Question 1

What is Acute kidney Injury?

Accepted Answer

AKI alone is not a diagnosis it is a syndrome with multiple potential causes – often multifactorial.

One or more of:

Rise in serum creatinine of 26 micro mol/L (umol/L) or greater, within 48h
50% or greater rise in serum creatinine (more than 1.5x baseline) known or presumed to have occurred within the past 7 days
Fall in urine output to <0.5 mL/kg/hour for more than 6 hours

Question 2

How is Kidney function measured?

Accepted Answer

1. Serum Creatinine What it measures: Creatinine is a waste product produced by muscles. The kidneys filter creatinine from the blood, so elevated levels can indicate impaired kidney function. Normal range: Typically 45-84umol/L in adults (varies by age, sex, and muscle mass). Insensitive for measurement of CKD 2. Glomerular Filtration Rate (GFR) What it measures: GFR estimates how well the kidneys are filtering waste from the blood. It’s calculated using serum creatinine levels, age, gender, and other factors. Normal range: 90–120 mL/min/1.73 m² (lower values indicate reduced kidney function). GFR may be over-estimated in those with lower muscle mass Measure AKI with creatinine, not glomerular filtration rate (GFR) 3. Cystatin C What it measures: An alternative marker for kidney function, less affected by muscle mass than creatinine. It is used to estimate GFR, particularly in people with unusual muscle mass. Possibly better in early detection of CKD and AKI Only removed in filtration (and not secreted by tubules) More research needed; hasn’t yet become routine part of practise

Question 3

What are the different stages of acute kidney disease?

Accepted Answer

Stage 1 (Mild)
Serum Creatinine: 1.5 to 1.9 times baseline, or an increase of ≥27 µmol/L from baseline.

This means if a person’s baseline creatinine is 100 µmol/L, stage 1 would be reached if the serum creatinine increases by 27 µmol/L or more, making it at least 127 µmol/L.

Urine Output: Less than 0.5 mL/kg/h for 6 to 12 hours.

Stage 2 (Moderate)
Serum Creatinine: 2.0 to 2.9 times baseline, or an increase of ≥54 to 150 µmol/L from baseline.

For example, if the baseline creatinine is 100 µmol/L, stage 2 would occur if the creatinine rises by at least 54–150 µmol/L, bringing it to 154–250 µmol/L.

Urine Output: Less than 0.5 mL/kg/h for more than 12 hours.

Stage 3 (Severe)
Serum Creatinine: 3.0 times baseline, or an increase of ≥354 µmol/L, or initiation of dialysis.

For example, if the baseline creatinine is 100 µmol/L, stage 3 would be reached if the serum creatinine increases by at least 354 µmol/L, bringing it to 454 µmol/L or more.

Urine Output: Less than 0.3 mL/kg/h for 24 hours or anuria for more than 12 hours.

Question 4

What are the clinical consequences of AKI?

Accepted Answer

Mortality increases with increasing stage of AKI
A diagnosis of AKI in 5.4% of admissions.
Overall mortality rate of 23.8%
- 16.1% stage 1
- 36.1% stage 3
Renal recovery dependent on severity of AKI:
80% recovery seen in stage 1 AKI
59% recovery seen in stage 3 AKI

Question 5

What are the three categories that AKI can fall into?

Accepted Answer

Pre-renal — due to reduced perfusion of the kidneys and/or hypotension.

Intra-renal (intrinsic) — due to structural damage to/within the kidney.

Post-renal — due to acute urinary tract obstruction

Question 6

What is Pre Renal AKI?

Accepted Answer

Most common cause of AKI

Mechanism = decreased renal perfusion= decreased glomerular filtration rate

Multiple causes
- decreased circulating volume
- decreased cardiac output (eg cardiac failure)
- Systemic vasodilatation (eg sepsis)
- Arteriolar changes(eg ACE-i or NSAID use). Drugs may cause altered glomerular haemodynamics. For pateints with acute illnesses they may be using combined NSAID and ACE inhibitor therapy which can lead to:
- NSAID-mediated vasoconstriction of the afferent arteriole
- ACE inhibitor mediated vasodilation of efferent arteriole
Which will lead to Reduced glomerular pressure thus reduced GFR.

Hypotension, systemic vasodilation and hypovolaemia also reduce glomerular pressure.

Question 7

What is the gold standard of renal artery stenosis investigation?

Accepted Answer

Gold standard diagnostic investigation renal arteriography Less invasive scans acceptable eg US doppler, CT or MRI

Question 8

How is renal artery stenosis treated?

Accepted Answer

1. Medical Management (Initial Approach) Antihypertensive Treatment: ACE inhibitors or angiotensin II receptor blockers (ARBs) are commonly used to control blood pressure and protect kidney function. However, they should be used cautiously in bilateral renal artery stenosis or when kidney function is severely compromised. Other antihypertensive agents like beta-blockers, calcium channel blockers, and diuretics may be used as adjuncts to control blood pressure. Statins: Statins should be considered if there is evidence of atherosclerosis, as they help reduce cholesterol levels and the risk of further plaque buildup in the renal arteries. Antiplatelet Therapy: Aspirin or other antiplatelet drugs may be prescribed to reduce the risk of thrombosis and further progression of atherosclerotic disease in the renal arteries. 2. Revascularization Procedures NICE guidelines recommend revascularization procedures in the following circumstances: Percutaneous Transluminal Angioplasty (PTA): Percutaneous angioplasty is the preferred approach for revascularization in patients with unilateral renal artery stenosis. The procedure involves inserting a catheter into the renal artery and inflating a balloon to open up the narrowed area. In some cases, a stent may be placed to maintain artery patency. Surgical Bypass: Surgical revascularization may be indicated in cases where angioplasty is not suitable, such as in severe stenosis, or where other options are ineffective. Stent Placement: A stent may be used in conjunction with angioplasty if the stenosis is severe or recurrent, to keep the renal artery open and improve blood flow. 3. Indications for Revascularization (as per NICE): Symptomatic renovascular hypertension: Refractory to optimal medical management. Progressive renal impairment: When there is evidence of worsening kidney function (e.g., increasing serum creatinine levels). Severe or worsening symptoms: Such as recurrent pulmonary edema or heart failure due to renovascular hypertension. Ischemic nephropathy: Evidence of chronic kidney injury due to insufficient blood supply to the kidneys. 4. Lifestyle Modifications Diet and Weight Management: A low-sodium diet, weight reduction, and a healthy, balanced diet are encouraged to help manage blood pressure and prevent further kidney damage. Smoking Cessation: Since smoking exacerbates atherosclerosis and vascular damage, patients should be advised to stop smoking. 5. Regular Monitoring Blood Pressure Monitoring: To assess the effectiveness of antihypertensive treatment and monitor for target organ damage. Kidney Function: Regular monitoring of kidney function (e.g., serum creatinine and eGFR) to detect worsening or improvement in kidney function.

Question 9

What are the different types of fluid therapy?

Accepted Answer

1. Resuscitation (Volume Replacement): Crystalloids (e.g., Normal Saline, Lactated Ringer’s) for rapid volume expansion. Colloids (e.g., Albumin, Hydroxyethyl Starch) for longer-lasting volume expansion in severe cases. 2. Routine Maintenance Therapy: Used for patients who can't eat or drink. Isotonic fluids like D5W (Dextrose 5% in water) and electrolyte solutions (e.g., D5 0.45% NaCl) to maintain hydration and electrolyte balance. 0.18% sodium chloride/ 4% dextrose 3. Replacement Therapy: For correcting fluid and electrolyte deficits due to vomiting, diarrhea, or burns. Oral Rehydration Solutions (ORS) for mild dehydration, or IV crystalloids for severe cases.

Acute Kidney Injury Flashcards