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1. Internal Medicine I > 8. Tubulointerstitial and cystic kidney diseases > Flashcards

8. Tubulointerstitial and cystic kidney diseases Flashcards

1
Q

What are the causes of acute tubular necrosis?

A
  • Prolonged ischemia,
  • nephrotoxins,
  • sepsis,
  • radio-contrast material,
  • drugs such as aminoglycosides, vancomycin, mTOR-inhibitors, amphotericin B
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2
Q

What is the site of injury in acute tubular necrosis (ATN)?

A

The site of injury is the proximal tubule and medullary TAL.

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3
Q

What are the causes of acute tubular necrosis?

A

Hemodynamic factors, endothelial injury, tubular epithelial injury, and inflammatory factors.

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4
Q

What is the differential diagnosis for acute tubular necrosis?

A
  • High urine Na (> 40-50 mmol/L)
  • Low urine osm (<350 mOsm/L)
  • BUN / creat 10:1
  • High FeNa (fraction excretion of Na)
  • Granular, muddy brown casts
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5
Q

What are the prevention and treatment options for acute tubular necrosis?

A
  • Avoid prolonged ischemia/nephrotoxic agents,
  • monitor volume status,
  • diuretics in case of volume overload,
  • renal replacement therapy if needed.
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6
Q

Prognosis of ATN?

A

Spontaneous recovery in 1-3 weeks (can use dialysis in the meantime)

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7
Q

Pathomechanism of radiocontrast induced nepthropathy?

A

prolonged vasoconstriction -> medullary hypoxia -> tubular epithelial cell toxicity

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8
Q

Clinical picture of radiocontrast induced nephropathy?

A

Non-oliguric ATN, 2-3 days after contrast administration

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9
Q

What is the recommended prevention for radiocontrast-induced nephropathy?

A
  • Cautious if GFR < 30 mL/min
  • adequate hydration and loop diuretics
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10
Q

What is the pathomechanism of aminoglycoside-type nephrotoxin-induced ATN?

A

The drug accumulates in proximal tubular cell lysosomes, interferes with cellular energetics, and induces oxidative stress.

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11
Q

What is the clinical picture of aminoglycoside-type nephrotoxin-induced ATN?

A

Non-oliguric ATN.

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12
Q

What is the pathomechanism of ethylene glycol-type nephrotoxin induced ATN?

A

Ethylene glycol is metabolized to toxic products. This leads to tubular precipitation and obstruction.

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13
Q

What is the clinical picture of nephrotoxin-induced ATN caused by ethylene glycol?

A

ATN with severe anion gap metabolic acidosis and calcium oxalate crystals in urine.

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14
Q

What is the recommended management for ethylene glycol-induced ATN?

A

Intravenous ethanol or alcohol dehydrogenase inhibitor

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15
Q

What is the clinical picture of heme pigment nephropathy?

A

Oliguric ATN with elevated plasma CK and LDH.

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16
Q

What are the risk factors for heme pigment nephropathy?

A
  • Rhabdomyolysis (muscle trauma, seizures, statin use, McArdle disease),
  • massive hemolysis.
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17
Q

What is the management of heme pigment nephropathy?

A
  • Correct metabolic abnormalities (hyperkalemia, hyperuricemia),
  • maintain fluid balance,
  • initiate renal replacement therapy if needed.
18
Q

What is the etiology of acute tubulo-interstitial nephritis?

A
  • Drugs (>75%),
  • infection-related (5-10%).
  • ATIN associated with systemic diseases
19
Q

What is the clinical picture of ATIN?

A
  • Oliguria
  • Leukocyturia / eosinophiluria
  • Hematuria
  • Joint and lumbar pain
  • Weakness
  • Weight loss
20
Q

What are the clinical triad of acute tubulo-interstitial nephritis?

A

fever ± eosinophilia ± skin rash

21
Q

How is the diagnosis of acute tubulo-interstitial nephritis made?

A
  • clinical picture,
  • renal biopsy
22
Q

What is the treatment for ATIN?

A
  • Discontinuation of the drug (in case of immune checkpoint inhibitors, temporary drug withdrawal)
  • Treat infection if infection related
  • Corticosteroids if immune or idiopathic
23
Q

What is the most common renal injury in multiple myeloma?

A

Myeloma cast nephropathy

24
Q

What is the clinical picture of myeloma cast nephropathy?

A
  • Acute kidney injury,
  • mild proteinuria (<2-3 g/day),
  • monoclonal light chains in urine (NOT DETECTED BY DIPSTICK),
  • hypercalcemia,
  • anemia.
25
Q

What is the treatment for myeloma cast nephropathy?

A
  • Hydration
  • treatment of hypercalcemia,
  • urine alkalization (pH >7),
  • avoidance of NSAIDs, furosemide,
  • plasma exchange/hemodialysis
26
Q

What are the clinical features of chronic interstitial nephritis and isolated tubulopathies?

A
  • Mild symptoms and signs, slowly progressing renal failure with insidious onset,
  • renal anemia at relatively early stage,
  • hypertension.
27
Q

What is Fanconi syndrome?

A

Fanconi syndrome is a rare disorder characterized by proximal tubular dysfunction.

28
Q

What are the types Fanconi syndrome?

A
  • Acquired Fanconi syndrome
  • Hereditary (storage diseases)
  • idiopathic
29
Q

What is the treatment for Fanconi syndrome?

A
  • bicarbonate
  • phosphate
  • potassium
  • vitamin D3 supplementation.
30
Q

What are the signs and symptoms of proximal tubular dysfunction?

A

Tiredness, muscle weakness, bone pain, and in hereditary forms, excessive thirst, polydipsia, and polyuria.

31
Q

What is Type 2 renal tubular acidosis (RTA)?

A

Decreased HCO3-reabsorption in the proximal tubules, leading to ion disturbances such as hypokalaemia + hyperchloraemia + acidosis and normal anion gap (12 ±4mmol/ L).

32
Q

What is the therapy for Type 2 renal tubular acidosis (RTA)?

A
  • bicarbonate supplementation
  • thiazide diuretics to decrease bicarbonate loss,
  • K-supplementation / K-sparing diuretics.
33
Q

What are the signs and symptoms of hypokalaemic nephropathy?

A
  • Polyuria / polydipsia
  • Decreased renal concentrating capacity
  • Hypochloremia
  • Metabolic alkalosis.
34
Q

What is the therapy and prognosis for hypokalaemic nephropathy?

A

It is reversible with potassium replacement.

35
Q

When should rare diseases affecting the loop of Henle / distal tubules be considered?

A

In young patients with tiredness, muscle cramps, polydipsia, excessive thirst

36
Q

What is the laboratory finding in rare diseases affecting the loop of Henle / distal tubules?

A

Hypokalaemia, hypochloraemia, metabolic alkalosis.

37
Q

What are some inherited hypokalemic salt-losing tubulopathies?

A
  • Bartter syndrome
  • Gitelman syndrome
38
Q

What are some cystic kidney diseases?

A
  • Polycystic kidney disease
  • Simple / complex renal cysts
  • Medullary sponge kidney
39
Q

What are the consequences of ADPKD?

A
  • Cysts can develop along the entire length of the nephron, leading to renal failure.
  • Additionally, multiple liver, pancreatic, and ovarian cysts can occur, and there is a risk of subarachnoid hemorrhage due to intracerebral aneurysms.
40
Q

What is the clinical presentation of ADPKD?

A
  • ADPKD can be asymptomatic or have few symptoms for a long time.
  • It can cause loin pain, macroscopic hematuria, hypertension, kidney stones, frequent UTIs, polyuria, and polydipsia.
41
Q

What is the treatment for ADPKD?

A
  • increased fluid intake (>3 L/day),
  • optimal blood pressure control (ACEI/ARB),
  • V2R antagonists in case of rapid progression.
42
Q

What are Bosniak categories for complex renal cysts?

A

Bosniak categories are used to classify complex renal cysts on CT scans

1. Internal Medicine I (20 decks)

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