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MBBS IV - Junior Clerkship WCS > JC79 (Medicine) - Chronic kidney diseases > Flashcards

JC79 (Medicine) - Chronic kidney diseases Flashcards

1
Q

Clinical definition of CKD

A
  • GFR < 60 mL/min/1.73m2 for ≥ 3 months (Normal range = 90 – 120 mL/min/1.73m2)
  • Evidence of kidney damage such as albuminuria for ≥ 3 months
  • Abnormal findings on renal imaging present for ≥ 3 months
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2
Q

Define range of GFR for 5 stages of renal failure

A 
Stage 1 - Normal >90 
Stage 2 - Mild decrease 60-89
Stage 3 - Moderate decrease 45-59
Stage 3b - moderate to Severe decrease 30-44
Stage 4 - Severe decrease 15-29 
Stage 5 - End-stage - <15

** must be sustained for >90 days **

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3
Q

How does albuminuria affect prognosis of CKD

A

Higher persistent albuminuria = worse prognosis and higher risk of progression in CKD

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4
Q

Basic functions of nephron unit

A

Remove nitrogenous waste product
Conserve Sodium and water
Maintain electrolyte balance
Maintain acid-base balance

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5
Q

Albuminuria

- Cut-offs for normal vs diabetic pt.

A

Urine Albumin-creatinine ratio > 30mg/mmol = significant albuminuria in normal pt.

Urine ACR >3mg/mmol = microalbuminuria in diabetic pt., need ACEI or ARB

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6
Q

3 formulas for estimated GFR

A

Cockcroft and Gault Creatinine Clearance: age, serum creatinine, weight

Modification of Diet in Renal Disease Study (MDRD)

CKD- EPI or CKD- EPIcys

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7
Q

Most common causes of CKD

A
  • DM nephropathy (45%) **
  • Hypertension/ Renal artery stenosis (RAS) (27%)
  • Chronic Glomerulonephritis (10%)
  • Chronic pyelonephritis
  • Interstitial disease (5%)
  • Polycystic kidney disease (2%)
  • Drug induced (TCM)
  • Myeloma (CARB), Vasculitis, SLE
  • Obstruction, nephrolithiasis
  • Hereditary diseases (e.g. Alport’s)
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8
Q

Define pre-renal causes of CKD

A

Hypovolemia
• Hemorrhage
• Vomiting/ Diarrhea
• Diuretics

Hypervolemia but low effective circulating volume
• Heart failure with reduced ejection fraction (HFrEF)
(Cardiorenal syndrome)
• Decompensated liver disease with portal hypertension (Hepatorenal syndrome)

Low Afferent arteriole vasodilatation
• NSAIDs - Inhibits COX enzymes and thus decreased synthesis of prostaglandins (PG)
• ACEI/ ARB
• Cyclosporine

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9
Q

Define renal causes of CKD

A

Renal vascular disease:
 Hypertensive nephrosclerosis
 Ischemic nephropathy - Renal artery stenosis

Glomerular disease:
 Proliferative glomerulonephritis (Nephritic pattern)
 Non-proliferative glomerulonephritis (Nephrotic pattern)

Tubular-interstitial diseases: 
 Polycystic kidney disease (PKD)
 Reflux nephropathy
 Nephrocalcinosis - Result of hypercalcemia or hypercalciuria
 Sarcoidosis
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10
Q

List proliferative and non-proliferative primary glomerulonephritis

A

 Proliferative glomerulonephritis (Nephritic pattern)
• Post-streptococcal glomerulonephritis (PSGN)
• IgA nephropathy
• Membranoproliferative glomerulonephritis

 Non-proliferative glomerulonephritis (Nephrotic pattern)
• Minimal change disease (children)
• Focal segmental glomerulosclerosis
• Membranous nephropathy (adult)

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11
Q

Post-renal causes of CKD

A

Obstructive uropathy
 Prostatic disease
• Benign prostatic hyperplasia
• Prostatic cancer

 Metastatic disease

+ other obstructive pathologies…etc

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12
Q

Common renal symptoms between AKI and CKD

How to distinguish from AKI

A

Edema (hypoalbuminemia and RAAS activation)

Hypertension (fluid retention and low plasma volume triggers compensatory RAAS activation for salt and water retention

Oligouria

"”CKD has complications in CVD, Neuro, Haemat, endocrine…etc””
Anuria is never observed in CKD alone, always indicate AKI

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13
Q

Determinants of CKD progression

Typical GFR deterioration rate

A

Underlying cause
Baseline serum creatinine and severity of proteinuria
Hypertension severity
Renal fibrosis and aging

Rate: From 1ml/min to 7ml/min over 1 year

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14
Q

Mild CKD does not require management as it does not correlate with mortality.

True or False?

A

False

Mild CKD and albuminuria increases risk of cardiovascular death

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15
Q

Cardiovascular complications of CKD

A

Uremic pericarditis*/ Hypertension/ Hyperlipidemia/ Cardiomyopathy/ Accelerated atherosclerosis/ Volume overload/ Congestive heart failure

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16
Q

Neurological complications of CKD

A

Uremic encephalopathy* (Mental status change/ Coma/ Decreased in memory and attention)/ Neuropathy/ Seizure/ Impaired sleep

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17
Q

Hematological and endocrine complications of CKD

A

Hematological
Uremic bleeding* (Platelet dysfunction and EPO deficiency)/ Anemia

Endocrinological
Hyperkalemia/ Hyperphosphatemia/ Hypocalcemia/ Metabolic acidosis/ Secondary hyperparathyroidism/ Renal osteodystrophy

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18
Q

Dermatological complications of CKD

A

Dermatological
Pruritus*/ Calciphylaxis/ Nephrogenic systemic fibrosis (NSF)/
Uremic frost (white crystals in and on the skin)

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19
Q

Constitutional symptoms of CKD

A

Fatigue/ Anorexia/ Nausea and vomiting*/ Metallic taste/ Fetor uremicus
Nocturia/ thirst

20
Q

Outline history taking for CKD

A

Medical history
• Hypertension (Hypertensive nephrosclerosis)
• DM (DM nephropathy)
• Previous AKI
• Cardiovascular/ Cerebrovascular/ Peripheral vascular disease for renovascular disease

Drug history
• NSAIDs/ Cisplatin/ Cyclosporine

Family history
• Polycystic kidney disease
• IgA nephropathy
• Hereditary nephropathy
• C3 glomerulonephritis
21
Q

Drug-induced kidney failure

  • Define time cut-off for acute, subacute and chronic
  • Pathogenesis pathways
A 
Acute = <7 days 
Subacute = 7-90 days 
Chronic = >90 days

Pathogenesis pathways:

  • Hypersensitivity
  • Vasoconstriction and hypoxic damage
  • Glomerular disease
  • Tubular toxicity
  • Nephrolithiasis and Crystalluria
22
Q

List example of drug-induced AKI

A 
Protease inhibitor 
Cisplatin 
Aminoglycosides 
Acyclovir 
Calcineurin inhibitor ...etc
23
Q

Major clinical features of CKD

A

Constitutional: Fatigue, Nocturia and thirst, fluid retention and edema, General pruritis

CVS: Hypertension, LVH, Congestive HF

Anaemia (NcNc)

CKD- Mineral bone disorder: includes abnormal PTH, bone biochemistry, vascular calcification

24
Q

Diagnostic investigations for CKD

A
  1. Ultrasound Kidney: Small/dysplastic/shrunken kidney
  2. CT angiogram for vascular causes of CKD
  3. Renal biopsy with histological diagnosis
25
Q

Treatment targets for CKD (what needs to be treated/controlled in CKD)

A
  • Delay renal failure
  • Treat cardiac, neurological, vascular risk, prevent CKD complications
  • Control albuminuria by ACEi or ARB
  • Control DM, HTN
  • Correct electrolyte and acid-base disturbance
  • Correct Lipid profile
26
Q

Typical CBC, Lipid, Electrolyte, ABG, PTH, RFT profile in CKD

A

CBC - NcNc anaemia

Lipid - Hypertriglyceridemia (reactive to low albumin)

HypoNatremia
HyperKalemia (K+ shift due to metabolic acidosis)
HypoCalcemia (low Calcitriol production, sec. to hyperphosphatemia)
HyperPhosphatemia (low renal excretion)

ABG: Metabolic acidosis + ↑ Anion gap

PTH: ↑ PTH level due to secondary hyperparathyroidism

RFT: ↑ Urea/ BUN and creatinine level; ↓ GFR

27
Q

List all serological and urine tests for CKD

A 
CBC with diff. 
Lipid profile 
Electrolyte with Ca and PO4
ABG 
Serum PTH 
RFT: Urea/ BUN and creatinine, GFR 
Urinalysis: quantitative protein test

Autoimmune markers: ANA/ anti-dsDNA/ C3/4/ ANCA/anti-GBM
Serum free light chain assays
Serum/ Urine protein electrophoresis with immunofixation

LFT: hepatorenal syndrome, high ALP
HBV and HCV (urgent HD)

28
Q

Imaging and sampling Ix for CKD

A

Renal biopsy for histological Dx with light microscopy, EM and immunofluorescence

Imaging:
X-ray or CT KUB
USG kidney

***MRI avoided- administration of gadolinium is associated with potentially severe syndrome of nephrogenic systemic fibrosis (NSF) **

29
Q

Dietary modifications for CKD

A

Calories: 30 – 35 kcal/kg/day

Vitamins: Ascorbic acid, Folate, Calcitriol

Low Sodium: reduce to <2g (<90mmol) for Hypertensive
Low Potassium: < 1 mmol/kg/day
Low PO4: < 800 mg/day

Low protein:

  • for CKD stage 3-5: reduce uremic toxins and clinical symptoms
  • Diabetic Nephropathy: 0.8g/kg
30
Q

Lipid control for CKD

  • Drug option
  • Indication
  • Risk of no control
A

Indications:

  • > 50 years old
  • CKD 3-5

Drugs: Statin +/- Ezetimibe

Risk: 10% CVD risk in 10 years

31
Q

Diabetic control in CKD

  • Treatment/ drug options
  • eGFR cut-offs for different treatments
A
  1. Lifestyle control: physical activity, nutrition, weight loss
  2. First-line:
    - Metformin**
    - SGLT2 inhibitor **
  3. Additional drugs:
    - GLP-1 receptor agonist preferred
    - DPP-4 inhibitor
    - Insulin
    - Sulphonylurea
    - TZD
    - Alpha- glucosidase inhibitor

Cut-off:

  • Discontinue/ do not initiate Metformin or SGLT2 inhibitor if eGFR <30
  • Stop Metformin or SGLT2 inhibitor if on dialysis
32
Q

Electrolyte and acid-base correction therapy for CKD

A

Hyperkalemia
• Calcium gluconate/ Dextrose-insulin infusion/ Sodium bicarbonate/ Resonium C
• Restriction of dietary K+ intake, discontinuation of ACEI/ ARB

Hypocalcemia
• Calcium gluconate or calcium carbonate if symptomatic
• Restriction of dietary PO43- intake

Hyperphosphatemia
• PO43- binding agents

Metabolic acidosis
• Sodium bicarbonate or sodium citrate
• Initiation of dialysis

33
Q

Anaemia treatment in CKD

  • Target Hb
  • Tx options
A

Symptomatic anemia
• Target Hb = 10-11 g/dL

Treatment:
• Blood transfusion preferably during dialysis using packed cells
• Erythropoiesis stimulating agents/ ESA (EPO therapy) in refractory anemia
• Iron supplementation (transferrin saturation >20%)

34
Q

CKD- Bone mineral disease

- Tx options

A

Active vitamin D analogues - Alfacalcidol

Calcimimetics

Parathyroidectomy

Phosphate Binders and dietary phosphate restriction

35
Q

Outline Vitamin D metabolism in skin, liver and kidney

A
36
Q

CKD-MBD

  • Features
  • Pathogenesis
A

Definition:
• Abnormalities of Ca2+, PO43-, PTH and vitamin D metabolism
• Abnormalities in bone turnover, mineralization, volume linear growth or strength

Pathogenesis:
- Hyperphosphatemia + Vitamin D deficiency (1a hydroxylase) + Secondary hyperparathyroidism

37
Q

Phosphate binding agents for CKD

  • Types
  • Indication of use for each type
A

Main types: Calcium binding and Non-calcium binding

Indications:
LOW Ca2+ = Calcium acetate or calcium carbonate

HIGH Ca2+ = Sevelamer (Renagel)/ Lanthanum (Fosrenol) - NON-calcium-NON-aluminium containing binders

38
Q

MoA of non-calcium containing phosphate binding agents

A

 Sevelamer is a non-absorbable cationic polymer that bind PO43- in intestinal lumen through ion exchange limiting absorption
 Lanthanum is a rare-earth element that lowering PO43- level

39
Q

Clinical manifestations of CKD-BMD

A 
Bone: 
Ostetis fibrosa cystica 
Adynamic bone disease 
Osteoporosis 
Mixed uremic osteodystrophy 
Gout and pseudogout

Vascular calcification:
Coronary artery calcification (death)
Calciphylaxis (small vessel calcification in fat and skin)

40
Q

Pathogenesis of Osteitis fibrosa cystica, Adynamic bone disease, Osteomalacia and Mixed uremic osteodystrophy in CKD-BMD

A

Osteitis fibrosa cystica
o (↑ PTH) High bone turnover due to secondary hyperparathyroidism

Adynamic bone disease
o (↔/↓ PTH) Low bone turnover, reduced bone volume and mineralization
o Due to excessive suppression of parathyroid gland by vitamin D use, calcium-based phosphate binder or calcium-dialysis solution

Osteomalacia
o (↔/↓ PTH) Low bone turnover and abnormal mineralization
o Due to use of aluminum-based phosphate binder

Mixed uremic osteodystrophy
o High or low bone turnover and abnormal mineralization

41
Q

List bone abnormalities caused by CKD-BMD

A

Subperiosteal resorption
Fracture
Bone pain
Metastatic calcifications

42
Q

Management options of CKD-BMD

A
  • Low dietary PO4 intake
  • Calcium-containing PO4 binding agents such as calcium acetate
  • Calcitriol or vitamin D analogues
  • Calcimimetics (stimulate parathyroid CaSR to decrease PTH secretion) - e.g. Cinacalcet
  • Total parathyroidectomy with autotransplantation
43
Q

Calciphylaxis

Definition
Ix
Tx

A

Calcification of media of small-to-medium-sized vessels of dermis and subcutaneous fat, causes skin ischemia and necrosis with painful lesions

Ix: Skin biopsy

Tx:
Sodium thiosulfate* (IV/ Intralesional)
Cinacalcet or parathyroidectomy for hyperparathyroidism
NON-calcium-containing phosphate binder for hyperphosphatemia

44
Q

Which treatment for CKD-BMD is appropriate if there is Calciphylaxis

Which treatment is not indicated

A

Aim for lower Ca: Canacalcet** (Calcimimetics)
Lower Ca, PTH, PO4

Not indicated:
Calcium-containing phosphate binding agents
Vitamin D analogues/ Calcitriol

45
Q

What causes of abnormal skin complexion in CKD

A

 Coexistence of anemia and retention of β-melanocyte-stimulating hormone
 Pigment deposition (urochromogens)

46
Q

Indications for emergency dialysis in CKD

A
  • Respi: Acute pulmonary edema
  • CVS: Uremic pericarditis or cardiac tamponade
  • CNS: Uremic encephalopathy
  • Endo: Severe metabolic acidosis
  • Endo: Hyperkalemia

MBBS IV - Junior Clerkship WCS (131 decks)

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