Renal

Question 1

Where does ADH act?

Answer 1

V2 receptors in the thick ascending loop of henle, DCT, cortical collecting duct and medullary collecting duct

Question 2

What happens when ADH is released?

Answer 2

Release of aquaporin 2 which binds to the luminal surface leading to water resorption into the circulation.

Question 3

What is Tolvaptan?

Answer 3

V2 receptor blocker, stopping the action of ADH - used in polycystic KD

Question 4

What are the lab findings in SIADH?

Answer 4

Low serum Na, Low plasma osmolality, high usine osmolality (>100), high urine Na

Question 5

Where / how do loop diuretics work?

Answer 5

Blockade of Na-K-2Cl transporter in the loop of henle.

Question 6

What is the effect of loop diuretics on calcium?

Answer 6

Also block calcium reabsorption so there is increased calcium in the urine - risk of stones

Question 7

Where and how do thiazides act?

Answer 7

Blockade of the Na-Cl cotransporter in distal convoluted tubule. (works synergistically with loop diurectic BC DCT comes later)

Question 8

What is the effect of Thiazides on Calcium?

Answer 8

Increase Ca resorption in the DCT and PCT so can be good for hypercalciuria + recurrent stones

Question 9

What is gittleman syndrome?

Answer 9

Defects the same as thizide - Defect in DCT in Na/Cl transporter
Low K+, metabolic alkalosis

Question 10

What is Barters syndrome?

Answer 10

B for BABY
Defect in loop of Henle Na/K/2Cl transporter ( defect the same as therapy with loop). Hypokalaemia, metabolic alkalosis. Also low Ca, Mg

Question 11

What is the effect od aldosterone in the kidney?

Answer 11

Increases the number of Na/K channels in principal cells both on the tubular and basolateral surfaces.
Promoting Na absorption and K+ excretion

Question 12

What is type 1 renal tubular acidosis?

Answer 12

Defect in the distal hydrogen ion excretion
Low K
Metabolic acidosis
Hypercalciuria, hypocitraturia, nephrolithiasis

Question 13

What is type 2 RTA?

Answer 13

Proximal type - reduced capacity to rectain filtered bicarbonate ( normal subjects do not have bicarb in urine). Bicarb excreted in urine
Low K

Question 14

What is type 4 RTA?

Answer 14

Secondary to hypoaldosteronaemia - also have hyperkalaemia

Question 15

how to treat RTA 1?

Answer 15

Bicarb tablets to bind retained hydrogen ions

Question 16

What is used to treat PKD in high risk patients?

Answer 16

Tolvaptan is a vasopressin V2-receptor (V2R) antagonist with proven beneficial results in ADPKD

Question 17

What are general treatment principles for PKD?

Answer 17

• Lower BP with ACEi/ARB - 110/70
• Drink >3L water / day to maintain hypoosmolar urine / supress ADH

Question 18

What PKD patients are prescribed tolvaptan?

Answer 18

Age >18
eGFR >25, but declining either 5 in one year or 2.5 per year/5 years
Limited data for use in >55y/o
4 years of use delays dialysis by 1 year

Question 19

What are contraindicators to Tolvaptan?

Answer 19

Liver disease ( 3xULN), use of CYP3a4 inhibitors, hypernatraemia at baseline, inability to respond to thirst, diuretic use

Question 20

How do patients with PKD present clinically?

Answer 20

can present with hypertension, hematuria, proteinuria, or kidney function impairment. Flank pain, due to kidney hemorrhage, obstructive calculi, or urinary tract infection, is the most common symptom reported by patient

Question 21

What neurologic condition is associated with PKD?

Answer 21

Intracranial aneurysms, hypertensive haemorrhage

Question 22

What are the feautres of minimal change GN?

Answer 22

Loss of podocytes on EM, pure nephrotic syndrome, normal light microscopy,

Question 23

Treatment for minimal change GN?

Answer 23

Steroids, if no / minimal response to steroids rituximab or cyclophosphamide

Question 24

What is serum soluble urokinate type plasminogen activator receptor ( suPAR) a marker of?

Answer 24

Disease activity in FSGS
Renal disease occurs when sufficient circulating suPAR activates podocytes B3 integrin causing foot process effacement, proteinuria and FSGC like GN

Question 25

PLA2R antibodies are measured in what disease?

Answer 25

Membranous nephropathy

Question 26

What is one of the adverse effects of cyclophosphamide?

Answer 26

Haematuria and bladder cancer

Question 27

What is secondary membrnous nephropathy?

Answer 27

Not caused by PLAR2 antibody, so if membranous nephropathy but negative pLAR2 need to look for secndayr causes such as lymphoma, adenocarcinoma

Question 28

What are the nephrotic syndorme diseases?

Answer 28

FSGS, Minimcal change and primary/secondary membranous

Question 29

How do you treat IgA nephritis syndrome?

Answer 29

Onset within hours of sore throat.
Accompanied with HTN
Treatment is RAAS blockage w ACEi or ARB

Question 30

How do you treat membranoproliferatice GN?

Answer 30

• Immunosuppression
  ○ No benefit in familial MPGN
• In C3GN consider anticomplement treatment - eculizumab
• MPGN with immuno complex deposition - consider steroid/Plasma exchange/rituximab

Question 31

What diseases cause rapidly progressive GN?

Answer 31

ANCA vasculitis, antiGBM disease, SLE

Question 32

What is the management of rapidly progressive GN?

Answer 32

Urgent inv and diagnosis is jey ( renal biopsy)
IV Methyl pred x 3 then PO
Cyclophosphamide
Plasmaexchange in anti-GBM + in AAV if there is associated pulmonary haemorrhage