AKI And CKD Flashcards
Difference between AKI and CKD
AKI- decrease in GFR which usually occurs within hours to weeks and is usually reversible
CKD is chronic kidney disease in which GFR is decreased over the course of over 6months, and is usually irreversible
Renal function is measured by…
Serum creatinine (U+E test)
Urination rate per hour
GFR (estimated through the serum creatinine value)
Causes of acute kidney injury AKI (pre, renal and post)
Pre renal AKI- caused by impaired perfusion (Shock)
Renal AKI- injury to the glmoeruli and tubules
Post renal AKI- caused by obstruction to urine excretion
Causes of shock
Hypovolemia
Sepsis = vasodilation=hypotension
Cardiac failure= ↓ blood output= ↓ perfusion
Embolis (obstruction to renal artery)
Body’s response to ↓ GFR and perfusion
Macula densa cells sense ↓ perfusion
JG apparatus
Renin release
Angiotensin II release with aldosterone = vasoconstriction and retention of sodium and water
Effect of the afferent arteriole and efferent arteriole in AKI
Vasodilation due to prostaglandins (afferent)
Vasoconstriction due to Ang II (efferent)
↑ resistance = ↑ pressure = ↑ GFR
Aldosterone effect on the kidneys
Causes the ↑ uptake of sodium ions in the DCT, causing ↑ water retention as a result which ↑ blood volume and rectifies any ↓ in BP
Features in prerenal AKI
↑ Na+ and water reabsorbtion
↑ urine osmolality
↑ urine specific gravity
↓ urine production
↓ fractional excretion of Na+
Renal AKI definition (ATN- acute tubular necrosis)
Inability of tubular cells to reabsorb/filter due to cell death, as a result of poor perfusion or toxicity
What causes poor perfusion in ATN acute tubular necrosis
Surgery
Hypotension
Sepsis= vasodilation = ↓ perfusion
What does ATN result in
↓ Na+ H2O reabsorption = ↓ volume of ECF
↓ urine osmolality
↑ urine output (damage to tubular cells = ↓ reabsorbtion of H2O)
↑ fractional Na+ excretion
Signs of Acute Tubular necrosis
↑ sodium in urine
↑ urine due to lack of reabsorption
Hyperkalemia (no swapping g with Na+)
Metabolic acidosis (H+ rentention and no secretion of HCO3- ions)
↓ GFR = fluid overload (oedema, pulmonary oedema)
Causes of renal toxicity
Radiocontrast dye
DAMN drugs
Myoglobin from muscles, which results from crush injuries
Post renal AKI definition
Obstruction to urinary excretion due to stones, ↑ prostate size or ureter tumour
Treatment of post renal AKI
Check for catheter
Add catheter if necessary, check the obstruction isn’t above this
Treat underlying cause, stones, prostate enlargement or tumour
Treat UTI/ Prevent
What kills patients with AKI
Hyperkalemia - ATN, no excretion in urine= ventricular fibrillation
Metabolic acidosis - ↓ excretion of H+ and lack of HCO3- reabsorbed
Pulmonary oedema- ↓ homeostatic control of fluid
Treatment of kidney failure
IV fluids
Avoid DAMN drugs
Treat hyperkalaemia
O2
Treat sepsis if there
Chronic kidney disease definition
Decrease in GFR which occurs over months or years and is usually irreversible
Measurement of renal function
Serum creatinine (u and e blood test)
GFR (estimated through the serum creatinine)
Symptoms of chronic kidney disease (kidney functions and related systems)
Bone pain (vit d deficiency)
Nausea, anorexia, weight loss (toxins)
Itch (toxins)
Breathlessness (pulmonary oedema)
Leg swelling (fluid retention)
Fatigue (2° anaemia from ↓ EPO production)
Signs of abnormal kidney function (anaemia, fluid retention)
Pallor (anaemia)
Hypertension (fluid retention)
Oedema (fluid retention)
Proteinurea
Causes of CKD (infection, other diseases, damage to glmoeruli/tubular cells, inheritance)
- Diabetic kidney disease
- Hypertension/atherosclerosis
- Glomerulonephritis
- Poly cystic kidney disease (inherited renal disease)
- Pyelonephritis, reflux nephropathy
Risk factors associated with CKD
Diabetes
Hypertension
Dyslipidemia
Family Hx
CARDIAC DISEASE
Smoking
Male
Age
How does diabetes cause CKD (Basement membrane) diabetic nephropathy
Diabetes causes hyperglycaemia
Hyperglycaemia = thickening of the basement membrane of the glomeruli, and expansion of the mesangial cells
Diabetic hypertension = ↑ BP (vasodilation of the afferent and vasoconstriction of the efferent)
Albumins leak into the filtrate= proteinurea toxic to tubules… causing tubular atrophy and interstitial fibrosis
Why does proteinurea cause tubular cell atrophy and interstitial fibrosis?
Albumins (proteinurea) are toxic to the tubular cells, causing death.
This can be caused due to diabetic nephropathy
Treatment of diabetic nephropathy (hypertension and hyperglycaemia)
Better management of the diabetes, insulin injections/metformin
ACEi or ARB to ↓ the RAAS effects of ↑ blood pressure in glmoerulus (↓ vasoconstriction of the efferent arteriole)
Eg ramopril
Consequences of ↓ GFR in chronic kidney disease
Fluid retention
- heart failure
- oedema (pulmonary, limbs and ascites)
Retention of metabolites
- uraemia (additional metabolites in system)
- urate in system causes gout
- ↑ serum creatinine
- prolonged drug half-life= easier drug toxicity
Drug prescribing in CKD
- Prolonged drug half-life = possible toxicity
- ↓ dosage/↑ time between doses
- Stop DAMN drugs
DAMN drugs
Diuretics
ACEi/ARB
Metformin
NSAIDs
Consequences of reduced renal tubular function
↓ fluid reabsorbtion
- polyurea
- nocturia
↓ potassium excretion
- hyperkalaemia
↓ acid excretion and ↓ HCO3- formation
- metabolic acidosis
How does renal bone disease form (osteomalacia)
Vitamin D is activated by thr kidneys
In CKD, this does not happen
↓ calcium abrogation in the gut
Leads to ↓ mineralisation of bone
OSTEOMALACIA
Consequences of hyperparathyroidism in renal bone disease (calcium, vitamin D and osteoclasts)
With ↓ Ca2+ and ↓ activated Vit D, parathyroid is stimulated
This leads to osteoclasts stimulation by PTH and breakdown of bone to ↑ calcium levels
Osteoblasts don’t lay down calcium due to ↓ in activated vit D = osteomalacia
Osteomalacia defiantion
The softening of bones due to inadequate mineralisation
Management of CKD (hypertension, anaemia, CVD, hypers, kidney)
Dialysis (haemo, peritoneal)
Kidney transplant
Anti-hypertensives
ACEi/ARB
Statins (hyperlipidaemia)
EPO injections (anaemia)
Activated vit d (osteomalacia)
Phosphate binding drugs (hyperphosphataemia)
Restrict intake of potassium (hyperkalaemia)
Therapies for end stage renal disease
Haemodialysis
- ateriovenous fistula/central venous catheter
Peritoneal dyalysis
- Catheter into abdomen
- incision below umbilicus
Kidney transplant (iliac fossa)
