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SMP - APP Part 2 > Lectures 11-12 & 15-16 - Renal Pathophysiology I-IV > Flashcards

Lectures 11-12 & 15-16 - Renal Pathophysiology I-IV Flashcards

1
Q

6 renal functions?

A
  1. Maintain water balance
  2. Regulate the quantity and concentration of the ECF ions
  3. Maintain plasma volume
  4. Acid-base balance
  5. Excrete waste products
  6. Secretion of renin, erythropoietin etc.
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2
Q

3 cell types of the glomerulus? How does each act as a filtration barrier?

A
  1. Podocytes => epithelial cells with foot processes that interdigitate to form filtration slits to block molecules from being filtrated based on size
  2. Mesangial cells => smooth muscle cells (do not usually contract) that lay down the glomerular basement membrane, which is negatively charged and repulses negatively charged molecules (i.e. cells and proteins)
  3. Endothelial cells => fenestrations between these cells to let molecules through based on size
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3
Q

What is found in the renal cortex?

A
  1. Glomeruli
  2. Proximal and distal tubules
  3. Loops of Henle
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4
Q

What is found in the renal medulla?

A
  1. Loops of Henle

2. Collecting ducts

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5
Q

Which is more homogenous: cortex or medulla?

A

Medulla

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6
Q

Normal GFR?

A

100-125 mL/min

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7
Q

Major determinants of GFR? Most important?

A
  1. Oncotic pressure
  2. ***Glomerular capillary hydrostatic pressure
  3. Kf = measure of surface area
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8
Q

What can decrease GFR?

A

Age (75-100 mL/min) and pathology

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9
Q

How does renal autoregulation work? Purpose?

A
  1. Myogenic mechanisms
  2. Tubulo-glomerular feedback via the juxtaglomerular apparatus

Purpose: to maintain constant blood flow through the glomerulus independent of systemic blood pressure

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10
Q

How does tubuloglomerular feedback work?

A

Flow in the distal tubule in between the afferent and efferent arterioles of the glomerulus is sensed by macula densa cells of the distal tubule => low flow stimulates renin release by juxtaglomerular cells into the afferent arteriole

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11
Q

Other than the macula densa cells, what other 2 factors stimulate the juxtaglomerular cells to secrete renin?

A
  1. Sympathetic innervation on beta-adrenergic receptors

2. Decreased pressure on baroreceptors in afferent arteriole

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12
Q

What are the 5 mechanisms by which Angiotensin II increases BP?

A
  1. Stimulates sympathetic activity
  2. Stimulates tubular NaCl reabsorption, K+ excretion, and H2O retention
  3. Stimulates aldosterone secretion by the adrenals => #2
  4. Stimulates arteriolar vasoconstriction
  5. Stimulates pituitary gland to secrete ADH => H2O absorption in the collecting duct
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13
Q

What % of kidney failure is caused by diabetes?

A

45%

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14
Q

Second leading cause of kidney failure?

A

HT

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15
Q

Ranking of kidney disease as a leading cause of death in the US?

A

9

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16
Q

How has the incidence of end stage renal disease changed over the years? Why?

A

Significant increase => following the incidence of DM and HT

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17
Q

% of DM patients with kidney issues?

A

30%

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18
Q

What causes marked geographic variations in adjusted prevalent rates of kidney disease?

A

Race and DM

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19
Q

Which races are more prone to end stage renal failure?

A
  1. Blacks
  2. Native Americans
  3. Asians
  4. Whites
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20
Q

Definition of acute renal failure (ARF)?

A

Sudden decrease in GFR, resulting in:

  1. Increase in the plasma concentration of metabolic waste products (azotemia and creatinine) normally excreted by the kidneys
  2. Reduced production of urine => oliguria or anuria
  3. Retention of water, H+, and minerals => metabolic acidosis and HT
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21
Q

What are the causes of ARF? Treatment?

A

Causes of ARF are varied and treatment depends on identifying the mechanism involved

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22
Q

When does ARF usually evolve?

A

Almost always in the hospital in 1-25% of critically ill patients

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23
Q

Mortality rate of ARF patients?

A

28-90%

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24
Q

3 types of ARF? What to note?

A
  1. Pre-renal: decreased renal perfusion
  2. Post-renal: obstruction to urine flow
  3. Parenchymal renal disease

NOTE: not mutually exclusive, all three of them may be present at the same time => important, even if it seems obvious why the renal function is falling, to look for evidence of all three

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25
Q

Other name for parenchymal ARF?

A

Intrarenal ARF

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26
Q

What can cause pre-renal ARF?

A
  1. Hypotension
  2. Volume depletion: fluid loss, bleeding, etc.
  3. Primary cardiac pump failure
  4. Decreased systemic vascular resistance (e.g. sepsis)
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27
Q

How to treat pre-renal ARF?

A

Improve renal perfusion via volume replacement or dialysis

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28
Q

Pathogenesis of pre-renal ARF? BUN and creatinine levels?

A

Decreased BP => decreased GFR => Ang II + ADH + aldosterone + SNS activation via baroreceptors => Na+ and water retention + arteriolar vasoconstriction => oliguria

Reduced blood flow causes elevated creatinine and BUN. Additionaly, BUN reabsorption is increased because of the lower flow; BUN is disproportionately elevated relative to creatinine => BUN/Cr > 20/1

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29
Q

Causes of post-renal ARF?

A
  1. Kidney stones

2. Cancers of the urinary tract or nearby organs (e.g. prostate)

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30
Q

Is pre-renal ARF reversible?

A

YUP

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31
Q

10 common causes of intra-renal ARF?

A
  1. Acute tubular necrosis
  2. Cortical necrosis
  3. Acute glomerulonephritis
  4. Malignant hypertension
  5. DIC
  6. Renal vasculitis
  7. Allograft rejection
  8. Drug allergy
  9. Infection
  10. Tumor
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32
Q

What 4 renal structures can be affected by intrinsic ARF aka intra-renal ARF?

A
  1. Glomerulus
  2. Vessels
  3. Interstitium
  4. Tubules
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33
Q

Explain the pathophysiology of postrenal ARF.

A

Tubular obstruction => insult (ischemia) causes sloughing of cells and cast formation => retrograde increase in pressure and reduction of GFR => backward flow of filtrate

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34
Q

What are the 3 phases of post-renal ARF? Describe each.

A
  1. Early phase: reflex adaptation to maintain GFR despite rising tubular hydrostatic pressure via afferent arteriolar dilitation to enhance glomerular perfusion (only 12 – 24 hours)
  2. Late phase: after 12 –24 hours, the afferent vasodilatation ceases => progressive fall in renal perfusion: glomerular blood flow and GFR drop => may result in anuria => if prolonged, the ischemia leads to progressive permanent nephron loss
  3. Recovery phase (after relief of the urinary obstruction): with release of the pressure, the pre-renal vessels relax, perfusion is restored, and GFR increases in the nephrons which survive => tubular pressure returns to normal => dilatation of the calyces and collecting system may remain permanently
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35
Q

BUN and creatinine levels in post-renal ARF?

A

Normal range: 10-20/1

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36
Q

BUN and creatinine levels in intra-renal ARF?

A

Renal damage causes reduced reabsorption of BUN, therefore lowering the BUN/Cr ratio => <10/1

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37
Q

Normal plasma creatinine level?

A

1 mg/dL

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38
Q

Normal BUN level?

A

10-20 mg/dL

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39
Q

What is chronic kidney disease (CKD)?

A

Gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes due to diseases affecting the kidney either:

PRIMARILY
1. Chronic glomerulonephritis
2. Interstitial nephritis 
SECONDARILY
3. Hypertensive vascular disease
4. Diabetes
5. Partial urinary tract obstruction
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40
Q

Are primary or secondary causes of CKD more common?

A

Secondary causes more common

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41
Q

What can progression of CKD lead to?

A

Progression may continue to end-stage renal disease (ESRD)

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42
Q

Describe the progression of chronic renal failure.

A
  1. Reduced renal reserve
  2. Renal insufficiency: GFR is reduced (< 50% of normal) and mild azotemia, nocturia, mild anemia
  3. Renal failure: azotemia, acidosis, impaired urine dilution, severe anemia, hypernatremia, and hyperkalemia (GFR below 20%)
  4. End stage renal failure: near absence of GFR, all organ systems are effected
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43
Q

Pathophysiology of chronic renal failure progression?

A

Renal injury leading to:

  1. Progressive loss of nephron mass and filtration surface area => decreased GFR
  2. Systemic HT => proteinuria => increased proximal tubule protein uptake => renal microvascular injury
  3. Renal growth factor and cytokine activation => influx of monocytes and macrophages => fibrosis

All 3 => ESRD

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44
Q

What is uremia? Causes?

A

Uremia refers to a number of symptoms caused by a decline in renal function with the accumulations of toxins (with azotemia, acidosis, hyperkalemia, HT, anemia, and hypocalcemia) => sign of failing excretory system and other metabolic and endocrine abnormalities

Causes unknown, and it appears that urea and creatinine build up plays little to no role

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45
Q

7 symptoms of uremia?

A
  1. Anorexia
  2. Nausea
  3. Vomiting
  4. Diarrhea
  5. Weight loss
  6. Edema
  7. Neurologic changes
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46
Q

What is important to note about sodium regulation?

A

Sodium must be regulated within narrow limits so the nephron is very efficient at reabsorbing sodium

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47
Q

What happens to Na+/H2O reabsorption when GFR declines?

A

A decreased fraction of filtered Na and water must be reabsorbed to keep them in balance

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48
Q

How are sodium and water balances affected by chronic renal failure?

A

Kidneys become less flexible and urinary dilution and concentration are impaired

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49
Q

How is calcium balance affected by chronic renal failure?

A

Vitamin D levels decrease as the kidney synthesis decreases => diminished absorption of calcium from the gut => overproduction of parathyroid hormone => plasma phosphate levels increase because of the decrease in GFR => phosphate levels bind to plasma calcium levels => further decreases calcium levels

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50
Q

How is potassium balance affected by chronic renal failure? What is the risk? How to fix this?

A

Aldosterone-mediated potassium secretion unable to function at such a low GFR => hyperkalemia

The heart function risk increases as the disease progresses and must be controlled by dialysis

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51
Q

How is the acid-base balance affected by chronic renal failure? Result?

A

Kidneys secretes acids in large amounts so as the kidney fails, ammonia synthesis decrease =>
acidosis => compensation, but acidosis must be treated with dialysis if severe

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52
Q

How are bones affected by chronic renal failure?

A

Renal osteodystrophy:

1, Elevated serum phosphate levels

  1. Decreased serum calcium levels
  2. Impaired activation of vitamin D
  3. Hyperparathyriodism

=> bone pain and higher fracture risk

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53
Q

Hematologic alterations caused by chronic renal failure? How is this treated?

A

Decrease in the production of erythropoietin => inadequate production of RBC => normochromic-normocytic anemia presenting with:

  1. Lethargy
  2. Dizziness
  3. Low hematocrit
  4. Left ventricular hypertrophy

Treatment: synthetic erythropoietin

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54
Q

What do most CRF patients die of?

A

Cardiovascular issues caused by the renal issues

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55
Q

How is the CV system affected by CRF?

A
  1. Hypertension resulting from excess fluid volume and sodium levels due to elevated renin
  2. Dyslipidemia = abnormal lipids in the blood: decrease in HDLs and increase in LDLs and VLDLs => higher risk of atherosclerosis
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56
Q

How is the nervous system affected by CRF? Both in CNS and PNS?

A
  1. Mild sleep disorders
  2. Impaired concentration
  3. Memory loss
  4. Impaired judgement may occur in some individuals
  5. Some may experience frequent hiccups, muscle cramps and twitching due to alterations in electrolyte and metabolic product elevation

YUP

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57
Q

How is endocrine function and reproduction affected by CRF?

A

Uremic males and females have a decrease in sex steroids:

  1. Females: amenorrhea and inability to maintain a pregnancy
  2. Males: decreased libido and impotence, and sometimes infertility
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58
Q

How is the immune system affected by CRF? Why?

A

Generalized immunosuppression due to unknown reasons:

  1. Increased susceptibility to infection
  2. Deficient response to vaccination
  3. Impaired wound healing
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59
Q

How to fix endocrine/reproduction and immune effects of CRF?

A

Dialysis

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60
Q

How is GI function affected by CRF?

A
  1. Non-specific GI complications: anorexia, nausea, and vomiting, along with a metallic taste in the mouth (especially with high BUN levels)
  2. Uremic gastroenteritis: bleeding ulcerations along mucosa that result in significant blood loss (upper GIT)
  3. Uremic fetor: form of bad breath caused by urea breakdown by salivary enzymes
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61
Q

How to treat high BUN in CRF patients?

A

Low protein diet

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62
Q

Treatment of GI issues caused by CRF?

A
  1. Dietary protein restriction
    OR
  2. Regular dialysis
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63
Q

9 treatments for CRF?

A
  1. Preserve remaining nephron function
  2. Dietary management: low protein, sodium, fluid, potassium, phosphate, and acid
  3. Sodium and fluid management
  4. Potassium management
  5. Erythropoietin
  6. Control hypertension
  7. Careful prescribing of drugs that are potentially nephrotoxic
  8. Dialysis
  9. Transplant
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64
Q

How does dialysis work?

A

Dialysis fluid separated by semi-permeable membrane (blocking RBCs, WBC, and proteins) from blood passing through slowly to equilibrate

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65
Q

Other name for dialysis fluid?

A

Dialysate

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66
Q

2 types of dialysis?

A
  1. Hemodialysis

2. Peritoneal dialysis

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67
Q

Difference between azotemia and uremia?

A

Azotemia is an elevation in BUN and Cr due to low GFR with decreased or absent urine, fatigue, decreased alertness, confusion, pale skin, tachycardia, dry mouth, thirst, swelling, orthostatic BP

Uremia is a broader term referring to the pathological manifestations of severe azotemia => azotemia, as well as acidosis, hyperkalemia, hypertension, anemia, and hypocalcemia along with other findings

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68
Q

What is hematuria?

A

Presence of blood in the urine

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69
Q

What is lipiduria?

A

Presence of lipids in the urine

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70
Q

What is bacteriuria?

A

Presence of bacteria in the urine

71
Q

What is pyuria?

A

Presence of leukocytes in the urine

72
Q

What is the difference between diffuse and focal glomerular diseases?

A

Diffuse = all glomeruli affected

Focal = selected glomeruli affected

73
Q

What is the difference between local/segmental and global glomerular diseases?

A

Global = entire glomerulus affected

Local/segmental = only part of the glomerulus is affected

74
Q

What are proliferative glomerular diseases?

A

Hypercellularity found in the glomerulus (either endogenous cells, immune, or bacterial cells)

75
Q

What are membranous glomerular diseases?

A

Diseases with increase in thickness of the glomerular basement membrane

76
Q

What do proliferative glomerular diseases of mesangial cells lead to?

A

Membranous disease

77
Q

What are sclerotic glomerular diseases?

A

Diseases with fibrous let down replacing cells

78
Q

What 4 nephrotic syndrome subtypes?

A
  1. Minimal change disease
  2. Membranous glomerulonephritis
  3. Focal segmental glomerulosclerosis
  4. Membranoproliferative glomerulonephritis
79
Q

Other name for membranous glomerulonephritis?

A

Membranous nephropathy

80
Q

Other name for minimal change disease?

A

Lipoid nephrosis

81
Q

Describe the pathogenesis of nephrotic syndrome.

A

Altered glomerular permeability => increased filtration of plasma proteins (> 3.5 g/day) => proteinuria =>

  1. Hypoalbuninemia (liver does not compensate) => edema (=> reduced BV => RAAS activation => salt/water retention) + hepatic synthesis of lipoproteins: LDLs and VLDLs (=> hyperlipoproteinemia)
  2. Hypercoagulable state
  3. Decreased immunoglobulins
82
Q

How to diagnose different nephrotic syndrome subtypes?

A

Kidney biopsy

83
Q

Population affected by membranous glomerulonephritis?

A

Adults, most commonly in 60s +

84
Q

Pathogenesis of membranous glomerulonephritis?

A

Endogenous immune complex initiates an immune response => inflammation with neutrophils and MOs infiltrate => release of cytokines and growth factors => mesangial cells stimulated => thickening of the glomerular basement membrane, especially in the form of thickened capillary loops

85
Q

Is membranous glomerulonephritis diffuse or focal? Global or segmental?

A

Diffuse

Global

86
Q

Is the glomerulus normocellular in membranous glomerulonephritis?

87
Q

Treatment for membranous glomerulonephritis?

88
Q

Pathogenesis of membranoproliferative glomerulonephritis?

A

Exogenous immune complex initiates an immune response => inflammation with neutrophils and MOs infiltrate => release of cytokines and growth factors => increase in number of mesangial cells => thickening of the glomerular basement membrane

89
Q

Population affected by membranoproliferative glomerulonephritis?

90
Q

Histology for membranous glomerulonephritis? 2

A
  1. Glomerulus is normocellular

2. Increase in extracellular substance, especially in the form of thickened capillary loops

91
Q

Histology for membranoproliferative glomerulonephritis? 2

A
  1. Diffuse hypercellularity with increase in mesangial cells
  2. The glomerular capillary loops show two basements membranes giving the loops a tram track appearance
92
Q

Treatment for membranoproliferative glomerulonephritis?

93
Q

Population affected by minimal change disease?

A

Most common in young children (2-6), more common in males

94
Q

Treatment for minimal change disease?

95
Q

Pathogenesis of minimal change disease?

A

Usually after a recent respiratory infection or after receiving routine immunizations => change in GBM charge (proteoglycans on outside of podocytes) => fusion of foot processes + glomerular capillary basement membranes are leaky to low molecular weight proteins such as albumin

96
Q

Histology for minimal change disease? 2

A
  1. The glomeruli appear normal on light microscopic examination
  2. Visceral epithelial cell shows fusion of the foot processes
97
Q

Cause of focal segmental glomerulosclerosis?

A

Idiopathic, but associated:

  1. Sickle cell disease
  2. Cyanotic heart disease
  3. IV drug abuse
98
Q

Population affected by focal segmental glomerulosclerosis?

A

AAs in the US

99
Q

2 extra symptoms with focal segmental glomerulosclerosis?

A
  1. HT

2. Decreased renal function

100
Q

Histology for focal segmental glomerulosclerosis? 2

A
  1. One half of the glomerular tuft is sclerosed

2. The other half of the glomerular tuft is normal showing patent capillary loops

101
Q

Treatment for focal segmental glomerulosclerosis?

A

BP management

102
Q

Describe the pathogenesis of nephrItic syndrome.

A

Inflammatory rupture of glomerular capillaries => increased filtration of plasma proteins + HEMATURIA => proteinuria =>

  1. Hypoalbuninemia (liver does not compensate) => edema (=> reduced BV => RAAS activation => salt/water retention) + hepatic synthesis of lipoproteins: LDLs and VLDLs (=> hyperlipoproteinemia)
  2. Hypercoagulable state
  3. Decreased immunoglobulins
103
Q

Is the proteinuria more pronounce in nephrotic syndrome or nephritic syndrome?

A

Nephrotic syndrome

104
Q

6 symptoms of nephritic syndrome?

A

Proteinuria

Hematuria

Azotemia

RBC cast

Oliguria

Hypertension

105
Q

4 subtypes of nephritic syndrome disorders?

A
  1. Acute proliferative glomerulonephritis
  2. Rapidly progressive glomerulonephritis
  3. IgA nephropathy
  4. Chronic glomerulonephritis
106
Q

Other name for acute proliferative glomerulonephritis?

A

Poststreptococcal, postinfectious glomerulonephritis

107
Q

Other name for rapidly progressive glomerulonephritis?

A

Crescentic glomerulonephritis

108
Q

Other name for IgA nephropathy?

A

Berger Disease

109
Q

Pathogenesis of acute proliferative glomerulonephritis?

A

Streptococcal infection (outside the kidney: pharyngitis or skin infection) leads to immune complex formation => neutrophils infiltrate => endothelial cells and mesangial cells proliferate

110
Q

Extra 4 symptoms in acute proliferative glomerulonephritis?

A
  1. Malaise
  2. Nausea
  3. Dark urine
  4. Edema
111
Q

Histology for acute proliferative glomerulonephritis?

A
  1. Increase in cellularity due to neutrophils and to proliferation of endogenous endothelial cells and mesangial cells
  2. Large subepithelial deposits
112
Q

What is the most common glomerular renal disease throughout the world? What to note?

A

IgA nephropathy

NOTE: may have not reached the threshold at which symptoms appear though

113
Q

Pathogenesis of IgA nephropathy?

A

Often preceded by an infection associated with the mucosum => vast deposits of IgA in the mesangium of the glomerulus => proliferation of mesangial cells

114
Q

Population affected by acute proliferative glomerulonephritis?

115
Q

Treatment for acute proliferative glomerulonephritis?

A
  1. Steroids

2. Strep antibiotics

116
Q

Histology for IgA nephropathy? 3

A
  1. Glomerulus is architecturally not very remarkable expect for mild mesangial expansion due to the increased numbers of mesangial cells
  2. Electron micrograph shows many discrete electron dense deposits located in the mesangium
  3. Immunofluorescence for IgA => whole glomerulus marked
117
Q

Population affected by IgA nephropathy?

118
Q

Treatment for IgA nephropathy?

119
Q

What can all nephrotic and nephritic syndromes lead to?

A

Chronic glomerulonephritis

120
Q

Feature of chronic glomerulonephritis?

121
Q

How to tell what caused glomerulonephritis?

A

Often the kidneys/glomeruli are so badly damaged that it is impossible to determine the type of glomerulonephritis that was the forerunner (even using immunofluorescence and electron microscopy)

122
Q

Histology for chronic glomerulonephritis? 4

A
  1. Glomeruli are solidified either partially or wholly into spherical structures
  2. Tubules show much loss and atrophy (with thickened basement membrane), and some cast formation
  3. Arteries show intimal thickening
  4. Interstitium shows fine fibrosis and contains variable numbers of inflammatory cells
123
Q

Kidney appearance for chronic glomerulonephritis?

A

Atrophic kidney with a thin cortex

124
Q

How does a tubular injury cause decreased glomerular filtration? 3

A
  1. Back-leak of filtration across damaged epithelium
  2. Decreased renal blood flow
  3. Decreased filtration properties of glomerulus
125
Q

2 types of tubulointerstitial nephritis?

A
  1. Acute pyelonephritis

2. Chronic pyelonephritis and reflux nephropathy

126
Q

What is tubulointerstitial nephritis often caused by? Which is more common?

A

Often caused by bacterial infections either ascended from the bladder or through the bloodstream:

  1. Hematogenous infection is less common and results from seeding of the kidneys due to septicemia or bacterial endocarditis.
  2. Vesicoureteral reflux occurs more readily with an uretheral obstruction or cystitis as the urinary bladder pressure is increased and the normal vesicoureteral valve is compromised
127
Q

Which will be affected first in tubulointerstitial nephritis: renal cortex or medulla? Implication?

A

Medulla => first symptom is inability to concentrate urine

128
Q

What parts of the kidney does tubulointerstitial nephritis affect?

A
  1. Tubules and interstitial space (glomeruli spared)

2. Renal pelvis is prominently involved

129
Q

8 symptoms of pyelonephritis?

A
  1. Chills
  2. Fever
  3. Headache
  4. Back pain
  5. Tenderness
  6. General malaise
  7. Dysuria
  8. Frequency and urgency
130
Q

Appearance of kidneys with acute pyelonephritis?

A

Patchy lighter colored areas (filled with pus) when compared to the normal darker colored areas

131
Q

Histology of acute pyelonephritis?

A
  1. Acute and chronic inflammation affecting the renal parenchyma
  2. Interstitium is widened by inflammatory cells
  3. Inflammatory cells consisting largely of neutrophils in the tubular lumens
132
Q

What is chronic pyelonephritis?

A

Urine outflow obstruction of any kind with superimposed ascending infection

Recurrent infection results in inflammation and scarring of the renal parenchyma

133
Q

Kidney appearance with chronic pyelonephritis?

A

Cystic appearing structures: dilated calyces, reflecting hydronephrosis

134
Q

Histology of chronic pyelonephritis? 2

A
  1. Many tubules are dilated with hyaline casts giving the kidney a thyroid-like appearance
  2. Patchy areas of collected chronic inflammatory cells are present
135
Q

Treatment for acute pyelonephritis?

A

Antibiotics

136
Q

Treatment for chronic pyelonephritis?

A
  1. Antibiotics (can be prophylactic)

2. Surgical fixing of the vesicoureteral valve

137
Q

What is renal tubular acidosis?

A

Tubular problems leading to acidosis and its subsequent complications:

  1. Proximal tubular disorder
  2. Distal tubular defects
138
Q

What are 2 renal blood vessel diseases?

A
  1. Benign nephrosclerosis

2. Malignant hypertension and malignant nephrosclerosis

139
Q

What is benign nephrosclerosis?

A

May naturally occur with age as a result of years of mild, uncontrolled chronic hypertension => progresses slowly, so symptoms may not be noticed unless the condition progresses to malignant nephrosclerosis (seldom is associated with significant proteinuria or increased serum creatinine or reduced renal function)

140
Q

Treatment for benign nephrosclerosis?

A

Anti-hypertensive therapy

141
Q

What happens if HT is uncontrolled in benign nephrosclerosis?

A

Chronic renal failure

142
Q

When looking at histology pictures with the blue and purple staining (tif stain), what do the colors mean?

A

Blue = fibrous material (should only be outside the glomerulus)

Purple = proteoglycans (should be in tubules and glomerulus)

143
Q

Histology for benign nephrosclerosis? 2

A
  1. Sclerosis of renal arterioles and small arterioles: medial and intimal thickening, as a response to hemodynamic changes and genetic defects
  2. Few glomeruli may undergo ischemic wrinkling (low functioning)
144
Q

What is malignant nephroclerosis?

A

Defined as a diastolic pressure > 130 mmHg or long-term mild hypertension

Associated with encephalopathy, retinopathy, cardiovascular abnormalities and renal failure (with significant proteinuria and azotemia)

Progresses very quickly and the damaged arteries are unable to provide enough oxygen to the kidney tissues, resulting in ischemic renal injury and renal failure

145
Q

% of hypertensive patients with malignant nephroclerosis?

146
Q

Treatment for malignant nephrosclerosis?

A
  1. Aggressive anti-hypertensive therapy

2. Dialysis

147
Q

Histology for malignant nephrosclerosis? 2

A
  1. Thickening of the arterial wall is associated with a hyperplastic arteriolosclerosis => “onion skin” appearance
  2. Glomeruli are completely fibrotic => non-functioning
148
Q

Leading cause of renal failure?

149
Q

Do both DMT1 and 2 cause renal failure?

150
Q

What DM patients are at greater risk of progression to renal failure?

A

Those with poor BP control

151
Q

Treatment for renal failure seen with DM?

A
  1. Once proteinuria is diagnosed => keep BP under control (to levels less than 130/80) with ACE inhibitors and/or angiotensin receptor blockers (ARBs) (most effective for DM patients)
  2. When uncontrolled: dialysis
152
Q

What is diabetic nephropathy?

A
  1. Leakiness of glomerular capillaries: microalbuminuria-proteinuria
  2. Glomerulosclerosis and tubulointerstitial fibrosis
  3. Arteriolar sclerosis

=> renal failure, hypertension, CVD

153
Q

Pathogenesis of diabetic nephropathy?

A

Hyperglycemia => non-enzymatic glycosylation => advanced glycation end-product (AGEs) formation (e.g. HbA1C, collagen) => cross-linking between AGEs => fibrosis, inflammation, and release of cytokines => tissue damage

154
Q

What are 2 renal cystic diseases? Which is more dangerous?

A
  1. Autosomal dominant adult polycystic kidney disease

2. ***Autosomal recessive childhood polycystic kidney disease

155
Q

What is autosomal dominant polycystic kidney disease?

A

Caused by dominant mutations in PKD1-3 genes, for tubular basement membrane proteins => some dilation in tubules (at any point), cysts in the kidney, liver, and pancreas

156
Q

Symptoms of autosomal dominant polycystic kidney disease?

A

Usually non-symptomatic until 3rd or 4th decade and then manifests with hypertension, and 90% of deaths occur by cardiovascular events

157
Q

What is autosomal recessive childhood polycystic kidney disease?

A

Caused by recessive mutations in PKHD1 gene, for very important tubular basement membrane protein => some dilation in ALL collecting ducts => hypertension and decrease in urine-concentrating ability seen in utero and in the first few months of life + high levels of Epo

158
Q

Lifespan of patients with autosomal recessive childhood polycystic kidney disease?

159
Q

Appearance of kidney with autosomal recessive childhood polycystic kidney disease?

A

Fusiform, cylindrical channels occupy most of the kidney parenchyma

160
Q

Are kidney stones more common in males or females?

161
Q

2 types of renal stones? Describe each.

A
  1. Urolithiasis: stones in ureter, bladder, or urethra

2. Nephrolithiasis: stones in kidney

162
Q

3 theories help to explain stone formation? Describe each.

A
  1. Saturation theory: individuals have too much salt or calcium, or not enough calcium, or are not hydrated enough
  2. Matrix theory: some individuals are genetically predisposed to have kidneys that put out matrices that promote crystallization
  3. Inhibitor theory: some individuals are genetically predisposed to making less inhibitors of stone formation or less efficient inhibitors
163
Q

What is hydronephrosis?

A

Dilation of the kidney with urine, caused by backward pressure on the kidney when the flow of urine is obstructed by stones in the renal pelvis, cancers of the bladder, cervix, uterus, prostate, pancreas, or other pelvic organs

164
Q

2 types of hydronephrosis? Describe each.

A
  1. Acute hydronephrosis: usually partial obstruction, oliguria
  2. Chronic hydronephrosis: oliguria, anuria, elevated pressure from obstruction may ultimately damage the kidney leading to acute renal failure, associated with vague intestinal symptoms, such as nausea, vomiting, and abdominal pain
165
Q

What is clear cell carcinoma?

A

Most common renal neoplasm seen in adults and can be as small as 1 cm or less and discovered incidentally, or it can be as bulky as several kilograms

166
Q

5 possible symptoms of clear cell carcinoma?

A
  1. Pain
  2. Palpable mass
  3. Hematuria
  4. May be clinically silent for years
  5. May present with symptoms of metastasis, most commonly to the lungs
167
Q

Histology for clear cell carcinoma?

A

Tubular cells accumulate glycogen and lipids, their cytoplasm appear “clear”, lipid-laden

168
Q

What is Wills tumor? Treatment?

A

Tumor usually arises as a result of failure of blastemal tissue to differentiate into normal renal structures, and is usually large at the time of detection => the neoplasm is aggressive and metastasizes widely, but is responsive to surgery and chemotherapy

169
Q

Population affected by Wills tumor?

A

Children, usually under age 5

170
Q

4 symptoms of Wills tumor?

A
  1. Pain due to size
  2. Fever
  3. High BP
  4. Constipation
171
Q

What are renal stones usually made of?

A

Calcium oxalate

172
Q

Is calyx dilation reversible?

173
Q

Is membranoproliferative glomerulonephritis diffuse or focal? Global or segmental?

A

Diffuse

Global

SMP - APP Part 2 (7 decks)

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