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September lectures yr 3 (2018) > Chemical pathology of renal disease > Flashcards

Chemical pathology of renal disease Flashcards

1
Q

What kidneys are affect early in AKI and late in CKD?

A

Excretion and homeostasis

  • waste products of metabolism
  • fluid and electrolyte balance
  • acid-base balance
  • removal of drugs and toxins
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2
Q

What kidneys functions are not normally disturbed by AKI?

A

endocrine functions but in the later stages of CKD they are disrupted

  • renin-angiotensin system
  • erythropoietin production
  • hydroxylation of vitamin D
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3
Q

What is stage 1 AKI?

A

creatinine rises >26.5 micromol/L in 48 hours OR 1.5-1.9x baseline

urine output - <0.5ml/kg/h for 6-12hours

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4
Q

What is stage 2 AKI?

A

creatinine rises 2-2.9x baseline

urine output - <0.5ml/kg/h for >12hours

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5
Q

What is stage 3 AKI?

A

creatinine rises >353.6 micromol/L OR 3x baseline OR need for renal replacement therapy

urine output - <0.3ml/kg/h for >24 hours or anuria for >12 hours

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6
Q

How can the 3 main causes of AKI be divided?

A

Pre-renal
Renal
Post-renal

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7
Q

What is pre-renal damage?

A

damage due to underperfusion of an otherwise normal kidney
Therefore as the kidney is normal the metabolic consequences are reduced
Over 1 million nephrons in each kidney which are highly sensitive to toxic and hypoxic injury so underperfusion is very damaging

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8
Q

What are the causes of pre-renal AKI?

A

hypovolemia - due to hemorrhage or dehydration

sepsis and vasodilation

renal artery stenosis and atherosclerosis

pump failure

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9
Q

What is intrinsic renal damage and what are the causes?

A

Damage can be of the tubules or the glomerulus

  • ischemia
  • nephrotoxicity from drugs, poisons, myoglobin, and paraproteins (myeloma)
  • pyelonephritis - direct infection of the kidney itself
  • trauma
  • early stage CKD - glomerulonephritis and interstitial nephritis
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10
Q

What are involved in post renal damage?

A

post-renal obstruction

  • kidney stones
  • tumour
  • prostatic hypertrophy
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11
Q

What are the key biochemical findings for an AKI caused by pre-renal damage?

A 
urine volume: low 
urine:plasma osmolality: >2:1
urine [Na]: <15
Plasma Na: high 
Elevation of urea vs creatinine: urea>>creatinine
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12
Q

What are the key biochemical findings for an AKI caused by intrinsic renal damage?

A 
urine volume: initially high
urine:plasma osmolality: <1:1
urine [Na]: >40
Plasma Na: low
Elevation of urea vs creatinine: urea=creatinine
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13
Q

What is the treatment for pre-renal damage AKI?

A

Give fluid to increase renal perfusion

whereas if you did this in intrinsic AKI then it would cause fluid overload and can potentially kill the pt

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14
Q

In intrinsic AKI what are some of the key clinical features?

A

acidosis - occurs as 100mmol/day of acidic waste products of metabolism are retained - becomes life threatening when pH <7
hyperkalaemia - occurs as K isn’t excreted - becomes life threatening when it increases >8mmol/L

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15
Q

As AKI progresses due to lack of treatment what can happen ?

A

nitrogenous waste builds up and patients experience nausea, malaise and confusion
also begin to retain electrolytes and water due to the reduction in GFR - leads to hyponatraemia as more water is retained than salt
Fluid overload can follow on from this

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16
Q

How is an AKI managed?

A

first find cause
stop any NSAIDS, ACE inhibitors or angiotensin receptor inhibitors and any other nephrotoxic drugs
correct any life threatening fluid, electrolyte and acid-base abnormalities

pre-renal = renal perfusion needs to be restored
intrinsic = renal function should be supported with dialysis
post-renal=any obstruction should be removed

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17
Q

What is CKD and what are the causes?

A

gradual, irreversible changes in renal function
causes: hypertension, diabetes, polycystic kidneys, recurrent pyelonephritis and reflux nephropathy, glomerulonephritis, interstitial nephritis and drugs

18
Q

How is CKD staged?

A

determined by serum creatinine and GFR

  • early disease - GFR is more sensitive as creatinine levels don’t begin to rise until relatively late in the disease
  • creatinine levels are used to monitor disease later on
19
Q

How is eGFR calculated?

A

using MDRD formula - calculated based on age, sex, plasma creatinine and a correction factor for ethnicity and paeds

20
Q

What is the albumin/creatinine ratio?

A

this may replace GFR estimate in the future
A1 <3
A2 3-30
A3 >30

21
Q

What are the different stages of CKD?

A 
1 - GFR >90ml/min 
2- 60-90
3a- 45-60
3b- 30-44
4- 15-30
5-<15
22
Q

What are the consequences for stages 3-5?

A

3a - hypertension due to water retention, increased CVD risk
3b - low calcium due to decreased vitamin D
4- anaemia, anorexia, and hyperphosphataemia
5- salt and water retention, acidosis and hyperkalaemia

23
Q

How are stages 1-3 CKD managed?

A

monitoring GFR and urinary albumin:creatinine ratio
Also monitoring of bone health and cardiovascular risk
Any causes treated - e.g. diabetic control and anti-hypertensive treatments

24
Q

What are the more severe biochemical changes that occur in stages 3-4 CKD?

A

Largely due to reduced GFR
- elevated ACR, elevated cholesterol and triglycerides (increasing cardiovascular risk) and impairment of immune function
Several endocrine changes occur too

25
Q

How are patients with stages 3-4 CKD managed?

A
  • need to take 1,25-OH vitamin D due to decreased hydroxylation = leads to low calcium and secondary hyperparathyroidism
  • increased PTH leads to osteomalacia and osteitis fibrosa due to increased calcium reabsorption
  • decreased GFR leads to an increased phosphate level, these form precipitous with calcium which can cause metastatic calcification
  • erythropoietin production also drops causing anaemia
26
Q

What symptoms start to develop in stage 5 CKD?

A

Uremic symptoms - due to high levels of creatinine and urea

Phosphate and potassium will be high and patient will be acidotic

27
Q

What are the main areas that specialists focus on when treating patients with CKD at stage 3b +?

A

correcting endocrine and metabolic abnormalities with hormone replacement (alfacalcidol and EPO), phosphate binders are given to prevent metastatic calcification, diet modified to reduce potassium and fluids monitored
acid base balance corrected with bicarbonates
dialysis (haemo or peritoneal) and kidney transplant are used as renal replacement

28
Q

When do CKD patients become oliguric?

A

not until the very late stages

29
Q

What is the GFR like in glomerular disease and what is the consequence of this?

A

very little GFR therefore fluid overload and oliguria

30
Q

What is the water balance like in polycystic kidneys?

A

in this kidney disease the nephrons remain healthy so there will be an initial osmotic diuresis, causing polyuria

31
Q

What happens to the water balance in tubular damage to the kidneys?

A

there is ineffective water absorption causing polyuria

32
Q

What are the key characteristics of AKI?

A

rapid onset
hospitalized
risk increased but not caused by multi morbidity
CKD predisposes to AKI
creatinine and urine output used to classify

33
Q

What are the key characteristics of CKD?

A 
Gradual onset 
patient in community 
often caused by multi morbidity 
AKI contributes to CKD deterioration 
eGFR and ACR used to classify
34
Q

What are the features of pre-renal AKI in terms of:
- urea/creatinine
- electrolyte balance and acid base balance
- fluid balance
- endocrine abnormality
?

A
  • urea/creatinine = urea&raquo_space; creatinine
  • electrolyte and acid base = hypernatraemia
  • fluid balance = hypovolemia
  • endocrine abnormality = none
35
Q

What are the features of renal AKI in terms of:
- urea/creatinine
- electrolyte balance and acid base balance
- fluid balance
- endocrine abnormality
?

A
  • urea/creatinine = urea = creatinine
  • fluid balance = hypervoleamia
  • electrolytes . acid base = hyperkalaemia, hyponatriaemia, acidosis
  • endocrine abnormality = none
36
Q

What are the features of CKD in terms of:
- urea/creatinine
- electrolyte balance and acid base balance
- fluid balance
- endocrine abnormality
?

A
  • urea/creatinine = urea= creatinine
  • electrolyte balance and acid base balance = hyperkalaemia and acidosis
  • fluid balance = euvolaemia (until late)
  • endocrine abnormality = persistent
37
Q

What is renal glycosuria?

A

due to lack of glucose uptake

38
Q

What are examples of generalised and selective kidney disorders that do not constitute renal failure?

A 
generalized = faconi syndrome 
selective = cysteinuria (lack of amino acid uptake)
39
Q

What are the 3 main forms of renal tubular acidosis?

A

causes acid base and electrolyte balance disturbance
1) type 1 = distal - causes hypochloracaemic hypokalemic acidosis and kidney stones - due to failure to secrete H+ causing acidosis and excess K+ being lost in exchange for Na
Tx = bicarbonate and K

2) type 2 - proximal = leads to alkalosis - due to bicarbonate leak
3) type 4 is hyperkalaemia due to low aldosterone and renin

40
Q

When can you get high or low urea other than renal problems?

A

High - protein load and upper GI bleed

low - low protein diet and anorexia

41
Q

When can you get high or low creatinine other than renal problems?

A

high - muscle breakdown

low - small muscle mass

September lectures yr 3 (2018) (56 decks)

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