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PHA 315 > Nephrotoxicity > Flashcards

Nephrotoxicity Flashcards

1
Q

Functions of the kidney

A
  • Filtration and excretion of metabolic waste products (urea and ammonium)
  • Regulation of necessary electrolytes, fluid, and acid-base balance.
  • Stimulation of red blood cell production.
    -Regulation of blood pressure via the renin-angiotensin-aldosterone system, controlling reabsorption of water and maintaining intravascular volume.
  • Reabsorption of glucose and amino acids
  • Hormonal functions via erythropoietin, calcitriol, and vitamin D activation.
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2
Q

Types of nephrotoxicity

A

Acute glomerulonephritis (GN)
Acute kidney injury (AKI) or Acute Renal Failure (ARF)
Acute tubular necrosis (ATN)
Chronic Kidney Disease

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3
Q

Markers of glomerular nephrotoxicity

A

Collagen IV
Cystatin C
Total protein

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4
Q

Markers of proximal tubular nephrotoxicity

A

Alpha- GST
Clusterin
Microalbumin
Osteopontin
Alpha 1 microglobulin

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5
Q

Markers of loop of Henle nephrotoxicity

A

NHE3
Osteopontin

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6
Q

Markers of collecting duct nephrotoxicity

A

Calbindin d28
RPA-1

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7
Q

3-part sequence of ATN - Acute Tubular Necrosis

A

Initiation
Maintenance
Recovery

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8
Q

Describe the initiation phase of ATN

A

Acute decrease in glomerular filtration rate (GFR) to very low levels, with a corresponding sudden increase in serum creatinine and blood urea nitrogen (BUN) concentrations.

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9
Q

Describe the maintenance phase of ATN

A

Sustained severe reduction in GFR that persists for a variable length of time, most commonly 1-2 weeks.

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10
Q

Describe the recovery phase of ATN

A

The recovery phase of ATN is characterized by regeneration of tubular epithelial cells.

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11
Q

Nephrotoxicants causing pre-renal damage

A

Diuretics
Angiotensin receptor agonists
Antihypertensive drugs

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12
Q

Nephrotoxicants causing vasoconstriction damage

A

NSAID
Cyclosporine
Tacrolimus
Amphoterin B

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13
Q

Nephrotoxicants causing tubular damage

A
  • Aminoglycosides
  • Cisplatin
  • Pentamidine
  • Radiocontrast agents
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14
Q

Nephrotoxicants causing endothelial damage

A

Cyclosporine
Mitomycin
Conjugated oestrogens

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15
Q

Nephrotoxicants causing interstitial nephritis

A

Antibiotics
NSAIDs
Diuretics

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16
Q

Nephrotoxic metals

A

Cadmium
Chromium
Mercury
Lead
Arsenic

17
Q

Mechanism of action of nephrotoxicity

A

ACTTIR

Altered intraglomerular hemodynamics
Tubular cell toxicity
Inflammation
Crystal nephropathy
Rhabdomyolysis
Thrombotic microangiopathy

18
Q

GFR depends on

A

4 factors:
(1) adequate blood fl ow to the glomerulus
(2) adequate glomerular capillary pressure
(3) glomerular permeability
(4) low intratubular pressure.

19
Q

Ways through which GFR is reduced

A

(B), Afferent arteriolar constriction decreases GFR by reducing blood flow, resulting in diminished capillary pressure.

C), Obstruction of the tubular lumen by cast formation increases tubular pressure; when tubular pressure exceeds glomerular capillary pressure, filtration decreases or ceases.

(D) Back-leak occurs when the paracellular space between cells increases and the glomerular filtrate leaks into the extracellular space and bloodstream

20
Q

Drugs that cause tubular cell toxicity do so by

A

impairing mitochondrial function, interfering with tubular transport, increasing oxidative stress, or forming free radicals

21
Q

Examples of drugs that cause tubular cell toxicity

A

Hespera, cisplastin, tenofovir.

22
Q

Examples of drugs that cause glomerulus inflammation

A

Medications such as gold therapy, hydralazine, NSAIDs have been reported.

23
Q

Examples of drugs that cause crystal nephropathy

A

Antibiotics (e.g., ampicillin, ciprofloxacin, sulfonamides)
Antivirals (e.g., acyclovir, foscarnet, ganciclovir [Cytovene])

24
Q

Examples of drugs that cause rhabdomyolysis

A

Cocaine
Heroin
Methamphetamine
Alcohol

25
Q

Mechanisms of renal injury secondary to drug-induced thrombotic microangiopathy include

A

an immune-mediated reaction or direct endothelial toxicity.

26
Q

Drugs most often associated with this thrombotic microangiopathy include

A
  • antiplatelet agents (e.g., clopidogrel [Plavix]
  • cyclosporine
  • mitomycin-C
27
Q

In vivo models to study renal function

A

Continuous micro perfusion
Stopped-flow micro perfusion
Free-flow micro puncture
Confocal microscopy

28
Q

Ex vivo models to study renal function

A

Isolated perfused kidney
Isolated perfused tubules

29
Q

In vitro models to study renal function

A
  • Renal slices
  • Glomerular cells
  • Tubular epithelial cells
  • Fibroblasts
30
Q

Renal protective strategies

A
  • Avoid routine use of clinically confirmed nephrotoxic drugs like NSAIDS, cyclosporine low-dose dopamine, diuretics
  • Avoid routine use of high-volume doses of contrast media
  • Avoid long periods of hypotension
31
Q

How man takes in nephrotoxicants

A

Pesticide/Fertilizer Farmland Well Water Drinking Kidneys

Some are inhaled or absorbed through the skin forming glyphosate-metal complex within circulation. In the kidneys, the complex causes oxidative stress, apoptosis, necrosis leading to glomerular sclerosis and collapse, proximal tubular damage and interstitial damage. All these = CKD.

32
Q

Nephrotoxicant drugs that cause crystalluria

A

Methotrexate
Sulfonamide

PHA 315 (6 decks)

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