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*Urinary System > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

Again - functions of kidney (3 homeostasis, 2 function, 1 regulation)

A

Body fluid homeostasis

Acid-base homeostasis

Electrolyte homeostasis

Excretory function

Endocrine function

Regulation of vascular tone

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2
Q

3 things to measure in kidney disease? How do we measure?

A
  • FILTRATION (excretion) function - use estimates of GFR (eGFR) from creatinine blood test
  • FILTRATION (keep in/barrier) function - check for presence of blood or protein in urine
  • ANATOMY - histology, imaging
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3
Q

4 methods for measuring excretory renal function?

A
  • inulin clearance (inulin is 100% filtered; not rly used in clinical practice as not practical (need constant infusion and catheter) but in books seen as gold standard)
  • isotope GFR (not practical as make the person radioactive - used if really want to know kidney function e.g. if they want renal transplant)
  • 24hr urine collection plus blood test
  • GFR estimating equations (measure serum creatinine; reciprocal relationship between GFR and creatinine - use eqns)
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4
Q

Describe relationship between serum creatinine and GFR

A

Reciprocal

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5
Q

Problem with creatinine?

A

Creatinine is generated from breakdown of muscle and not everyone has same muscle mass; dependent on age, ethnicity gender, weight, etc

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6
Q

Creatinine will not be raised above normal range until what percentage of total kidney function is lost?

A

60%

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7
Q

What demographic has a naturally higher serum creatinine?

A

African american (they have a higher muscle mass)

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8
Q

What is eGFR?

A

Estimated GFR - this is important to remember because it is NOT a direct measure of GFR (so is vulnerable to being incorrect - if person is not average for their sex, age, race, look at the patient! i.e. someone with leg amputation will have much ess creatinine as lost all that muscle)

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9
Q

What is the system for assessing kidney function?

A

International CKD Classification System

(to remember - start from bottom - 25ml/min increments)

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10
Q

3 formulae to estimate GFR from serum creatinine? (dont need to memorise actual equations - just say name)

A

Cockcroft Gault (generally used by pharmacists for drug dosing; includes weight so not practical on population level)

MDRD 4 variable equation

CKD-EPI equation (slightly more accurate than MDRD 4)

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11
Q

What substances cross GBM?

A

Water

Electrolytes

Urea

Creatinine

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12
Q

What substances cross GBM but are reabsorbed in proximal tubule

A

Glucose

Low molecular weight proteins (α2 microglobulin)

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13
Q

What substances do not cross GBM?

A

Cells (RBC, WBC)

High molecular weight proteins (albumin, globulins)

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14
Q

How is the barrier function of kidneys measured? What do they measure exactly?

A

Urinalysis (dipstick) - blood, protein

Protein quantification - protein creatinine ratio (PCR)

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15
Q

Definition of CKD?

A

Defined by either the presence of kidney damage (abnormal blood, urine or x-ray findings) or GFR <60ml/min/1.73m2 that is present for 3 months or longer (3 months important because can be AKI if less)

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16
Q

Try n name aetiologies of CKD (6) (more but these r the ones on slide)

A
  • Diabetes (most common)
  • Glomerulonephritis (and all its causes)
  • Hypertension
  • Systemic disease (immunological/haematological)
  • Renovascular disease
  • Genetic disorders e.g. polycystic kidney disease most common
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17
Q

4 step clinical approach to CKD

A
  • Detection of underlying aetiology (treatment for specific disease)
  • Slowing rate of renal decline (generic therapies)
  • Assessment of complications related to reduced GFR (prevention and treatment)
  • Preparation for renal replacement therapy
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18
Q

Signs and symptoms of CKD? (loads)

A

Appearance - pallor secondary to anaemia

Hypertension

SOB due to fluid overload

Kidneys - next card

Itch + cramps - advanced; likely due to biochemical changes = neuronal irritation

Cognitive changes

GI - anorexia, vomiting, taste disturbance

Urine output - polyuria (tubular conc ability impaired), oilguria, nocturia (impaired solute diuresis or oedema), proteinuria (frothy urine)

Haematuria (immune injury to glomerular capillary wall)

Peripheral oedema

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19
Q

What kidney changes can be seen in CKD? (5)

A
  • kidney shape on imaging may give clues to cause
  • bilaterally small = intrinsic disease e.g. GN
  • unilaterally small = renal arterial disease
  • clubbed calyces and cortical scars = reflux w chronic infection/ischaemia
  • enlarged cystic kidneys = cystic KD
20
Q

Proteinuria - what does tubular damage v glomerular damage result in?

A

Tubular - low grade proteinuria typically <2g, of low molecular weight proteins (e.g. beta-2 microglobulin)

Glomerular - loss of selectivity to protein filtration often exacerbated by hyperfiltration; losses >3.5g regarded as nephrotic range

21
Q

Haematuria - how is glomerular bleeding differentiated from lower tract bleeding?

A

Microscopy showing dysmorphic red cells and casts

22
Q

What causes peripheral oedema in CKD?

A

Renal sodium retention

Exacerbated by reduced oncotic gradient in nephrotic syndrome, cos of hypoalbuminaemia

23
Q

RLY good diagram for symptoms of CKD

A
24
Q

What are the components of history that should be obtained in detection of underlying aetiology

A

Previous evidence of renal disease, family history, systemic diseases, drug exposure, pre/post renal factors, uraemic symptoms

25
Q

What indicates previous renal disease?

A

Raised urea/creatinine

Proteinuria/haematuria

Hypertension

LUTs

Family History

26
Q

What history of systemic diseases may be found in CKD?

A

Diabetes mellitus

Collagen vascular disease (scleroderma, SLE, vasculitis)

Malignancy (myeloma, breast, lung, lymphoma)

Hypertension

Amyloidosis

Sickle cell disease

27
Q

Exposure to what drugs may be found in CKD?

A

NSAIDs

Penicillins/aminoglycosides

Chemotherapeutic drugs

Narcotic abuse

ACEi / ARBs

28
Q

Examples of pre/post renal factors?

A

Congestive cardiac failure

Diuretic use

Nausea, vomiting, diarrhoea

Cirrhosis

LUTS / pelvic disease

29
Q

What are uraemic symptoms?

A

Nausea, anorexia, vomiting

Pruritis

Weight loss

Weakness, fatigue, drowsiness

30
Q

What are the components of examination that aid detection of underlying aetiology (not as important as history but useful)?

A

Vital signs (fever, BP), volume status, systemic illness, obstruction (percussable bladder, enlarged prostate, flank masses)

31
Q

Indicators of depleted v overloaded volume status?

A

Depleted = orthostatic BP, skin turgor/temperature

Overloaded = raised JVP, crepitations, ascites, oedema

32
Q

Indicators of systemic illness?

A

-Rash – malar (lupus), purpuric (vasculitis), macular (AIN)

–Auscultation

–Cardiac murmurs (endocarditis)

–Abdomen

–Bruits, palpable organs

–Extremities

–Livedo reticularis (vasculitis, atheroembolism),

–splinter haemorrhages (endocarditis)

–Pulses

–Absent (vascular disease)

–Bones and joints

–Tender (malignancy)

–Inflammed (lupus)

–Gouty tophi

33
Q

4 KEY tests done in detection of underlying aetiology of CKD

A

Blood tests (U+Es, FBC)

Urine tests (urine dip, urine PCR or ACR (protein quant), 24 hr collection)

Histology (renal biopsy)

Radiology (USS etc)

34
Q

Ultrasound indicating progressive obstruction

A

Far right - long term obstruction leading to loss of renal cortex - thin, end-stage kidney

35
Q

Main stategies for slowing rate of renal decline

A

BP control (most important) - high BP is enemy of kidney! (damage to tufts, glomeruli sclerose, leftover glomeruli put under stress, they then sclerose etc leading to end stage KD!)

Control proteinuria (ACEI/ARB)

Treat underlying cause

(others - llopurinol, dietary protein restriction, fish oils, lipid lowering, control acidosis)

36
Q

Complications related to reduced GFR

A

Acidosis, anaemia, bone disease, CV risk, death + dialysis, electrolytes, fluid overload, gout, hypertension, iatrogenic issues

37
Q

Management of complicationsr elated to reduced GFR?

A

Acidosis - bicarb

Anaemia - EPO injection and iron

Bone disease - diet (potassium management) and phosphate binders (also vit D tablets)

CV risk - BP, aspirin, cholesterol, exercise, weight

Death + dialysis - counsel and prepare

Electrolytes - diet and consider drugs

Fluid overload - salt and fluid restriction, diuretics

Gout - optimise +/- meds

Hypertension - weight, diet, fluid balance, drugs

Iatrogenic issues - BE AWARE

38
Q

What causes bone disease in CKD?

A

kidney’s function to excrete phosphate is impaired (reduced serum calcium) - combo of low calcium and high phosphate stimulates PTH = bone resorption

impaired ability to hydroxylate vitamin D (low levels of 1 a hydroxylase- leads the reduced absorption of calcium) - high phosphate results in reduced 1 a hydroxylase = low vitamin D

39
Q

How does the delivery of sodium change when GFR falls?

A

When GFR falls there is reduced delivery of sodium to the distal tubule, where it usually exchanges with potassium

40
Q

How does an ACE i affect potassium levels?

A

Causes retention of potassium

41
Q

What level of potassium can induce fatal cardiac arrhythmia?

A

When potassium is greater than 7mmol/l

42
Q

Management of hyperkalaemia?

A

Acute

  • Stabilise - calcium Gluconate
  • Shift - salbutamol, insulin-Dextrose
  • Remove - dialysis, calcium resonium

Chronic

  • Diet, drug modifications
43
Q

Which drugs cause acute kidney injury on top of CKD?

A

Antibiotics

Contrast agents

44
Q

Risk of uraemia building?

A

Uraemic pericarditis

45
Q

How to prepare patient for end stage renal disease and renal replacement therapy

A
  • Education and info
  • Selection of modality (HD/PD? transplant? conservative care?)
  • Planning access
  • Deciding when to start RRT
  • MDT IS KEY !!

*Urinary System (26 decks)

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