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Integrative Nutrition & Pathophysiology > INP midterm - KIDNEY DISEASE > Flashcards

INP midterm - KIDNEY DISEASE Flashcards

Flashcards for the first half of the INP course. This set will cover KIDNEY DISEASE

1
Q

Describe the primary functions of the glomerulus.

A
  • Working unit of filtration: blood enters through afferent arteriole, exits through efferent arteriole
  • Hydrostatic pressure opposes oncotic pressure
    o Oncotic pressure determined by proteins in blood, most notable albumin
  • Usually a limit to size of molecules that can pass through filtrate (proteins usually too big to be filtered)
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2
Q

Describe the primary functions of the the proximal tube.

A
  • Major site of reabsorption – sodium and glucose
  • SGLT 1 & 2 co-transporters
  • Sodium/H+ Antiporter – H+ generated from carbonic acid (CO2+H2O, enzyme: carbonic anhydrase)
  • Basolateral Na/K-ATPase pump maintains gradient
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3
Q

Describe the primary functions of the loop of Henle.

A
  • Sodium reabsorption – especially in the thick ascending limb (TAL)
  • Na/K/2Cl co-transporter
  • Na/K-ATPase pump: maintains gradient
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4
Q

Describe the function of the kidney as it relates to sodium.

A
  • kidney maintains sodium concentration via reabsorption/excretion – maintains blood pressure
  • Excretion depends on:
    o Dietary sodium intake
    o Perceived blood volume
  • Na/K-ATPase pump – maintains electrochemical/concentration gradients that drive reabsorption
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5
Q

Describe the function of the kidney as it relates to water.

A

Plasma osmolality controls secretion of ADH (released from posterior pituitary)
o ADH: increases permeability of
collecting duct – increases water
reabsorption by kidney
§ Syndrome of Inappropriate ADH: increases blood volume & Hyponatremia

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6
Q

Describe the function of the kidney as it relates to acid/base balance.

A
  • Increased Na reabsorption = Increased H+ excretion à more alkaline (higher pH)
  • Bicarbonate: generation requires carbonic anhydrase and glutamine
    o majority reabsorbed in proximal tubule –requires sodium and ATP
    o Some reabsorbed in distal tubule
    o Usually no bicarbonate in urine
-       Acid/Base balance affected by:
        o   Dietary acid load
        o   Volume contraction
        o   Ventilatory failure
        o   Hypokalemia
        o   Increased aldosterone secretion
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7
Q

Describe the function of the kidney as it relates to potassium (electrolyte).

A
  • Reabsorption highest in proximal tubule and TAL of loop of Henle
  • Main sites of regulation = distal tubule and cortical collecting tubule (CCT)
  • K+ secretion depends on:
    o Delivery of sodium
    § Except when:
    · Severely K+ depleted
    · Tubule is severely damaged, in which case sodium does not promote excretion of potassium
    o Presence/absence of aldosterone – (Aldosterone increases secretion/excretion of K+)
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8
Q

Describe the function of the kidney as it relates to magnesium (mineral).

A
  • Filtered and reabsorbed by kidney – main site of reabsorption = TAL of Loop of Henle
    o Na/K/2Cl co-transporter increases electronegative gradient – facilitates voltage-dependent flux of Mg through tight junctions
-       Magnesium levels lowered by:
     o   Diuretics
     o   Kidney transplantation drugs
     o   Recovery from kidney failure
     o   Other drugs
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9
Q

Describe the function of the kidney as it relates to urea.

A
  • Actively transported in kidney

- Kidney failure –> elevated BUN

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10
Q

Describe the function of the kidney as it relates to creatinine.

A
  • Filtered and secreted by kidney

- Bad estimate of eGFR (estimated glomerular filtration rate)

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11
Q

Describe the function of the kidney as it relates to ammonia.

A
  • Generated from glutamine

- Buffers H+ in urine

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12
Q

Describe the function of the kidney as it relates to calcium.

A
  • Majority complexed to phosphate/citrate – some ionized (free)
  • Majority reabsorbed in proximal tubule by passive diffusion (60-70%)
  • Some reabsorbed in CCT (20%)
    o Affected by parathyroid hormone (PTH) and 1,25-OH Vit. D3 (active vitamin D)
  • Remainder in distal tubule
    o Affected by thiazide diuretics, PTH, and 1,25 OH Vit. D3
  • PTH levels are dysregulated when kidneys are damaged
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13
Q

Describe the function of the kidney as it relates to phosphate.

A
  • Phosphorous usually elevated in kidney disease
    o Hyperphosphatemia can be treated by increasing Ca++ intake – binds phosphate
  • Regulated by dietary calcium intake
  • Majority reabsorbed in proximal tubule (Na/PO4 co-transporter)
    o Expression of co-transported modulated by:
    § dietary phosphorous intake
    § FGF23 (fibroblast growth factor)
    § PTH
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14
Q

What are the endocrine functions of the kidney as discussed in class?

A
  • renin secretion
  • erythropoietin synthesis
  • 1-hydroxylation of 25-OH vitamin D à 1,25-OH Vit. D
  • insulin metabolism
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15
Q

What is renin?

A
  • an enzyme secreted in response to decreased Na, sensed by the macula densa cells, which implies low blood volume/low GFR
  • results in increased Na+/water reabsorption
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16
Q

Explain erythropoietin synthesis in the kidney.

A

o Synthesized by peritubular cells of kidney in response to hypoxia

o Binds to EPO receptor on red cell precursors in bone marrow

o Kidney failure –> dec. EPO –> Anemia

17
Q

What does insulin metabolism have to do with kidney?

A
  • insulin is reabsorbed at the proximal tubule and degraded to oligopeptides
  • some insulin is reabsorbed at the distal tubule, which stimulates the reapsorption of
    • sodium
    • phosphate
    • glucose
  • kidney failure prolongs insulin action (T1/2)
18
Q

1-hydroxylation of 25-OH vitamin D –> 1,25-OH Vitamin D.

Explain.

A 
o   Activity increased by:
     §  Hypocalcemia
     §  Hypophosphatemia
     §  Increased PTH
     §  Increased GH

o Activity decreased by:
§ Kidney failure
§ High FGF23

o People with kidney failure given supplement of active vitamin D

o 25 hydroxylation takes place in liver

19
Q

What are the primary symptoms and complications of nephritis (a glomerular disease)?

A
  • Ex. Post-infectious (esp post- strep infection), SLE (lupus), etc.
  • Hallmark: Inflammation of glomerular capillary – usually acute onset
  • Usually resolves with time or treated with steroids
  • Symptoms
    o Urinary casts/hematuria
    o HTN/Edema
20
Q

What are the nutritional considerations for nephritis?

A

o NO protein restriction

o Volume retention treated with diuretics + salt restriction (2g/day)
§ may increase ADH –> hyponatremia

o possible benefits from omega-3 fatty acids (not definitively proven):
§ Fish oils & IGA nephropathy
§ Flaxseed oil & SLE (lupus) nephritis

21
Q

What are the primary symptoms and complications of nephrosis (a glomerular disease)?

A
  • Diagnosis (must have at least 3 of the following symptoms for nephrotic syndrome diagnosis)
    o >3.5 g proteinuria/m^2/day (anything > 500 mg is abnormal)
    o HTN
    o HLD
    o Edema
    o Hypoalbuminemia
  • Hallmark: loss of podocyte foot processes on electron microscopy + subsequent leaking of protein due to loss of filtration barrier
    o Foot processes prevent protein leakage
  • hypoalbuminemia, hypercholesterolemia, edema
  • loss of anti-thrombin 3/ other clotting factors à, thrombotic disorders
  • HTN and kidney insufficiency/failure can develop
22
Q

What are the nutritional considerations for nephrosis?

A

o Hypoproteinemia – high protein diet (1.5g/kg/day) à increased urinary protein excretion
§ Protein restriction has been tried (.8-1.0 g/kg/day) à decreased urinary protein excretion without compromising muscle mass
§ Elimination diets in kids (gluten or dairy) – mixed results

o Edema: (secondary to low oncotic pressure)
§ Sodium restriction may help, but risk of hyponatremia

o HLD: (mech. Unclear)
§ One thought is that liver increases production of cholesterol along with albumin
§ Or loss of sterol regulatory elements
§ Likely: increased PCSK9, decreased LDL receptors
§ Dietary fat restriction (<30%, <10% saturated fat) + conventional lipid lowering therapy (statins/ ezetimibe)
· Shouldn’t use statins to lower cholesterol when albumin is low
§ Other approaches: fish oils (DHA/EPA), plant sterols/stanols

23
Q

What is the definition of acute kidney injury?

A

Deterioration of kidney function that occurs over hours to days and results in accumulation of nitrogenous wastes

24
Q

What is acute tubular necrosis?

A

o most common type of acute kidney injury

o Requires multiple insults to kidney

o Recovery over weeks to months if underlying disease is treated

25
Q

What are the primary nutritional issues in acute kidney injury?

A
  • Hypercatabolic – require increased caloric intake
    o Excessive intake, particularly of CHOs –> increased CO2, which can worsen acidosis (Recommendation = 30-40 kcal/kg/day)
  • TPN (total parenteral nutrition) sometimes used
    o Cannot give lipids with peripheral administration
    o D10 glucose solution with amino acids often given with lipids during dialysis à decreases catabolic rate
  • Kidney Replacement Therapy: typically hemodialysis, sometimes CAVH, CVVH< or CAVHD (rely on patient’s BP)
  • Dialysis allows for increased protein intake (up to 2g/kg) – protein restriction may delay recovery
  • Early ATN usually oliguric (urine volume <500 mL/ 24 hours)
    o Suggested sodium restriction (460-920 mg/day) – difficult because many meds administered with saline solution
    § Free water may lead to hyponatremia – higher risk with syndrome of inappropriate ADH (high ADH secretion)
  • Hypercatabolism/necrotic tissue à potassium release
    o Suggested restriction (1170 – 1950mg/day)
    o Hyperkalemia Treatment:
    § Calcium gluconate
    § Redistribution: bicarbonate & insulin/glucose – forces some K+ out of bloodstream, into cells
    § Dialysis
26
Q

What are kidney stones?

A
  • Stone formation results from supersaturation of the urine with a substance, nucleation, aggregation (crystal growth), crystal retention, and stone formation
  • Stone formation depends on promotors, inhibitors and complexors in the urine
27
Q

What is the most common type of kidney stone?

A

Calcium ocalate (~60%)

28
Q

Who is more likely to get kidney stones?

A
  • Men more likely than women
  • Whites more likely than non-whites
  • Age 40-70
29
Q

How should kidney stones be treated?

A
  • Dissolution therapy (special bath)
  • Lithotripsy
  • Calcium Stones:
    o Do NOT prescribe low calcium diet – makes stone formation worse (increases oxalate)
    o Intake: 1200 mg/day from dietary sources – avoid supplements
30
Q

How can kidney stones be prevented?

A
  • Maintain urine volume (2 – 2.5 L/day)
  • Avoid soda containing phosphoric acid
  • Avoid grapefruit juice (increases oxalate absorption)
  • Tea: max 2 cups/day (high oxalate)
  • Eat oxalate and calcium together
  • Hyperoxaluria:
    o Fat malabsorption à increased oxalate absorption (fat binds calcium in gut)
    § Gastric/intestinal bypass surgery
    § IBD
    § Short gut syndrome
  • Limit animal protein:
    o High animal protein –> increased acid load –> increased excretion of calcium, urate, oxalate, and acid
  • decreased citrate (stone inhibitor)
  • Lemon water or potassium citrate = stone inhibitor/ opposes hypocitraturia
31
Q

What are the nutritional considerations associated with chronic kidney disease?

A
  • Reduce excessive Vit. C intake (< 2g/day) – (ascorbic acid can be converted to oxalate)
  • 1200 mg calcium/day from food
  • 2g sodium/day
  • .8g/kg protein (some plant sources)
  • B6> 40mg/day
  • Avoid colas and phosphate containing beverages
  • DASH diet good
32
Q

What is dialysis?

A

treatment for kidney failure that rids your body of unwanted toxins, waste products and excess fluids by filtering your blood

33
Q

What are the three types of dialysis?

A

1) Hemodialysis (classic version)
2) Continuous Cyclical Peritoneal Dialysis (CCPD)
3) Continual Ambulatory Peritoneal Dialysis (CAPD)

34
Q

What are the complications with CAPD dialysis?

A

o Peritonitis

o Poor peritoneal exchange rate

o Worsening blood glucose control

o Patient burn-out – some opt to switch to hemodialysis

o Umbilical hernia

o leak

35
Q

Discuss the nutritional considerations associated with drugs used for renal transplant (you do not need to know the drugs).

A
  • glucose intolerance
  • increased protein catabolism
  • sodium retention
  • decreased renal absorption of Ca (cal lead to osteoporosis/increased PTH)
  • hypertriglyceridemia/hypercholesterolemia
  • hyperkalemia
  • new onset diabetes
  • hypomagensia
36
Q

What are the dietary recommendations for transplant recipients?

A

o Avoid excess protein intake (<1g/kg) if kidney insufficiency, no restriction if normal

o If hypertensive – sodium restriction (2g/day)

o If hyperkalemic – potassium restriction (2g/day)

o Calcium supplementation – 1200-1500 mg/day

o Magnesium supplementation – 400-800 mg/day as oxide or chelate

o Limited cholesterol and sat. fat intake

o Weight gain in first 6 months is a serious issue

37
Q

How does CCPD work?

A
  • similar to CAPD – machine does exchanges throughout the night – dwell period is during the day
  • better for kids – yields better growth
  • no sodium restriction (up to 6g/day lost in dialysate)
38
Q

How does hemodialysis work?

A

blood pump creates hydrostatic pressure that allows for external filtration of blood using membranes – usually takes 3-4 hours and must be done 3 times per week

  • Dialysate solutions contain:
    o Bicarbonate buffers
    o Sodium, calcium, potassium (concentrations can be varied)
    o Glucose
  • fluid restriction important

Integrative Nutrition & Pathophysiology (15 decks)

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