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year 5 pathology > Renal Part 2 > Flashcards

Renal Part 2 Flashcards

1
Q

AKI vs CKD

A
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1
Q 
Acute Renal Failure (MEDICAL EMERGENCY)
AKI definition (name of criteria, stages and 2 markers)
A

AKI = rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis

KDIGO stages

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2
Q

Pre-renal AKI:
hall mark
Normal response to REDUCED circulating volume physiology

A

Hallmark = reduced perfusion pressure (no structural abnormalities)

  • as part of generalised reduction in perfusion pressure
  • or renal ischaemia

Baroreceptor activation

  • activation of RAAS
  • Vasopressin release
  • SNS activation → (1) vasoconstriction (2) increased CO (3) renal sodium retention
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3
Q

Renal blood flow pressure control by 2 MAIN MECHANISMS

A
  • Myogenic Stretch – if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that high pressure into the Bowman’s capsule, thereby keeping the GFR steady
  • Tubuloglomerular Feedback – high chloride concentration in the early distal tubule (sign of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and reduced chloride level in the distal tubule
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4
Q

Causes of pre-renal AKI)

A

True volume depletion (e.g. haemorrhage)

Oedematous state (e.g. HF, liver failure)

Hypotension

Selective renal ischaemia (e.g. Renal Artery Stenosis)

Drugs affecting renal blood flow:

  • ACEi/ARBs = reduce efferent constriction. ACEi very contraindicated in RAS
  • NSAIDs/Calcineurin inhibitors (e.g. ciclosporin/tacrolimus) = decreased afferent dilatation
  • Diuretics = affect tubular function, decreased preload
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5
Q

Pre-Renal AKI vs Acute Tubular Necrosis (ATN)

A

Pre-Renal AKI is NOT associated with structural renal damage

  • Responds immediately to restoration of circulating volume
  • However, a prolonged AKI insult → ischaemic injury (ATN)
  • ATN does NOT respond to restoration of circulating volume
  • Epithelial cell casts would be seen in the urine on microscopy
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6
Q

Post-renal AKI case presentation

A 68-year-old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys (hydronephrosis). What is the likely cause AKI?

A

BPH due to hydronephrosis being present in both kidneys

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7
Q

Post-renal AKI: hallmark

A

Physical obstruction (at any level) to urine outflow

  • iata-renal obstruction
  • prostatic/urethral obstruction
  • retroperitoneal fibrosis/Ormond’s disease
  • ureteric obstruction (bilateral)
  • blocked urinary catheter
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8
Q

Post-renal: pathophysiology

A

GFR is dependent on the hydraulic pressure gradient

Obstruction results in increased tubular pressure

This results in an immediate decline in GFR

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9
Q

Post-renal AKI prognosis

A

Immediate relief restores GFR with no structural damage

Prolonged obstruction results in:

  • glomerular ischaemia
  • tubular damage
  • long-term interstitial scarring
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10
Q

Intrinsic renal AKI: pathophysiology (abnormality could be anywhere in the nephron)

A

Vascular disease (e.g. vasculitis)

Glomerular disease (e.g. glomerulonephritis)

Tubular disease (e.g. ATN) = MOST COMMON

Interstitial disease (e.g. analgesic nephropathy - long-term excessive use of analgesics)

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11
Q

Intrinsic renal AKI: common mechanisms of renal injury

A

Direct tubular injury (common) = ischaemia/toxins:

  • commonly ischaemia
  • endogenous toxins → myoglobin (i.e. rhabdomyolysis from muscle injury), Ig
  • exogenous toxins → contrast mediums (ahminoglycosides, amphotericin, acyclovir)

Immune dysfunction causing renal inflammation (common)

  • glomerulonephritis
  • vasculitis (i.e. 40 y/o presenting with systemic purpura and AKI diagnosis)

Infiltration/abnormal protein deposition

  • amyloidosis (causes nephrotic syndrome)
  • lymphoma
  • multiple myeloma
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12
Q

AKI RAAS SYSTEM RESPONSE

A
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13
Q

Rhabdomylosis

A

cola coloured urine, bruising (e.g. on thigh)

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14
Q

A 40 year old female presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure?

A

Systemic vasculitis

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15
Q

Most frequent cause of AKI

A

pre-renal and ATN

16
Q

5 biggest causes of mortality and morbidity in AKI

A

decreased renal perfusion pressure

medications

radiographic contrast media

postoperative

sepsis

17
Q

complications of AKI

A

partial recovery of renal function

discharged requiring chronic dialysis

discharged with increased serum creatinine

death (20%)

18
Q

Why do some AKIs resolve and others don’t?

A

Acute wounds heal via: haemostasis → inflammation → proliferation → remodelling

pathological responses are characterised by an imbalance between scarring and remodelling

replacement of renal tissue by scar tissue results in chronic disease

19
Q

CKD stages and parameters/markers

Why is stage 1 and 2 lower prevalence than 3

A

1 and 2 often undiagnosed

20
Q

Causes of CKD

A

DIABETES, HYPERTENSION (atherosclerotic renal disease)

chronic glomerulonephritis

infective/obstructive uropathy

polycystic kidney disease

21
Q

Roles of the kidney

A

Excretion of water-soluble waste

water balance

electrolyte balance

acid-base homeostasi s

endocrine functions (EPO, RAAS, Vit D)

  • 25 hydroxylase in liver
  • 1a hydroxylase in kidneys - sarcoid macrophages express this → sarcoidosis hypercalcaemia
22
Q

Consequences of CKD (4 processes)

A

(1) Progressive failure of homeostatic function

  • (1a) Acidosis
  • (1b) Hyperkalaemia

(2) Progressive failure of hormonal function

  • (2a) Anaemia
  • (2b) Renal bone disease

(3) Cardiovascular disease

  • Vascular calcification (renal osteodystrophy)
  • Uraemic cardiomyopathy

(4) Uraemia and death

23
Q

CKD complication: Renal acidosis and tx

A

Metabolic acidosis (failure of renal excretion of protons) →

  • Muscle and protein degradation
  • Osteopaenia due to mobilisation of bone calcium (because protons can be stored in bone)
  • Cardiac dysfunction
  • TREATMENT: oral sodium bicarbonate
24
Q

CKD complication: hyperkalaemia (common consequence of CKD esp. in diabetics)

A

Hyperkalaemia causes membrane depolarisation

This impacts on:

  • Cardiac function
  • Muscle function

Medications that cause hyperkalaemia:

  • ACE inhibitor
  • Spironolactone (potassium-sparing diuretics)
25
Q

CKD complication: anaemia (of CKD)

A

Progressive decline in EPO-producing cells

Usually occurs when GFR <30 ml/min

Causes normochromic, normocytic anaemia

  • This helps distinguish it from other causes of anaemia (e.g. iron deficiency, B12 deficiency)
  • TREATMENT: use artificial erythropoiesis-stimulating agents (ESAs)
    • Erythropoietin alfa (Eprex)
    • Erythropoietin beta (NeoRecormon)
    • Darbopoietin (Aranesp)

NOTE: reasons for CKD not responding to an erythropoiesis-stimulating agent:

  • Iron deficiency, TB, malignancy, B12 and folate deficiency, hyper-parathyroidism
26
Q

CKD complication: renal bone disease examples

A

Complex entity resulting in reduced bone density, bone pain and fractures:

  • Osteitis fibrosa cystica = caused by osteoclastic resorption of calcified bone and replacement by fibrous tissue. A feature of HPT.
  • Osteomalacia = insufficient mineralisation of bone steroid as body is trying to mobilise calcium from the bone
  • Adynamic bone disease = excessive suppression of PTH (from overtreatment) results in low turnover and reduced osteoid
  • Renal osteodystrophy
27
Q

Renal bone disease pathophysiology

A

Unable to: excrete phosphate from kidneys / make vitamin D

FGF-23/klotho produced → lower vitamin D → 2nd HPT

Excess phosphate → complexes with Ca2+ → hypocalcaemia

Phosphate-calcium crystals deposit → renal osteodystrophy

28
Q

Tx of renal bone disease

A

Phosphate control (bring it down) → dietary, phosphate binders

Vitamin D receptor activators:

  • 1-alpha calcidol
  • Paricalcitol

Direct PTH suppression

  • Cinacalcet (increases sensitivity of the calcium-sensing receptors)
29
Q

CKD complications: CVD (vascular calcification, uraemia cardiomyopathy)

A

This is the MOST IMPORTANT consequence of CKD (it is most likely thing to kill them)

The risk of a cardiac event seems to be directly related to GFR

Atherosclerosis:

  • Traditional risk factors such as cholesterol and hypertension contribute towards the risk
  • Renal vascular lesions are characterised by heavily calcified plaques (rather than lipid-rich atheromas)

Uraemic Cardiomyopathy (THREE phases):

  • LV hypertrophy → LV dilatation → LV dysfunction
30
Q

Treatment of CKD (3)

translpantation

harm-dialysis

peritoneal dialysis

A
31
Q

CKD tx transplantation: what is the contraindication

A

only contraindication is active sepsis

32
Q

CKD tx haemodialysis

A

blood passed through dialysed which removes most waste products

done about 3x per week for around 6 hours

you can have home dialysis

33
Q

CKD tx peritoneal dialysis

A

can be done at home

peritoneal cavity filled with fluid and peritoneal membrane is used as the dialysing membrane

increased risk of:

  • b2 macroglobulin amyloidosis
  • papillary RCC

year 5 pathology (27 decks)

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