Chronic Kidney Disease (CKD) Flashcards
What are the most common causes of CKD? (hence should be asked in history). 6+
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)
What are the 5 modifiable risk factors for the progression of CKD in this patient?
AKI
Proteinuria
HTN
Hyperuricaemia
Smoking
In PRICMCP for CKD patient, what symptoms would you ask for that led to the initial diagnosis? (4)
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.
What are symptoms of uraemia? (5)
itch
lethargy
anorexia/nausea
SOB/chest pain (pericarditis)
confusion (encephalopathy)
What are the complications of CKD? Go.
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
What are the dialysis questions in history? (8)
Duration
Type
Where
Dry & current weight
Weight gain between dialysis
Passing urine
Complications
Coping
Plan for transplant
CKD + dialysis - PRICMCP***.
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.
CKD examination? (8)
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
What is your approach for investigating this patient with CKD/dialysis?
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
How would you explain to the patient what eGFR of 30 means?
This means that you have 30% of normal kidney function.
Normal eGFR is ~100ml/min.
What do you think the risk of progression in this patient with CKD?
This patient has a significant risk of rapid progression given that he/she is… (risk factors)
- Proteinuria
- AKI
- HTN
- Smoking
- Have a disease that increases the glomerular pressure (diabetes, obesity)
In a 85-yo man with single kidney, what would be the expected eGFR?
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.
When is eGFR not accurate? (3)
When there is AKI
When patient is over or under weight
Any other cause of muscle mass loss (e.g. amputation)
How would you classify GN? What do you know about GN?
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
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)
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.
Difference between nephrotic vs. nephritic syndrome in terms of pathological (1) & biochemical features (i.e. urine)?
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
What are the 2 most common causes of Nephrotic syndrome?
Primary (80%): Membranous GN (most common), FSGS, MPGN
Secondary: Diabetes (most common by far), SLE, malignancies, MM, infection.
3 most common causes of nephritic syndrome?
IgA nephropathy
Lupus nephritis
Crescenteric GN associated with vasculitis (GPA, EGPA, MPA, GPS)
What is your approach to managing this patient with CKD?
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.
Patient with diabetic nephropathy + hypertension. You have started ACEi/ARB and Cr increased from 100 to 128. Would you cease ACEi?
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)
What is your approach to managing this patient’s HTN with CKD, including pharmacological agents?
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
What are the causes of Anaemia in this patient with CKD? (5)
Erythropoietin deficiency
Iron deficiency, result out bleeding
ACD
BM suppression
Malnutrition (folate deficiency)
How would you investigate suspected osteomalacia? (focussed)
XR - decreased density, looser’s zones
CMP: low Ca, phosphate and vit D (pan-low)
High ALP
What is dynamic bone disease caused by in CKD on dialysis?
This is due to reduced bone formation.
Oversuppression of Phosphate using binders is the main cause.
What are the Calcium, Phosphate, PTH target in CKD?
Calcium 2.1-2.4
Phosphate <1.6 (normal)
PTH 2-3 ULN
What is the management for renal osteodystrophy? (4)
Basically try and normalise Ca/PTH/Phos then consider pharmacological.
- Normalize Calcium, 2.1-2.4
- Lower Phosphate with binders or increasing dialysis time: Calcium carbonate, Sevelemer, Lanthanum, avoid aluminum.
- Hyperparathyroidism: Cinacalcet (lowers Ca/PO4/PTH), consider Parathyroidectomy if PTH >100
- Bisphosphonates are controversial: as it may make the bone more dynamic. But if evidence of osteoporosis - can use.
Treatment of Calciphylaxis?
Sodium Thiosulphate
Fertility on dialysis? What do you know?
Fertility improves with good dialysis
Even better with transplant
If dialysis patient get pregnant, need daily dialysis
Risk of premature
DDx for membrane stops working in PD patient?
Membrane failure - often occur after few years
Constipation
Mechanical factors with Tenchoff catheter
How would you manage following symptoms of ESRF?
Itch
Nausea
Neuropathic pains
Hiccups
Itch: moistrisers, antihistamines, gabapentine, evening primrose oil
Nausea: antiemetics
Neuropathic pains: gabapentinoids
Hiccups: Haloperidol
PD adequacy is assessed by (5)?
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)
What phosphate binders do you know of? (3)
Calcium Carbonate
Sevelamer (for patient on dialysis)
Lanthanum (for patient on dialysis)
Which AV fistula would you recommend?
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)
