Prevalence
Definition of CKD
Structural or functional abnormalities of the kidneys for >3 months, as manifested by either:
1. Kidney damage, with or without decreased GFR, as defined by
pathologic abnormalities markers of kidney damage, including abnormalities in the composition of the blood or urine or abnormalities in imaging tests
Definition
OR
GFR < 60
Screening
Glomerular Filtration
You MUST calculate the GFR! Use an equation MDRD or C-G
Hemoglobin < 12.0 g/dL Serum albumin < 3.5 g/dL Serum phosphorus > 4.5 mg/dL
Screening
Proteinuria
Good evidence for screening with annual micro-albumin in DM Consider screening in HTN, age> 55
Proteinuria
Protein in urine is associated with a more rapid decline in renal function This decline can be slowed by ACE-I or ARB even without diabetes Can be helpful in diagnosis if not DM
Causes of CKD
Diabetes
Non-diabetic
Hypertension?? Transplant
Glomerular
Tubulointerstitial
Vascular
Low-flow states
Medications? Family history? Risks of HIV and Hepatitis Rashes, joints, renal bruit Screen again for diabetes Look at urine micro for clues Consider ESR, SPEP, ANA, ANCA Renal ultrasound
CKD Stages
Stage 1
GFR > 90
2 3 4 5
Goals of Care
1.
2.
3.
Slow decline in renal function Prevent cardiovascular disease Detect and manage complications
Formation
osteoblasts matrix
Quiescence
Mineralisation
Pathogenesis
Kidney failure disrupts systemic calcium and phosphate homeostasis and affects the bone, GIT and parathyroid glands. In kidney failure there is decreased renal excretion of phosphate and diminished production of calcitriol (1,25dihydroxyvitamin D)
The increased phosphate and reduced calcium, feedback and lead to secondary hyperparathyroidism, metabolic bone disease, soft tissue calcifications and other metabolic abnormalities
PO4
GFR 1,25 DHCC
Calcitriol
Ca
PTH
Secondary hyperparathyroidism
Most with CKD and mildly elevated PTH are asymptomatic When present classified as either
1. Musculoskeletal 2. Extra-skeletal
Accelerates:
High PO4 or Low Ca2+, calcitriol, HCO3, oestrogen Via PTH*, IL-1,6 & TNF
Formation
osteoblasts matrix
Quiescence Retards:
Calcitriol*, Age, Diabetes, Al3+, PTHx
Mineralisation
*Acts via osteoblasts
Due to excess PTH Increased bone turnover activity (greater number of osteoclasts and osteoblasts) and defective mineralization. Associated with bone pain and increased risk of fractures. Severe symptomatic disease is currently uncommon with modern therapy.
Osteomalacia
From aluminium based phosphate binders From contamination of water in diasylate solutions
Characterized by low osteoblastic activity and bone formation rates Seen in up to 40% HD and 50% PD May be due to excess suppression of the parathyroid gland with therapies, particularly calcium-containing phosphate binders and vitamin D analogues. Typically maintain a low serum intact PTH concentration, which is frequently accompanied by an elevated serum calcium level. Felt to represent a state of relative hypoparathyroidism
To slow decline
Low salt diet (for HTN) Low protein diet in CKD 4 & 5
Nutrition consult!
To slow decline
ACE-I or ARB Diuretics thiazide for GFR > 30 - furosemide for GFR < 30
To slow decline
Prescribe an ACE-I or ARB for proteinuria + CKD even in the ABSENCE of diabetes
Goals of Care
1.
2.
3.
Slow decline in renal function Prevent cardiovascular disease Detect and manage complications
Prevent CV disease
Most common cause of death is CV disease and not renal failure.
No evidence that tx affects renal fxn Guidelines: ATP3 -> LDL goal < 100
Goals of Care
1.
2.
3.
Slow decline in renal function Prevent cardiovascular disease Detect and manage complications
When to refer
Diabetes & CKD but no retinopathy GFR decline of 50% in one year Stage 3 or 4 CKD
Key Points
Calculate the GFR! Look for reversible cause if no DM Get to know the KDOQI guidelines & think about the complications