Chronic Kidney Disease Flashcards
What is chronic kidney disease (CKD)?
Reduction in kidney function or structural damage (or both) present for more than 3 months, with associated health implications.
Kidney damage may cause fluid and electrolyte imbalance, and leakage of protein and/or blood into the urine, resulting in proteinuria and haematuria.
What are the causes of CKD?
- Diabetes
- Hypertension
- Age related decline
- Glomerulonephritis
- Polycystic kidney disease
- Medications (e.g. NSAIDs, PPI and lithium)
What medications can cause CKD?
NSAIDs, PPI and lithium.
What are the risk factors for CKD?
- Age >50 years
- Male sex
- Black or Hispanic ethnicity
- Family history
- Smoking
- Obesity
- Long-term analgesic use
- Diabetes
- Hypertension
- Autoimmune disorders
What are the signs of CKD?
- Oedema
- Coca-cola urine
- Foamy-appearing urine
- Pallor
- Hypertension
- Peripheral neuropathy
What are the symptoms of CKD?
- Fatigue
- Nausea and/ or vomiting
- Pruritus
- Anorexia
- Restless legs
- Loss of appetite
Why is pruritus a symptom of CKD?
Due to an accumulation of toxic waste products in the circulation and under the skin, such as urea that is not excreted by the kidney.
Why does CKD lead to changes in urine?
Note: coca-cola urine and foamy-appearing urine
Coca-cola urine→ due to haematuria.
Foamy-appearing urine→ due to proteinuria.
What investigations should be ordered for CKD?
- Renal chemistry
- Estimation of GFR
- Serum cystatin C and cystatin C-based estimation of GFR
- Urinanalysis
- Urinary albumin
- Renal ultrasound
Briefly describe the classification of CKD based on GFR
G1: GFR >90 mL/minute/1.73 m² and evidence of kidney damage based on pathological diagnosis, abnormalities of radiographic imaging, or laboratory findings such as haematuria and/or proteinuria
G2 GFR 60 to 89: mL/minute/1.73 m²
G3a GFR 45 to 59: mL/minute/1.73 m²
G3b GFR 30 to 44: mL/minute/1.73 m²
G4 GFR 15 to 29: mL/minute/1.73 m²
G5 GFR <15: mL/minute/1.73 m²
Briefly describe the classification of CKD based on albumin excretion rate (AER) or albumin to creatinine ratio (ACR)
A1 AER <30 mg albumin/24 hours or ACR <3 mg/mmol (<30 mg/g): normal to mildly increased
A2 AER 30 to 300 mg albumin/24 hours or ACR of 3 to 30 mg/mmol (30 to 300 mg/g): moderately increased
A3 AER >300 mg albumin/24 hours or ACR >30 mg/mmol (>300 mg/g): severely increased.
Why investigate using renal chemistry?
Includes sodium, potassium, chloride, bicarbonate, urea, creatinine and glucose. Serum creatinine alone is insufficient to determine CKD, and may be falsely low in conditions of low muscle mass, as in older or malnourished people, or patients with liver failure.
Elevated serum creatinine and electrolyte abnormalities.
Why investigate using eGFR?
A GFR estimating equation using serum creatinine is recommended for initial assessment.
<60 mL/minute/1.73 m².
Why investigate using serum cystatin C and cystatin C-based estimation of GFR?
Warranted in specific circumstances when GFR estimates based on serum creatinine are thought to be inaccurate, such as in people with extremes of muscle mass (e.g., bodybuilders, people with muscle wasting disorders, older or malnourished people).
Reduced muscle mass will lead to overestimation; increased muscle mass to underestimation of the GFR.
Why investigate using urinalysis?
Screening test to determine for pathological markers of kidney damage excreted in the urine.
Haematuria and/or proteinuria.
Why investigate using urinary albumin?
Classification of CKD requires quantification of urinary albumin as based on albumin excretion rate (AER) or albumin to creatining ration (ACR). Moderately increased albuminuria is a risk factor for the development of progressive CKD and coronary artery disease associated with diabetes and hypertension.
Moderately increased (AER 30-300 mg/day; ACR 30-300 mg/g).
Why investigate using renal ultrasound?
Helps to diagnose CKD if kidney atrophy is present and diagnoses obstruction with hydronephrosis or bladder retention.
Small kidney size; presence of obstruction/hydronephrosis; kidney stones.
What are the aims of managing CKD?
- Slow the progression of the disease
- Reduce the risk of cardiovascular disease
- Reduce the risk of complications
- Treating complications
How can disease progression be slowed down?
- Optimise diabetic control
- Optimise hypertensive control
- Treat glomerulonephritis
What are the complications of CKD?
- Anaemia
- Renal bone disease
- Cardiovascular disease
- Peripheral neuropathy
- Dialysis related problems
How are the complications of CKD prevented?
- Exercise, maintain a healthy weight and stop smoking
- Special dietary advice about phosphate, sodium, potassium and water intake
- Offer atorvastatin 20mg for primary prevention of cardiovascular disease
How are the complications of CKD treated?
- Oral sodium bicarbonate to treat metabolic acidosis
- Iron supplementation and erythropoietin to treat anaemia
- Vitamin D to treat renal bone disease
- Dialysis in end stage renal failure
- Renal transplant in end stage renal failure
Briefly describe the management of hypertension and CKD
ACE inhibitors are the first line in patients with chronic kidney disease. These are offered to all patients with:
- Diabetes plus ACR > 3mg/mmol
- Hypertension plus ACR > 30mg/mmol
- All patients with ACR > 70mg/mmol
Aim to keep blood pressure <140/90 (or < 130/80 if ACR > 70mg/mmol).
What needs to be monitored if a patient has CKD and requires ACEi?
Serum potassium needs to be monitored as chronic kidney disease and ACE inhibitors both cause hyperkalaemia.
