Chronic Kidney Disease Flashcards
What is the definition of CKD?
kidney damage or GFR <60ml/min per 1.73m2 for 3 months or more
What are the issues around using serum creatinine levels as measure of CKD?
- exponential relationship between GFR and serum creatinine can result in slow recognition of a large loss of renal function (a big loss of GFR can cause minimal reduction in serum creatinine)
^ can result in late renal referrals - effect of muscle mass can result in overestimation of function in those with decreased mass (eg. elderly, amputees, RA partients etc.)
^ seemingly normal serum creatinine levels with low GFR
What factors are taken into consideration when calculating eGFR?
- serum creatinine levels
- if Afro-Carribean descent
- if female
What are the problems with eGFR?
- only validated in white and Afro-Carribean population
- mean age was 50 (not validated for very young/old)
- wide confidence intervals so discretion around true values
- doesn’t take weight into account (used for drug dosing but shouldn’t)
- not valid for AKI
- not valid for pregnancy
What is responsible for tubular filtration in the kidneys?
- tubular endothelium
- basement membrane
- podocyte processes
Why is proteinuria not always the most accurate in assessing CKD and how is it modified to be more accurate?
- proteinuria normal in fever, exercise, or normal physiology
- spot urine protein concentration compared with urine creatinine concentration to make a ratio (ACR and PCR)
- this accounts for any changes that cannot be controlled for
List the clinically important ACR/PCR values
- normal ACR <2.5
- normal PCR <20
- albuminuria = ACR >30 (if heavy, use PCR to follow progress)
- nephrotic proteinuria = PCR >300 (3g/24hr)
Describe the possible causes of CKD
- diabetic nephropathy (caused by nodular lesions in the glomerulus and sclerosis)
- renovascular disease/ischaemic nephropathy (narrowing of carotid arteries and renal vasculature resulting in ischaemia)
- chronic glomerulonephritis/IgA nephropathy
- reflux nephropathy/chronic pyelonephritis (back flow of urine which causes reflux and scarring of the kidney over time)
- ADPKD (cysts and pressure on surrounding tissue)
- obstructive uropathy (chronic back pressure causing kidney damage - tumour causes)
What are the symptoms of advanced CKD?
- pruritus
- nausea, anorexia, weight loss
- fatigue
- leg swelling
- nocturia
- joint/bone pain
- confusion
(low GFR 10-15)
What are the signs of advanced CKD?
- peripheral and pulmonary oedema
- pericardial rub
- rash/excoriation
- hypertension
- tachypnoea
- cachexia
- pallor and or lemon yellow tinge
What are the general principles of management of CKD?
- targeted screening for CKD
- interventions to slow rate of progression and reduce CVD risk
- medicines to replace impaired individual functions of the kidney
- advanced planning for future renal replacement therapy
What are the methods of slowing progression of CKD?
- BP control (ACEi/ARB - be aware of ACEi on tubules)
- diabetic control
- diet
- smoking cessation
- lowering cholesterol
- treating acidosis
When do we worry about anaemia in CKD and how is it treated?
- eGFR <30 (reduction in EPO and reduced absorption and handling of iron)
- iron replacement as well as B12 and folate
- target Hb 100-120g/l (higher levels associated with CV events)
Describe how secondary hyperparathyroidism can occur due to CKD
- declining kidney function causes a direct increase in phosphorus (as kidneys are unable to remove from blood resulting in accumulation) and a decrease in vitamin D synthesis (due to reduction in precursor produced by the kidney)
- over time this causes a decreased rate of Ca absorption, increased release from bone and increased PTH release and hyperplasia
How is SHPT due to CKD treated?
- activated vitamin D: alfacalcidol
- occasionally Mg supplements
- phosphate binders (calcium based - calcium carbonate/acetate, non-calcium - sevelamer, lanthanum, aluminium)
- calcimimetic: cinacalcet
- parathyroidectomy
