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Pathophysiology - Urinary Tract > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is the definition of Chronic Kidney Disease (CKD)? How does it relate to GFR?

A

Kidney damage or decreased kidney function for three or more months

Kidney damage is either defined be a specific marker, or is a reduction in GFR to less than 60 mL/min*** for three months(half normal)

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2
Q

What are the six possible markers of kidney damage that would define CKD (other than GFR reduction)?

A
  1. Albuminuria
  2. Urine sediment abnormalities - RBC casts, WBC casts, oval fat bodies
  3. Electrolyte or other abnormalities caused by tubular disorders - i.e. RTA, Fanconi, nephrogenic DI
  4. Pathological abnormalities by kidney biopsy
  5. Imaging abnormalities (CT, ultrasound, etc)
  6. History of kidney transplant
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3
Q

What is the definition of albuminuria for chronic kidney disease? Is this a common cause for CKD diagnosis?

A

Albumin excretion rate of >30 mg/day
or
Urine albumin to creatinin ratio >30mg albumin / gram creatinine

Normal for both is <10

Yes -> most common cause

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4
Q

What imaging abnormalities might be found for diagnosis of CKD?

A

Polycystic kidney disease, hydronephrosis, small echogenic kidneys, renal masses

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5
Q

How is GFR semi-precisely estimated in a clinical test?

A

Clearance of creatinine, with urine collected over 24 hours (not perfect because creatinine is slightly secreted)

Ccr = Ucr*V/Pcr

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6
Q

What is the Cockcroft-Gault equation for estimating GFR based on creatinine?

A

Ccr = (140-age)(body wt in kg) / (72 * serum creatinine in mg/dL) * 0.85 if female

0.85 in females because women are less muscular for the same body weight -> less creatinine should be being produced

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7
Q

Based on the Cockrcroft-Gault equation, if two people have the same serum creatinine, what will be the person with the highest GFR (ideally)?

A

Young male who is very heavy (high body wt)

Basically young male body builders

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8
Q

What equation takes into account a patient’s race, BUN, and albumin as well? What affect does race have?

A

Modification of Diet in Renal Disease equation (MDRD)

If you are black, your GFR is increased -> kidneys are overactive

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9
Q

What equation is thought to be more accurate than MDRD if eGFR > 60 mL/min?

A

CKD-EPI equation

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10
Q

Is serum creatinine a good marker for GFR alone? When can it not be used?

A

No -> it must be used in combination with age, sex, wt

Cannot be used whenever it is unstable

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11
Q

If a person is very muscular and eats a lot of meat, will predicted GFR change?

A

Yes -> GFR will be estimated to be too low by the equation -> buildup of creatinine due to high intake

In reality, the GFR will be higher

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12
Q

What drugs can influence GFR calculation and why?

A

Cimetidine and trimethoprim

-> block tubular secretion of creatinine, raising serum creatinine levels -> causes an artificial fall in calculated GFR even though it hasn’t changed

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13
Q

What is a new endogenous marker which may take the place of creatinine in the future?

A

Cystatin C -> produced by all nucleated cells, rate of production is relatively constant

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14
Q

How does criteria for CKD change with age in terms of GFR?

A

It doesn’t -> stays at 60 mL/min

-> even though your GFR drops when you age, it should still stay above 60

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15
Q

What are the two factors which help classify patients with CKD? What is this staging useful for?

A
  1. GFR
  2. Degree of albuminuria

Staging useful for risk stratification and guiding management of patients

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16
Q

What happens as you go from stage G1-G5, and what is G5 marked by? What is this called?

A

Progressive decline in GFR

G5 is marked by GFR<15 -> dialysis-dependent kidney failure (renal replacement therapy)

If you need renal replacent therapy (kidney transplant or dialysis), it is called End Stage Renal Disease

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17
Q

What effect does albuminuria have on all-cause mortality depending on GFR?

A

Independent of GFR, a rise in albuminuria (A1->A3) will cause a rise in all-cause mortality, cardiovascular mortality, progressive kidney disease, AKI

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18
Q

What are the two most common causes of CKD?

A

Diabetes and hypertension

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19
Q

What initiates CKD in general and what happens immediately afterwards?

A

Loss in number of functioning nephrons (whatever the cause)

  • > decreased perfusion pressure and solute delivery to macular densa due to loss of functioning in nephrons leads to afferent arteriolar vasodilation to increase blood flow, and activation of RAA system. AT2 will vasoconstrict the efferent arteriole
  • > increases GFR = hyperfiltration of remaining functional nephrons
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20
Q

What are the consequences of the increased intraglomerular pressure and hyperfiltration in the remaining functional nephrons?

A

This maintains the GFR initially, but leads to capillary wall stretching, which promotes mechanical injury to endothelial cells, mesangial cells, and podocytes

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21
Q

What happens when there is mechanical injury to endothelial cells in CKD?

A

Disintegration or detachment of endothelium leads to local exposure of GBM, and ECM is exposed to bloodstream.

Leads to microthrombi with thrombosis -> glomerular tuft becomes partially or totally fibrotic after organization

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22
Q

What happens when there is mechanical injury to mesangial cells in CKD?

A

Synthesis of cytokines, growth factors, and inflammatory eicosanoids.

Mechanical stretch also stimulates collagen production

  • > fibrosis and progressive destruction of glomeruli
  • > when complement and Ig’s leak in it can maintain the inflammation
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23
Q

What leads to albuminuria in CKD?

A

Mechanical injury to podocyte -> rupture of slit diaphragm, impairing glomerular barrier function, with podocyte rupture, necrosis, or apoptosis.

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24
Q

How does plasma protein leak into the interstitium in CKD?

A

Loss of podocytes favors fixation of glomerular tuft to parietal layer of bowman’s capsule.

As the glomerular tuft becomes stuck to the wall, sclerosis allows plasma proteins to leak into the interstitium

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25
Q

What are the consequences of plasma proteins leaking into the interstitium due to podocyte loss in CKD?

A

This “misdirected filtration” will collect surrounding the glomerulus and around extensive portions of tubular segments
-> inflammatory reaction and subsequent fibrosis

26
Q

Once CKD is in progress, can it be stopped?

A

Hell no homie! Once enough normal glomeruli have been loss, the hyperfiltration will just cause gradual progression of the disease

Progression starts once roughly 50% of GFR has been lost

27
Q

How does proteinuria itself contribute to CKD?

A

Proteinuria stimulates increased proximal tubule protein reabsorption rate

  • > need to make more proteolytic enzymes to reuptake them
  • > enzymes will destroy the tubules and leak into interstitium, causing more inflammation and fibrosis
28
Q

How does hypertension by itself contribute to progression of CKD? How does this relate to CKD management?

A

Hypertension increases the GFR, which further damages tubules, causing more renin release by remaining tubules, worsening hypertension, and further worsening damage in a vicious cycle

Treatment of hypertension is a mainstay of CKD treatment

29
Q

What are two genetic / hereditary factors which can predispose to CKD and how? Which mutation is worse in ADPKD?

A
  1. Decreased number of nephrons at birth
  2. Problem genes which predispose to kidney disease
    i.e. Apoprotein L1 for FSGS / HIV nephropathy
    or
    PKD1 is worse than PKD2 mutation in ADPKD
30
Q

How do obesity and iron toxicity contribute to CKD?

A

Obesity - massive obesity will increase hyperfiltration and CKD progression

Iron toxicity - glomerular damage will lead to increased filtration of transferrin complex (normally not transferred) -> high iron leads to hydroxyl free radical formation in tubule

31
Q

How does CKD affect sodium balance?

A

Inability to adapt to acute changes in sodium loss or increase sodium loading

  • > Generally Na+/H20 retention
  • > will also not be able to stop secreting a base level of sodium in diarrhea (unable to adapt)
32
Q

How is water balance affected by CKD?

A

Impaired urinary concentration and dilution, with moreso impaired concentration
-> water deprived patients will be more prone to hypernatremia

33
Q

Is hyperkalemia generally a problem in CKD? Why or why not? When is it a problem?

A

No -> as GFR declines, aldosterone-mediated K+ secretion increases, and also colon begins secreting more K+

Hyperkalemia doesn’t become a problem til GFR drops <20 mL/min

34
Q

What are some conditions which may cause hyperkalemia even if GFR is high?

A
  1. Diabetes - hyporeninemic hypoaldosteronism
  2. Renal diseases affecting distal nephron (sickle cell, obstructive nephropathy)
  3. Acidosis
  4. Hemolysis
  5. Increased intake
  6. K+ sparing diuretics and NSAIDs
  7. Oliguria / volume depletion

-> all should be avoided in CKD

35
Q

What is done to correct hyperkalemia when it develops in CKD?

A

Low potassium diet, loop diuretics, kayexalate, correction of metabolic acidosis

36
Q

What happens to acid-base balance in early vs late CKD?

A

Early - non-anion gap metabolic acidosis -> ammonia production is not adequate due to too low # of nephrons

Late - anion gap metabolic acidosis -> GFR becomes so low that sulfate, urate, hippurate, and phosphate are retained

37
Q

Why does metabolic acidosis worsen kidney disease progression?

A

Activates complement (acidic conditions, like PNH) and increases production of endothelin-1, which cause inflammation and fibrosis

38
Q

What are two factors which cause anemia in CKD?

A
  1. Decreased synthesis of erythropoietin by peritubular fibroblasts
  2. Decresaed RBC survival -> due to RBC microvascular trauma and oxidative stress
39
Q

What are disorders of the bone called in CKD?

A

CKD-MBD - Chronic Kidney Disease Mineral and Bone Disorder

40
Q

What is the underlying factor which drives secondary hyperparathyrodism in CKD? What other hormone acts with it?

A

Phosphate retention due to declining GFR
-> PTH upregulated to help secrete phosphate

FGF23 - another hormone which increases urinary phosphate excretion

41
Q

What produces FGF23 and what does it do?

A

Produced by osteocytes

  • > promotes urinary phosphate excretion
  • > inhibits calcitriol formation which thereby reduces phosphate absorption by GI tract
42
Q

What happens to calcitriol levels in CKD and why?

A

They decrease due to:

  1. Increased FGF23
  2. Decreased calcitriol production due to decreased nephron mass
  3. Phosphate retention directly inhibits 1-alpha-hydroxylase
43
Q

What does decreased calcitriol due to PTH levels?

A

Increases it because:

  1. Will decrease levels of ionized calcium -> stimulates PTH
  2. Low calcitriol DIRECTLY stimulates PTH
44
Q

What happens to the calcium sensing receptors in CKD?

A

They are reduced in number and thus become less sensitive

-> higher serum Ca+2 levels are needed to suppress PTH, so PTH rises

45
Q

What overall happens to phosphorus, calcium, and PTH as CKD progresses?

A

Phosphorus - early on, phosphate levels are maintained at low levels by increasing PTH secretion, but later rises due to inadequate secretion

Calcium - Falls, due to lack of calcitriol from increased FGF and other factors

PTH - progressively rises

46
Q

What bone disease happens secondary to secondary hyperparathyroidism?

A

Osteitis fibrosa cystica
-> increased osteoclasts, abnormal bone turnover and fibrosis, with formation of bone cysts and hemorrhagic elements which make them appear brown in color

-> this is the disease caused by renal osteodystrophy, the primary problem caused by CKD

47
Q

What part of the bone changes in renal osteodystrophy -> osteitis fibrosa cystica and give some skeletal examples?

A

Subperiosteal thinning of bones

  • > Resorption of phalanges
  • > resorption of distal clavicle
  • > salt and pepper appearance of skull (lesions of bone)
48
Q

What supplements / dietary changes are given to prevent calcium balance diseases in CKD?

A

Low phosphorous diet

Calcium-containing phosphate binders for GI tract -> precipitate out the phosphate from the food

-> inhibition of phosphate absorption

49
Q

How does extraskeletal calcification happen passively in CKD, and why does this worsen outcomes?

A

Passively -> increased phosphate levels will precipitate out with calcium in blood vessels and cardiac valves
= metastatic calcification
-> leads to increased cardiovascular morbidity and mortality

50
Q

How can extraskeletal calcification be an active process?

A

Elevated phosphorus (as well as elevated urea and other products) leads to upregulation of osteoblast production of a specific core binding factor Cbfa1

  • > vascular smooth muscle cells are made into osteoblast-like cells
  • > new osteoblast like cells produce bone matrix and lead to calcification
51
Q

What is calciphylaxis and what will it cause?

A

Medial calcification of small arterioles of the skin, happens in advanced CKD
-> leads to occlusion of vessels and ischemic, painful ulcerations of skin

52
Q

What is the leading cause of death in CKD and why?

A

Cardiovascular disease, due to increases in both traditional and nontraditional risk factors

Traditional risk factors - HTN, diabetes, etc

Nontraditional risk factors - hyperphosphatemia, valvular calcification, chronic inflammation

53
Q

What are the earliest symptoms of CNS complications of CKD?

A

Mild disturbances in memory and concentration, as well as sleep disturbance, starting around stage 3

54
Q

What are the late stages of neuromuscular complications in CKD?

A

Neuromuscular irritability, with cramps, twitching, asterixis (flapping), myoclonus, seizures, and coma

Stage 4 - sensory > motor peripheral neuropathy

55
Q

What GI abormalities are associated with CKD?

A

Unpleasant metallic taste due to ammonia in saliva -> dysgeusia

Gastritis, ulceration, nausea, vomiting, GI bleeding

56
Q

What happens to glucose metabolism in CKD and why? Will patients need more or less insulin as GFR drops?

A

Insulin resistance -> due to accumulation of uremic toxins

Decreased insulin degradation - insuulin normally taken up by PCT cells and degraded
-> when GFR declines, insuline half-life is prolonged

In ESKD, less insulin is needed due to longer halflife

57
Q

What happens to reproductive function in CKD?

A

Women - high rate of spontaneous abortion, inability to carry pregnancy to term

Men - oligospermia, reduced testosterone, sexual dysfunction

58
Q

What does CKD do to growth in children?

A

Increased resistance to growth hormone -> growth retardation in children

59
Q

What happens to the skin in CKD?

A

Pruritis - due to uremia

60
Q

What are the indications for renal replacement therapy in patients with CKD?

A
  1. Volume overload refractory to diuretics
  2. Persistent hyperkalemia refractory to medical treatment
  3. Severe metabolic acidosis which is refractory
  4. Uremic symptoms and signs: pericarditis, encephalopathy, neuropathy
61
Q

How does hemodialysis work?

A

Patient’s blood passes through a hemodialysis filter, and metabolic waste / extra chemical move down their concentration gradient out of the body

Need to do it several hours a day three times a week

62
Q

How does peritoneal dialysis work?

A

Uses peritoneal membrane as a semi-permeable membrane to diffuse out urea / toxins

-> Fluid is put into peritoneal cavity, allowed to equilibrate for several hours, and then replaced with new fluid

Pathophysiology - Urinary Tract (14 decks)

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