RENAL 227 Acute Renal Failure

Question 1

What is renal failure?

Answer 1

A failure of renal excretory function due to GFR depression. There is an abrupt deterioration in renal parenchymal function

Question 2

What does the RIFLE criteria stand for?

Answer 2

Risk, Injury, Failure, Loss and End Stage Kidney Disease

it is criteria for each level

Question 3

What factors affect outcome in ARF?

Answer 3

Age, DM, HTN, CCF, pre-existing renal disease and sepsis

Question 4

What are some extra renal effects of ARF?

Answer 4

Pulmonary: Oedema and ARDS and Infection
CNS: Altered consciousness, coma, confusions and convulsions
CVS: HTN, pericarditis, arrythmia, hypertrophy, HF and MI

Question 5

What is indicative of ARF in the blood?

Answer 5

Uraemia - high serum urea concentration

Question 6

What can you group causes of ARF into?

Answer 6

Pre-renal

Intrinsic and Post-renal

Question 7

What are the pre-renal causes of ARF?

Answer 7

impaired perfusion of the kidneys

e.g. hypovolaemia, hypotension, inefficient cardiac pump, vascular disease, third space sequestration, drugs

Question 8

What drugs and why do certain drugs increase tendency towards pre-renal ARF?

Answer 8

ACEI and NSAIDS
because they impair autoregulation -
NSAIDS = constriction of afferent arteriole therefore not maintaining pressure difference/ inability to regulate flow through
ACEI = blocks efferent constriction

Question 9

What is 3rd space sequestration?

Answer 9

Where ECF ends up in a place other than intravascular or interstitial space?
e.g:
severe pancreatitis –> retroperitoneal space
intestinal obstruction –> in GI tract
Crush injury –> into damaged muscle
Peritonitis –> into peritoneum

Question 10

What is post-renal ARF?

Answer 10

ARF due to obstruction of the urinary tract from calyces to the external urethral orifice

Question 11

What are the 3 main causes of Intrinsic AKI?

Answer 11

Acute tubular necrosis
Radiocontrast nephropathy
Acute tubulo-interstitial nephritis

Question 12

Describe acute tubular necrosis?

Answer 12

Can be due to ischaemia or nephrotoxicity

Necrosis of tubular cells but they have the ability to regenerate but there is no current treatment

Question 13

What are some causes of ATN?

Answer 13

Ischaemia: hypotension, hypovolaemia, shock, sepsis
nephrotoxiticity: aminoglycosides, radiocontrast, cisplatin, rhabdomyolosis

Question 14

What are the risk factors for radiocontrast nephropathy?

Answer 14

pre-existing renal disease, DM

Question 15

What happens in radiocontrast nephropathy?

Answer 15

There is transient vasodilation followed by prolonged vasoconstriction

Question 16

How might you prevent radiocontrast nephropathy?

Answer 16

low osmolality contrast media, IV fluids, antioxidants, n-acetylcysteine, diuretics and NaCO3

Question 17

What is acute-tubulo interstitial nephritis usually due to?

Answer 17

Drugs: penicillins, cephalosporins, sulfonamides, rifamipicin, furosemide and NSAIDS
Usually present with fever, rash, arthralgia, eosinofillia and a cellular infiltrate in the tubulointerstitium

Question 18

What are the two main life threatening complications of ARF?

Answer 18

Metabolic acidosis and hyperkalaemia

Question 19

How do you calculate the serum anion gap and what should it normally be?

Answer 19

cations - anions
Na+K -Cl-HCO3
should normally be 6-13meq/l

Question 20

What does a normal anion gap in a metabolic acidosis indicate?

Answer 20

That HCO3 is being lost but replaced by CL- therefore no change
causes: ddiarrhoea, renal tubular acidosis

Question 21

What does an increased anion gap in metabolic acidosis indicate?

Answer 21

increased acid production other than increased Cl-

e.g. lactic acidosis, DKA and renal failure

Question 22

What is the clinical effect of a metabolic acidosis?

Answer 22

muscle weakness, altered mental states, kussmauls breathing, hyperkalaemia and hypotension

Question 23

What is given cardioprotectively in hyperkalaemia?

Answer 23

IV Calcium gluyconate

Question 24

What is the role oif IV dextrose insulin/ Beta agonists in treating hyperkalaemia?

Answer 24

Shifts potassium into the intracellular compartment

Question 25

What is rhabdomyolosis?

Answer 25

Breakdown of muscle and release of these products into the circulation - these are harmful to the kidney (myoglobin, potassium, phosphate, urate and creatinine kinase)

Question 26

What are some causes of rhabdomyolosis?

Answer 26

Crush injury, immobilisation, compartment syndrome, marathon runners, hypokalaemia, prolonged convulsions, hypothermia, alcohol, opiates, statins etc etc etc

Question 27

What is the pathophysiology behind rhabdomyolosis?

Answer 27

Obstruction with haem pigment cast and proximal tubule injury by haem iron 10-12L of fluid may accumulate in damaged tissue withyin 24-48 hours

Question 28

How do you diagnose rhabdomyolosis?

Answer 28

History, red brown urine, increased CK and LDH hyper: K, PO4, uric acid hypo: calcium (deposited in damaged muscle)

Question 29

How do you treat/prevent rhabdomyolosis?

Answer 29

fluids to improve renal perfusion and urine output - wash out obstructions forced diuressi but can worsen hypocalcaemia and be careful in those with limited renal function anyway

Question 30

What might cause a hyponatraemia with high ADH?

Answer 30

Hypovolaemic states: diarrhoea etcc hypervolaemia states: HF and liver cirrhosis SiADH, MDMA and hypothyroid

Question 31

Why does HF and cirrhosis result in a high ADH in hyponatraemia?

Answer 31

baroreceptors sense decreased perfusion pressure therefore increasing ADH release and RAAS system despite the excess fluid a Na less than 125 is a poor prognostic factor in HF

Question 32

What may cause a hyponatraemia with a low ADH?

Answer 32

renal failure (impaired free water excretion), polydipsia and beer drinking

Question 33

How do you calculate serum osmolality?

Answer 33

(2x serum [Na]) + serum glucose +plasma urea

Question 34

What is osmotic demyelination syndrome?

Answer 34

due to rapid correction of severe hyponatraemia (