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Year 3 > Acute Kindey Injury > Flashcards

Acute Kindey Injury Flashcards

1
Q

Which nephrotoxic drugs cause vasoconstriction of the afferent arteriole?

A

NSAIDs inhibit the action of prostaglandin for vasodilation of afferent arteriole

Tacrolimus, a calcineurine inhibitor used in cancer treatment to act as an immunosuppressant.

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2
Q

Which nephrotoxic drugs cause vasodilation of the Efferent arteriole?

A

ACE inhibitors and ARBs which inhibit angiotensin II, resulting in vasodilation of efferent arteriole and vasoconstriction of afferent arteriole. ACE inhibitors reduce GFR and reduce the release of hyperkalemia, reducing loss of K+ out of the bloodstream and in the urine.

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3
Q

Which nephrotoxic drugs cause acute tubular necrosis, an intrarenal AKI?

A

-> Aminogloycosides such as gentamycin which inhibit protein synthesis of 30s ribosomes of bacteria. It damages tubular cells of kidney directly for intrarenal AKI and has ototoxicity for hearing damage. Aminoglycosides accumulate in the tubules.
-> Vancomycin inhibits bacterial wall cell synthesis of gram positive bacteria.
-> Aciclovir is an anti-viral drug which inhibits the viral DNA polymerase for replication. It accumulates in renal damage
-> Contrast dyes
->Statins act to inhibit the synthesis of cholesterol but this may increase the risk of rhabdomyolysis which results in acute tubular necrosis within intrarenal AKI.
-> Amphotecirin B, an anti-fungal medication which binds to sterols in the cell membrane of fungi to cause leaking.

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4
Q

Which Analgesics are Nephrotoxic?

A

NSAIDS and COX inhibitors
Opioid analgesics
Gabapentin, anticonvulsant which inhibits the release of of excitatory neurotransmitters. It causes rhabdomyolysis and is excreted solely by the kidneys.

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5
Q

What is the effect of lithium on the kidneys?

A

Lithium is used in mania however should be avoided completely in impaired kidney function because it accumulates in the principal cells of the collecting duct to block the action of anti-durietic hormone, leading to polyuria and Nephrotoxic diabetes insipidus.

Lithium can induce hyperparathyroidism and result in osteolysis and hypercalcaemia.

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6
Q

Which cardiovascular drugs cause kidney damage?

A

Anti-hypertensives can cause renal hypoperfusion and lead to pre-renal AKI.

Digoxin inhibits the Na+/k+ ATPase exchanger that cause accumulation of K, therefore during kidney injury, digoxin will worsen hyperkalemia

Statins act to inhibit the synthesis of cholesterol but this may increase the risk of rhabdomyolysis which results in acute tubular necrosis within intrarenal AKI.

Phenytoin is a sodium channel blocker which may lead to acute interstitial nephritis in cardiovascular disease

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7
Q

What is renal clearance?

A

Renal clearance is the volume of plasma completely cleared of a drug per unit of time. This is calculated via Urinary excretion x volume/plasma volume

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8
Q

What is used to estimate GFR?

A

Extraction ratio of serum creatinine in the kidneys is used to estimate the GFR, as well as age and sex. This is based on the patient’s actual concentration of creatinine in urine divided by expected plasma concentration of creatinine for their age and sex However, since some creatinine is secreted, it is a slight overestimation.

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9
Q

What is the gold standard for renal function?

A

Inulin.

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10
Q

What is filtration?

A

Filtration in the kidney is the movement of unbound substances from the efferent arteriole to the glomerulus. This is dependent on kidney GFR function and conc of drug bound to albumin

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11
Q

What is secretion?

A

Secretion is the movement of substances from the Peritubular capillaries to the kidney tubules. For polar drugs, these require energy transporters.

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12
Q

What is reabsorption?

A

Reabsorption in the kidney is the movement of substances from the kidney tubules in the DCT back to bloodstream, typically the Peritubular capillaries, a branch of the efferent arterioles.

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13
Q

What are the complications with renal failure?

A

Reduced synthesis of substances like enzymes for Vitamin D synthesis, leading to hypocalcaemia and secondary hyperparathyroidism.

Hyperkalemia and hyponatremia

Insulin is partially metabolised in the kidneys so reduction in kidney function causes a rise in insulin which reduces insulin requirement dosages in diabetics.

Anaemia

Less drug excretion = higher serum drug concentration so greater risk of side effects

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14
Q

What is an indicator of acute kidney injury?

A

Increase in creatinine of 0.3 mm/dl in 48 hours OR Increase from 1.5x from the baseline indicates acute kidney injury.
A fall in urine output to less than 0.5kg/hr for more than 6 hours.

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15
Q

What does a higher ratio of urea than creatinine indicate?

A

Pre-renal AKI

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16
Q

What does a higher ratio of creatinine than urea?

A

Intrarenal AKI or a late post-renal AKI.

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17
Q

What is an indicator for pre-renal AKI?

A

High urine osmolality
AND
Low urine Na+/ Fractional excretion of Na+ less than 1%
AND
Higher ratio of urea than creatinine.

-> indicates preserved tubular cell function for water reabasorption or decrease in circulating volume and may be a pre-renal AKI or early stage post-renal AKI.

Pre-renal causes of AKI are related to low blood flow due to cardiac failure, hypovolemia or scarring of the kidney

Reduced blood flow reduces filtration of urea and creatinine into the glomeruli. Since the tubular cells are still functional, creatinine can still be excreted however urea continues to be reabsorbed which causes a drastic increase in urea. Urea reabsorption drives the reabsorption of sodium and water into the blood and triggers the RAAS system. Aldosterone will drive Na+ and ADH will drive water reabsorption. Urine will be concentrated but have a low fractional extraction ratio of sodium.

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18
Q

What is an indicator for intrarenal AKI?

A

Low urine osmolality
AND
High urine Na+/fractional excretion of Na/+ greater than 1%
AND
Higher ratio of creatinine than urea

Indicates damaged tubular cell function for water/Na+ reabsorption in intrarenal AKI.

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19
Q

Which electrolytes are affected in AKI?

A

Hyperkalemia, hyperphosphataemia and hypermagnesaemia because they are primarily excreted in the kidneys
Metabolic acidosis due to inability to excrete H+
Hypocalcaemia
Hyponatremia and dehydration due to loss of Na+ and water in urine

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20
Q

What does eosinophiluria indicate?

A

Presence of eosinophils in urine indicates acute interstitial disease, an intrarenal AKI.

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21
Q

What do muddy brown casts indicate?

A

Acute tubular necrosis.

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22
Q

How is urea formed?

A

Urea is formed in the liver from ammonia and removed in the body at the PCT during exchange, with the rest excreted in the urine

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23
Q

How is creatinine formed?

A

Creatine is formed from the metabolism of creatinine phosphate in skeletal muscle to be partially re absorbed in the PCT and the rest excreted in the DCT

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24
Q

What are the causes of pre-renal AKI?

A

Hypovolemia, due to:
->Congestive heart failure
->Liver failure which reduces albumin production that causes a loss of negative colloid osmotic pressure and re absorption of fluid
->Acute pancreatitis due to inflammatory cytokines release causing vasodilation
-> Shock due to production of inflammatory cytokines which cause blood vessels to become leaky
->Blockage of the renal artery from an embolus due to atrial fibrillation, stenosis of the vessel or diabetes
->Hepatorenal syndrome where liver failure causes portal hypertension and diverts blood away from non vital organs like the kidney
-> Worsened by anti-hypertensives and ACE inhibitors.

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25
Q

What is the pathophysiology of pre-renal AKI?

A

An indicator of pre-renal AKI is an increase in the urea:creatinine ratio, renal hypoperfusion, absence of casts and return to normal within 48 hours of correction of hypoperfusion.

This is because reduced blood flow reduces filtration of urea and creatinine into the glomeruli. Since the tubular cells are still functional, creatinine can still be excreted however urea continues to be reabsorbed which causes a drastic increase in urea. Urea reabsorption drives the reabsorption of sodium and water into the blood and triggers the RAAS system. Aldosterone will drive Na+ and ADH will drive water reabsorption. Urine will be concentration but have a low fractional extraction ratio of sodium.

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26
Q

What are the causes of intrarenal AKI?

A

Glomerulonephritis

Acute interstitial nephritis

Acute tubular necrosis

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27
Q

What is glomerulonephritis?

A

Inflammation of the glomeruli and the vessels of the kidney, which includes conditions like Nephrotic syndrome which has a range of causes and includes minimal change disease, focal segmental glomerulosclerosis and other conditions which results in proteinuria, oedema, hypoalbuminaemia (increased risk of bleeding) and hyperlipidaemia.

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28
Q

What is acute interstitial nephritis?

A

Inflammation of the renal interstitium surrounding the tubules due to:
Infection
drugs like NSAIDs, PPIs, rifampicin, loop diuretics
Multiple myeloma, where tumours of plasma B cells block the tubules due to amyloidosis deposits Sarcoidosis can also cause interstitial nephritis due to granuloma formation in kidney interstitum

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29
Q

What is the cause of acute tubular necrosis?

A

Use of nephrotoxic substances like iodine contrast agents, infection or ischaemia from pre-renal AKI
Haemolysis can cause haemoglobin to precipitate in the kidney tubules, creating tubular casts and causing obstruction, reducing oxygen and perfusion.
Rhadomyolysis where myoglobin interacts with Tamms-Horsfall protein and cause tubular casts to form in acidic urine, leading to tubular obstruction, reducing oxygen and perfusion.

30
Q

What is the pathophysiology of intrarenal AKI?

A

Damage to the tubular cells and necrosis which causes sloughing of the tubular cells to form casts in the tubules which increases intra-pressure. This disrupts the pressure gradient in the tubules for filtration at the glomeruli that lowers GFR and prevents tubule function for excretion of creatinine and urea reabasorption. This causes the BUN: creatinine ratio to increase. There is a lower GFR however activation of RAAS system does not prevent the loss of Na+ and water due to inability for tubular cells to function for reabsorption so sodium and water and urea are lost in urine and there is a low osmolality. Fractional excretion of Na+ is high.

31
Q

What is the cause of post-renal AKI?

A

Bladder obstruction such as BPH and kidney stones

Prostate cancer

32
Q

What is the pathophysiology of post renal AKI?

A

In the early stages of post-renal AKI, obstruction to kidneys results in back pressure which prevents filtration in the glomerulus. Preserved function of kidney tubular cells allows creatinine excretion and Na+ and water reabsorption to the bloodstream. The indicators are a high urea and BUN:creatinine ratio, high urine osmolality and low fractional excretion of Na+, similar to pre-renal AKI.
In the late stages of post-renal. AKI, high presssure in kidneys causes damage to tubular cells and also reduces glomeruli filtration. Low GFR and less excretion of creatinine and reabsorption of urea will mean less reabsorption of sodium.Increase in blood creatinine causing increase in BUN:creatinine ratio and Higher urea, water and fractional excretion of sodium in urine.
Reduced urine osmolality.

33
Q

What is the management of AKI?

A

Cessation of Nephrotoxic medication.
Monitoring fluid levels and treating with bolus dose if hypovolemic
-> indicated by decreased BP, urine output, loss of raised JVP, prolonged capillary refill time
Patient showing signs of Hypervolemia with crackling on auscultation, increase in BP and JVP, peripheral oedema and gallop heart rate with 3 clear heart sounds due to rapid ventricular filling.
-> Managed with diuretics, oxygen supplementation to address pulmonary oedema, fluid restriction and monitoring fluid levels and creatinine levels
Referral for renal replacement therapy if kidney function has deteriorated.

34
Q

How should hyperkalemia be managed?

A

Hyperkalemia above 6.5 Mmol and hyperphosphataemia should be managed with calcium gluconate on IV which stabilises cardiac cell membranes

35
Q

What are the signs of hyperkalemia on ECG?

A

Broadening of QRS complex, increased PR interval, small or absent P waves and asystole and tall tented t waves

36
Q

What are the major complications of AKI?

A

-> Azotema is the build up of nitrogenous compounds in the blood like creatinine, ammonia and urea. Uraemia is a complication of azotemia.
Infection and sepsis due to the role of the kidneys in immune homeostasis
* Anaemia
* Oedema
* pericardial effusion due to accumulation of toxic metabolites from lowered GFR

37
Q

What are the symptoms of uraemia?

A

-> Platelet dysfunction
* Grand mal Seizures due to encephalopathy
* Asterexis where flapping of the hands when hyperextended
* Pericarditis that may lead to pleural effusion
* Metabolic acidosis due to inability of kidneys to excrete H+
* Hyperkalemia due to inability of kidneys to excrete Na+

38
Q

What is the normal range for urea to creatinine?

A

A normal range for BUN: creatinine is from 12:1 to 20:1.

->Urea and creatinine are filtered in the glomerulus. Urea will be reabsorbed in the PCT to cause a rise in urea but creatinine levels in the blood will decrease further because creatinine will be excreted from the blood to the kidney tubules.
Therefore, urea/BUN should be greater than creatinine because urea is reabsorbed.

39
Q

What is the BUN?

A

Blood urea nitrogen test (BUN) is the level of nitrogen in the blood, where normal range is between 7-20 mg . Greater levels may indicate dehydration, liver or kdiney disease

40
Q

What is the normal serum creatinine level?

A

Serum creatinine test for creatinine levels in the blood; higher levels indicate dehydration, kidney disease or urinary tract obstruction.
-> Men range is 0.7-1.3
-> Women range is 0.6-1.1

Creatinine is freely filtered in the glomerulus and reduce

41
Q

What does urine cast indicate?

A

The type of urine casts indicates the region and cause of kidney damage.

42
Q

What does hyaline cast indicate?

A

Hyaline casts are clear clumps of proteins which can occur when standing for long periods, exercising or stress. Abnormal amounts indicates proteinuria due to CKD.

43
Q

What does fatty cast indicate?

A

Fatty casts indicate nephrotic syndrome.

44
Q

What do epithelial cast indicate?

A

Epithelial casts indicate renal tubular disease, glomerulonephritis and heavy metal poisoning or eclampsia

45
Q

What do RBC casts indicate?

A

RBC casts indicate nephritic syndrome/glomerulonephritis, renal tumour or acute tubular necrosis.

46
Q

What is a normal protein and creatinine ratio?

A

Normal protein/creatinine ratio is less than 0.15 because protein should not be in urine.

47
Q

What is the cause of proteinuria?

A

Protein in the urine rises during excercise due to increase in catecholeamines which increase the concentration of the glomerular capillary membrane.

Proteinuria can occur in situational circumstances like standing for long periods, excessive, stress or cold baths or a protein rich diet.

Persistent proteinuria indicates renal disease
-> Microalbumin that is high means it is a glomerular disease.
-> B2 globulin protein that is high means it is a tubular disease

48
Q

What does early morning proteinuria indicate?

A

Proteinuria only early in the morning indicates orthostatic hypertension, with excessive neurohumoral activation while standing.

49
Q

When is renal ultrasound used?

A

Assess kidney size
Identify masses for lesions
Screen for hydronephrosis
Screening for autosomal dominant polycystic kidney disease
Used in renal Doppler ultrasound for blood flow and assessing for renal vein thrombosis

50
Q

When is renal CT scan used?

A

Investigation of renal haematuria
Detection of retroperitoneal fibrosis
Detection of renal infection, infarction and papillary necrosis
Detection of renal stones
Detection of renal vein thrombosis
Assess for adrenal causes of hypertension

51
Q

When is renal MRI used?

A

For patients unable to tolerate radiographic contrast agents because MRI uses gadolinium, an iodine free contrast agent
Detect renal vein thrombosis and stenosis and masses, superior to CT scans
Assess for phaemochromocytoma

52
Q

How is kidney disease generally investigated?

A

Clinical assessment for volume status through assessing skin turgour, JVP and echocardiogram and third heart sound on cardiovascular examinations
FBC for urea, electrolytes, serum creatinine, and blood urea nitrogen (BUN)
CRP
Blood cultures
CT and ultrasound for imaging of the kidneys and diagnostic biopsy
Urine dip test
Urine analysis

53
Q

How can tubular function be assessed?

A

Level of B2 microglobulin in urine.

54
Q

What are possible causes of haematuria?

A

Blood
Myoglobinuria
Porphyria
Drugs sch as rifampicin and phenazopyridine

55
Q

What are the causes of white urine?

A

Pyuria (pus present in the urine)
Crystals present in the urine

56
Q

What is urine specific gravity used as an indication for?

A

Concentration of solutes in the urine and can indicate the presence of radiocontrast agents, protein and glucose which have a lesser impact on urine osmolality.

57
Q

What does glucose in the urine indicate?

A

Diabetes mellitus
Type 2 Renal tubular acidosis
Canonical syndrome

58
Q

What is the urinary anion gap?

A

Used for a differential diagnosis of metabolic acidosis by estimating an increase or decrease in ammonium, based on the difference between cations like urinary sodium, potassium and anions like chloride, based on the equation:
(UNa -Uk) - UCl

59
Q

What is normal anion gap?

A

4-12 mmol/L

60
Q

What does a negative anion gap indicate?

A

Acidosis with High urinary excretion of chloride due to:
Low levels of albumin
Renal tubular acidosis due to an inability to excrete ammonium
Extrarenal loss of bicarbonate in pancreatic damage or diarrhoea

61
Q

What happens during metabolic acidosis?

A

Reduction in bicarbonate which stimulates an increase in chloride and anions to compensate

62
Q

What is the cause of an increased anion gap?

A

Rise in cations like Na+ and K+ due to reduced tubular function to excrete acids due to:
Diabetic ketoacidosis
Lactic acidosis
Kidney failure
Salicylate poisoning with aspirin, where there is an initial phase of respiratory alkalosis which is compensated by alkuluria that leads to potassium loss and increase in aciduria.

63
Q

How to distinguish between tubular and glomerular disease?

A

B2 microglobulin

64
Q

What does high B2 microglobulin in the urine indicate?

A

Tubular disease

65
Q

What does high B2 microglobulin in the blood indicate?

A

Glomerular disease.

66
Q

What determines the volume of the ECF?

A

Sodium ions, which constitute 90% of the ECF space

67
Q

What is the cause of hypochloremic metabolic acidosis?

A

Gastrointestinal loss from diarrhoea
Renal loss of bicarbonate with type. 2 renal tubular acidosis
Use of carbonic anhydrase inhibitors
Hypoaldosteronism
Potassium sparing diuretics

68
Q

What are the causes of lactic acidosis?

A

Shock
Mesenteric ischaemia
Hypoxia
Excessive energy expenditure with seizures, hyperthermia and extreme exertion
Malignancy, diabetic ketoacidosis and malignancy
Impaired lactate clearance with liver failure

69
Q

Which chemotherapeutic agent typically causes necrosis of renal tubular epithelial cells?

A

Cisplatin

70
Q

What are the causes of ketoacidosis

A

Type 1 diabetes
Starvation
Excessive alcohol intake in malnourished individual

Year 3 (33 decks)

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