Renal disease: pre-renal

Question 1

What are the three major causes of Acute Kidney Injury (AKI)?

Answer 1

AKI can be caused by pre-renal, renal, or post-renal factors.

Question 2

What are the main causes of pre-renal AKI?

Answer 2

Pre-renal AKI is mainly caused by reduced perfusion to the kidneys and can be the result of an acute systemic illness. The urine dipstick usually shows a bland result. This form of AKI is usually acute and potentially reversible, accounting for 55-60% of AKI incidence.

Question 3

What are the main causes of renal AKI?

Answer 3

Renal AKI can be caused by autoimmune diseases, acquired or inherited renal diseases, nephrotoxic drugs, or disease of the renal blood vessels. Most glomerular diseases occur without warning or a prodromal illness. The urine dipstick usually shows blood and protein present. This form of AKI often presents acutely but can result in chronic kidney disease, accounting for 35-40% of AKI incidence.

Question 4

What are the main causes of post-renal AKI?

Answer 4

Post-renal AKI is caused by an obstruction to the flow of urine, such as ureteric stones, benign prostate obstruction, ureteric strictures, or pelvic malignancy. It is usually diagnosed radiologically or in patients with a known urological history. The urine dipstick is often blood positive. This form of AKI can present either acutely or chronically and accounts for less than 5% of AKI incidence.

Question 5

What is Acute Kidney Injury (AKI) and what factors contribute to it?

Answer 5

AKI occurs when there is a sudden decrease in glomerular filtration rate (GFR), which is maintained by sufficient blood flow to the kidneys and nephron. If this is compromised, AKI can occur. The condition is usually reversible. GFR depends on a pressure gradient between the incoming blood at the afferent capillaries and the pressure in Bowman’s space, known as net filtration pressure.

Question 6

What is pre-renal AKI and when does it occur?

Answer 6

Pre-renal AKI occurs when there is reduced perfusion to the kidneys through the afferent arteriole. This can happen regardless of whether the patient has hypovolaemia, euvolaemia, or hypervolaemia. The causes of pre-renal AKI can be divided into different sections.

Question 7

What are the main causes of pre-renal AKI due to absolute hypovolaemia?

Answer 7

Causes of pre-renal AKI due to absolute hypovolaemia include:

Haemorrhage (shock) from trauma, surgery, postpartum, or gastrointestinal issues
Gastrointestinal losses, such as diarrhoea and vomiting
Renal losses, caused by drug-induced or osmotic diuresis, diabetes insipidus, and adrenal insufficiency
Losses through skin and mucous membranes, as in burns, hyperthermia, or other insensible losses
“Third-space” losses, such as pancreatitis and hypoalbuminaemia.

Question 8

What are the main causes of pre-renal AKI due to decreased cardiac output?

Answer 8

Causes of pre-renal AKI due to decreased cardiac output include:

Diseases of the myocardium, valves, pericardium, or conducting system
Pulmonary hypertension, pulmonary embolism, positive pressure mechanical ventilation
Systemic vasodilation: Sepsis, liver failure, anaphylaxis
Drugs: antihypertensives, anaesthetics, drug overdoses.

Question 9

What are the main causes of pre-renal AKI due to renal vasoconstriction?

Answer 9

Causes of pre-renal AKI due to renal vasoconstriction include noradrenaline, liver disease, sepsis, and hypercalcaemia.

Question 10

What are the main causes of pre-renal AKI due to renovascular diseases?

Answer 10

Renovascular diseases causing pre-renal AKI include atherosclerosis, thromboembolic disease, and renal artery dissection.

Question 11

What drugs can cause pre-renal AKI by impairing autoregulation and glomerular filtration rate?

Answer 11

Drugs that impair autoregulation and glomerular filtration rate, thus causing pre-renal AKI, include angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs that inhibit prostaglandin synthesis during renal hypoperfusion, diuretics, angiotensin II receptor blockers like candesartan, cyclosporin, and tacrolimus.

Question 12

What are the primary causes of pre-renal AKI?

Answer 12

The primary causes of pre-renal AKI include:

Intravascular volume depletion or absolute hypovolaemia
Decreased cardiac output
Renal vasoconstriction
Renovascular diseases, and
Drugs that impair autoregulation and glomerular filtration rate by affecting the vascular tone of afferent and efferent arterioles.

Question 13

What drugs are known to cause Acute Tubular Necrosis (ATN)?

Answer 13

Drugs that can cause Acute Tubular Necrosis (ATN) include:

Antibiotics like Vancomycin, Acyclovir, Foscarnet, Pentamidine, Aminoglycoside-Gentamicin, and Amphotericin B.
Organic solvents such as Ethylene Glycol and Toluene.
Anti-inflammatory painkillers like NSAIDs including COX 2 inhibitors.
Antihypertensives like ACE inhibitors (in patients with Bilateral Renal Artery Stenosis).
Chemotherapeutic agents such as Cisplatin and Ifosfamide.
Immunosuppressants like Cyclosporin, Tacrolimus, and IV immunoglobulin.
Radiocontrast agents.

Question 14

Which drugs are known to cause tubular cell toxicity, interstitial nephritis, and crystal toxicity in AKI?

Answer 14

Tubular cell toxicity can be caused by Aminoglycosides, Amphotericin B, and Cisplatin.
Interstitial Nephritis can be caused by NSAIDs and Rifampicin.
Crystal Toxicity can be caused by Acyclovir and Ampicillin.

Question 15

How can ACE inhibitor therapy result in worsening renal function?

Answer 15

ACE inhibitor therapy can worsen renal function in certain settings due to their action in decreasing glomerular filtration pressure. This can occur in conditions with already compromised renal perfusion such as bilateral renal artery stenosis or heart failure.

Question 16

What leads to the development of Renal AKI?

Answer 16

Renal AKI develops when there is a disruption to the anatomy or function of the nephron. It can occur independently or as a consequence of pre-renal AKI. The causes are usually defined by the area of the nephron where the disruption occurs.

Question 17

What is the most common cause of Renal AKI and how does it occur?

Answer 17

The most common cause of Renal AKI is Acute Tubular Necrosis, which is an ischaemic or toxic injury to the proximal convoluted tubule.

Question 18

What are the common causes of Acute Interstitial Nephritis?

Answer 18

Acute Interstitial Nephritis is commonly induced by drugs like NSAIDs and penicillins, infections such as Tuberculosis, or it can be immune mediated, as seen in conditions like Systemic Lupus Erythematosus or Sarcoidosis.

Question 19

What are the main causes of Glomerular Disease in Renal AKI?

Answer 19

Glomerular Disease in Renal AKI can occur due to Nephrotic Syndrome/Nephritic Syndrome, Primary diseases like anti-glomerular basement membrane disease, or Secondary systemic diseases that are immune complex mediated, like IgA nephropathy.

Question 20

What can cause Tubular Obstruction leading to Renal AKI?

Answer 20

Tubular Obstruction leading to Renal AKI can occur due to conditions like Myeloma or Rhabdomyolysis.

Question 21

How does Post-Renal AKI occur?

Answer 21

Post-Renal AKI occurs following an acute obstruction of urinary flow. This leads to an increase in intra-tubular pressure and a reduction in Glomerular Filtration Rate (GFR). Acute urinary tract obstruction also leads to impaired renal blood flow and inflammatory processes that contribute to diminished GFR.

Question 22

What are the causes of Post-Renal AKI?

Answer 22

Post-Renal AKI can occur due to obstructions in different parts of the urinary system: Ureter (stones, Retroperitoneal fibrosis, malignancy, ureterocoele), Bladder (malignancy), Prostate (cancer, benign prostate enlargement), Urethra (stricture disease, posterior urethral valve), or Extrinsic compression of ureters (pelvic malignancy, lymph nodes).

Question 23

What are the symptoms of Pre-Renal AKI?

Answer 23

The symptoms of Pre-Renal AKI include severe dehydration symptoms such as sunken eyes, dry skin, decreased skin elasticity, and dry mouth and eyes. There might also be tachycardia and dizziness when standing or sitting up, which is known as orthostatic hypotension.

Question 24

What is the difference between Pre-renal insult and Acute tubular necrosis (ATN) in Acute Kidney Injury (AKI)?

Answer 24

Pre-renal insult and ATN both result in AKI, but they differ in causes and characteristics. Pre-renal insult is caused by physiological or pathological factors, often has predisposing systemic factors, and can be reversible. It presents with high urine osmolality (>500 osmol/kg), oliguria, and fractional excretion of sodium <1%. On the other hand, ATN is a pathological condition, often reversible, but can lead to chronic kidney disease (CKD). It presents with low urine osmolality, normal urinary sodium concentration, non-oliguria or normal urine volume, and fractional excretion of sodium > 2%.

Question 25

How is the Fractional Excretion of Sodium (FeNa) calculated?

Answer 25

The Fractional Excretion of Sodium (FeNa) can be calculated using the following formula: FeNa = (Urinary Sodium x Serum Creatinine / Serum Sodium x Urinary Creatinine) x 100. It is expressed as a percentage (%). FeNa < 1% typically indicates pre-renal insult, while FeNa > 2% is suggestive of acute tubular necrosis (ATN).

Question 26

What is Acute Kidney Injury (AKI) and how is it staged?

Answer 26

Acute Kidney Injury (AKI) is a condition where there is a sudden decrease in glomerular filtration rate (GFR), compromising the kidneys' ability to filter waste from the bloodstream. AKI can be staged based on serum creatinine (Cr) levels. The stages are: Stage 1 (Risk): Increase in serum creatinine by ≥0.3 mg/dl or increase to 1.5-1.9 times baseline within 7 days. Stage 2 (Injury): Increase in serum creatinine to 2.0-2.9 times baseline. Stage 3 (Failure): Increase in serum creatinine to 3.0 times baseline, or increase in serum creatinine to ≥4.0 mg/dl, or initiation of renal replacement therapy, or decrease in estimated GFR to <35 ml/min/1.73 m2 in patients <18 years.

Question 27

What is Chronic Kidney Disease (CKD) and what are its causes?

Answer 27

Chronic Kidney Disease (CKD) is a condition in which the kidney's ability to filter waste from the bloodstream gradually diminishes over a period of years. This typically develops due to chronic illnesses such as diabetes and hypertension. Other causes include chronic glomerulonephritis, hereditary renal diseases, chronic tubulo-interstitial nephritis, congenital anomalies of the kidneys, chronic pyelonephritis, renal stone disease, obstructive uropathy, and chronic infections of kidneys (like Tuberculosis).

Question 28

How is the staging of Chronic Kidney Disease (CKD) done based on GFR?

Answer 28

The stages of CKD are defined based on Glomerular Filtration Rate (GFR) and are as follows: Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2) Stage 2: Mild decrease in GFR (60-89 mL/min/1.73 m2) Stage 3a: Moderate decrease in GFR (45-59 mL/min/1.73 m2) Stage 3b: Moderate decrease in GFR (30-44 mL/min/1.73 m2) Stage 4: Severe decrease in GFR (15-29 mL/min/1.73 m2) Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysiis)

Question 29

What is Renal Vascular Disease and what are its manifestations?

Answer 29

Renal Vascular Disease affects the blood flow to and from the kidneys, causing kidney damage, kidney failure, and high blood pressure. Its manifestations include: Renal artery stenosis (RAS): Narrowing of the renal artery which can cause kidney injury and high blood pressure. Renal artery thrombosis: Formation of a blood clot in the renal artery. Renal vein thrombosis: Formation of a clot in the renal vein. Renal artery aneurysm: Usually small and asymptomatic, often found during tests for other conditions. Atheroembolic renal disease: Emboli obstructing small renal arteries, common cause of kidney problems in older adults. Renin production: Decreased blood flow from renal vascular disease may cause excess renin production leading to raised blood pressure.

Question 30

What are the causes of Renal Vascular Diseases?

Answer 30

The main causes of Renal Vascular Diseases are: Atherosclerosis: hardening and narrowing of the arteries due to plaque buildup. Diabetes: long-term diabetes can cause damage to the blood vessels, including the renal arteries. Hypertension: high blood pressure can lead to damage of the blood vessels in the kidneys. Morbid obesity: being severely overweight can contribute to atherosclerosis and hypertension, leading to kidney damage. Infection: infections can lead to inflammation and damage to the renal arteries or veins. Inflammatory or other underlying disease: diseases such as lupus, vasculitis, or other conditions can cause inflammation and damage to the kidneys' blood vessels.

Question 31

What investigations are generally performed in Acute Kidney Injury (AKI)?

Answer 31

The common investigations performed in Acute Kidney Injury are: Haematological: Full blood count (FBC) Serological: Urea and Electrolytes (U&E), C-Reactive protein (CRP) Multiple Myeloma screen - blood and urine Blood and Urine cultures: to check for infection Urine Microscopy: to look for red and white blood cells, casts, and crystals Urine dipstick for presence of Haematuria (blood in urine), Proteinuria (protein in urine), and Leukocyturia (white blood cells in urine).

Question 32

What additional investigations might be needed in Acute Kidney Injury (AKI)?

Answer 32

The additional investigations in Acute Kidney Injury might include: Immunological tests: Such as Serum Anti Neutrophil Cytoplasmic Antibody (ANCA), Serum Anti Neutrophil Antibody (ANA), Serum dsDNA (double stranded DNA) to check for autoimmune conditions. Viral Serology: Tests for Hepatitis B/C, HIV may be done to check if these infections are the underlying cause of AKI. Radiological: Chest X-ray may be done to check for associated conditions. Ultrasound scan Kidney Ureter Bladder (KUB), CT KUB may be done to assess the anatomy of the urinary system and look for obstructions. Renal Biopsy: This might be done for intrinsic renal diseases to assess the exact cause of AKI.

Question 33

How are the results of investigations interpreted in Acute Kidney Injury (AKI)?

Answer 33

The interpretation of investigations in Acute Kidney Injury includes: Blood tests: Elevated urea and creatinine levels indicate AKI. The serum potassium level can also be elevated. Arterial Blood gas: Metabolic acidosis may be observed, characterized by decreased pH and bicarbonate levels. Full blood count: Low hemoglobin concentration indicates anaemia, often seen with haemorrhage. Raised white blood cells are typically seen with infections. Positive blood cultures indicate a bacteraemia (presence of bacteria in the blood). C-reactive protein: This can be raised in infection or inflammation.

Question 34

What can be identified from urine microscopy in AKI and what do these findings indicate?

Answer 34

The following findings can be identified from urine microscopy in AKI: Hyaline casts: These may be found in pre-renal insult and in cast nephropathy in multiple myeloma. Epithelial cell casts: These are indicative of Acute Tubular Necrosis (ATN). Red blood cell (RBC) casts: These are associated with glomerular diseases. White blood cell (WBC) casts: These are indicative of tubulointerstitial disease or pyelonephritis.

Question 35

How is renal artery stenosis visualized in imaging?

Answer 35

Renal artery stenosis can be visualized in imaging such as Magnetic Resonance Imaging (MRI). Normal renal arteries will show clear, unobstructed passages on a Renal Magnetic Resonance Angiogram (MRA). In contrast, atherosclerosis with renal artery stenosis (RAS) will display a narrowing or blockage in the renal arteries on Renal MRA.

Question 36

What are the steps in the management of Acute Kidney Injury (AKI)?

Answer 36

The management of AKI includes the following steps: Ensure appropriate volume status and haemodynamic parameters. Monitor serum creatinine and urine output. Avoid hypoglycaemia. Discontinue all nephrotoxic drugs. Consider alternatives to radiocontrast procedures. Perform non-invasive and invasive diagnostic workups as needed. Check for changes in drug dosages. Consider admission to the Intensive Care Unit. Consider Renal replacement therapy.

Question 37

What are the treatment options for pre-renal Acute Kidney Injury (AKI)?

Answer 37

The treatment options for pre-renal AKI include: Maintaining appropriate fluid balance. Maintaining sufficient blood pressure (with a target Mean Arterial Pressure (MAP) > 80 mmHg). Administering antibiotics for sepsis. Renal replacement therapy (RRT), which includes dialysis or haemofiltration. Indications for RRT include fluid overload, hyperkalaemia, metabolic acidosis, and uraemia.