Chronic Kidney Disease (CKD)
Definition
Specifics:
Stages:
0 = eGFR >90 with risk factors (eg HTN, diabetes)
1 = eGFR >90 with kidney damage
2 = eGFR 60-89
3 = eGFR 30-59
4 = eGFR 15-29
5 = eGFR <15
ESKD = stage 3-5
Risk Factors
Aetiology
Pathogenesis
--> inflam mediators --> fibrosis --> further destruction
Clinical Features
Management
1. Reduce BP (140/90 or 130/80 with albuminuria)
- ACEI (watch for K due aldosterone) --> reduces proteinuria
2. Avoid nephrotoxin (NSAIDs)
3. Do not restrict diet
4. Dialysis
5. Transplant
NOTE: Initiating ACEI, ok to have K<6.0mmol/L and up to 50% increase in creatinine
Diet
Medical
Source
Harrison's 17th Ed
Prof Matthew Jose 2013
Toronto Notes 2012
- Progressive reduction of nephron numbers
- Irreversible
Specifics:
- eGFR <60 for >3mo, regardless of evidence of kidney damage
- Evidence of kidney damage, regardless of eGFR
- Proteinuria
- Haematuria (not caused by post renal issues)
- Structural damage (imaging)
- Pathological damage (biopsy)
Stages:
0 = eGFR >90 with risk factors (eg HTN, diabetes)
1 = eGFR >90 with kidney damage
2 = eGFR 60-89
3 = eGFR 30-59
4 = eGFR 15-29
5 = eGFR <15
ESKD = stage 3-5
Risk Factors
- Hypertension
- Diabetes mellitus
- Autoimmune disease
- Older age
- African ancestry
- Fhx of renal disease
- Previous episode of acute renal failure
- Proteinuria
- Abnormal urinary sediment
- Structural abnormalities of the urinary tract
Aetiology
- Diabetic nephropathy (most common)
- Hypertension
- Atherosclerosis
Pathogenesis
- Mechanisms of underlying cause (eg nephrotoxin, hypovol)
- Hypertrophy and hyperinfiltration of remaining nephrons
--> inflam mediators --> fibrosis --> further destruction
Clinical Features
- Lethargy, dyspnoea (due to anaemia), pruritus (hyperPO4)
- Immune dysfunction (infections)
- Haematological (easy brusing)
- Electrolyte imbalances (hyper/hypoNa, metabolic acidosis, hyperK)
- Endocrine dysfunction (loss of libido, slower insulin clearance)
- Neuro (cramps, RLS)
- Cardiovascular disease (HF)
- Bone health (kidney converts 25(OH)2D --> 1-25(OH)2D (Calcitriol)--> dec GIT absorption of Ca2+ --> hypoCa2+/ inc PO4 forms CaPO4 --> hypoCa2+)
Management
1. Reduce BP (140/90 or 130/80 with albuminuria)
- ACEI (watch for K due aldosterone) --> reduces proteinuria
2. Avoid nephrotoxin (NSAIDs)
3. Do not restrict diet
4. Dialysis
5. Transplant
NOTE: Initiating ACEI, ok to have K<6.0mmol/L and up to 50% increase in creatinine
Diet
- Restrict: Protein, K+, PO4, Mg2+ (antacids)
- Na+ and water restriction
- Severe protein restriction not recommended
Medical
- Treatment of secondary hyperparathyroidism
- Calcium supplements (e.g. TUMSe) treats hypocalcemia when given between meals and
- binds phosphate when given with meals
- Consider calcitriol (1,25-dihydroxy-vitamin D) if hypocalcemic
- Sevelamer (phosphate binder) if both hypercalcemic and hyperphosphatemic
- Vitamin D analogues are being introduced in the near future
- Cinacalcet for hyperparathyroidism (sensitizes parathyroid to Ca2+, decreasing PTH)
- Sodium bicarbonate for metabolic acidosis
- Erythropoietin injections (Hct <30%) for anemia; target Hct 33-36%
- DDAVP for prolonged bleeding time if patient has clinical bleeding or invasive procedures
- ACEi for hypertension (target 130/80 or less), loop diuretics when GFR <25 mL/min
- Statins for dyslipidemia
- Adjust dosages for renally excreted medications (avoid nephrotoxic medications)
Source
Harrison's 17th Ed
Prof Matthew Jose 2013
Toronto Notes 2012