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LMP301 (Winter 2022) > L6 - Kidney Dysfunction/Disease > Flashcards

L6 - Kidney Dysfunction/Disease Flashcards

1
Q

4 Roles of the Kidney

A
  1. Filtration of blood
    • Remove wastes
    • Maintain appropriate [electrolyte]
    • Maintain acid/base balance
  2. Regulation of blood volume and blood pressure
    • Kidneys receive 20% cardiac output
    • (RAAS and ADH effect on Kidney)
  3. Activation of 25-hydroxyvitamin D (to 1,25dihydroxyvitamin D)
  4. Production of hormone erythropoietin
    • Kidneys sense Reduction in O2 delivery to tissues by blood and releases EPO
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2
Q

What is Kidney Disease/injury?

A

Abnormality of kidney structure or function that can occur abruptly and resolve or persists and become chronic

  1. Acute Kidney Injury
  2. Chronic Kidney Disease
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3
Q

What are the consequences? Compromise in the 4 roles

A
  1. Increase in waste in the circulation
  2. Disequilibrium of fluids and electrolytes
  3. Decreased vitamin D activation (decreased calcium absorption → hypocalcemia)
  4. Decreased erythropoiesis (→ anemia)
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4
Q 
What are biochemical evaluations of kidney
function and structure?
A

Urine Marker
1. Primary biomarker for kidney damage is urine albumin
• ACR: Urine albumin: Urine Creatinine: < 30 mg/(g of creatinine)
• AER: Urine Albumin/24hr urine collection: <30 mg/24hrs

Serum Marker
2. Primary biomarker for kidney function is glomerular filtration rate (GFR)
• eGRF < 60 mL/min/1.73m2
• Typically estimated (Calculated) from serum creatinine or cystatin measurements
• Indicator of number of functioning nephrons (functional capacity) that enable proper
filtration

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5
Q

Why do we care about eGFR?

A
  1. Easily understood by nurses, RT, physicians, others - best overall index
    of kidney function in health or disease GRF (< 60 mL/min/1.73m2)
  2. eGFR allows to better account biological variation in creatinine (dependent on muscle mass: age, gender, ethnicity?)
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6
Q

Creatinine

A

• Waste product from muscle breakdown of creatine
• Produced at daily constant rate and eliminated mostly by glomerular filtration
• Most utilized filtration marker
(Primary marker for evaluating and monitoring renal function (eGFR))

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7
Q

Cystatin

A
  • Alternative endogenous filtration marker;
  • Unlike creatinine, it is a protein that is a protease inhibitor (produced by almost all tissues)
  • Reduced influences of age, gender, weight, and muscle mass compared to serum creatinine
  • Not secreted by proximal tubular cells Immunoassay
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8
Q

Clearance of a substance (e.g. creatinine) from the plasma as it pass through the glomerulus at a given rate

A

(Urine Creatinine/Serum Creatinine)
×
(Urine Volume (mL)/Collection Time (min))

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9
Q

Measured GFR

A

by determining clearance rate of exogenous substance (e.g. Iohexol administration by IV)
• Invasive

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10
Q

Estimated GFR

A

by measuring endogenous substance
• – e.g. serum creatinine (or cystatin)
• Equations that transform serum creatinine into eGFR
• More convenient; no need for urine collection period

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11
Q

Urea- Waste product from protein break down

A

1) Formed by the liver and excreted by the kidney (40-50% reabsorbed by passive diffusion)
2) If GFR decreased, urea in the blood increases
3) How is it formed? From Ammonia (from protein catabolism) that is converted to urea via urea cycle in the liver.
4) Ammonia is toxic (can cross BBB) and needs to be detoxified by conversion to urea or
elimination thru NH4

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12
Q 
Tests to assess kidney
function - Why is it useful to measure?
A
  • Increased when kidney function is impaired

* Commonly measured in dialysis patients – addresses dialysis adequacy

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13
Q

Phosphorous

A

• Kidney are responsible for excretion of excess Phosphates
• Reabsorption occurs in predominantly in the proximal tubules (e.g Na+ dependent phosphate
cotransporters) → balance between intake and outtake
• Kidney function decline leads to decline in PO4(3-) excretion → serum PO4(3-) will rise (Not always seen early stages)

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14
Q

Calcium

A
  • PO4(3-) rise will suppress active form of Vitamin D (1, 25dihyrdroxyvitamin D)
  • Decreased in CKD (Not always seen early stages)
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15
Q

Hemoglobin

A

Anemia develops during CKD

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16
Q

Clinical Significance of Acute Kidney Injury (AKI)

A

1) Common yet under recognized (1.2 Million people/year)
2) Various etiologies
3) Costly
• Increased length of stay
• Increased risk of mortality
• Increased risk of chronic kidney
disease (CKD)

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17
Q

Diagnostic Criteria of AKI

A

1) Reduction in urinary output (little to anuria)
2) Increased serum creatinine

• Either of these criteria can be used to define the 3
stages of AKI (1 – 3)

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18
Q

Clinical Management

A
  • Treat the underlying disease
  • Discontinue or dose-adjust nephrotoxic drugs
  • Treat electrolyte disturbances
  • Optimize fluid balance and hemodynamics
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19
Q

Etiology of AKI

A 
1) Prerenal-AKI
• Decreased renal perfusion
2) Intrinsic-Renal
• Caused by processes within kidney
3) Postrenal
• Inadequate drainage of urine
20
Q

Prerenal AKI

A
  1. Kidneys do not get adequate blood supply (hypovolemia)
    • E.g. hemorrhage
    • E.g. dehydration, vomiting, reduced fluid intake
  2. Effective circulating volume depletion: kidneys not perfused despite
    volume is not depleted (e.g. hypervolemic scenarios)
    • E.g. congestive heart failure: heart does not pump adequately
    • E.g. cirrhosis: scarring of the liver impedes blood flow to kidney (hepato-renal
    syndrome)

• Note: if blood supply is restored in timely manner, kidneys will work again

21
Q

Intrinsic Renal Injury – direct insult to kidney

A 
1) Acute tubular necrosis
• Nephrotoxic medications
• Radiographic contrast agents
• Cardiac surgery
2) Diseases of the tubules or glomeruli (Glomerulopathies)
• Drugs, ischemia, infection, autoimmune disease, genetics
• Nephrotic syndrome
• Nephritic Syndrome
22
Q

Diseases of the Glomeruli

A

1) Nephrotic Syndrome
• Damage to the filtering mechanism of the glomerulus
• Protein wasting (proteinuria) → hypoproteinemia (decreased serum proteins) (hypoalbuminemia)
• Hypoproteinemia → intravascular fluid is hypotonic → edema
• Hyperlipidemia → Liver tries to increase the production of serum proteins (since they are being lost in the urine), and in doing so it also increases lipid productions

2) Nephritic Syndrome
• Hypertension, hematuria, proteinuria
• Systemic inflammatory/immune complex disease or infection (vasculitis, lupus)
(IgA Nephropathy - Deposition of IgA into the glomeruli)

23
Q

Hematuria: Blood in the Urine

A

1) Presence of three or more red blood cells (RBCs) per high-powered field in 2 of 3 urine samples
• Rule out menstrual contamination
2) Early indicator in ADPKD
• Most common inherited renal disorder
• Progressive increase in the number and size of renal cysts accompanied by gradual loss of kidney function
(falling eGFR)
3) Urine (dipstick) chemistry
• Make use of peroxidase activity of heme moiety from Hb or Myoglobin in the presence of H2O2

Chromogen on pad + H2O2 → oxidized chromogen (color change)

4) Urine microscopy can indicate the source of hematuria
• RBC casts often suggests renal (glomerular) source
• Cast: cylindrical or convoluted objects formed in the renal tubules composed of mostly proteins and cells

24
Q

What is Pseudohematuria or reasons for FP?

A

• Menstrual blood
• FP on dipstick: oxidizing agents (bleach), microbial peroxidase
• Hemolytic anemia (Hb in urine)
• Myoglobin
(precipitate out Hb using ammonia sulfate and retest. If still positive, then it’s myoglobin)

25
Q

Urinary Casts?

A

(A) Renal tubular epithelial cell cast, often seen with acute tubular injury/necrosis
(B) Muddy brown granular casts seen with severe acute tubular necrosis
(C)White blood cell cast seen with acute interstitial nephritis
(D)Red blood cell cast seen with acute glomerulonephritis

**Check image

26
Q

Stones and Crystals in Urine?

A

1) Nephrolithiasis (or urolithiasis): Process of Kidney stone formation
2) Most pass spontaneously, some do not (determined by size)
3) Formed when excretion of certain components (found in the stone) is
increased
• Most commonly Ca2+, PO4(3-), and oxalate are the most common chemical constituents

27
Q

Kidney Stones? What happens after formation of stones?

A

Stones stay in the kidney or travel down the
urinary tract.

Stones that don’t move may cause a back-up of
urine in the kidney, ureter, the bladder, or the
urethra → can be painful

28
Q

Post-Renal AKI

A

1) Refers to the ureters, bladder, and urethra
2) Blockage from passing kidney stones into ureters
3) Tumor in genitourinary system (e.g. bladder, prostate)
4) Can lead to hydronephrosis
• Build-up of urine leading to swelled kidneys
• Happens when urine cannot drain out from the kidney to the bladder from a blockage or obstruction

29
Q

Etiology of AKI

A 
1) Prerenal-AKI
• Decreased renal perfusion
2) Intrinsic-Renal
• Caused by processes within kidney
3) Postrenal
• Inadequate drainage of urine
30
Q

Future of AKI Diagnosis?

A

From Reactive to Pro-Active

31
Q

Other Markers of AKI?

A 
Tubular Stress/Injury
• TIMP2
• IGFBP-7
• NGAL
• L-FABP
• IL-18

Decreased Glomerular Filtration
• Creatinine, Serum
• Cystatin, Serum

32
Q

Chronic Kidney Disease?

A

1) Abnormalities of kidney structure or function, present for ≥ 3 months
with implications for health
• i.e. GFR < 60ml/min/1.73m2 for ≥ 3 months
• Albuminuria (common)
2) Kidney Failure is the “end” stage of CKD

33
Q

Chronic Kidney Disease on eGFR

A

**Check Image

34
Q

CKD Stages based on Albuminuria

A

**Check Image

35
Q

Risk Factors of Chronic Kidney Disease?

A
  • AKI
  • Hypertension
  • Diabetes
  • Cardiovascular disease
  • Old age
36
Q

Metabolic Acidosis of CKD?

A

1) Old term: uremic acidosis
2) Increase in severity of metabolic acidosis as GFR declines
3) Anion GAP is elevated or normal (non-anion gap)
4) Decrease in NH4+ excretion
5) Seen by increased Urea, decreased HCO3-
• Defined by <22 mmol/L of HCO3- in CKD patients
• Patients given oral bicarbonate (alkali) supplements

37
Q

CKD Reversibility

A
  • Most causes of CKD are irreversible (Chronicity ≠ Irreversibility)
  • Kidney failure can be reversed by transplantation
38
Q

CKD Long course

A

• Patients can have 1 or more episodes of AKI superimposed in CKD

39
Q

CKD Treatment

A

Aimed at slowing progression to kidney failure
• E.g. diet and lifestyle changes, improving blood glucose control in diabetes, blood
pressure control

40
Q

Renal Replacement Therapy

A 
Techniques to temporarily or permanently remove toxic substances from blood
1) Dialysis
• Hemodialysis
• Peritoneal dialysis
2) Kidney Transplant
41
Q

Hemodialysis

A

1) Blood is passed through a dialyzer (outside the body)
2) Instrument has checks to monitor rate of blood flow out and in

3) Heparin infusion to minimize clotting
• Other medications: EPO

4) Dialysis solution in the filter allows waste from your blood to be mixed and filtered
• Solution is adjusted based on laboratory results (Ca2+, PO4(3-),K+, HCO3-and PTH)
• Pre/Post dialysis chemistry tests

42
Q

Peritoneal Dialysis

A
  • Surgery to place a catheter in the abdominal cavity (peritoneum)
  • Peritoneum acts as the dialysis membrane
  • Dialysis solution (Dialysate) is infused through a catheter to allow for waste and fluid absorption
  • Dialyzate (now with wastes) are then drained through into a waste bag
  • Repeat with fresh dialysis solution
43
Q

Kidney Transplant

A

1) Best quality of life
2) Lab Medicine plays an important role Pre-transplant assessment; Aids for donor matching and anti-rejection drugs
• Lab tests to ensure recipient (and Donor) is appropriate (Blood typing, Human Leukocyte Antigen typing, Viral infectious disease (cytomegalovirus, Hepatitis B, Hepatitis C, and HIV))
• Cancer screening (colon cancer screen, pap test, mammogram)
• TB Skin test

44
Q

Post- Kidney Transplant

A

Patients placed on lifelong immunosuppressant
• E.g. Cyclosporine, tacrolimus, sirolimus
• Laboratory tests to measure immunosuppressant (drug) level in blood. Why?
• Therapeutic Drug Monitoring
• These drugs are nephrotoxic at high concentrations
• Low concentration may lack efficacy in preventing rejection
• Therefore, lab test used monitor to ensure [ drug ] within therapeutic range; (Not too low, not too high)
• Laboratory tests helps monitor and prevent rejection

45
Q

Candidates for Screening Vitamin D

Deficiency

A

Kidney Transplant patients
• Advised to avoid or protect themselves from sun
• Medications taken after transplant, e.g. prednisone reduce Vitamin D
• Should be screened and monitored
• Deficiency can predispose patients to increased risk of transplant rejection

LMP301 (Winter 2022) (10 decks)

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