Certain antibiotics (aminoglycosides)
  • Heavy metals (cis-platinum)
  • Carbon tetrachloride and solvents
27
Q

What can cause cortical necrosis?

A

Ischemia of cortex

  • Microvascular thrombosis, glomerular and tubule damage
  • Medulla may survive
  • Damage is patchy, some renal function may remain

Obstetrical disorders, DIC, HUS (E. coli infxn)

Anuria or oliguria is common

28
Q

What is seen here?

A

Cortical necrosis

29
Q

What conditions can cause urinary crystals?

  • Metabolic disease
  • Medications
  • Chemicals
  • Other
A

Metabolic disease

  • Cysteine
  • Hyperuricemia
  • Hypercalcemia

Medications

  • Indinavir
  • Foscarnet
  • Sulfa drugs

Chemicals

  • Antifreeze (oxalic acid crystals)

Triple phosphate crystals and staghorn calculi (chronic kidney infection with urea splitting agents)

30
Q

What can cause Cysteinosis? Cysteinuria?

A

Cysteinosis- autosomal recessive

  • Cysteine accumulates in cells
  • Proximal nephron damaged, unable to reabsorb filtered glucose, bicarb, AAs (Fanconi syndrome)

Cystinuria- autosomal recessive

  • Filtered cysteine not reabsorbed by proximal nephron
  • High urinary levels precipitate in pH neutral or acid urine, causing cysteine kidney stones
31
Q

What crystals are these?

A
32
Q

What is Myeloma Cast Nephropathy?

A
  • Plasma cell clone produces defective antibody parts, excessive kappa or lambda chains
  • Direct proximal tubule toxicity, cast formation in collecting duct
  • Associated bone lesions, proteinuria (kappa and lambda proteins not detected by urinary dip stick)
  • Anemia
  • Small anion gap (kappa and lambda are positively charged proteins)
33
Q

What is seen here?

A

Myeloma Cast Nephropathy

  • Due to toxicity of filtered light chain (kappa, lambda) proteins; Bence Jones
  • Directly toxic to proximal tubular cells
  • Precipitate int he distal and collecting tubules
34
Q

What is papillary necrosis?

A
  • Necrosis of papilla: long loops of Henle, vasa recta, collecting duct
  • Flank pain, tissue in urine
  • Sickle cell, analgesic abuse, pyelonephritis…
  • Not usually oliguric or anuric (humans have multiple papilla)
35
Q

What happens to the nephrone/tubule in renal papillary necrosis? GFR?

A
  • Loss of justamedullary nephrons
  • Cortical nephrons preserved
  • Tubular dysfunction but GFR maintained until disease advanced
36
Q

What is seen here?

A

Left: Normal

Right: Sickle cell renal disease

37
Q

Summary:

  • Tubule and interstitial diseases share a common inflammatory pathogenesis
  • Interstitial renal disease results in characteristic tubule defects
  • Multitudes of common substances can cause TIN-be suspicious and pay attention to prescribed and over-the-counter medications
A

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MS2 Renal (25 decks)

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