Renal physiology

Question 1

Substances absorbed in PCT

Answer 1

60% of Na
HCO3 reabsorption
All glucose and amino acids
Solute excretion : cations: Cr, Li, cimetidine
anions: urate, diuretics, radiocontrast media, penicillin., cephalosporin

Question 2

Site of action of loop diuretics

Answer 2

TAL of LH - Na-k-2CL transporter
25-30% Na reabsorption
Site of absorption of Ca and Mg -paracellular diffusion (claudin 16 gene)
Mutation of claudin 16 ->hypomagnesemia, nephrocalcinosis

Question 3

Bartter syndrome features

Answer 3

AR, normotensive
Hypokalemic metabolic alkalosis, hypercalciuria+/-hypomagnesemia, sodium loss
Increased renin and aldosterone due to low Na

Question 4

Bartter syndrome genetics

Answer 4

Type 1 -NKCC2 -neonatal
Type 2-ROMK -neonatal
Type 3-CLCNKB -classic
Type 4 -BSND - neonatal with deafness
Type 5 -CLCNKB, CLCNKA -neonatal with deafness

All present with hyokalemic metabolic alkalosis

Question 5

Site of action of thiazides, indapamide, metalazone

Answer 5

Distal tubule
NKCC1 channel - Na-Cl transporter
Also absorption of Ca and Mg at DT
Thiazide -cause increase Ca absorption, hypocalciuria -used to treat stones

Question 6

Absorption of Mg and Ca in DCT

Answer 6

Mg -TRPM6/M7 Channel
Inhibited by CNI esp Tacrolimus

Ca - TRPV5 channel,upregulated by PTH

Question 7

Genetics in Gitelman syndrome

Answer 7

Autosomal recessive , late in life
Musculoskeletal presentation
(NKCC1 chl) Na-Cl channel in DT
Salt wasting , hypokalemic metabolic alkalosis
Hypomagnesemia, hypocalciuria
Normotensive
Increased renin , aldosterone
Urine prostaglandin E normal

Question 8

Pseudohypoaldosteronism Type 2 features

Answer 8

AD inheritance, HTN -2-3rd decade
NAGMA
DCT: inhibition of ROMK->Hyperkalemia, stimulation of NCC -increased Na
hypercalciuria
High aldosterone levels
Rx-thiazides

Question 9

Absorption in cortical collecting duct

Answer 9

2 cell types-Principal cells(Na+K chls, water balance), intercalated cells (pH balance)
Sodium absorption via ENaC
ADH acting onV2 receptors - insertion of aquaporin ch
Aldosterone receptor -increases Na channels
ANP binds - decrease Na channels
Li enters via ENaC
Diuretics -Amiloride and triamterene act to close Na chl

Question 10

Liddle syndrome

Answer 10

AD inheritance
Inability to catabolise ENaC -increased Na absorption
Early onset hypertension + hypokalemic metabolic alkalosis
Decreased renin and aldosterone
Rx- amiloride/ triamterene

Question 11

Apparent mineralocorticoid excess/liquorice)

Answer 11

Deficiency of 11beta-HSD2 (required to convert cortisol to cortisone)
Excess cortisol -> increased mineralocorticoid activity

Question 12

Indication of vasopressin receptor antagonists

Answer 12

SIADH
C/c hyponatremia when other Rx failed
S/E hepatotoxicity
Agents -tolvaptan, conivaptan

Question 13

Causes of Type1 RTA

Answer 13

Autoimmune -SLE, sjogrens, RA
Hereditary hypercalciuria, hyperparathyroidism, Vit D intoxication
Thyroid disorders
Hypergammaglobulinemia, Sickle cell anemia
Drug- Amphotericin, Ifosphamide,NSAID,PPI, Li
Obstructive uropathy
Chronic hepatitis
Renal transplantation

Question 14

Features of Type 2RTA

Answer 14

Failure of prox tubular HCO3 reabsorption
Milder acidosis than Type 1
Urine pH<5.5
Rx- high dose HCO3
Often associated with Fanconi’s syndrome
Confirmatory test -Frac excretion of HCO3>25%

Question 15

Causes of Type 2 RTA

Answer 15

Drugs -Adefovir, tenofovir, aminoglycosides
Fanconi’s syndrome
Multiple myeloma, amyloidosis
Heavy metal poisoning
Interstitial nephritis -drugs, infections (CMV,lepto)

Question 16

Type 4 RTA features

Answer 16

Aldosterone deficiency/distal tubule resistance to aldosterone
Decreased Na absorption
Acidosis impairs ammonium production
Hyperkalemia, acidosis
Urine ph<5.5

Question 17

Causes of Type 4 RTA

Answer 17

Diabetic nephropathy
NSAIDS, ACEI,ARBs, heparin
Spironolactone, Bactrim ,tacrolimus
Tubulointerstitial disease -SLE, amyloid

Question 18

Most common type of renal stone

Answer 18

Calcium oxalate >calcium phosphate> urate