S6: acid/base balance in kidney & AKI Flashcards
State the normal range of plasma pH
pH 7.35-7.45
Describe alkalemia and effects on calcium
Lowers free calcium by causing Ca2+ to come out of solution
-increases neuronal excitability, fire APs at slightest signal
Sensory changes – numbness/tingling & muscle twitches
If severe, sustained contractions (tetany) can paralyse respiratory muscles
Describe acidemia and effects on calcium
Increases free calcium by causing Ca2+ ions to go into solution
Increases plasma potassium ion concentration – affects excitability eg. arrythmias
Increasing H+ denatures proteins
Describe pH homeostasis
Three mechanisms to control pH of the blood – buffers, ventilation & renal regulation of H+ and HCO3-
Renal regulation is slower than buffers and ventilation (1-2 days)
Kidneys alter pH in two ways
-directly: excreting or reabsorbing H+
-indirectly: changing the rate at which HCO3- is reabsorbed or excreted
Describe the dihydrogen phosphate buffer
Excess luminal phosphate can bind a large portion of hydrogen ions, buffering them as H2PO4- before excretion
Excretion of H+ increases blood pH
Describe the excretion of hydrogen ions in the form of ammonium
Glutamine is converted to glutamate and ammonium in the PCT
Ammonium dissociates to ammonia and H+ ions, allowing it to pass the membrane and enter the lumen
Once in lumen, it reforms ammonium
Allows H+ to be excreted, increasing blood pH
Describe bicarbonate reabsorption in the PCT
H+ ions are secreted into the lumen via Na+/H+ exchanger to combine with any filtered bicarbonate
Forms carbonic acid, catalysed by carbonic anhydrase
Carbonic acid dissociates into CO2 and H20, which can both diffuse into the cell
Carbonic acid is reformed in the cell, which then dissociates into H+ and HCO3-
HCO3- can then be transported into the blood whilst the H+ ions can be transported into the lumen for the cycle to repeat
Describe bicarbonate production by the kidney
Metabolic activity of cells produces a large amount of CO2
Reacts with water to produce HCO3-, which enter plasma & H+ ions to be transported into the lumen
Useful as it provides H+ ions to drive HCO3- reabsorption
Describe respiratory acidosis
Occurs when alveolar hypoventilation results in CO2 retention and elevated pCO2
Any compensation must come from renal mechanisms that secrete H+ and reabsorb HCO3-
Describe respiratory alkalosis
Much less common than acidotic conditions
Often because of hyperventilation when alveolar ventilation increases without a matching increase in metabolic CO2 production
Primary cause = excessive artificial ventilation
Any compensation must come from renal mechanisms
-HCO3- not reabsorbed in proximal tubule
-late DCT/CD HCO3- secreted, H+ reabsorbed (with potassium)
Describe metabolic acidosis
Occurs when dietary and metabolic input of H+ exceeds H+ excretion – lactic acidosis & ketoacidosis
Can also occur if body loses HCO3- (diarrhoea)
Respiratory compensation instant, increased ventilation, pCO2 decreases due to hyperventilation
Renal compensation – late DCT/CD secretion of H+ (& potassium), reabsorption of HCO3-
Describe the anion gap
Difference between measured cations and anions, normally 10-18mmol/L
(Na+ + K+) – (Cl- + HCO3-)
Gap is increased if HCO3- is replaced by other anions
If a metabolic acid (eg. lactic acid) reacts with HCO3- the anion of the acid replaces the HCO3- -> this is not measured, the gap increases
In renal causes of acidosis, the anion gap will be unchanged -> not making enough HCO3-, but this is replaced by Cl-
Describe metabolic alkalosis
Caused by excessive vomiting of acidic stomach contents & excessive ingestion of bicarbonate – containing antacid
Respiratory compensation is rapid, hypoventilation means the body retains CO2 -> creates more H+ and HCO3- -> restores pH but produces more HCO3-
Renal compensation mechanisms -> HCO3- not reabsorbed in PT & in late DCT/CD – HCO3- secreted & H+ reabsorbed (with potassium)
Describe the common causes of metabolic alkalosis
Vomiting – causes loss of stomach acid and therefore H+ ions
Burns
Milk-alkali syndrome – leads to increased HCO3- in the blood
Diuretic usage
Describe the symptoms of metabolic acidosis
Hyperventilation – lungs to increase pH by blowing off CO2 to reduce its concentration in blood
Confusion
Tachycardia
Describe the symptoms of metabolic alkalosis
Hypoventilation – lungs try to decrease pH by increasing the concentration of CO2
Confusion
Tetany
Tremor
Describe potassium balance linked to acid/base balance
Acidosis and hyperkalaemia: high H+, means it is exchanged for potassium causing hyperkalaemia (& vice versa)
Alkalosis and hypokalaemia: low H+, means it is exchanged for potassium causing hypokalaemia (& vice versa)
Define AKI
Sudden deterioration of renal function over hours to days
Urea and creatinine rise rapidly
Usually associated with oliguria/anuria
Usually reversible, but not always
Describe the staging of AKI
1 – creatinine 1.5 – 1.9 times baseline, urine output < 0.5ml/kg/hour for 6-12 hours
2 – creatinine 2.0-2.9 times baseline, urine output < 0.5ml/kg/hour for > 12 hours
3 – creatinine 3 times baseline, urine output < 0.3ml/kg/hour for > 24 hours OR anuria > 12 hours
Stage according to the most severe classification outcome
List pre-renal causes of AKI
Hypoperfusion of the kidney
Sepsis, ACEi, hypovolemia, shock, renal artery stenosis, CCF, NSAIDs
List intrinsic renal causes of AKI
Parenchyma of the kidney is damaged
Acute tubular necrosis, acute interstitial nephritis, glomerular disease, vasculitis
Describe acute tubular necrosis
Ischemia secondary to any pre-renal cause
Rhabdomyolysis
Drug toxicity eg. gentamicin
List post-renal causes of AKI
Obstruction of outflow of urine
Calculus, ureteric/urethral stricture, BPH, tumour & retro-peritoneal fibrosis
Describe fluid assessment for AKI
General – colour, RR
Peripheral – hand temp, CRT & POSTURAL BP
Face & neck – sunken eyes, JVP
Chest & back – dull percussion, sacral oedema
Abdo & limbs – ascites, ballotable kidneys, urine output
List the complications of AKI
Metabolic acidosis
Hyperkalaemia
Volume overload
Uraemia
Describe investigations for AKI
Bedside – bladder scan, ECG
Bloods – VBG, CK
Imaging – ultrasound KUB, CT, CXR
Procedures – nephrostogram, cystoscopy
Describe the management for AKI
Pre-renal: IV fluid replacement to correct hypovolaemia & optimise renal blood flow until euvolaemic, diuretics
Renal: correct electrolytes, renal replacement therapy, call nephrology
Post-renal: urinary/supra-pubic catheter, ureteric stents, nephrostomy
Describe acute interstitial nephritis
Inflammation and oedema of the renal interstitium
Drugs, infections, hypercalcaemia, myeloma
