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YEAR 3 - SEMESTER 2 > Case 10 - Chronic renal failure > Flashcards

Case 10 - Chronic renal failure Flashcards

1
Q

What is the definition of chronic kidney disease?

A

An estimated or measured glomerular filtration rate (GFR) <60 mL/min/1.73m2 that is present for at least 3 months, with or without evidence of kidney damage.

OR

Evidence of kidney damage, with or without decreased GFR that is present at least 3 months, as evidenced by:

  • Albuminuria
  • Haematuria
  • Structural abnormalities (eg on kidney imaging tests) or
  • Pathological abnormalities (eg on kidney biopsy)
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2
Q

What are the 2 most common cause of end-stage kidney disease in Australia?

A

Diabetes

Chronic hypertension

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3
Q

What is the typical presentation of someone with CKD?

A

Usually asymptomatic.

HTN or CKD complications (e.g. elevated serum creatinine) may be discovered during a routine evaluation or as tests for another issue

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4
Q

What is the timeline demarcating AKI vs. CKD?

A

AKI = <3 months

CKD = >3 months

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5
Q

Why are patients usually asymptomatic until they reach the later stages of CKD?

A

Kidneys have exceptional compensatory ability

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6
Q

Name 5 risk factors for CKD

A
  • Diabetes
  • HTN
  • Smoking
  • Obesity
  • Advanced age (>60)
  • AKI
  • FHx of CKD
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7
Q

The presence of certain abnormalities/clinical markers are required for >3 months in order to diagnose someone with CKD. Name these abnormalities.

A
  1. Albuminuria (measured using ACR)
  2. Electrolyte imbalances
  3. Retention of nitrogenous wastes (urea, creatinine, ammonia, etc)
  4. Acid-base imbalances
  5. Decreased EPO production
  6. Imaging showing structural abnormalities (e.g. polycystic kidneys)
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8
Q

Name the 2 CATEGORIES of clinical manifestations that patient with CKD may develop

A
  1. Manifestations of Na+ / H2O retention

2. Manifestations of uraemia

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9
Q

Describe the early, nonspecific manifestations which may appear in CKD

A
  • Weakness
  • Fatigue
  • Anorexia
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10
Q

List the manifestations of Na+ / H2O retention that may appear in CKD

A
  • Pulmonary oedema
  • Peripheral oedema
  • Hypertension
  • Heart failure
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11
Q

What is uraemia?

A

The constellation of signs/symptoms that manifest in ESKD

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12
Q

Describe the constitutional symptoms of uraemia

A
  • Headache
  • Weakness
  • Fatigue
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13
Q

Describe the GIT manifestation of uraemia

A
  • NV
  • Anorexia
  • Uraemic fetor (ammonia / urine-like breath odour)
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14
Q

Describe the dermatological manifestations of uraemia

A
  • Pruritus
  • Skin colour changes (e.g. hyperpigmentation or pallor due to anaemia)
  • Uraemic frost
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15
Q

What is uraemic frost?

A

High levels of urea in the blood leading to urea being secreted in sweat. Once it evaporates there may be tiny crystallised yellow-white urea deposits on the skin

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16
Q

Describe the serous manifestations of uraemia

A

Serositis causing:

  1. Uraemic pericarditis
  2. Pleuritis
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17
Q

Describe the neurological manifestations of uraemia

A
  • Encephalopathy (coma, seizures, somnolence)
  • Asterixis
  • Parasthesia (caused by peripheral neuropathy)
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18
Q

Describe the haematological manifestations of uraemia

A
  • Anaemia (due to increased destruction of RBCs)

- Leukocyte dysfunction (frequent infections, easy bleeding)

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19
Q

What are the 4 most common causes of CKD in Australia?

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
  • Polycystic Kidney Disease
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20
Q

Can you have a normal GFR but still be diagnosed with CKD?

A

YES - in this case, urine albumin excretion will be abnormal

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21
Q

Evidence of kidney damage for >3 months is one of the definitions of CKD. List the parameters used to define kidney damage

A
  • Albuminuria
  • Haematuria after exclusion of urological causes
  • Structural abnormalities (eg on kidney imaging tests)
  • Pathological abnormalities (eg on kidney biopsy - not routinely done)
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22
Q

Which lab abnormalities are most common in CKD?

A
  • Increased serum creatinine

- Increased blood urea & nitrogen

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23
Q

What is the most frequently assessed marker of kidney damage in clinical practice?

A

Albuminuria, as measured using the ACR / Albumin-creatinine ratio

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24
Q

What are the definitions of a normal ACR, microalbuminuria, and macroalbuminuria?

A

NORMAL ACR: <2.5 in males, <3.5 in females

MICROALBUMINURIA: <2.5-25 in males, <3.5-35 in females

MACROALBUMINURIA: >25 in males, >35 in females

units: mg/mmol

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25
Q

What you might expect to find in the following laboratory tests in someone with CKD?

  1. CBE
  2. Biochemistry
  3. Coagulation screen
  4. Urine ACR
  5. Fasting lipids
  6. Urinalysis
A
  1. CBE: normochromic, normocytic anaemia
  2. Biochemistry: inc. BUN + creatinine, hyperkalemia, possible hyperphosphatemia and hypocalcemia
  3. Coagulation screen: increased bleeding time
  4. Urine ACR (first-morning void): raised
  5. Fasting lipids: dyslipidaemia
  6. Urinalysis: abnormal urine sediment, waxy casts
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26
Q

Describe the pathophysiology of CKD resulting from diabetic nephropathy

A
  1. Excess blood glucose
  2. Non-enzymatic glycation: glucose molecules stick to proteins
  3. Hyaline arteriosclerosis –> narrowing of afferent arteriole
  4. Increased resistance in the nephrons
  5. High-pressure state causes mesangial cells to secrete more structural matrix
  6. Expands the size of the glomerulus
  7. Glomerulosclerosis diminishes the nephron’s ability to filter blood –> CKD
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26
Q

Name 2 causes of CKD that aren’t HTN or diabetes

A

Systemic diseases: lupus, RA

Medications: NSAIDs

Infections: HIV

Toxins: tobacco

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27
Q

Outline the 2 mechanisms of kidney damage in chronic hypertension (below + above protective autoregulatory threshold)

A

BELOW AUTOREGULATORY THRESHOLD: benign nephrosclerosis (sclerosis of the afferent arterioles & small arteries) –> thickening –> decreased perfusion –> ischaemic damage

ABOVE AUTOREGULATORY THRESHOLD: acute injury –> malignant nephrosclerosis –> bunch of bad shit happens –> failure of autoregulatory mechanisms –> damage

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28
Q

What is glomerulonephritis?

A

A group of diseases characterised by glomerular cell proliferation, inflammation, and leukocyte infiltration.

Characteristically presents with nephritic syndrome, but isolated nephrotic syndrome and nephrotic-nephritic syndromes can also occur.

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29
Q

Name 6 complications of CKD

A
  1. Chronic kidney disease-mineral & bone disorder (CKD-MBD)
  2. Secondary hyperparathyroidism
  3. Anaemia of chronic kidney disease
  4. Delayed growth (in children)
  5. Cardiovascular disease
  6. ESRD (end-stage renal disease)
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30
Q

Use the acronym Kidney OUTAGES to list some of the complications of CKD

A

Kidney - hyperKalaemia

O - renal osteodystrophy (CKD-MBD)
U - uraemia
T - triglyceridaemia
A - acidosis (metabolic)
G - growth delay
E - erythropoietin (anaemia)
S - sodium/water retention
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31
Q

How does CKD lead to arrhythmias?

A

CKD –> decreased K+ secretion –> hyperkalemia –> defective electrical conduction through cardiac myocytes –> arrhythmias

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31
Q

How does CKD lead to anaemia?

A

CKD –> less EPO production –> decreased RBC production –> anaemia

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32
Q

How does CKD lead to renal osteodystrophy? (a form of metabolic bone disease seen in patients with chronic renal insufficiency characterized by bone mineralization deficiency due to electrolyte and endocrine abnormalities)

A

CKD –> decreased calcitriol production –> decreased intestinal calcium absorption –> hypocalcemia –> renal osteodystrophy

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33
Q

What are the components of nephritic syndrome?

A
  • HAEMATURIA with acanthocytes (dysmorphic RBCs)
  • RBC CASTS IN URINE
  • PROTEINURIA (<3.5g/day)
  • HYPERTENSION
  • OEDEMA
  • Sterile pyuria
  • Oligouria
  • Azotemia
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34
Q

List 4 factors that influence serum creatinine

A
  • Age
  • Sex
  • Muscle mass
  • Diet
  • Medications (e.g. trimethoprim)
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35
Q

Should creatinine levels be used to detect renal impairment?

A

NOOOOOO

You can have normal creatinine despite having RENAL IMPAIRMENT

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35
Q

Should creatinine levels be used to detect renal impairment?

A

NOOOOOO

You can have normal creatinine despite having RENAL IMPAIRMENT

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36
Q

How does kidney impairment impact the plasma concentration of a drug?

A

CLEARANCE is reduced in renal impairment, so the CONCENTRATION of the drug INCREASES

C(steadystate) = dosing rate / clearance

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37
Q

Which types of opioids are preferentially used in renal impairment? Why?

A

In patients with renal impairment, prefer to use: oxycodone, fentanyl.

Opioids such as codeine and morphine are metabolised by the liver BUT produce METABOLITES that are cleared by the kidneys. These active metabolites build up and can cause complications (e.g. seizures)

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38
Q

Renal impairment can increase the ADVERSE EFFECTS of certain drugs, regardless of concentration. Gives some examples of adverse drug effects that are affected by CKD and why this occurs.

examinable

A
  1. HYPERKALEMIA: in CKD, there is already less K+ clearance. Spironolactone and other K+ sparing diuretics can exacerbate this.
  2. SALT & WATER RETENTION: fluid retention already occurs in CKD. Drugs such as NSAIDs and COX-II inhibitors contribute to this.
  3. DRUGS ASSOCIATED W/ACIDOSIS: metformin, acetazolamide
  4. ANTICOAGULANTS/ANTIPLATELETS: bleeding diathesis associated with uraemia
39
Q

Give 3 examples of drugs that do not work in renal impairment, and explain why

A
  1. Thiazide diuretics: need to be filtered by the glomerulus in order to work. Less filtration due to CKD = less effect
  2. Loop diuretics: higher dose (usually double) required to work
  3. Antibiotics for UTI: trimethoprim is filtered, so less effective. Prefer to use drugs which are not just filtered but also ACTIVELY SECRETED, e.g. amoxicillin + cephalosporins
39
Q

Give 3 examples of drugs that do not work in renal impairment, and explain why

A
  1. Thiazide diuretics: need to be filtered by the glomerulus in order to work. Less filtration due to CKD = less effect
  2. Loop diuretics: higher dose (usually double) required to work
  3. Antibiotics for UTI: trimethoprim is filtered, so less effective. Prefer to use drugs which are not just filtered but also ACTIVELY SECRETED, e.g. amoxicillin + cephalosporins
40
Q

Describe the consequences of someone with renal failure taking glimperide

A

GLIMPERIDE - a sulphonylurea

ISSUE 1 - is hepatically-cleared but has active metabolites that are renally-cleared

ISSUE 2 - produces insulin, which is renally-cleared and can accumulate in CKD

ISSUE 3 - patients w/renal impairment have less homeostatic mechanisms to counteract hypoglycaemia, so hypo can be prolonged

41
Q

Name 3 drugs that can interfere with kidney function/decrease GFR and HOW (triple whammy)

A
  1. Diuretics - dehydration/hypovolemia
  2. Vasodilatory prostaglandins (e.g. NSAIDs, other COX-II inhibitors) - PGs help cause afferent arteriole dilation (which is necessary in CKD since there are less nephrons and each nephron needs to filter more blood/work harder - vasodilation helps them do this). Afferent arteriole constriction is induced by these drugs, leading to decreased GFR
  3. Vasodilators of the efferent arteriole (e.g. ACEII, ARBs) - means there is less pressure across the glomerulus, resulting in renal impairment (usually in CKD you CONSTRICT the efferent arteriole to maintain a pressure gradient)
42
Q

Name 3 nephrotoxic drugs

A
  • Aminoglycosides
  • NSAIDs
  • Vancomycin
43
Q

Name 2 drugs that APPEAR to cause renal impairment by competing with creatinine for clearance by the kidneys

A

Trimethoprim

Fenofibrate (for dyslipidaemia)

43
Q

Name 2 drugs that APPEAR to cause renal impairment by competing with creatinine for clearance by the kidneys

A

Trimethoprim

Fenofibrate

44
Q

What are 3 methods of adjusting medications for someone who has renal impairment?

A
  1. Increase dose (e.g. frusemide)
  2. Use a different drug
  3. Reduce daily total dose (smaller doses at same time intervals, or larger doses at longer time intervals)
45
Q

eGFR vs. GFR

A

eGFR: automatically calculated, will appear in biochem and takes into account age + gender + renal function (but NOT patient size - so if your patient’s GFR is different from someone of AVERAGE size, it will not be accurate)

GFR: takes into account the weight of the individual patient

46
Q

Compare the pathophysiology of nephrotic vs. nephritic syndrome

A

NEPHROTIC: damage to podocytes –> STRUCTURAL damage to glomerular filtration barrier –> leading to renal loss of protein

NEPHRITIC: inflammatory response in the glomerulus –> GBM disruption –> RBC loss & decreased GFR

47
Q

List 5 clinical features of NEPHROTIC syndrome

A
  • Oedema
  • Frothy urine / HEAVY proteinuria
  • Hypoalbuminaemia (due to renal losses)
  • Hyperlipidaemia
  • Hyper-coagulable state (loss of antithrombin III)
  • Increased susceptibility to infections (loss of IgG)
48
Q

List 5 clinical features of NEPHRITIC syndrome

A
  • Haematuria!!! With acanthocytes
  • Light proteinuria (<3.5g/day)
  • RBC casts in urine
  • Hypertension
  • Mild-moderate oedema
  • Oliguria
  • Azotemia
  • Sterile pyuria (WBCs in the urine despite no bacteria)
49
Q

What defines a mixed nephrotic-nephritic picture?

A

Patients presenting with characteristics of nephritic syndrome and NEPHROTIC-RANGE proteinuria (>3.5g/day)

50
Q

Name 4 common causes of NEPHROTIC syndrome

A
  • Minimal change disease
  • FSGS
  • Membranous nephropathy
  • Diabetic nephropathy
51
Q

Name 3 common causes of NEPHRITIC syndrome

A
  • IgA nephropathy
  • Poststreptococcal glomerulonephritis
  • Goodpasture syndrome
  • Alport syndrome
  • Lupus nephritis (Can cause nephrotic and nephritic)
52
Q

Clinical manifestations of IgA nephropathy are usually triggered by which infections?

What is the proposed pathophysiology?

A
  • URTI
  • GIT infections

Infection –> IgA is the principal immunoglobulin in mucosa –> defective IgA circulative after an infection –> forms immune complexes in the kidney –> glomerulonephritis (Type III hypersensitivity: immunoglobulin/antibody-mediated)

53
Q

4 aspects of an infective urinary history (FUND)

A

Frequency
Urgency
Nocturia
Dysuria

54
Q

How does nephritic syndrome lead to hypertension?

A

Inflammation of the glomerulus –> GBM disruption –> decreased GFR –> macula densa detects low Na+ –> RAAS activation –> hypertension

55
Q

When is a renal biopsy indicated?

A
  • No clear cause of CKD

- Signs of severe or progressive disease

56
Q

Which investigations would you order in someone suspected to have IgA Nephropathy in order to diagnose the condition? What would they show?

A
  1. Urinalysis: signs of nephritic sediment, microhaematuria, minor proteinuria
  2. Laboratory tests: serum IgA levels (usually elevated)
  3. Renal biopsy: light microscopy showing mesangial proliferation, immunofluorescent microscopy showing mesangial IgA deposits, electron microscopy showing mesangial immune complex deposits
57
Q

Describe the renal biopsy findings in IgA Nephropathy

Light microscopy:
Immunofluorescent microscopy:
Electron microscopy:

A

Light microscopy: mesangial proliferation
Immunofluorescent microscopy: mesangial IgA deposits
Electron microscopy: mesangial immune complex deposits

58
Q

What is the pharmacological management of IgA nephropathy?

A
  • ACEi or ARBs

- Glucocorticoids (for those at HIGH risk of PROGRESSION. Not given if they have severe, irreversible kidney damage)

59
Q

Can renal cysts be benign?

A

YES - these are known as simple cysts

60
Q

Serum creatinine levels do not start rising until GFR is reduced by…

A

~ 50%

https://www.amboss.com/us/knowledge/Diagnostic_evaluation_of_the_kidney_and_urinary_tract/

61
Q

Name the 4 leading causes of end-stage kidney disease

A

Diabetes (38%)
Glomerulonephritis (16%)
Hypertension (13%)
Polycystic disease—presence of multiple cysts in the kidney (6.6%).

62
Q

Describe the RAAS system

A

LOW RENAL PERFUSION detected by one of the following mechanisms: macula densa cells sense low Na+, reduced perfusion pressure detected by baroreceptors in afferent arteriole, SNS stimulation of JGA

  1. Renin released from JG apparatus
  2. Angiotensinogen (from the liver) is cleaved into angiotensin I by renin
  3. Angiotensin-converting-enzyme (ACE) converts angiotensin I to angiotensin II
  4. Ang II has a number of effects on different cells (including aldosterone release)

Increases BP

63
Q

Name the peptide that inhibits renin release

A

Atrial natriuretic peptide (ANP) - released by stretched atria in response to increased BP

64
Q

Name the sites of action of Angiotensin II (5)

A 
ARTERIOLES: vasoconstriction
ADRENAL GLANDS: aldosterone release
HYPOTHALAMUS: increased thirst sensation + ADH release
NEPHRONS: increased Na+ retention
SNS: noradrenaline release
64
Q

Name the sites of action of Angiotensin II

A 
ARTERIOLES: vasoconstriction
ADRENAL GLANDS: aldosterone release
HYPOTHALAMUS: increased thirst sensation + ADH release
NEPHRONS: increased Na+ retention
SNS: noradrenaline release
65
Q

Name 4 calcium channel blockers

A

Ah, Very Nice Drugs

Amlodipine, verapamil, nifedipine, diltiazem

(Note: dihydropyridines end in ‘-dipine’)

66
Q

What are the 2 types of calcium channel blockers and how do their side effects differ?

A

DIHYDROPYRIDINES (amlodipine, nifedipine): primarily act on vascular smooth muscles.
SE: peripheral oedema!!!, headache, flushing, reflex tachycardia

NONDIHYDROPYRIDINES (verapamil, diltiazem): primarily act on ventricles
SE: bradycardia, AV block, (verapamil can also cause hyperprolactinaemia and constipation)

both can cause gingival hyperplasia

‘Verapamil mainly acts on Ventricles whereas Amlodipine mainly acts on Arteries’

67
Q

Should a diuretic be prescribed for amlodipine (and other dihydropyridine)-induced peripheral oedema?

A

NOOOOOO

68
Q

Angiotensin II causes constriction of both the afferent and efferent arteriole. Which arteriole is more greatly constricted?

A

EFFERENT arteriole subject to greater vasoconstriction

69
Q

When a patient is commenced on an ACE inhibitor or angiotensin-II-receptor blocker, they can experience a rise in serum creatinine. Why is this, and should the ACEi/ARB be stopped?

A

When patients have chronic renal impairment they have nephron loss, and hence each nephron is having to filter a larger amount. This is partly achieved by INCREASING the glomerular pressure so that there is increased pressure across each nephron.

Medications such as ACE inhibitor and Angiotensin Il blockers cause VASODILATION by blocking the effect of angiotensin ll. This results in dilatation of primarily the EFFERENT arteriole, which results in a REDUCTION in the glomerular filtration pressure. As a result there is less glomerular filtration (i.e. less GFR) and the creatinine rises.

Depending on the degree of fall in renal function (and this requires clinical judgement so there is no right or wrong percentage) the aim would be to try to continue the ACEi/ARB. This is because although there is a short term fall in GFR, in the long term, the reduction in glomerular pressure (think of it as glomerular hypertension) protects the glomerulus against future glomerulosclerosis, and further falls in GFR.

So the initial fall in renal function is really a short term pain for a long term gain.

TL;DR = renal impairment –> each nephron working harder –> compensate by increasing glomerular filtration pressure.

ACEi cause reduction in glomerular filtration pressure, so less GFR, leading to rise in BUN. Long-term the reduction in filtration pressure protects against further glomerulosclerosis so net benefit is positive

70
Q

What are the 2 most important prognostic factors in renal disease? Which medication helps?

A

HYPERTENSION and PROTEINURIA are the 2 most important prognostic factors.

ACEi both reduce blood pressure and reduce GFR (and therefore proteinuria) by causing DILATION of the efferent arteriole.

71
Q

What effect do NSAIDs have on the nephrons?

A

Constricts the afferent arteriole, reducing renal perfusion and GFR

72
Q

Which drugs make up the ‘triple whammy’?

A
  • NSAID
  • Diuretic
  • ACEi or ARB
73
Q

Describe the mechanism through which each of the 3 drugs in the ‘triple whammy’ can cause AKI

A
  1. ACEi and ARBs decrease GFR by dilating the efferent arteriole
  2. Diuretics contribute to AKI by causing hypovolemia
  3. NSAIDs block COX-II, inhibiting prostacyclin synthesis. Prostacyclin USUALLY causes afferent arteriole DILATION, so NSAIDs will result in afferent arteriole CONSTRICTION
74
Q

Handy memory tool for the effect of prostaglandins and angiotensin on afferent and efferent arteriole

A

AFFERENT ARTERIOLE (AA): prostAglAndins (dilate AA)

EFFERENT ARTERIOLE (EA): angiotEnsin (constrict EA)

75
Q

The anaemia of CKD is…?

A

Normocytic, normochromic

76
Q

What can be given to treat anaemia due to CKD?

A

Erythropoietin-stimulating agents (ESAs)

77
Q

What is the leading cause of death in people with ESKD?

A

Cardiovascular disease

78
Q

Under which circumstances might creatinine NOT be a good measure of kidney function?

A

Breaking down more muscle: physical activity, cachexia

Drugs (e.g. gentamicin)

Hypertension

79
Q

Describe the lifestyle changes that will be beneficial for someone with CKD

A
  • Low sodium diet
  • Low-protein diet (but not if they have nephrotic syndrome)
  • Glycaemic control
  • Lipid control
  • Healthy diet + exercise
  • Smoking cessation
80
Q

Give examples of pre-renal, intra-renal, and post-renal causes of kidney injury/failure

A

PRE-RENAL: decreased GFR, decreased blood volume (e.g. shock, ischaemia)

INTRA-RENAL: injury to renal tubule, e.g. acute tubular necrosis (due to drugs, toxins, ischaemia)

POST-RENAL: urinary outflow obstruction (kidney stones, prostate, tumour)

81
Q

Describe the biochemistry changes that occur in CKD

A
  • Hyperkalemia
  • Hyperphosphatemia and hypocalcemia
  • Hypernatremia
  • Elevated creatinine and BUN
  • Metabolic acidosis
82
Q

How does high phosphate cause low calcium?

A

Phosphate binds to calcium

83
Q

Why does metabolic acidosis result from CKD?

A

Kidneys aren’t excreting as many H+ ions, causing them to build up

84
Q

Name 4 nephrotoxic substances that patients with CKD should be instructed to avoid

A
  1. NSAIDs
  2. Antifungals
  3. Antibiotics (aminoglycosides, cephalosporins, vancomycin)
  4. Antivirals (aciclovir)
85
Q

What are the 2 options for dialysis? What are the principles underlying dialysis?

A

Haemodialysis and peritoneal dialysis

Uses DIFFUSION to remove urinary substances, toxins, and extra water from the patient’s body

86
Q

What can be done to manage hyperphosphatemia?

A

Phosphate chelating agents / phosphate binders

87
Q

What is azotemia?

A

Laboratory abnormality due to an increase in urea, nitrogen and/or creatinine, due to decreased renal excretion.

88
Q

What is the function of aldosterone? Which electrolytes does it affect?

A

Increases Na+ reabsorption by principal cells of the DCT and collecting duct. Cl- passively follows as a result.

It also increases K+ secretion by the principal cells.

89
Q

What is the most common type of primary glomerulonephritis?

A

IgA nephropathy

90
Q

What is the most common clinical feature/presentation of IgA nephropathy?

A

Gross/frank haematuria

Other (less frequent) presentations:

  • Microscopic haematuria & proteinuria
  • Nephrotic/nephritic syndrome
91
Q

Compare IgA Nephropathy vs. Post-Streptococcal Glomerulonephritis

A

IgA Nephropathy: episodes of gross haematuria, flank pain, low-grade fever occur DURING OR IMMEDIATELY AFTER URTI or GIT infection

PSGN: symptoms occur ~10-30 days after an acute infection

92
Q

Name 3 sources of infection that can trigger PSGN

A

Prior infection with Group A beta-haemolytic streptococci:

  • Throat infections (tonsilitis, pharyngitis)
  • Soft tissue infections (impetigo, erysipelas)
  • Osteomyelitis
93
Q

What can be seen in a urinalysis of someone with IgA nephropathy?

A
  • Nephritic sediment
  • Microhaematuria
  • Minor proteinuria
94
Q

Compare the Urine MC&S findings in nephrotic vs. nephritic syndrome

A

NEPHROTIC:

  • Nephrotic sediment (lipiduria, fatty casts with Maltese cross appearance)
  • Renal tubular epithelial cell casts

NEPHRITIC:

  • Haematuria
  • Acanthocytes
  • Red blood cell casts
  • Mild-moderate proteinuria
  • Sterile pyuria
95
Q

How does the pathophysiology of nephritic syndrome cause oedema and HTN?

A

Inflammation of the glomerulus –> disruption of GBM –> increased permeability –> loss of RBCs + decreased GFR –> haematuria, oliguria, azotemia –> increased renin d.t. decreased perfusion –> oedema, HTN

YEAR 3 - SEMESTER 2 (12 decks)

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