Renal System Flashcards
How are the control of fluid balance regulated?
Thirst mechanism
Hormone
- ADH (increase ADH = decrease H20 = > reabsorption; decrease ADH = increase H20 = < reabsorption)
- Aldosterone (increase H20 = decrease Aldo.)
Atrial Natriuretic Peptide
What are the mechanical causes of edema?
Increase capillary hydrostatic pressure
- high BP, pregnancy
Decrease plasma osmotic pressure due to loss of plasma protein
- loss of albumin lead to decrease plasma osmotic pressure
Obstruction of lymphatic system
- tumor
Increase capillary permeability
- due to inflammatory response (V.D)
What are the causes of fluid deficits/ dehydration?
Can be due to both inadequate intake / excessive loss OR both
- losses are more common & affects the extracellular compartment
- vomiting / diarrhea
- excessive sweating (decrease Na+ & H20)
- diabetic ketoacidosis (glucose in urine)
- insufficient fluid intake
What is the definition of Acute Kidney Injury (AKI)?
Increase in SCr more than or equals to 0.3mg/dL (more than or equals to 26.5) within 48hr OR
Increase in SCr more than or equals to 1.5x baseline, which is known to / presumed to occur within previous 7 days OR
Urine volume less than 0.5ml/kg/hr for 6 hours
What are the types of AKI?
- Non-oliguric AKI - AKI with urine output >400ml/day
- Oliguria - <400ml/day of urine
- Anuria - <100ml/day of urine
What are the stages of AKI (KDIGO staging)?
Stage 1
- SCr 1.5-1.9x baseline OR more than 26 milli mol/L
- Urine output <0.5ml/kg/hr for 6-12 hrs
Stage 2
- SCr 2-2.9x baseline
- Urine output <0.5ml/kg/hr for more than or equals to 12hrs
Stage 3
- SCr higher than 3x baseline OR initiation of RRT OR patients younger than 18y/o with eGFR <35ml/min/1.73m2
What is the definition of CKD?
Abnormalities in structure or function of the kidney for > 3 months with implications for health
What are the criteria for CKD?
Presence of albuminuria
- A1 - normal to mild increase; <30mg/g; <3mg/mmol
- A2 - moderately increased; 30-300mg/g; 3-30mg/mmol
- A3 - severely increased; >300mg/g; >30mg/mmol
GFR - <60ml/min/1.73m2; category G3a - 5
- G3a - 45-59ml/min (mildly to moderately decreased)
- G3b - 30-44ml/min (moderately to severely decreased)
- G4 - 15-29ml/min (severely decreased)
- G5 - <15ml/min (kidney failure)
What are the possible kidney injury areas?
Pre-renal - inadequate perfusion resulting in not enough blood to sustain pressure to allow filtering
Renal - cellular / intrinsic damage which makes filtering mechanism not possible
Post-renal - obstruction of ureter leading to issues with urine drainage (system backed up)
What are the 5 renal causes?
Small vessel disease - inflammation (vasculitis)
Glomerular disease - inflammation to glomeruli
Acute tubular necrosis - toxins / ischemia
Acute interstitial nephritis
Intratubular Obstruction
What are the sequence of events that occur during AKI?
Ischemia -> initiation of cell injury (tubular obstruction) -> extension (coagulopathy & inflammation) -> maintenance (proliferation, migration, differentiation) -> recovery
What is the pathophysiology of post-renal AKI?
Back-up of system leads to increase ureteric & tubular pressure
What is the definition of Radiation Nephropathy?
Renal injury & loss of function caused by ionising radiation
- Acute radiation nephritis can progress to CKD & subsequently ESRF
What is the accepted threshold dose of photon irradiation that can cause radiation nephropathy?
Exposure of both kidney to a total dose of 23Gy, fractioned in 20 doses over 4 weeks
What is the criteria to be met for CKD to occur due to radiation nephropathy?
- CKD would not occur if irradiated volume is <30% of both kidneys
- Constant exposure to low radiation can cause kidney injury after many years of follow up
- Renal failure from radiation nephropathy would not occur if only 1 kidney is irradiated with a threshold / higher dose BUT radiation injury will still occur
What are the clinical presentation of external beam radiation?
Acute radiation nephropathy - 6-12 months
Chronic radiation nephropathy - more than or equals to 18 months
Malignant hypertension - 12-18 months
Benign hypertension - more than or equals to 18 months
What is the definition of Contrast Induced Nephropathy (CIN)?
A generally reversible form of AKI that occurs soon after administering radio contrast media
What is the typical presentation of CIN?
Acute decline in renal function that occurs 48-72 hrs (SCr peaks at 3-5 days) after IV injection of contrast medium w/o an alternative explanation
What are the risks of CIN?
Patient related risks
- CKD
- Diabetes mellitus
- Intravascular volume depletion
- Reduced cardiac output
- Concomitant nephrotoxins
Procedure related risks
- Increased dose of radiocontrast
- Multiple procedures within 72 hours
- Intra-arterial administration
- Type of radio contrast
What are the preventive measures of CIN?
eGFR >/= 60ml/min - very low risk (avoid dehydration)
eGFR 45-59ml/min - low risk (preventive measure for patients receiving IA contrast media
eGFR <45ml/min - moderate risk (IV hydration)
eGFR <30ml/min - high risk (IV hydration)
What is the most prevalent cause of CKD?
- Diabetes
- HBP
- Others
Describe the pathophysiology of CKD
Systemic hypertension -> increase intraglomerular pressure -> proteinuria -> progressive glomerular & tubulointerstitial damage -> loss of nephrons -> RAAS activated -> AA dilation & EA constriction -> increase intraglomerular pressure
To prevent CKD progression - prescribe ACEi, angiotensin receptor blockers to decrease proteinuria
What are the areas of evaluation to diagnose renal failure?
Checking history - family, drug, past medical history, symptoms of complications of renal failure
Physical examination - swelling, signs of uraemia, distended bladder
Investigation - blood, urine, imaging, renal biopsy
What are the functions of kidney?
- Regulation of RBC production
- Regulation of BP
- Acid-base metabolism
- Regulation of bone-mineral metabolism (Ca2+)
- excretion of metabolites waste products & water
What are the complications of renal failure?
Acidosis
Anemia
Blood pressure
Bone (mineral bone)
Cardiovascular complications
Constitutional factos
Diet
Electrolyte imbalance (Hyperkalemia)
Fluid overload
How does kidney failure lead to anemia?
- Kidney fail to reduce erythropoietin hormone -> affect bone marrow stimulation for RBC production
- RBC lifespan decrease (60-90 days)
- Uraemic toxins induce platelet dysfunction & increase bleeding tendency
- Treatment - SC erythropoietin injections; iron supplement
How does kidney failure lead to metabolic acidosis?
Kidney unable to prices enough ammonia in Proxima tubules to excrete acid into urine -> aggravated bone disease, protein/muscle wasting, CKD progression
Treatment - sodium bicarbonate to reduce acid level in blood -> reduce CKD progression rate
How does kidney failure lead to blood pressure complications?
Damaged kidney cannot excrete waste & fluid which lead to a buildup in the body (increases BP)
RA system activated to maintain BP to to sustain GFR
Treatment
- Low salt diet
- Medications - ACEi, beta blocker
- Calcium channel blockers
- Diuretic
How does kidney failure lead to mineral bone disease?
Decrease in GFR -> low Vit. D activity & high PO43- ->low Ca2+ -> high PTH -> increase bone reabsorption -> increase Ca2+ & PO43- -> increase soft tissue calcification
- Increase bone reabsorption lead to increase risk of fractures
- Increase soft tissue calcification -> CVS risk, endocrine failure, tendon rupture
- Treatment - supply calciferol, restrict PO43-, PO43- binders, dialysis
How does kidney failure lead to electrolyte complications?
Hyperkalemia
- reduce excretion from kidney due to EA constriction
- require low K+ diet
Hyperphosphatemia
- reduce excretion from kidney
- require phosphate binder to reduce absorption of phosphate
Hypocalcemia
- decrease intestinal absorption of Ca2+ due to low calcitrol levels from decrease do Vit. D activity
Describe the transition from CKD to ESRF
CKD -> Stage 4 CKD (long term plan) -> Stage 4 CKD (GFR <20) -> ESRF
What are the options for CKD & ESRF?
- Peritoneal dialysis
- Haemodialysis
- Kidney transplant
What is the importance of renal replacement therapy timing?
- Avoid unplanned initiation of RRT
- might have infective complications associated with vascular catheters
- increase morbidity - Allow for timely dialysis access placement
- Allows transplantation referral for consideration of preemptive renal transplant
What are the types of renal transplantation?
- Living donor renal transplant
- Deceased donor renal transplant
- Standard criteria - kidney considered to be of good quality & suitable for transplantation
- Expanded criteria - kidney considered to be of lower quality & may have higher risk of complications after transplantation
- Donation after cardiac death
How does dialysis work?
- Fluid moves through semi-permeable membrane (dialyzer / peritoneal membrane)
- Dialysate solution contains electrolyte level that resembles the level in the human body
How does peritoneal dialysis work?
- PD catheter is inserted permanently into the abdomen
- ~2L of PD solution is filled into & drained out of the abdominal cavity
- Each exchange takes ~30 minutes (10 mins inflow; 20 mins outflow); can dwell up to ~1.5-4 hrs depending on PD formed
- Dialysis fluid consist of glucose which creates the tonicity of dialysate solution
What are the types of PD?
Continuous Ambulatory PD
- dialysis exchange up to 3-4x during the day
- PD solution allowed to dwell up to 4-6 hrs in abdomen before draining
- either ‘cap-up’ at night or have a night dwell
Automated PD
- performed using a cycler when patient sleep at night
- attached to the machine for ~8-10 hrs
- Continuous cycling PD - dialysis with day dwell
- Intermittent PD - dialysis with ‘day dry’
What are the complications of PD?
Infective complications - PD peritonitis, exit site infection, tunnel infection
Non-infective complications
- Metabolic - hyperglycaemia (due to fluid containing glucose), insulin resistance, weight gain, dyslipidaemia
- Mechanical - hernias, leaks, catheter obstruction, abdominal pain
- Membrane complications - encapsulating peritoneal sclerosis, membrane failure
How does Haemodialysis work?
- Performed up to 3-4x a week with each session lasting ~4hrs depending on patient size & medical condition
- Method - 2 needles inserted into vascular access
- Patient is connected via tubing to the dialysis machine through a vein in the arm
What are the different vascular access to haemodialysis?
- Vascular catheters - temporary non-tunnelled vs tunneled
- Arteriovenous Fistua (AVF)
- Brachiobasilic
- Brachiocephalic
- Radiocephalic - Arteriovenous Graft - looped vs straight
What are the complications of vascular catheters?
- Catheter related bloodstream infection
- Exit site/tunnel tract infection
- Central Venous stenosis
- Right atrium / mural thrombosis
- Occlusion - blood clot/ fibrin sheath/ kink
What are the complications of AVF / graft?
Non-infection complications
- High outflow to the heart -> cardiac failure
- Steal syndrome - inadequate blood flow to the hands & finger
- Central vein stenosis
- Thrombosis
- Primary failure
What are the types of HD?
Intermittent HD
- 3 times a week in centre for ~4 hrs
Nocturnal HD
- 3 times a week in centre for ~6-8 hrs
What are the interdialytic complications?
- BP - hyper / hypo
- Cardiac arrhythmia - due to electrolyte shift
- Dialysis disequilibrium syndrome - decrease urea in blood ->fluid shift into brain -> cerebral edema
- Air embolism
- Haemolysis
- Muscle cramp
- Dialyser reaction
What are the implications of drug dosing for renal impairment?
- Fluid accumulation affect Vd of drug (lower Vd)
- Increase Vd may be a result to decrease protein binding
- May lead to non renal clearance of medication
Dosing should be adjusted to GFR of patient; adjust maintenance dose
- reduce dosing & lengthen dosing intervals
What are the types of renal drug dosing?
- Diuretics - to increase urine output
- Antimicrobials - different types of antibiotics
- Oral hypoglycemic agents - to manage blood glucose levels in patients with type II diabetes
- Analgesics - to manage pain
