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RnU > CKD, AKI, Transplantation > Flashcards

CKD, AKI, Transplantation Flashcards

1
Q

Low GFR < 60 ml/ min for 70 days, CKD or AKI?

A
  • Defined as GFR of < 60ml/min for > 90 days/3 months
    • If < 90 days may be AKI
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2
Q

How is CKD classified

A

Classification includes both eGFR and urinary albumin: creatine ratio (ACR) eg. G3a A3
As raised serum creatinine reflects compromised renal function with reduced GFR

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3
Q

Non-renal cause of CKD

A

Diabetes, hypertension

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4
Q

what is measured to test for proteinuria, how is it quantified

A

Albumin, quantify using albumin/creatine ratio

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5
Q

first line investigation in patients with albumin in dipstick

A

ACR, (then test kidney renal function)

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6
Q

Treatment for proteinuria

A

ACE inhibitors and corticosteroids

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7
Q

Should treatment be given if ACR is <30

A

No, may occur transiently. but need to prevent diabetic nehropathy

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8
Q

What does presence of proteinuria WITH BLOOD imply
What does proteinuria in HTN imply

A

Glomerular disease (problems with filtering)
Albuminuria suggest a primary renal cause in Hypertension → SEC Hypertension

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9
Q

What is nephrotic syndrome

A
  • Clinical syndrome comprising oedema, heavy proteinuria, hypoalbuminemia (low levels of albumin IN BLOOD)
    • May not have blood in urine
      (MAINLY GLOMERULAR PROBLEMS)
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10
Q

is GFR normal or abnormal in nephrotic syndrome

A

Depends on whether there is impairment of excretory function

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11
Q

One sign of nephrotic syndrome, dominant symptoms

A

stretch marks in legs during protein leaking. severe lethargy, reduced exercise tolerance, nausea and loss of appetite

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12
Q

What causes congenital Nephrotic syndrome

A

Mutations in nephrin in podocyte

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13
Q

How are the test results in systemic vasculitis

A

Tends to have more blood than protein - indicates inflammation

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14
Q

what antibody us systemic vasculitits associated with , what other symptoms

A

ANCA, May have painful lesions over joints (in both hands and feet) and rashes

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15
Q

Are CKD patients more likely to be hypo or hyperkalaemic
What other drugs or diseases can exacerbate this?

A
  • Hyperkalaemia common as GFR declines to less than 25
    • May occur at GFR > 25
      • Diabetes and type 4 RTA
      • ACE inhibitors → should consider reducing ACE inhibitors
      • High K Diet→ reduce consumption of high K food, increase low na food
        • High K diet will affect Na delivery to DCT
          Related to distal sodium delivery, decreased DND with decreased GFR
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16
Q

Is acidosis or alkalaemia more likely in CKD

A
  • Most Acidosis in CRF is due to animal protein in food → phosphates and sulfates generated as they break down
    • Inability to acidify urine in CKD
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17
Q

Bone disease as complication of CKD => What types??

A

Renal osteodystrophy

  • High turnover bone disease
    • Secondary hyperparathyroidism (Osteitis Fibrosa)
  • Low turnover bone disease
    • Osteomalacia
      • Due to low calcium
    • Adynamic bone disease
    • Aluminium bone disease
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18
Q

Treatment of renal osteodystrophy

A

phosphate restriction- meat and dairy , take calcium or non-calcium binders with meals, vitamin d therapy directly to override hydroxylation (alfacalcidiol), may require parthyriodectomy ??

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19
Q

What risk does CKD increase?

A

CVD

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20
Q

What is renal clearance? Diff vs GFR

A

VOLUME of plasma completely cleared of a substance per unit time
GFR = clearance if substance is completely lost to urine = C urine x UO / C plasma

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21
Q

MDRD vs Cockcroft gault equation for estimating GFR
What are the equations

A

MDRD does not require weight, only requires plasma creatinine
Cockcroft= eGFR = (140-age) * (weight)* 1.22 or 1.04 / Cr

22
Q

What is AKI characterized by

A

Acute oliguria and increases in plasma urea and creatinine

23
Q

Normal response to water deprivation test

A
  • plasma osmolality static but urine osmolality rises ( conc. of urine)
  • DI→ plasma osmolality rises as urine remains dilute
    • CDI→ responsive to DDAVP
24
Q

What does RTA type 1 result in and how to test

A
  • Renal Tubular Acidosis Type 1 (exclusively affects tubules) can lead to pH of urine being more than 5.5 (usually less than 5.5)
    • Due to distal tubular cells being unable to secrete H+(Abnormally permeable to H+)
  • an be tested through Ammonium Chloride loading test
    • Used to confirm suspected RTA type I
    • NH4Cl administration leads to metabolic acidosis
    • If pH of urine> 5.5 persists then RTA type 1 confirmed
25
Q

What is pre-renal AKI

A
  • Reduced real or “effective blood volume”
    • Kidneys are working fine but do not get sufficient blood supply
26
Q

Glomerular causes of renal AKI

A
  • Rapidly progressive glomerulonephritis
    • Immune aetiology characterised by “glomerular crescents”
27
Q

allergic cause of tubulointerstitial damage and treatment

Non allergic cause?

A

Acute allergic interstitial nephritis,
- PPIs (omeprazole), antibiotics, diuretics, NSAIDs
- May have eosinophilia (no rash)
- Often respond well to steroids

ATN- drugs, hypoperfusion eg. ACEI

28
Q

post-renal causes of AKI and first line method of exclusion

A

Obstruction, ultrasound

29
Q

what kind of AKI does myeloma cause

A

Post renal=> intra renal obstruction

30
Q

Treatment of multiple myeloma

A
  • Similar to primary hyperparathyroidism, but instead of surgery:
    • Reduce tumour mass by chemotherapy and/ or radiotherapy (reduces bone resorption)
    • Consider autologous bone marrow transplant
31
Q

what protein test for myeloma

A

Bence Jones

32
Q

treatment for rapidly progresive glomerulonephrotis

A

Immunosupression

33
Q

Indications for dialysis in severe AKI

A
  • Severe “uraemia”
    • No prospect of immediate improvement
      • Low amount of urine passed
    • Uraemic encephalopathy or seizures
    • Uraemic pericarditis
  • Hyperkalaemia unrespove to medical treatment (>6.5)
  • Instituted for fluid overload esp pulmonary oedema as they cannot respond to diuretics/ fluid restriction during AKI
  • Severe acidosis⇒ cells cant work well in myocardium, results in myocardial depression and hypotension
34
Q

What is CKD defined as

A
  • GFR of < 60ml/min for > 90 days/3 months
  • If < 90 days may be AKI
35
Q

When is CKD diagnosed despite GFR being over 60

A
  • Persistent proteinuria/microalbuminuria
  • Haematuria
  • Renal anatomical/genetic abnormality eg. biopsy-proven GN, or PKCD, or ultrasound or radiology
  • hypertension
36
Q

What drugs can cause CKD

A

NSAIDs, contrasts, gentamicin, phosphate enemas

37
Q

when should you test for proteinuria ( 2 disease, 1 symptom)

A

HTN, DM, Ascites/oedema

38
Q

CV complications of ESRD

A

LV hypertrophy, stroke

39
Q

Treatment of anaemia from CKD

A
  • EPO replacement therapy
    • All patients with Hb < 105 and adequate iron stores should be on EPO
      • In the form of long lasting EPO, give 3 times a week if on dialysis
  • f poor response to EPO
    • Check iron stores/CRP/B12+folate/PTH/Aluminium/? malnutrition/?malignancy
40
Q

is phosphate low or high in renal osteodystrophy and why

A

High, due to increased resorption of bone. Po4 not removed properly by kidneys despite being high

41
Q

What problem can PTH result in wrt bone

A

Osteitis Fibrosa

42
Q

What happens in renal osteodystrophy if too responsive to Vit D treatment

A

Adynamic bone disease as whole bone process is shut off

43
Q

Consequences of hyperphosphataemia

A

Vascular calcification which worsens BP

  • Non-compliant vessels
  • Systolic hypertension - L Vent Hypertrophy
  • Diastolic hypotension - MI
  • Calciphylaxis
    • Phosphate and vascular calcification
44
Q

What is the relationship between plasma creatinine and GFR

A

Reciprocal

45
Q

How can urine Na help to determine type of AKI

A

Urine sodium can be used to determine whether tubular function is appropriate
If low, suggests that tubules are appropriately re absorbing Na+ and water, may be pre-renal failure caused by hypotension.
If high, suggests tubular dysfunction or damage, or inadequate aldosterone action eg. established renal failure

46
Q

Causes of hypotension not related to hypovolaemia that can cause pre-renal AKI

A

Liver failure and septic/cardiogenic shock

47
Q

Tubulointersitial causes of AKI

A

Acute tubular Necrosis
-Tubular toxins eg. Gentamicin, cisplatinum,(nephrotoxic and used for cancers), NSAIDs ( limit blood flow and can be direct allogernic to kidneys) and radio- contrast dye
- Severe prolonged hypotension ( sepsis or MI etc.)
- Renal hypoperfusion( ACEI, ARBs, diuretics etc)

48
Q

What renal cause of AKI is related to thrombosis

A
  • Haemolytic uraemic syndrome (HUS)
    • E.coli related ⇒ may get better
49
Q

Post renal causes of AKI

A
  • Obstruction - multiple levels ⇒ Bilateral obstruction of obstruction or a single kidney ( transplant only one kidney) to result in AKI
  • Ureter
    • Calculi, tumour, extrinsic compression ( retroperitoneal fibrosis, tumour)
  • Bladder lesions- tumour
    • Stones ⇒ May have no pain at all
  • Prostate - hypertrophy (common), cancer
  • Myeloma spread to kidney ⇒ Intrarenal obstruction
50
Q

How does PTH change in mutliple Myeloma

A

suppressed due to hypercalcaemia

RnU (9 decks)

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