Renal Flashcards

1
Q

How does the fractional excretion of sodium (FeNa) aid in differentiating pre-renal from intrinsic renal AKI?

A

FeNa greater than 1% suggests intrinsic renal injury, while FeNa less than 1% indicates pre-renal etiology.

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2
Q

What distinguishes pre-renal from intrinsic renal acute kidney injury (AKI) based on clinical features?

A

Pre-renal AKI presents with signs of volume depletion and decreased urine output, while intrinsic renal AKI manifests with features such as proteinuria and cellular casts.

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3
Q

What role does renal ultrasound play in the diagnostic workup of AKI, particularly in identifying post-renal causes?

A

Renal ultrasound helps identify features of obstruction such as hydronephrosis, hydroureter, and dilated renal pelvis, aiding in the diagnosis of post-renal AKI.

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4
Q

What are the key laboratory investigations in suspected rhabdomyolysis-induced AKI, and how is it managed?

A

Key investigations include serum creatine kinase (CK) levels and urine myoglobin. Management focuses on aggressive fluid resuscitation to prevent myoglobin-induced renal tubular obstruction and acute tubular necrosis (ATN) progression.

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5
Q

Describe evidence-based strategies for preventing contrast-induced nephropathy (CIN) in high-risk patients undergoing radiological procedures.

A

Preventive strategies include hydration with isotonic saline, minimizing contrast volume, and considering alternative imaging modalities in high-risk patients to mitigate renal vasoconstriction, tubular toxicity, and oxidative stress associated with CIN.

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6
Q

How does dehydration cause an AKI?

A

Dehydration decreases blood volume- decreased perfusion of the kidneys.

This reduces the delivery of oxygen and nutrients to the kidney tissues, impairing kidney function.

Dehydration triggers the RAAS. Activation of the RAAS leads to vasoconstriction of the renal arteries and increased reabsorption of sodium and water in the kidneys, further reducing kidney perfusion.

Concentrated urine with higher levels of solutes, such as urea and creatinine. The high concentration of solutes can damage the renal tubules and impair their function, leading to AKI.

Increased risk of intravascular volume depletion: Dehydration can lead to intravascular volume depletion, which increases the risk of prerenal AKI. Prerenal AKI occurs when there is inadequate blood flow to the kidneys, leading to reversible kidney dysfunction.

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7
Q

How do you make a diagnosis of chronic kidney disease?

A

A diagnosis of chronic kidney disease is made when eGFR is below 60 on two blood tests three months apart.

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8
Q

What bacterial infection is screened for before a renal transplant?

A

Tuberculosis

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9
Q

Why do you get cerebral oedema with dynamic disequilibrium syndrome?

A

During hemodialysis, lots of urea is removed from the blood. The urea in the brain doesn’t move out as quickly, so water rushes into the brain tissue due to the osmotic gradient difference

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10
Q

What does the presence of nitrites indicate?

A

Nitrites Formation: Certain bacteria can convert nitrates (normally present in urine) into nitrites.

This conversion is performed by the enzyme nitrate reductase.

Common Gram-Negative Bacteria:
Escherichia coli (E. coli): The most common cause of UTIs.
Klebsiella species
Proteus species
Implications of Positive Nitrites
Gram-Negative Bacteria: A positive nitrite test strongly suggests the presence of Gram-negative bacteria, as these are typically the bacteria that possess nitrate reductase.

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11
Q

Describe how Anti-diuretic hormone (ADH) regulates fluid balance

A
  • Osmoreceptors in the hypothalamus sense changes in blood osmolality
  • When there is an increased osmolarity, ADH is released
  • ADH binds to vasopressin receptors in the collecting duct and enhances the permeability, increases water reabsorption
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12
Q

What type of anaemia do you get with CKD?

A

Normocytic anaemia
Can have a normal MCV!!

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13
Q

What are the characteristics of acute interstitial nephritis?

A

Acute interstitial nephritis is an inflammatory reaction in the interstitium of the kidney, commonly following the administration of drugs such as non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs) or penicillin-based antibiotics (as is the case here).

Characteristic investigation results include white cells in the urine and white cell casts detectable on urine microscopy. A definitive diagnosis is made with a renal biopsy, though often unnecessary, as the condition reverses when the offending agent is stopped.

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14
Q

With IgA nephropathy, why is frank hematuria associated with a good prognosis?

A

In IgA nephropathy, frank haematuria (visible blood in urine) is often associated with a good prognosis because it usually indicates a more acute, self-limiting flare rather than chronic, progressive kidney damage.

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15
Q

What is McArdle’s disease?

A

McArdle’s disease, also known as glycogen storage disease type V, is a genetic metabolic myopathy. Symptoms include muscle pain, cramps, fatigue and poor exercise tolerance. Exercise may provoke myoglobinuria, which may look like cola-coloured urine.

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16
Q

What is peripheral anasarca?

A

Peripheral anasarca refers to severe, generalized swelling (edema) that occurs in the subcutaneous tissues throughout the body, often most pronounced in the lower limbs. It is typically a result of fluid accumulation due to underlying conditions that affect fluid balance.

17
Q

Simply, what is the difference between type 1, 2 and 4 renal tubular acidosis?

A

Type 1: Problems getting rid of acid in the distal tubule.
Type 2: Problems reabsorbing bicarbonate in the proximal tubule.
Type 4: Issues with potassium and acid regulation due to aldosterone problems.

18
Q

What is the most likely composition of a staghorn calculus?

A

Magnesium ammonium phosphate (struvite)
Struvite is a substance which grows very quickly explaining why staghorn calculi are so large

19
Q

What type of shock would result in AKI from sepsis?

A

Distributive shock
Sepsis causes release of cytokines and a massive inflammatory response. This results in vasodilation and increased capillary permeability (distributive shock).

20
Q

What does goodpasture’s syndrome present as?

A

Haemoptysis and haematuria. It is also known as anti-glomerular basement membrane disease. It occurs when anti-glomerular basement membrane antibodies attack type IV collagen in the kidneys and lungs. In addition, a unique risk factor for this patient is his occupation. Exposure to solvents is a risk factor for Goodpasture syndrome, so people who have worked in dry cleaners or laboratories are at higher risk.

21
Q

What are side effects of Ciclosporin?

A

Gingival hypertrophy
Hypertrichosis
Nephrotoxicity

22
Q

How does a uremic tinge present on the skin?

A

The classic “uraemic tinge” gives the patient’s skin a brown-grey colour

23
Q

How would urogenital TB present?

A

This is most likely given her sterile pyuria and history of fever, night sweats and weight loss, which is typical of TB. Urine samples should be sent for acid-fast staining and PCR. A Mantoux test, interferon-gamma release assay and radiographic imaging should also be undertaken to check for other manifestations of TB

24
Q

What does pH and potassium have to be to referred onto dialysis?

A

<7.2
>7mmol/L

25
Q

What finding with a kidney stone would warrant immediate urology referral?

A

In this relatively young patient a creatinine of 200 μmol/L is concerning for an AKI, especially if accompanied by a reduction in eGFR. AKI suggests back-pressure which may need surgical intervention and should be discussed with the urology team.