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Renal System > The Urinary Tract, Kidney: Chronic Kidney Disease > Flashcards

The Urinary Tract, Kidney: Chronic Kidney Disease Flashcards

1
Q

How is chronic kidney disease defined as?

A

Kidney damage or decreased GFR of less than 60mL/min/1.73m^2 for at least 3 months

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2
Q

What is ESKD a result of?

A

Progressive scarring from any type of kidney disease (glomeruli, tubules, interstitium, and vessels being sclerosed)

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3
Q

What are the most common causes of chronic kidney disease?

A

Diabetes (up to 50%)
Hypertension (up to 30%)
Glomerular diseases
Urinary tract obstruction

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4
Q

What is the treatment of chronic kidney disease?

A

Dialysis or transplantation

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5
Q

What is the criteria for chronic kidney disease? (7)

A

Either one of the following must be present for > 3 months:
1. Albuminuria
2. Hematuria
3. Electrolyte abnormalities due to renal tubular disorders
4. Abnormalities detected on histopathology
5. Structural abnormalities detected on imaging
6. History of kidney transplant
OR
Decreased GFR with or without kidney damage

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6
Q

How can hypertension lead to chronic kidney disease?

A

Glomerular and vascular changes
Interstitial nephritis
Chronic hypertension

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7
Q

What is the pathogenesis of glomerular and vascular changes in relation to CKD?

A

Elevated systemic BP causes a hypertrophic response, leading to intimal thickening of the large and small vasculature

The mechanism is compensatory at first but later on leads to glomerular damage:
- Global sclerosis
- Focal segmental sclerosis

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8
Q

What is global sclerosis?

A

Ischemic injury to the nephrons causes death

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9
Q

What is focal segmental sclerosis?

A

Glomerular enlargement for compensation of the loss of nephrons in other areas of the kidney

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10
Q

What is the pathogenesis of interstitial nephritis in relation to CKD?

A

The vascular and glomerular disease leads to tubular atrophy and intense chronic interstitial nephritis

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11
Q

What is the effect of chronic hypertension on the kidneys?

A

Chronically, these changes lead to tubular and glomerular loss, causing nephron loss

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12
Q

What is the effect of nephron death?

A

Fewer available nephrons to maintain GF –> gradual decline in the GFR is noticed as nephrons continue to die

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13
Q

What is considered as malignant hypertension?

A

BP > 200/120mmHg

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14
Q

What is the pathogenesis of malignant hypertension?

A
  1. Long-standing hypertension,
  2. Increased permeability of the vessels to fibrinogen and other plasma proteins, endothelial injury, and platelet deposition –> which can lead to the appearance of fibrinoid necrosis of arterioles and small arteries and intravascular thrombosis OR
    Mitogenic factors from platelets and plasma cause intimal hyperplasia of vessels –> hyperplastic arteriosclerosis
  3. Kidneys become markedly ischemic
  4. Further elevation of the blood pressure via the RAAS activation
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15
Q

What is the morphology of malignant hypertension?

A

Fibrinoid necrosis
Hyperplasticity’s artriolosclerosis

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16
Q

What is fibrinoid necrosis?

A

Formation of pink fibrin of small renal arteries

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17
Q

What is hyperplastic arteriosclerosis?

A

Homogenous, granular eosinophilic appearance

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18
Q

What causes hyperplastic arteriosclerosis?

A

Proliferation of intimal cells after acute injury, which produces an onion-skin appearance

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19
Q

What is the morphology of hyperplastic arteriosclerosis?

A

Marked narrowing of interlobular arteries and larger arterioles,
Necrosis may also involve glomeruli as well as arterioles

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20
Q

What are the clinical symptoms of malignant hypertesnion?

A

Papilledema, encephalopathy, cardiovascular abnormalities, and renal failure

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21
Q

What are the early symptoms of malignant hypertension?

A

Increased intracranial pressure –> headache, nausea, vomiting, and visual impairment (scotomas or spots)

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22
Q

What are the renal manifestations of malignant hypertension?

A

Marked proteinuria and hematuria but no significant alteration in renal function
Presents with severe acute kidney injury and renal failure

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23
Q

What is the pathogenesis of CKD in regard to diabetes? (8)

A
  1. Hyperglycemia starts sticking to proteins in the blood –> non-enzymatic glycation
  2. The glucose can get through the endothelium, a process of glycation that involves the basement membrane of small blood vessels, making it thicken
  3. The process of glycation particularly affects efferent arteriole, causing it to get stiff and more narrow –> hyaline arteriosclerosis
  4. Creates an obstruction, making it difficult for the blood to leave the glomerulus, increasing the pressure within. Afferent arteriole dilates, allowing more blood flow and increasing the pressure even more
  5. High pressure in the glomerulus –> increase in GFR
  6. In response to high-pressure rate, the mesangial cells secrete more and more structural matrix –> expand the size of the glomerulus
  7. Thickening of the basement membrane makes it more permeable –> allow proteins such as albumin to be filtered out
  8. Diabetic nephropathy and GFR decraeses
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24
Q

What is considered the first stage of diabetic nephropathy?

A

The increased pressure in the glomerulus causing an increase in the GFR –> known as hyperfiltration

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25
Q

What happens if half of the number of nephrons is lost?

A

CKD progresses similarly regardless of etiology, initial hyperfiltration activates RAAS and causes proteinuria.
Angiotensin II and protein uptake at the tubule cause inflammation and fibrosis of the glomerulus and tubules.
Progressive decline in GFR and systemic complications occur

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26
Q

What is the pathogenesis of CKD in regards to nephron loss? (7)

A
  1. Decrease in nephron number
  2. Adaptive hyperfiltration at glomerulus
  3. Increased glomerular activity OR RAAS activation
  4. Increased filtration of proteins and molecules OR Increased single nephron GFR (in the early course) and hypertension
  5. Nephrotoxic inflammation/remodeling
  6. Tubulointestinal fibrosis and 2o FSGS
  7. Decreased GFR, decreased urine output and systemic complications
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27
Q

What is the result of increased filtration of proteins and macromolecules?

A

Proteinuria –> Dyslipidemia

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28
Q

What are the different stages of CKD>?

A

Stages 1 to 5

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29
Q

What is stage 1 of CKD like? What is the GFR like?

A

Kidney damage with NORMAL kidney function, GFR: 90 or higher

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30
Q

What is stage 2 of CKD like? What is the GFR like?

A

Kidney damage with MILD LOSS of kidney function, GFR: 89 to 60

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31
Q

What is stage 3a of CKD like? What is the GFR like?

A

MILD to MODERATE loss of kidney function, GFR: 59 to 45

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32
Q

What is stage 3b of CKD like? What is the GFR like?

A

MODERATE to SEVERE loss of kidney function, GFR: 44 to 30

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33
Q

What is stage 4 of CKD like? What is the GFR like?

A

SEVERE loss of kidney function, GFR: 29 to 15

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34
Q

What is stage 5 of CKD like? What is the GFR like?

A

Kidney FAILURE, GFR: < 15

35
Q

What are the gross features of CKD? (3)

A
  1. Kidneys are symmetrically contracted
  2. Damage in blood vessels or glomeruli
  3. Damage by chronic pyelonephritis
36
Q

What is the appearance of the kidneys if there is damage in blood vessels or glomeruli in CKD?

A

Kidney surface: red-brown and diffusely grsnular

37
Q

What is the appearance of the kidneys if there is damage by chronic pyelonephritis in CKD?

A

Uneven kidneys with deep scarring

38
Q

What are the microscopical features of CKD? (5)

A
  1. Glomerular sclerosis
  2. Interstitial fibrosis with lymphocytic infiltrates
  3. Tubules atrophy
  4. Loss of portions of the peritubular capillary network
  5. Arteries (thick-walled, narrow lumina)
39
Q

Which arteries are affected in CKD?

A

The small or medium sized ones

40
Q

In chronic glomerulonephritis what is shown with a Masson trichrome stain?

A

Complete replacement of virtually all glomeruli by blue-staining collagen

41
Q

In which stages of CKD are patients asymptomatic?

A

Stages 1 to 3, where the GFR > 30ml/min

42
Q

In which cases of CKD are the patients symptomatic?

A

Stages 4 & 5, where the GFR < 30ml/min

43
Q

What are the early signs of CKD?

A

Polyuria/oliguria (changes in urine output)
Hematuria
Edema
Because of the hyperfiltration compensatory mechanism

44
Q

What are the late signs of CKD?

A

Hypertesnion
Signs of anemia (pallor)
Signs of uremia

45
Q

What are the signs of uremia that affect the brain?

A

Uremic encephalopathy: low concentration –> confusion, lethargy, asterixis and coma

46
Q

What are the signs of uremia that affect the heart?

A

Pericarditis

47
Q

What are the GIT clinical presentations of CKD?

A

Nausea, vomiting, anorexia and diarrhea

48
Q

What are the reproductive system clinical presentations of CKD?

A

Erectile dysfunction, decreased libido, amenorrhea

49
Q

What are the blood system clinical manifestations of CKD?

A

Platelet dysfunction with a tendency to bleed, infections due to WBC dysfunction

50
Q

What are the peripheral neuropathy clinical manifestations of CKD?

A

Numbness, paraesthesia, restless leg syndrome

51
Q

What are the skin clinical manifestations of CKD?

A

Dry skin, pruritus, ecchymosis

52
Q

What are other clinical manifestations of CKD?

A

Fatigue, hiccups and muscle cramps

53
Q

What is the mechanism behind the generalized edema of CKD?

A

Water retention due to loss of GFR –> sodium and fluid retention –> fluid moves to extravascular space due to increased hydrostatic pressure –> pitting edema

54
Q

What is the mechanism behind pulmonary crackles in CKD?

A

Fluid accumulation causes pulmonary edema and loss of air space –> ventilation-perfusion mismatch.

55
Q

What is the mechanism behind anemia in CKD?

A

Renal failure –> loss of erythropoietin release

56
Q

What is the mechanism behind weight loss in CKD?

A

Protein-energy malnutrition due to metabolic acidosis –> loss of kidney function results in impaired H+ secretion from the body

57
Q

What is the mechanism behind hyperkalemia in CKD?

A

The inability of the kidneys to secrete potassium in the urine leads to life-threatening arrhythmias

58
Q

What is the mechanism of hyperphosphatemia in renal osteodystrophy?

A

Damaged kidneys fail to excrete phosphate
Also secondary to high parathyroid hormone levels

59
Q

What is the mechanism of hypocalcemia in renal osteodystrophy?

A

Secondary to low Vitamin D3, in early cases of CKD, low levels of calcitriol due to hyperphosphatemia. In later stages of CKD, low levels are hypothesized due to decreased synthesis of 1a-hydroxylase

60
Q

What is the function of 1a-hydroxylase?

A

Converts calcifediol to calcitriol in the kidneys

61
Q

What is the mechanism of secondary and tertiary hyperparathyroidism in renal osteodystrophy?

A

To compensate for low calcium because of low vitamin D levels

62
Q

What is the effect of increased parathyroid hormone secretion?

A

High bone turnover, always attempting to normalize the low calcium levels in the blood –> maladaptive –> extraosseous calcification and parathyroid hyperplasia (tertiary hyperparathyroidism)

63
Q

What is the mechanism behind the uremia complication: ecchymosis and GI bleeding?

A

Uremia-induced platelet dysfunction

64
Q

What are the presenting symptoms of complications of uremia: ecchymosis and GI bleeding?

A

Increased tendency to bleed and ecchymosis

65
Q

What is the mechanism behind the uremia complication: pericardial friction rub?

A

Uremic pericarditis

66
Q

What is the mechanism behind the uremia complication involving the brain?

A

Uremic encephalopathy; adverse effects of urea of CNS (mechanism is unclear)

67
Q

What are the presenting symptoms of pericardial friction rub?

A

Chest pain and malaise

68
Q

What are the presenting symptoms of uremic encephalopathy?

A

Headaches, confusion and coma

69
Q

What are thrombotic micronagiopathies?

A

Lesions that are seen in various clinical syndromes characterized by microvascular thrombosis accompanied by microangiopathic hemolytic anemia , thrombocytopenia and renal failure

70
Q

What are the two types of thrombotic microangiopathies?

A

Primary TMA
Secondary TMA

71
Q

What is Primary TMA?

A

Shiga-toxin mediated hemolytic uremic syndrome (HUS); atypical HUS and thrombotic thrombocytopenic purpura (TTP)

72
Q

What is secondary TMA?

A

Malignant hypertension and scleroderma-associated TMA

73
Q

What is the Shiga-toxin mediated HUS?

A

Intestinal infection with Shiga-toxin-producing E.coli and infections with Shigella dysenteriae type I

74
Q

Where is E.coli usually found?

A

Contaminated ground meat

75
Q

What is the pathogenesis of Shiga-toxin-mediated HUS? (low doses)

A

The toxin activates endothelial cells, leading to leukocyte adhesion, increased endothelin production, and decreased nitric oxide production, as well as other changes that may promote platelet adhesion and activation

76
Q

What is the effect of increased endothelin production and decreased nitric oxide production?

A

Vasoconstriction

77
Q

What is the pathogenesis of Shiga-toxin-mediated HUS? (high doses)

A

The toxin causes endothelial cell death

78
Q

What is the result of all the alterations that take place in Shiga-toxin mediated HUS?

A

Formation of thrombi, which tend to be the most prominent in glomerular capillaries, afferent arterioles and interlobular arteries

79
Q

What is atypical HUS?

A

Genetic abnormalities in complement regulatory proteins (mostly factor H but also factor I, and membrane cofactor protein)

80
Q

What is the pathogenesis of atypical HUS?

A

Antibodies to complement regulatory proteins (anti-factor H or C5 to 9 MAC)

Excessive activation of complement, with ensuing microvascular injury and microvascular thrombosis

81
Q

What is thrombotic thrombocytopenic purpura (TTP)?

A

Genetic or acquired deficiency of a protease, ADAMTS13

82
Q

What is the function of ADAMTS13?

A

Cleaves multimers of von Willebrand factor (carrier for factor 8) on the surface of endothelial cells

83
Q

What is the result of TTP ?

A

Abnormally large vWF multimers activate platelets spontaneously, leading to platelet aggregation and thrombosis in multiple organs, including the kidneys

84
Q
A

Renal System (24 decks)

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