renal essay - acute kidney injury

Question 1

What tends to the be the first sign of an acute kidney injury?

Answer 1

Fluid retention

Question 2

What are the symptoms of uraemia (build up of nitrogenous wastes in the blood) in AKI?

Answer 2

anorexia, nausea/vomiting, seizures, myoclonic jerks, coma

Question 3

How does urine output change over the course of an AKI?

Answer 3

Initially urine output is maintained due to compensatory mechanisms, but then nephron damage or obstruction causes oliguria. During AKI recovery, there is usually massive polyuria causing electrolyte imbalance.

Question 4

What are the general principles of management in AKI?

Answer 4

regulate volume and cardiac output, avoid catheterisation to reduce sepsis risk, renal support with dialysis

Question 5

What is a pre-renal AKI?

Answer 5

Low blood pressure and reduced renal perfusion cause low GFR and damage to tubules of an otherwise healthy kidney

Question 6

What are some causes of pre-renal AKI?

Answer 6

Hypovolemia, hypotension/shock, low cardiac output, renal artery contriction

Question 7

What systems will be activated by a drop the initial drop in perfusion in a pre-renal AKI?

Answer 7

Renin-Angiotensin II, aldosterone, ADH, renal sympathetic nerves

Question 8

What is the process of volume restoration with renin and ang II in response to low renal perfusion?

Answer 8

1. renin released from JGA in response to reduced renal perfusion pressure at the afferent arteriole
2. renin cleaves angiotensinogen to ang I, and ACE converts Ang I to Ang II
3. Ang II contricts the efferent arteriole, reducing filtered load,
4. tubular reabsorption of sodium increases, which increases water reabsorption
5. vasocontriction occurs in the vasculature of the body, increasing total peripheral resistance and raising BP further.

Question 9

What is the process through which Aldosterone increases sodium and water retention?

Answer 9

1. Ang II triggers the release of aldosterone from the adrenal glands
2. Aldosterone acts on Na+/K+ transporters on principal cells of distal tubule, increasing sodium and chloride reabsorption, while increased excretion of K+
3. Upregulate sodium channels in the collecting duct, further increasing reabsorption

Question 10

What is the process through which ADH increases sodium and water retention?

Answer 10

1. Ang II acts on the hypothalamus to trigger thirst and ADH release
2. ADH acts of the collecting duct and distal tubules, inserting aquaporins to increase water reabsorption
3. At high concentrations, ADH will trigger arteriolar vasoconstriction in the periphery to raise BP

Question 11

What is the process through which renal sympathetic nerves increase sodium and water retention?

Answer 11

1. further activate RAAS in response to low volume, by increase the release of renin
2. increase sodium reabsorption in the tubules
3. increase renal vascular resistance to drop GFR and renal blood flow.

Question 12

What pathology does renal hypo-perfusion eventually lead to?

Answer 12

Acute Tubular Necrosis

Question 13

Which parts of the nephron are susceptible to renal hypo-perfusion and acute tubular necrosis, and why?

Answer 13

Late proximal tubules, thick ascending limbs in the medulla, because they have high oxygen demands due to their active transport processes. Vascular endothelium may also be damaged

Question 14

How does Acute Tubular Necrosis alter urine output?

Answer 14

Necrotic debris/casts will accumulate in the lumen of the distal tubule, impeding urine output and worsening kidney damage.

Question 15

How does Acute Tubular Necrosis alter electrolyte and acid-base balance?

Answer 15

Damage to the distal tubule causes a metabolic acidosis and hyperkalemia

Question 16

What is the histological morpholgy in pre-renal AKI?

Answer 16

Normal glomeruli, necrotic tubular epithelial cells, necrotic debris and cell apoptosis

Question 17

What investigations are used to diagnose a pre-renal AKI?

Answer 17

Lying & standing BP, JVP, body weight, urine biochemistry/output

Question 18

What are the clinical findings in the early stages of a pre-renal AKI?

Answer 18

postural hypotension, JVP not visible, weight loss, high urine osmolarity/oliguria, low urine sodium (may become elevated in acute tubular necrosis due to distal tubule damage)

Question 19

What are the principles of management in pre-renal AKI?

Answer 19

Correct underlying hypotension/hypovolemia, correct acid/base abnormalities (dextrose/insulin for hyperkalemia, sodium bicarb for acidosis), dialysis

Question 20

What is intrarenal AKI?

Answer 20

Intrinsic structural damage to renal structures, most commonl the tubules, that impairs filtration and absorption

Question 21

What are some of the causes of intrarenal AKI?

Answer 21

glomerulonephritis, vasculopathies, interstitial nephritis, nephrotoxin acute tubular necrosis

Question 22

What investigations can be used to diagnose an intrarenal AKI?

Answer 22

renal biopsy, toxicology, immunology, urinalysis, biochemistry, ABG

Question 23

What are the general principles of management of an intrarenal AKI?

Answer 23

Remove/treat source of injury, immunosupressive treatment for immunological pathologies, correcting acid/base and electrolyte/fluid abnormalitie

Question 24

What is a post-renal AKI?

Answer 24

Injury to the kidney caused by pressure from an obstruction of urine flow in the kidney or urinary tract

Question 25

What are some of the causes of post-renal AKI?

Answer 25

cell debris/crystals in tubules, strictures, nephrolithliasis, clots, tumors, neurogenic bladder, prostatic hypertrophy

Question 26

How does urinary obstruction lead to kidney damage and AKI?

Answer 26

Increased intratubular pressure reduces filtration and tubular flow. Back pressure will reduce GFR at the glomerulus

Question 27

What investigations can be done to diagnose post-renal AKI?

Answer 27

urine output, urine microscopy, ultrasound/abdominal exam/prostate exam, plasma creatinine, eGFR

Question 28

What are the possible clinical findings in post-renal AKI?

Answer 28

Anuria or oliguria, haematuria, elevated uric acid, tumors/masses/prostatic hypertrophy, pain

Question 29

What is the most important management consideration immediately following the removal of an obstruction in post-renal AKI?

Answer 29

There will be massive post-obstructive diuresis, which can cause electrolyte abnormalities and volume depletion

Question 30

How may an MI lead to AKI?

Answer 30

MI may lead to heart failure - which reduces perfusion to the kidneys by reducing cardiac output and blood pressure

Question 31

How does MI lead to mitral valve dysfunction and therefore a murmur?

Answer 31

MI causes ischaemic damage to the papillary muscles of the mitral valve, leading to mitral regurgitation

Question 32

How does mitral regurgitation lead to heart failure (both left and right)?

Answer 32

1. Regurgitation increases pressure in the left atrium, which results in atrial hypertrophy.
2. Increased volume in the left ventricle will cause hypertrophy and eventually dilation and heart failure.
3. Back pressure into the lungs causes pulmonary oedema and hypertension.
4. Pulmonary hypertension puts strain on the right heart, which hypertrophies and eventually fails too, causing peripheral oedema and a raised JVP.

Question 33

What is the process through which heart failure causes volume retention (which exacerbates oedema and heart dysfunction)?

Answer 33

heart failure/IHD reduced cardiac output and blood pressure, reducing renal blood flow. the RAAS system is activated by reduced GFR, causing sodium and water retention which increases the preload on the heart, worsening heart function

Question 34

What are the first line treatments for an AKI caused by heart failure?

Answer 34

Frusemide - removes excess fluid to relieve pulmonary and peripheral oedema.

Question 35

What are the second line treatments for AKI caused by heart failure, and why?

Answer 35

ACE Inhibitors - promotes systemic vasodilation to reduce preload and work on the heart
Beta-Blockers - decrease heart rate to increase time in diastole and improve coronary perfusion and overall heart functioning

Question 36

How can ACE inhibitors prevent renal ischaemia?

Answer 36

While they cause a transient decrease in GFR initially by vasodilating the efferent arteriole, they also promote downstream renal perfusion which prevents ischaemia and progression to Acute Tubular Necrosis