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MBBS I CPRS > L77 - Kidney Diseases II > Flashcards

L77 - Kidney Diseases II Flashcards

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1
Q

What are the 2 major groups of processes in renal tubule diseases?

A

1) Acute tubular injury and acute renal failure

2) Tubulointerstitial nephritis

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2
Q

What is Acute tubular injury and acute renal failure mostly due to?

A

Ischaemic or toxic injury

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3
Q

What is Tubulointerstitial nephritis mostly caused by?

A

Inflammatory reactions of tubules and interstitium

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4
Q

What is another name for acute tubular injury?

A

Acute tubular necrosis

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5
Q

How does acute tubular injury present?

A

As Acute renal failure

Tubular injury is the most common cause of acute renal failure

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6
Q

Describe acute renal failure?

A

Clinicopathologic entity with clinical acute deterioration of renal function

Associated with morphologic evidence of tubular injury

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7
Q

Give 3 examples of ischaemia that causes acute renal failure?

A

Decreased effective circulating blood volume (e.g. shock)

Diffuse involvement of intrarenal blood vessels (e.g. malignant hypertension)

Thrombosis (e.g. thrombotic microangiopathy)

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8
Q

Give examples of direct toxic injury that causes acute renal failure?

A

drugs
Radiocontract dyes
heavy metals
Organic solvents

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9
Q

Give 3 examples of urinary obstruction that causes acute renal failure?

A

By prostatic hypertrophy

Tumour

Blood clot

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10
Q

Apart from ischaemia, urinary obstruction, direct toxic injury, name one cause of acute renal failure?

A

Acute Tubulointerstitial nephritis

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11
Q

[Acute tubular injury appearance under light microscopy?

A

Necrotic tubular epithelium sloughed in tubules

Dilated tubules with flattened tubular epithelium

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12
Q

3 stages of acute tubular injury?

A

Initiation phase

Maintenance phase

Recovery phase

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13
Q

What is initiation phase in acute tubular injury?

A

Slight decline in urine output with rise in blood urea and creatinine

(lasting for about 36 hours)

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14
Q

What is maintenance phase in acute tubular injury?

A

Decrease in urine output 40-400 mL/day (oliguria),

salt and water overload,

rising blood urea and creatinine,

hyperkalemia

metabolic acidosis

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15
Q

What is Recovery phase in acute tubular injury?

A

Steady increase in urine volume, up to 3L/day,

leading to loss of large amount of water, sodium and potassium

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16
Q

What is the outcome in acute tubular injury?

A

supportive care&raquo_space; most patients can recover

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17
Q

What can delay recovery in acute tubular injury?

A

conditions like sepsis, extensive burns and multi-organ failure

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18
Q

What is affected in Tubulointerstitial nephritis?

A
  • Inflammatory injuries of the tubules AND interstitium

* Glomeruli are spared

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19
Q

How does acute Tubulointerstitial nephritis manifest?

A

presented as acute or
subacute worsening of renal function:

  • Raised blood urea and creatinine level
  • Usually 2 weeks after drug exposure
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20
Q

What is the number 1 cause of Tubulointerstitial nephirits?

A

Drugs

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21
Q

What are other causes of Tubulointerstitial nephritis?

A
  • Infections
  • Metabolic diseases
  • Neoplasm
  • Physical factors
  • Immunologic reactions
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22
Q

What infections can cause Tubulointerstitial nephritis?

A

Acute and Chronic pyelonephritis

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23
Q

What Metabolic diseases can cause Tubulointerstitial nephritis?

A

Nephropathy:

1) Urate
2) Acute phosphate
3) Hypokaelemic
4) Oxalate
5) Acute phosphate

+ nephrocalcinosis

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24
Q

What neoplasms can cause Tubulointerstitial nephritis?

A

• Multiple myeloma (light chain cast nephropathy)

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25
What physical factors can cause Tubulointerstitial nephritis?
Chronic urinary tract obstruction
26
What immunologic reactions can cause Tubulointerstitial nephritis?
Sarcoidosis, Sjogren’s disease
27
What are the top causative drugs causing tubulointestinal nephritis?
All drug classes Especially NSAID, Antibiotic, Antivirals, Diuretics
28
WHat reaction occurs that cause tubulointerstitial nephrritis? How to allevaite problems?
Hypersensitivity reaction to medication Identification and withdrawal of the culprit drug
29
3 histology features of Tubulointestinal nephritis?
• Interstitial inflammation >>Abundant eosinophils points to drug cause • Tubulitis >> Inflammatory cells in between tubular cells • Interstitial edema (acute) or fibrosis (chronic)
30
Light microscopy appearance of drug-induced acute tubulointerstitial nephritis?
Large amount of inflammatory cells including eosinophils (stained red) in the interstitium and tubulitis edema
31
What does Pyelonephritis affect?
tubules, interstitium and renal pelvis
32
2 major forms of pyelonephritis?
* Acute pyelonephritis | * Chronic pyelonephritis
33
What is acute pyelonephritis? Caused by?
• Acute infection of kidney, generally caused by ascending bacteria infections
34
2 routes of acute pyelonephritis?
* Acute pyelonephritis | * Chronic pyelonephritis
35
What are some common predisposing causes of acute pyelonephritis?
• Lower urinary tract infection • Urinary tract obstruction (Stones/tumour) • Vesico-ureteric reflux
36
What are some less common predisposing causes of acute pyelonephritis?
• Pregnancy • Instrumentation / catheterization of urinary tract • Immunosuppression and deficiency
37
What are some presenting symptoms of acute pyelonephritis?
``` Fever Loin pain Shaking chills Nausea Vomiting Diarrhoea ```
38
What is a presenting symptoms of acute pyelonephritis Specific to bhildren?
Failure to thrive
39
Name the common pathogens that cause Acute pyelonephritis?
* Mycobacterium Tuberculosis (TB) *** | * Other bacteria and fungal infections
40
What are other bacteria (not Mtb) that can cause acute pyelonephritis?
* Escherichia coli (E. coli) * Proteus * Klebsiella * Enterobacter * Strptococcus faecalis * Staphylococcus
41
Gross appearance of urinary tract of acute pyelonephritis?
Multifoci abscess and pus formation
42
Light microscopic appearance of urinary tract of acute pyelonephritis?
Glomerulus preserved (infection extend up to Bowman's capsule) Large amount of neutrophils in interstitium and tubules + other inflammatory cells
43
Treatment of acute pyelonephritis?
appropriate antibiotic therapy depending on the inciting pathogen
44
Outcome of acute pyelonephritis?
• Symptoms usually disappear in a few days • Usually complete resolution without leaving significant effects on kidney function
45
Describe the healing process of acute pyelonephritis?
• Neutrophilic infiltrates replaced by macrophages, plasma cells and lymphocytes • Scattered scar formation
46
Name 2 complications of acute pyelonephritis?
• Pyelonephrosis >> Pus in renal pelvis, calyces and ureter • Perinephric abscess >> Extension of pus through renal capsule into perinephric tissue
47
Describe chronic pyelonephritis?
Chronic inflammation in tubules and interstitium (Tuberculosis excluded) >> Scarred kidney caused by repeated bacterial infections
48
What is chronic pyelonephritis associated with?
* Vesico-ureteric reflux | * Urinary tract obstruction (stone, stricture)
49
Is Chronic pyelonephritis bilateral or unilateral?
• Involvement usually unequal on the two sides
50
How does the scar formation in chronic pyelonephritis change the morphology of kidney?
Scar tissue is depressed/ shrunken
51
Symptoms of recurrent acute pyelonephritis?
* High fever * Shaking chills * Loin pain
52
What are the early stage symptoms of chronic pyelonephritis?
subtle/no symptoms in early stage >> Polyuria and nocturia due to loss of tubular function in concentrating urine and resorption of water
53
Name one symptom of chronic renal failure and end stage kidney disease?
Uraemia
54
Explain how chronic pyelonephritis lead to FSGS? FSGS = nephrotic
* Decrease in number of functional glomeruli due to loss of nephron unit * Compensatory hypertrophy by remaining glomeruli (due to increased renal blood pressure) * Progressive fibrosis involving portions of some glomeruli due to compensatory action >. FSGS
55
Are microscopic findings diagnostic for chronic pyelonephritis?
No
56
Treatment for chronic pyelonephritis?
* Treat possible underlying causes | * Treat recurrent acute pyelonephritis by antibiotic therapy
57
Outcome of Chronic pyelonephritis?
• Depends on extent of scarring: If loss of significant amount of renal tissue = End stage renal disease
58
What is the Dx for this case: 35/F Unknown herbal medicine intake Epigastric pain and vomiting with oligouria Normal kidney size and WBC levels
Tubulointerstitial nephritis? Need microscopy to diagnose
59
What are the microscopic features of light chain cast nephropathy?
Tubular casts rimmed by macrophages revealed by both PAS stain and H&E stain Lambda light chain restriction
60
What is Lambda light chain restriction?
In reactive lymphoid populations there is a mixture of kappa and of lambda positive cells, >> cells expressing kappa light chains outnumbering cells expressing lambda light chains >> lambda light chain restriction
61
What is the cause of light chain cast nephropathy?
Neoplasm > multiple myeloma = neoplasm of plasma cells
62
What age group does light chain cast nephropathy affect?
90% of cases greater than age of 50 years old (median age 70 years old)
63
Presentation of Light chain cast nephropathy?
Acute renal failure and proteinuria
64
Other renal diseases associated with monoclonal light chains?
* Amyloidosis (AL type) * Light chain deposition disease * Light chain proximal tubulopathy
65
Treatment for Light chain cast nephropathy?
* Treat underlying plasma cell neoplasm | * Hematopoietic stem cell transplantation in selected case
66
Outcome of Light chain cast nephropathy?
• 5-year survival rate: 20-25%
67
Name 4 important vascular diseases that lead to renal disease? * only remember top 4*
* Hypertensive nephrosclerosis * Malignant nephrosclerosis (malignant hypertension) * Diabetic nephropathy * ANCA-associated vasculitis (Atheroemboli, Renal artery stenosis, Thrombotic microangiopathy)
68
Diabetic nephropathy affects which structures?
Affecting both vessels and glomeruli
69
Pathology of Hypertensive nephrosclerosis causing Extravasation of plasma protein ?
Hypertension >> Sclerosis of renal arterioles and small arteries >> Hyalinization of arteriolar wall >> Extravasation of plasma protein through injured endothelium
70
Changes to renal arterioles in Hypertensive nephrosclerosis?
Intimal fibrosis and medial thickening
71
How does Hypertensive nephrosclerosis lead to gradual decline in renal function?
Affected vessels have thickened walls and narrowed lumens >> ischaemia and subsequent glomerulosclerosis and chronic tubulointerstitial injury >> gradual decline in renal function
72
Light microscopy appearance of Hypertensive Nephrosclerosis? **important**
Glomerulus: Glomerulosclerosis and Hyaline arterolosclerosis Arterioles: Intimal fibrosis and medial thickening of artery
73
What is Malignant nephrosclerosis associated with?
• Associated with malignant or accelerated hypertension
74
What is the criteria for malignant hypertension?
Systolic pressure greater than 200 mmHg and/or diastolic pressure greater than 120 mmHg
75
Presentation of malignant nephrosclerosis?
acute renal failure Papilloedema (optic disc swelling), retinal haemorrhages, encephalopathy, cardiovascular abnormalities
76
Light microscopic appearance of Malignant nephrosclerosis?
* Fibrinoid necrosis of arteriole | * Hyperplastic arteriolitis (onion-skin lesion)
77
Treatment of malignant nephrosclerosis?
• Prompt and aggressive antihypertensive medication
78
Which type of diabetes can lead to diabetic nephropathy?
• Both Type I and Type II Diabetes mellitus (DM)
79
3 histological features of Diabetic nephropathy on the glomeruli?
* Thickened GBM (increase ground substance) * Diffuse increase in mesangial matrix * Kimmelstiel-Wilson nodules (deposition of basement membrane nodules)
80
How does Diabetic nephropathy lead to gradual decline in renal function?
Leading to ischaemia and subsequent glomerulosclerosis > chronic tubulointerstitial injury > gradual decline in renal function
81
What forms in renal vasculature?
Leading to ischaemia and subsequent glomerulosclerosis and chronic tubulointerstitial injury
82
histological features of Diabetic nephropathy on the renal arterioles?
Hyalinosis of both afferent | and efferent arterioles
83
What is the EM appearance of GBM in Diabetic nephropathy?
GBM thickened to more than 1000nm, at least twice as thick as GBM
84
What type of glomerulonephritis is caused by ANCA-associated vasculitis?
rapidly progressive (crescentic) glomerulonephritis Type III, Pauci-immune
85
Why is ANCA-associated vasculitis Pauci-immune?
Lack of detectable anti-GBM antibodies or immune complex by direct immunofluorescence and electron microscopy
86
Name the 2 circulating antibodies in ANCA-associated vasculitis?
* c-ANCA (cytoplasmic) | * p-ANCA (perinuclear)
87
What is the full name of ANCA?
antineutrophil cytoplasmic antibodies
88
What are the 2 disease entities of ANCA-associated vasculitis?
granulomatosis with polyangiitis Microscopic polyangiitis
89
What replaces vessel walls in ANCA- associated vasculitis?
Fibrin
90
Pathology of ANCA-associated vasculitis?
Injury to glomerular tufts >> leakage of plasma protein stimulates Bowman’s capsule >> parietal epithelium proliferates >> hypercellular glomeruli with crescentic glomerulonephritis
91
Summarize the 3 selected diseases affecting mainly renal blood vessels?
- Hypertensive (and malignant) nephrosclerosis - Diabetic nephropathy - ANCA-associated vasculitis

MBBS I CPRS (78 decks)

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