Renal tubule disorders and diuretics

Question 1

Proximal tubule role

Answer 1

Reabsorption: 70% Na
HCO3-
Phosphate
Aas
Sugars
Uric acid

Question 2

Fanconi syndrome pathology

Answer 2

Generalised impairment of proximal tubule function resulting in urine containing high amounts of normally reabsorbed items (Na, HCO3-, phosphate, aas, sugars, uric acid)
Phosphate loss lead to bone demineralisation and growth impairment

Question 3

Fanconi syndrome treatment

Answer 3

Replace phosphate

Question 4

Proximal (type 2) renal tubular acidosis pathology

Answer 4

Failure of bicarb reabsorption but distal reabsorption intact so serum bicarb usually >12
Accompanied by Fanconi unless rare familial cause

Question 5

Proximal (type 2) renal tubular acidosis causes

Answer 5

Light chain disease
Drugs (tenofovir)
Heavy metals

Question 6

Proximal (type 2) renal tubular acidosis diagnosis

Answer 6

IV bicarb causes rapid rise in urine pH due to urinary bicarb loss

Question 7

Proximal (type 2) renal tubular acidosis treatment

Answer 7

Bicarb and K+ replacement

Question 8

Proximal tubule diuretics

Answer 8

Osmotic diuretics (mannitol) freely filtered but poorly reabsorbed, risk of pulmonary oedema if anuric
Carbonic anhydrase inhibitors (acetazolamide) can cause metabolic acidosis due to inc bicarb excretion

Question 9

TAL physiology

Answer 9

Reabsorbs Na+ 10-30% and other electrolytes

NKCC transporter is key

Question 10

Bartter syndromes pathology

Answer 10

Impaired salt transport in TAL, present from childhood and subtypes depending on which transporter affected, Type I is NKCC
Na reabsorption increases further along nephron in exchange for H+ and K+ resulting in hypokalaemic, hypochloraemic metabolic alkalosis

Question 11

Bartter syndrome treatment

Answer 11

Salt replacement

NSAIDs after volume repletion

Question 12

TAL diuretic

Answer 12

Loop diuretics (furosemide, bumetanide) block NKCC to increase water, Na, Cl, phosphate, Mg, Ca, K and H+ excretion
IV needed if GI tract too oedematous to absorb

Question 13

Distal tubule physiology

Answer 13

Reabsorbs Na 5-10% and other electrolytes

NaCl co-transporter is key here

Question 14

Gitelman syndrome pathology

Answer 14

Loss of function of NaCl co-transporter

Usually presents in adolescence/adulthood as incidental electrolyte abnormality finding

Question 15

Gitelman syndrome treatment

Answer 15

Electrolyte supplementation

Question 16

Distal tubule diuretics

Answer 16

Thiazide (bendroflumethiazide) and thiazide-like (indapamide, chlortalidone, metolazone) diuretics inhibit NaCl transporter
Ca and uric acid excretion reduced
Glucose intolerance can occur

Question 17

Cortical collecting duct physiology

Answer 17

Acid-base and K+ homeostasis

Aldosterone acts to retain Na+ and excrete K+

Question 18

Distal (type 1) renal tubular acidosis pathology

Answer 18

Failure of H+ excretion can be 1˚ (genetic) or 2˚ (to SLE/toxins)
Causes bone demineralisation, renal calculi, hypokalaemia

Question 19

Distal (type 1) renal tubular acidosis diagnosis

Answer 19

Urine fails to acidify (pH>5.3) despite metabolic acidosis

Question 20

Distal (type 1) renal tubular acidosis treatment

Answer 20

Bicarb replacement and management of underlying disease in 2˚

Question 21

Type 4 RTA pathology

Answer 21

Hyperkalaemia and acidosis due to hypoaldosteronism e.g. adrenal insufficiency, DM, anti-RAS, K+ sparing diuretics

Question 22

Type 3 RTA pathology

Answer 22

Carbonic anhydrase II deficiency so reabsorption of bicarb impaired in proximal tubule
Now thought to be combination of type 1 and 2 so not used as classification anymore

Question 23

Cortical collecting duct diuretics

Answer 23

K+ sparing (spironolactone, eplerenone, amiloride) aldosterone antagonists
Decrease Na+ and K+ excretion
Can cause hyperkalaemia + acidosis
Oestregenic effects with spironolactone