Renal: CKD Flashcards

1
Q

How is CKD staged?

A

1 = >90ml/min = normal or increased GFR with other evidence of renal disease

2 = 60-89ml/min = slight decrease In GFR with other evidence of renal damage

3a = 45-59ml/min = moderate GFR decrease with/without evidence of renal damage

3b = 30-44

4 = 15-29ml/min = severe GFR decrease with/without evidence of renal damage

5 = <15ml/min = established renal failure

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2
Q

What causes CKD?

A

DM = T2>T1

Glomerulonephritis = commonly IgA nephropathy

Unknown (20%) = many present late with small/shrunken kidneys

HTN, renovascular disease

Pyelonephritis and reflux nephropathy

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3
Q

What are the symptoms and signs of CKD?

A

Pallor

Uraemic tinge to the skin (yellowish)

Purpura

Increased BP

Cardiomegaly

Ballotable polycystic kidneys

Weight loss and poor appetite

Swollen ankles, feet or hands – as a result of water retention (oedema)

SOB

Tiredness

Haematuria

Polyuria, nocturia

Insomnia

Itchy skin

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4
Q

How should CKD be investigated?

A

Blood = Hb, ESR, U+Es, glucose, decreased Ca, increased phosphate, increased alk phos, PTH

Urine = dipstick, microscopy, C+S, albumin:creatinine

Imaging = USS (<9cm in CKD)

Histology = renal biopsy

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5
Q

How should CKD be managed?

A

Identifying and treating reversible causes = obstruction, nephrotoxic drugs, high Ca, lower CVS risks, tight glucose control in DM

BP = target <130/80, ACEi, ARB

CVS = statins for patients with raised lipids, aspirin

Diet = review by dietitian, K restriction if hyperkalaemia

Anaemia = replace iron/B12/folate, EPO

Acidosis = Na bicarb supplements

Oedema = high dose loop diuretic (furesemide), restriction on fluid and Na intake

Restless legs/cramps = check ferritin, gabapentin

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6
Q

What complications can arise from CKD?

A

Anaemia

HTN

Pulmonary oedema

CKD mineral bone disease

Secondary hyperparathyroidism

CVD

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7
Q

As a Dr how should you plan for the future for a CKD pt?

A

Start discussions of what options they have if they reach ESRF

Home care team input

Discuss disadvantages + advantages of types of RRT

  • Home therapies – APD, CAPD, Home HD
  • Unit-based therapies – Nocturnal HD, conventional HD
  • Active conservative management
  • Transplant

Refer for fistula
- Venous mapping

Refer for PD tube insertion

Work-up for transplant

  • Further tests
  • Refer to Transplant work-up clinic
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8
Q

How does the patient’s CKD affect any medications they need?

A

Statins = pts with high lipids

BP medication = target <130/80 - ACEi, ARBs

Anaemia = replace iron/b12/folate, EPO

Oedema = high dose loop diuretic (furosemide)

Restless leg/cramps = gabapentin

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9
Q

What is adult polycystic kidney disease?

A

Aetiology = genetic (ADPKD/ARPKD)

Pathophysiology = renal tubules become structurally abnormal, cysts develop, kidneys enlarge and lose function - over time

S/S = HTN, back or side pain, headache, abdo fullness, increased abdo size, haematuria, kidney stones, UTI

Investigations = BUN, Cr, eGFR, aCT, exam - enlarged liver, heart murmurs

Management = no current therapies proven effective to prevent progression, end stage - renal replacement therapy (RRT): dialysis and/or transplantation

Complications = HTN (activation of RAAS - use ACEi), kidney failure, liver cysts, mitral valve prolapse (1/4), diverticulosis, chronic pain, aneurysms, infected cysts

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10
Q

How can you differentiate between acute and chronic kidney damage?

A

Hx

Exam

Bloods = establish baseline (median value 1 year prior to event)

  • Hb - normocytic, normochromic
  • Acid-base balance
  • PTH, Ca, phosphate

Imaging = US
- CKD = shows loss of differentiation between cortex and medulla - thin cortex due to sclerosed nephrons

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