Clinical Chronic Kidney Disease Flashcards
(42 cards)
Epidemiology of CKD
-7% (10-20%)
-Increasing prevalence with age (>65)
-Patients above 70= 80% chance of some form of CKD
-The prevalence of CKD in patients with hypertension, diabetes and vascular disease is substantially higher
Definition of CKD and MDRD equation
-Irreversible damage to the structure +/- function of the kidneys
-Typically develops and progresses slowly over years
-Often manifests as an incidental biochemical finding (asymptomatic until advanced)
-Modification of Diet in Renal Disease (MDRD) equation measures eGFR, which uses the following variables:
=serum creatinine (differences in muscle)
=age
=gender
=ethnicity
=Pregnancy, muscle mass (Amputee/ body-builders), eating red meat 12 hours prior to sample affects result
Classification of CKD
1= Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests (normal U&Es, no proteinuria) are normal, there is no CKD)
2= 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a= 45-59 ml/min, a moderate reduction in kidney function
3b= 30-44 ml/min, a moderate reduction in kidney function
4= 15-29 ml/min, a severe reduction in kidney function
5= Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
Diagnosis and investigations of CKD
-Elevation in serum creatinine persistent for > 3 months
-Other markers of renal injury
=Albuminuria (ACR of 3 mg/mmol or more clinically important)
=Electrolyte abnormalities due to tubular dysfunction
=Structural abnormalities, e.g. cysts
-Exclude AKI: unexpectedly high urea and creatinine (when there is an increase from previous results or no prior results are available), renal function should be retested within 2 weeks to avoid missing AKI
-Screen for complications of CKD, such as anaemia and renal osteodystrophy
Criteria for renal USS
have accelerated progression of CKD (see recommendation 1.3.5)
have visible or persistent invisible haematuria
have symptoms of urinary tract obstruction
have a family history of polycystic kidney disease and are older than 20
have a GFR of less than 30 ml/min/1.73 m2 (GFR category G4 or G5)
are considered by a nephrologist to need a renal biopsy
General symptoms of CKD
-Usually asymptomatic until late stage 4 (incidental findings)
-Non-specific symptoms:
=Weakness and fatigue/ lethargy
=Oedema (ankle swelling, weight gain)
=Polyuria, nocturia (early symptom, loss of concentrating ability)
=Breathlessness (fluid retention/ metabolic acidosis/renal anaemia)
=Nausea / anorexia / altered taste/ loss of appetite
=Itching skin (advanced, secondary to uraemia)
=Muscle cramp (advanced)
=Restless legs
=Insomnia
=Confusion/ collapse/ coma death
-Can be hypertension and proteinuria (not always)
AKI vs CKD
-One of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD) is renal ultrasound - most patients with CKD have bilateral small kidneys. Exceptions to this rule include:
=autosomal dominant =polycystic kidney disease
=diabetic nephropathy (early stages)
=amyloidosis
=HIV-associated nephropathy
-Other features suggesting CKD rather than AKI
=hypocalcaemia (due to lack of vitamin D)
Describe stage 1 CKD
-GFR 90+
-Normal kidney function but urine or other abnormalities point to kidney disease
-Stages 1-3 (5-10% of the population?)
Need assessment, long term monitoring, control of blood pressure and CV risk factors
Describe stage 2 CKD
-GFR 60-89
-Mildly reduced kidney function; but must also have urine or other abnormalities (e.g. anatomical, genetic) to be classified as CKD
-Need assessment, long term monitoring, control of blood pressure and CV risk factors
Describe stage 3 CKD
-GFR 30-59
-Moderately reduced kidney function; may be subdivided into 3a, 3b according to GFR over or under 45; and proteinuric or not.
-Few or no symptoms still
-Common: estimates of incidence vary, but it may be round about 5% of the population, mostly elderly (incidence rises over 70)- most never develop ESRF
-Need assessment, long term monitoring, control of blood pressure and CV risk factors
Describe stage 4 CKD
-GFR 15-29
-Severely reduced kidney function
-0.2% of the population. Planning for end stage renal failure if progressive. Symptoms at lower GFRs.
Describe stage 5 CKD
-GFR 14 or less
-Very severe kidney failure. Sometimes used to imply end stage, ESRF or ESRD, but average GFR for starting dialysis is below 10
-0.2%
Risk factors for developing ESRF
-Deteriorating function β unsurprisingly, if GFR falls with time, ESRF is more likely
-Severe of CKD β worse kidney function is more likely to deteriorate further
-Proteinuria is a strong risk factor, risk increasing with the severity of proteinuria.
-Haematuria can be an indicator of kidney inflammation
-High blood pressure β and blood pressure reduction reduces risk
-Young age β younger patients with CKD are more likely to reach ESRD
-Increased cardiovascular risk
Complications of CKD
-Increased risk of heart attacks and all kinds of cardiovascular disease, and if a patient with CKD has a cardiovascular event, or an operation, the risk of doing badly is substantially increased.
=Hypertension is often an early feature.
-Fluid retention commonly becomes a major problem in late renal failure, requiring large doses of diuretics.
-Anaemia can be treated by recombinant erythropoietin injections after other causes have been excluded and adequate iron stores demonstrated. This often requires intravenous iron therapy. This is not usually a serious problem until GFR falls below 20
-Renal osteodystrophy
-Itching, neuropathy, pericarditis (late manifestations prevented or controlled by dialysis)
-Gastrointestinal symptoms β anorexia, progressing to nausea and ultimately vomiting =Usually late symptoms, GFR usually well below 20, and sometimes not becoming prominent until GFR <10. They may be helped by dietary modification but are often an indication that dialysis is required.
Common causes of CKD/ CRF
Any disease process which interrupts structure or function of kidneys (systemic vs intrinsic)
-In many cases the underlying diagnosis is unclear, especially among the large number of older patients with stage 3 CKD. Many patients diagnosed at a late stage have bilateral small kidneys. Renal biopsy is rarely undertaken in this group since it is more risky, less likely to provide a histological diagnosis because of the severity of damage, and unlikely to alter management.
-Systemic
=Diabetes (20-45%): large racial and geographical differences
=Hypertension (5-20%, causality controversial, may be secondary to another primary renal disease)
=Vascular disease (5%, mostly atheromatous)
=Inflammatory disorders (5-10% SLE, vasculitis)
=Unknown (5-10%)
=Chronic pyelonephritis
=Hypertension
=Adult PKD
-Intrinsic
=Congenital/ inherited: PKD, Alportβs syndrome, Reflux nephropathy, renal dysplasia (5-10%)
=Glomerular disease 10-20% (IgA nephropathy)
=Interstitial disease (20-30%): drug-induced, reflex nephropathy
=Inflammatory (vasculitis)
-Circulatory problems such as renal artery stenosis
-Inflammation within the kidneys β interstitial nephritis or glomerulonephritis
-Diabetes is very important cause β diabetic kidney disease also affects glomeruli
-Urinary tract obstruction β in ureters, bladder, or below β more on obstruction
-Inherited diseases β more info on inherited/congenital diseases
Risk factors for deterioration of renal function
-Worse renal function β higher serum creatinine (lower eGFR)
-Proteinuria β the higher, the greater the risk of progression
-Hypertension β the higher, the greater the risk
-Renal biopsy shows fibrosis, or continuing inflammation
-Young age β they have longer for trouble to develop
Management strategies to prevent progression of CKD
-Blood pressure control to stringent targets. More on BP control
-ACE inhibitors if there is proteinuria.
=NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs). A rise greater than this may indicate underlying renovascular disease.
-Prevention of acidosis by treatment with bicarbonate may play a role
-Furosemide
-Dietary restriction: intermediate course, recommending moderate protein restriction (0.6-0.8g/kg/day) but ensuring adequate calorie intake.
CKD bone disease
-Low vitamin D (1-alpha hydroxylation normally occurs in the kidneys), high phosphate, low calcium: due to lack of vitamin D, high phosphate, secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
-Several clinical manifestations may result:
=Osteitis fibrosa cystica (aka hyperparathyroid bone disease)
=Adynamic reduction in cellular activity (both osteoblasts and osteoclasts) in bone
may be due to over treatment with vitamin D
-Osteomalacia (due to low vitamin D)
-Osteosclerosis
-Osteoporosis
How is renal osteodystrophy prevented?
REDUCE PHOSPHATE AND PTH
-Prescription of alfacalcidol or calcitriol, vitamin D metabolites; controls hypocalcaemia (but may cause hypercalcaemia).
-Parathyroidectomy if needed
-Phosphate
=dietary restriction
=phosphate binders such as calcium carbonate (hypercalcaemia vascular calcification) or acetate preparations, or aluminium hydroxide (risk of aluminium toxicity, now generally reserved for short-term use), or sevelamer (RenagelΒ©), or lanthanum carbonate.
=Phosphate retention is not usually a severe problem until GFR is less than 20-25.
Why is diet important in CKD?
-As well as excreting the processed metabolites of the body, the kidneys also get rid of all excess fluid, salt etc that we take in over our daily requirements.
-Diet becomes increasingly important as renal function deteriorates, because the body becomes less able to deal with excessive intake first, and later, with the normal output of the body.
Describe the diet in different scenarios of CKD
-Deteriorating kidney function
=Restrict salt; moderate protein; in late stages, phosphate and potassium often become important issues.
=Where blood pressure control is possible, evidence no longer supports restricting protein below moderate levels. It does not seem to protect kidney function, and severe restriction of protein can be hazardous.
-Dialysis
=Salt, protein, fluid, potassium and phosphate are important to varying degrees depending on the type and frequency of dialysis, and on whether there is a little bit of residual renal function
-Transplantation
=With good kidney function, it is important to eat a healthy diet to minimise cardiovascular risk.
What is ESRF?
-Implies a level of renal function at which death is likely within weeks or months.
-Symptoms are those of severe chronic renal failure
-It is not the same as CKD stage 5: the average GFR for commencing dialysis in the UK is below 10ml/min, but there is wide individual variation, and some may require renal replacement therapy (RRT) much earlier
Management options in ESRF
-Haemodialysis
-Peritoneal dialysis
-Renal transplantation
-Conservative management
Decisions about management in ESRF
-Younger and βlow riskβ patients are favoured for transplantation. For some patients who are at a high risk of dying on dialysis, conservative management may provide a higher quality of life than renal replacement therapy, with little shortening of life.
-Risk is related to both age and co-existing diseases. Prognosis with renal replacement therapy tends to be very good in younger patients with no other serious diseases, especially after transplantation. However even in this group, mortality from cardiovascular disease is many times higher that of the general population. Infectious causes of death are the second major problem in patients on renal replacement therapy.
-High risk patients are the very elderly (over 80 years) or those of any age with two major comorbid conditions (clear evidence of coronary, cerebrovascular or peripheral vascular disease; diabetes; non-skin malignancy); or those aged 70-80y with one major comorbid disease. The median survival of the high risk group defined this way is generally under 18 months, although up to a quarter may survive >4y.
-Conservative management includes all usual measures to retard progression of renal disease and reduce symptoms, including particularly close attention to diet, and use of erythropoietin and other treatments to reduce symptoms.
