Session 10

Question 1

How do patients with renal disease usually present?

Answer 1

Without symptoms: usually detected via screening of at risk patients.

Question 2

What effect does acidosis have on patients breathing?

Answer 2

Kussmaul breathing patterns: strained breathing.

Question 3

How does impaired tubular function manifest in patients?

Answer 3

Usually an impaired ability to concentrate urine so more urine produced; can cause acidosis so breathing problems; can cause glycosuria even with normal blood glucose levels.

Question 4

How can renal disease cause glycosuria?

Answer 4

Tubular disease can lower the threshold for complete glucose resorption so glycosuria can result even if blood glucose levels are normal.

Question 5

How can kidney failure cause anaemia?

Answer 5

Less erythropoietin is released by the kidneys so there is less erythropoiesis in the bone marrow, less RBCs are produced and RBCs have a shorter lifespan so anaemia is caused.

Question 6

How will macroscopic haematuria due to renal disease normally appear?

Answer 6

Smoky brown colour.

Question 7

If urine appears red at the start of the stream and then normal, what is the likely cause?

Answer 7

Bleeding in the lower urinary tract.

Question 8

If urine is normal at the start of the stream and then red towards the end, what is the likely cause?

Answer 8

Bleeding from the bladder.

Question 9

What is the most likely cause of haematuria originating in the kidneys?

Answer 9

IgA nephropathy.

Question 10

What usually causes IgA nephropathy?

Answer 10

Infections elsewhere in the body, usually after an upper respiratory tract infection precipitates release of IgA in the kidneys.

Question 11

How does nephrotic syndrome usually present?

Answer 11

Triad of symptoms: proteinuria, hypoalbuminaemia and oedema (+/- hyperlipidaemia). Always have some form of glomerular disease. Can have oedema without orthopnoea, Muehrcke’s bands on fingernails, xanthelasma, fat bodies in urine, DVT.

Question 12

How can oedema due to heart failure and oedema due to nephrotic syndrome be distinguished?

Answer 12

Oedema due to nephrotic syndrome has no orthopnoea. May also have oedema of the face, this isnt present in oedema due to heart failure.

Question 13

Describe the features on examination of nephritic syndrome compared to nephrotic syndrome.

Answer 13

• Raised BP and JVP in nephritic, not in nephrotic.
• Less severe oedema in nephritic syndrome.
• Less severe proteinuria in nephritic syndrome.
• More severe haemauria in nephritic syndrome.
• Red cell casts only present in nephritic syndrome.
• High serum albumin in nephritic, low in nephrotic syndrome.

Question 14

Define acute kidney injury.

Answer 14

Clinical syndrome causing an abrupt decline in actual GFR. Serum creatinine is raised and urine volume is decreased.

Question 15

What causes pre-renal failure?

Answer 15

Decreased blood supply to the kidney; usually due to volume depletion, heart failure or cirrhosis.

Question 16

What causes intrinsic renal failure?

Answer 16

Disease of the renal parenchyma; usually due to ischaemia and toxic acute tubular necrosis.

Question 17

What causes post-renal failure?

Answer 17

Obstruction; may be from structures pressing on the kidney or urinary tract obstruction.

Question 18

Describe the main features of pre-renal AKI.

Answer 18

GFR reduced because of reduced renal blood flow; no cell damage; will respond to fluid resuscitation; causes acute tubular necrosis if untreated.

Question 19

How can NSAIDs precipitate pre-renal AKI?

Answer 19

Reduce prostaglandin production which prevents autoregulation of renal blood flow as afferent arteries cant be dilated.

Question 20

How can ACE-I and AIIR antagonists precipitate pre-renal AKI?

Answer 20

Prevent autoregulation of renal blood blow my preventing constriction of the efferent arterioles as they inhibit angII production/binding.

Question 21

Which areas of the kidney nephron are most susceptible to damage due to ischaemia, why?

Answer 21

Proximal convoluted tubule and thick ascending limb of the loop of Henle, both have very high oxygen demands for active transport and are poorly supplied by oxygen physiologically as they lie in the medulla.

Question 22

Why are areas of nephron in the kidney cortex not likely to be affected by ischaemia?

Answer 22

The cortex has a much better supply of oxygen than the medulla.

Question 23

How can muscle crush injuries lead to toxic ATN?

Answer 23

Myoglobin is released due to muscle crush injuries, can act as a nephrotoxin and cause damage to epithelial cells in the kidney tubules.

Question 24

Describe the appearance of myoglobinuria.

Answer 24

Urine appears dark brown, like flat coca cola.

Question 25

What is acute glomerulonephritis?

Answer 25

Immune disease affecting the glomeruli.

Question 26

What glomerular and arteriolar diseases can cause ATN?

Answer 26

Acute glomerulonephritis, haemolytic uraemia syndrome, malignant hypertension, pre-eclampsia, acute tubule-interstitial nephritis.

Question 27

How would obstructive AKI present on examination/investigation?

Answer 27

Increased intraluminal pressure, dilation of the renal pelvis (hydronephrosis), decreased renal function, may see the obstruction with imaging or palpate it on examination.

Question 28

What investigations are always performed if ?AKI?

Answer 28

Urea and creatinine levels, urinalysis (dipstick and microscopy if +ve dipstick).

Question 29

In which types of AKI may proteinuria and haematuria be present?

Answer 29

Intrarenal AKI.

Question 30

What may urine chemistry tests show in prerenal AKI?

Answer 30

Increased urine osmolarity, increased urine-to-plasma osmolarity, decreased urine sodium levels.

Question 31

What may urine chemistry results show in postrenal AKI?

Answer 31

Decreased urine osmolarity, decreased urine-to-plasma osmolarity, increased urine sodium.

Question 32

When would an USS be performed in an AKI patient?

Answer 32

If ?obstruction or unclear cause USS is performed within 24 hours.

Question 33

How is prerenal AKI treated?

Answer 33

Aggressively to prevent ATN from developing, usually aggressive fluid resuscitation.

Question 34

How are patients who are at risk of AKI treated?

Answer 34

Close monitoring, ensure adequate hydration, avoid nephrotoxins, detect any AKI early and identify its cause.

Question 35

What are the indications for dialysis in AKI patients?

Answer 35

High potassium refractory to treatment, metabolic acidosis, fluid overload refractory to diuretics, presence of dialyzable nephrotoxins, uraemia.