Renal

Question 1

What are the causes of AKI?

Answer 1

Pre-renal, renal + post-renal

Pre-renal: hypotension (shock), dehydration, heart failure
Renal: glomerulonephritis, interstitial nephritis, acute tubular necrosis
Post-renal: kidney stones, mass in abdo/pelvis, strictures, BPH/prostate cancer

Question 2

How is AKI diagnosed?

Answer 2

By measuring serum creatinine
>50% in 7 days
> 25mmol/L in 48hrs
<0.5ml/kg urine output for >6hrs

Question 3

What medications should be stopped in AKI?

Answer 3

NSAIDs
ACEi’s
Contrast dyes
Gentamicin

Question 4

Describe nephritic and nephrotic syndrome

Answer 4

NephrOtic syndrome = prOtein

• proteinurea (>3g/24hrs)
• peripheral Oedema
• hypercholesterolaemia
• serum albumin <25g/L

Nephritic syndrome = blood

• haematuria
• oliguria (decreased UO)
• fluid retention

Question 5

What are the most common causes of nephrotic syndrome in children and adults?

Answer 5

Children = minimal change disease
Adults = focal segmental glomerulosclerosis

Question 6

How does IgA nephropathy present?

Answer 6

Macroscopic haematuria associated with URTI in young patients
IgA deposits on histology

Question 7

What is the most common glomerulonephritis and what are the signs on histology?

Answer 7

Membranous glomerulonephritis,
IgG deposits on basement membrane

(peak in 20s and 60s, mostly idiopathic or 2dary to malignant, connective tissue disorders of drugs)

Question 8

When does post-streptococcal glomerulonephritis present and what causes it?

Answer 8

2-3weeks after step infection
tonsillitis or impetigo

(full recovery)

Question 9

How does goodpastures syndrome present and what is the antibody?

Answer 9

AKI + haemoptysis

Anti-GBM antibodies attack kidney and pulmonary basement membrane

Question 10

What is the difference between Goodpastures and Wegners vasculitis (granulomatosis with polyangitis) in presentation/diagnosis?

Answer 10

Same symptoms (haemoptysis + AKI)
Goodpastures = anti-GBM
Wegners (GPA) = ANCA

Question 11

How is Glomerulonephritis treated?

Answer 11

immunosuppression: steroids

BP control: ACEi or ARB (block RAAS)

Question 12

What re the signs on histology of rapidly progressive Glomerulonephritis?

Answer 12

Crescentic glomerulonephritis

Question 13

What is interstitial nephritis and what are the 2 causes?

Answer 13

Inflammation of the area surrounding the tubules (interstitium)

• acute interstitial nephritis
• chromic tubulointerstitial nephritis

Question 14

What causes acute interstitial nephritis and how does it present?

Answer 14

Causes: hypersensitivity reaction to infection or drugs (NSAIDs or Abx)

Presentation: AKI + hypertension

(treatment: steroids (reduce inflammation) + treat underlying cause)

Question 15

How does chronic tubulointerstitial nephritis present and what are the causes?

Answer 15

Causes: autoimmune, iatrogenic, infections, granulomatous
(chronic inflammation of tubules + interstitium)

Presentation: CKD

(Tx: treat underlying cause)

Question 16

What is the most common cause of AKI?

Answer 16

Acute tubular necrosis

Question 17

How is acute tubular necrosis treated?

Answer 17

Supportive - IV fluids, stop nephrotoxic medication (contrast, NSAIDs, Gent), treat complications

Cells will regenerate in 7-21days

Question 18

What are the causes of acute tubular necrosis?

Answer 18

Hypoperfusion: shock, sepsis, dehydration
Toxins: contrast, NSAIDs, gentamicin

Question 19

How is acute tubular necrosis diagnosed?

Answer 19

Urinalysis = muddy brown casts

Question 20

What are the 3 types of dialysis

Answer 20

Continuous ambulatory peritoneal dialysis:
- fluid inserted into peritoneal cavity, draws out toxins from blood, replace fluid several times a day (roughly 2L)

Automated dialysis
- machine constantly replaces dialysis fluid in peritoneum overnight (takes 8-10hrs)

Haemodialysis

• attach to blood filtering machine, usually 4hrs/day 3days/wk
• requires tunnelled cuff catheter (into jugular or subclavian vein) or AV fistula in forearm

Question 21

What are the indications for acute dialysis?

Answer 21

AEIOU

• acidosis
• electrolyte abnormalities
• intoxication (medication overdose)
• oedema - pulmonary
• uraemia symptoms (seizures/reduced consciousness)

Question 22

How is anaemia of CKD managed and why does it develop?

Answer 22

Decreased erythropoietin for stimulation of RBCs, so decreased RBC production

Tx: iron supplements/transfusions
erythropoietin
(avoid blood transfusions as can accuse sensitisation and reduce compatibility with renal transplants)

Question 23

How is renal bone disease managed and what causes it?

Answer 23

Decreased hydroxylation of VitD in the kidneys, so reduced calcium absorption. Parathyroid gland overreacts to produce excess PTH. PTH stimulates osteoclast activity to increase resorption of calcium from bone.

Tx: alphacalcidol (hydroxylated VitD)
bisphosphonates for osteoporosis

Question 24

Who gets tertiary hyperparathyroidism?

Answer 24

Renal disease

Question 25

When should ACEis be used in kidney disease?

Answer 25

AKI = stop
CKD = 1st line for hypertension
Glomerulonephritis = start in all cases (BP control very important, unless associated with AKI)

Question 26

What is the normal albumin creatinine ratio (ACR)?

Answer 26

<3mg/mmol