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Nephrology (Long) > Chronic Kidney Disease (CKD) > Flashcards

Chronic Kidney Disease (CKD) Flashcards

1
Q

What are the most common causes of CKD? (hence should be asked in history). 6+

A

Diabetes – 33%

GN – 24%

HTN – 14%

PCKD – 7%

Reflux nephropathy (any cystoscopies?)

Analgesic nephropathy

Vasculitis

Infiltrative: sarcoid/amyloid

Renovascular

Wield and wonderful: Alport’s (_deafness & persistent haematuri_a)

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2
Q

What are the 5 modifiable risk factors for the progression of CKD in this patient?

A

AKI

Proteinuria

HTN

Hyperuricaemia

Smoking

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3
Q

In PRICMCP for CKD patient, what symptoms would you ask for that led to the initial diagnosis? (4)

A

Ask “Have you been told what the cause of your kidney trouble is?” - will save a lot of time.

Protein or blood in urine

Swelling/oedema

Passing little amount of urine (oliguria)

On a routine blood test or during admission for other reasons.

Others are pretty vague, e.g. lethargy, anorexia, other complications.

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4
Q

What are symptoms of uraemia? (5)

A

itch

lethargy

anorexia/nausea

SOB/chest pain (pericarditis)

confusion (encephalopathy)

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5
Q

What are the complications of CKD? Go.

A

CKD - ABCDEF

Anaemia (EPO deficiency, ACD, iron deficiency), Acidosis

BP (HTN) & Bones: renal osteodystrophy (from osteomalacia, abnormal bone tun-over), vitamin D & calcium deficiency, 2o/3o hyper-PTH

Cardiac: inc risk of CAD, PVD, accelerated AS, CCF

Dialysis-related complications: peritonitis (PD), fistula thrombosis, infection, bleeding (HD), cardiac complications during dialysis.

Disability from neurological complication: PN, CTS, Restless leg syndrome

Electrolyte disturbances: hyper-K, hyper-Ca, hyper-Phos

Fluid Overload

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6
Q

What are the dialysis questions in history? (8)

A

Duration

Type

Where

Dry & current weight

Weight gain between dialysis

Passing urine

Complications

Coping

Plan for transplant

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7
Q

CKD + dialysis - PRICMCP***.

A

P: primary kidney disease, disease duration, initial symptoms (routine bloods, haematuria, proteinuria)

R: FH of primary kidney disease, secondary causes (e.g. HTN, DM, GN, analgesia, reflux, PCKD…etc)

I: renal biopsy if so when, why, what showed.

C: Anaemia, Bone disease, HTN, CVD/PVD/CVA, PN/RLS, electrolytes, fluid overload, dialysis-related complications

M:

  • Dialysis: type & access (graft vs native vein, previous access), duration (how many hours, how much fluids removed), location (satellite, in-centre or home), symptoms before & after dialysis, are they passing urine? dry + current weight. Coping? Complications.
  • Dialysis patient - are you on transplant list? if not why not?
  • Of complications
    • A: EPO, iron supplements/infusion
    • B: ACEi, antihypertensives, Bone: Calcium/Vit D
    • C: diuretics, salt/fluid restriction
    • DE: resonium, phosphate binders, lyrica…etc.
  • Of the disease

C:

  • dialysis (dry weight, weight gain between sessions, passing urine?). Any weight gain, increased gain between dialysis?
  • uraemia (itch, lethargy, anorexia/nausea, chest pain, encephalopathy)
  • fluid overload, IHD symptoms
  • how is the family/patient coping
  • is there a plan for a transplant? if not have you thought about it?

P: do you understand the prognosis/natural hx of CKD, complications.

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8
Q

CKD examination? (8)

A

Coherent patient with no evidence of Asterix to suggest encephalopathy.

Palmar creases / conjunctival pallor (anaemia)

BP was …., visual acuity was x/x. Ophthalmoscopy revealed changes suspicious of hypertensive retinopathy in fundoscopy (AV nicking, flame hemorrhages, cotton-wool spots, exudates)

Access (do not miss!): AVF in L/R arm that looks non-erythematous, non-tender. Bruit was present, or tenckhoff catheter, vascath (or old scars)

Uraemia: no Scratch marks, pericardial rub to suggest pericarditis

JVP + sacral oedema, Chest (fluid overload)

Abdomen: there was a diagonal scar in RIF/LIF with a palpable mass below it suggestive of kidney transplant. There was no tenderness.

Legs: evidence of gout, PN, fluid overload

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9
Q

What is your approach for investigating this patient with CKD/dialysis?

A

T: confirm renal function with EUC and previous trend to assess disease progression. Renal biopsy (if any)

E: exclude other secondary causes. Rule out infection, hypovolaemia, shock, bleeding, NSAIDs/PPIs (interstitial nephritis), obstruction - urine MCS, septic screen, review medications, renal USS/CT KUB looking for obstruction (size, scarring). Disease specific bloods (ANA, ENA, ANCA, complement, APS abs, Hep B/C, HIV, ASOT…etc)

S: UACR, UPCR, 24h urine collection to quantify proteinuria. Urine cast/dysmorphic RBCs looking for haematuria

Screen complications: Albumin (malnutrition), Hb + EPO (rule out insufficiency), iron studies, B12/folate, VBG/Bicarb (acid-base), ambulatory BP, PTH/Vitamin D/CMP (looking for hyper-PTH, hypercalcemia), EUC (raised urea). ALP (osteomalacia). ECG (LVH, ischaemia), CXR (fluid overload). DEXA, TTE/stress test. NCS looking for evidence of motor/sensory neuropathy.

T: other baseline blood tests

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10
Q

How would you explain to the patient what eGFR of 30 means?

A

This means that you have 30% of normal kidney function.

Normal eGFR is ~100ml/min.

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11
Q

What do you think the risk of progression in this patient with CKD?

A

This patient has a significant risk of rapid progression given that he/she is… (risk factors)

  1. Proteinuria
  2. AKI
  3. HTN
  4. Smoking
  5. Have a disease that increases the glomerular pressure (diabetes, obesity)
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12
Q

In a 85-yo man with single kidney, what would be the expected eGFR?

A

eGFR drops at a rate of 1ml/hr per year from 35.

So by 85, normal eGFR (100) would drop to by 50 = 50ml/min.

In a patient with single kidney, would be about 25mls/min.

If there is a discrepancy between the calculated & expected eGFR - suspect the presence of cause other than the aging.

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13
Q

When is eGFR not accurate? (3)

A

When there is AKI

When patient is over or under weight

Any other cause of muscle mass loss (e.g. amputation)

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14
Q

How would you classify GN? What do you know about GN?

A

Primary or Secondary

Primary is divided to focal & diffuse

Primary focal: FSGS (focal segmental glomerular sclerosis), IgA nephropathy

Primary diffuse: minimal change, membranous, proliferative (mesangio-capillary, mesangio-proliferative, crescentic, post streptococcal)

Secondary: Diabetes, SLE, Vasculitis, Goodpasture’s, Myeloma, Cryo, IE, HUS, HSP

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15
Q

Here is the result of kidney biopsy (showing e.g. membrano-proliferative or FSGS). How would you investigate this to work out what the aetiology is? (5 categories)

A

Investigations for secondary causes of GN includes:

Review Hx: FH or previous Heroin use (FSGS), penicillamine, NSAIDs or anti-TNFs (MPGN)

Autoimmune: ANA, ENA, APS abs, ANCA, cryoglobulins, anti-GBM abs

Infection: HIV, Hep B/C, syphilis serology, thin/thick blood film (indolent)

Imaging: Kidney USS looking for Reflux nephropathy (cause of FSGS)

Cancer: Look for evidence of malignancies if consistent with Hx.

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16
Q

Difference between nephrotic vs. nephritic syndrome in terms of pathological (1) & biochemical features (i.e. urine)?

A

Nephrotic – protein leakage across the glomeruli:

  • severe proteinuria (urine protein 3.5 g / 24 hours)
  • hypoalbuminaemia (<30)
  • oedema.
  • Hyperlipidaemia

Nephritic – inflammation or injury within the glomeruli allowing protein, RBCs, WBCs into the renal tubule; there is:

  • proteinuria
  • haematuria, pyuria
  • hypertension
17
Q

What are the 2 most common causes of Nephrotic syndrome?

A

Primary (80%): Membranous GN (most common), FSGS, MPGN

Secondary: Diabetes (most common by far), SLE, malignancies, MM, infection.

18
Q

3 most common causes of nephritic syndrome?

A

IgA nephropathy

Lupus nephritis

Crescenteric GN associated with vasculitis (GPA, EGPA, MPA, GPS)

19
Q

What is your approach to managing this patient with CKD?

A

Goals:

  • identify & treat reversible causes
  • slow disease progression
  • prevent complications

Confirm Dx: EUC, UACR/UPCR, trends and renal biopsy if any.

A: investigate & treat secondary causes + associations

  • Infection, hypovolaemia/dehydration, shock (AKI), remove precipitating drugs, obstruction
  • consider investigating for secondary causes (AI panel, infection panel, MM, dopplers)
  • exacerbating factors - compliance to FR.

Screen/investigate for complications

  • ABCDEF (anaemia, acidosis, bone, cardiac, neuro/RLS, electrolytes, fluid overload)

T: non-pharm

  • Education: nature of the progressive disease, need for RRT, complications - Kidney Health Australia: has info packs, self-management resources
  • Slow disease progression: manage HTN, smoking cessation, avoid unnecessary NSAIDs & contrast, prevent hyperuricemia
  • ***This means lifestyle changes are necessary - salt & fluid restriction, avoid alcohol, weight loss (if obese), moderate exercise
  • Diet [aim Alb >35]: low Na (<6g/d)/K/Phosphate diet, minimize purine-rich food/beer that worsens hyper-uricaemia. Refer to the renal dietician. Nephro supplement.
  • infection prophylaxis (vaccination, hygiene, contacts)
  • Support groups, exercise programs
  • Neuropathic/muscle pains: stretching exercise, hot-cold compresses, massages
  • RLS: massages, relaxation techniques

T: Pharm (focused on Mx of complications, preparation to dialysis & renal transplant)

  • A: EPO, iron supplements (target Hb 100, ferritin >100, tSAT >20%), sodium Bicarbonate (titrate to Bicarb >22), watch fluid status
  • B: Ca/Vit D replacement, Calcitriol, phosphate binders to maintain Ca/phos at normal level tx OP, parathyroidectomy (if PTH >800-1000 persistently)
  • C: aggressive CV risk factor Mx - statins, BP medications (aim BP <125/75), aspirin if high Framingham.
  • D: ensure iron replete, dopamine agonist for RLS (pramipexole, rotigotine)
  • E: phosphate binders, resonium [aim K < 6]
  • F: cautious use of diuretics based on fluid balance
  • Dialysis: prepare when eGFR <30 ⇒ educate, refer, prepare vascular access when eGFR 20, commence eGFR 7-10.
  • Transplant: consider when eGFR <15
  • Treat underlying aetiology

Involve: renal dietician, renal palliative care, transport/pool appointments

Complication screening: regularly monitor for ABCDEF + need for dialysis & transplant

Ensure F/U provide support.

20
Q

Patient with diabetic nephropathy + hypertension. You have started ACEi/ARB and Cr increased from 100 to 128. Would you cease ACEi?

A

Depends on the clinical context. Would still assess volume status & rule out infection, hypovolaemia…etc.

Assuming volume neutral - would continue.

Increase in Cr up to 30% may indeed indicate a degree of renal protection (reduced glomerular pressure increases Cr but protects kidneys in the long run)

21
Q

What is your approach to managing this patient’s HTN with CKD, including pharmacological agents?

A

Rule out poor compliance, secondary causes

ACEi/ARB 1st line, risk in Cr is expected

Loop Diuretics to reverse volume overload

CCB (dihydropyridine) - slows disease progression (better than thiazide)

Aldosterone R antagonists - if reasonable renal function. Watch K

Regular loop +/- thiazide can be considered to help reduce K

22
Q

What are the causes of Anaemia in this patient with CKD? (5)

A

Erythropoietin deficiency

Iron deficiency, result out bleeding

ACD

BM suppression

Malnutrition (folate deficiency)

23
Q

How would you investigate suspected osteomalacia? (focussed)

A

XR - decreased density, looser’s zones

CMP: low Ca, phosphate and vit D (pan-low)

High ALP

24
Q

What is dynamic bone disease caused by in CKD on dialysis?

A

This is due to reduced bone formation.

Oversuppression of Phosphate using binders is the main cause.

25
Q

What are the Calcium, Phosphate, PTH target in CKD?

A

Calcium 2.1-2.4

Phosphate <1.6 (normal)

PTH 2-3 ULN

26
Q

What is the management for renal osteodystrophy? (4)

A

Basically try and normalise Ca/PTH/Phos then consider pharmacological.

  1. Normalize Calcium, 2.1-2.4
  2. Lower Phosphate with binders or increasing dialysis time: Calcium carbonate, Sevelemer, Lanthanum, avoid aluminum.
  3. Hyperparathyroidism: Cinacalcet (lowers Ca/PO4/PTH), consider Parathyroidectomy if PTH >100
  4. Bisphosphonates are controversial: as it may make the bone more dynamic. But if evidence of osteoporosis - can use.
27
Q

Treatment of Calciphylaxis?

A

Sodium Thiosulphate

28
Q

Fertility on dialysis? What do you know?

A

Fertility improves with good dialysis

Even better with transplant

If dialysis patient get pregnant, need daily dialysis

Risk of premature

29
Q

DDx for membrane stops working in PD patient?

A

Membrane failure - often occur after few years

Constipation

Mechanical factors with Tenchoff catheter

30
Q

How would you manage following symptoms of ESRF?

Itch

Nausea

Neuropathic pains

Hiccups

A

Itch: moistrisers, antihistamines, gabapentine, evening primrose oil

Nausea: antiemetics

Neuropathic pains: gabapentinoids

Hiccups: Haloperidol

31
Q

PD adequacy is assessed by (5)?

A

Uraemic symptoms

Fluid overload

Urea/PO4/K+

UF: UF failure is defined as <400mls of fluid shifted on a high strength bag.

Cr clearance (in the blood vs. bag)

32
Q

What phosphate binders do you know of? (3)

A

Calcium Carbonate

Sevelamer (for patient on dialysis)

Lanthanum (for patient on dialysis)

33
Q

Which AV fistula would you recommend?

A

Native AV fistula should always be attempted first.

Start distally: radio-cephalic (wrist) then proximally to brachiocephalic

If native graft cannot be fashioned → use synthetic graft (but higher risk of infection and thrombosis)

Nephrology (Long) (5 decks)

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