Renal Disorders Flashcards

(52 cards)

1
Q

What are intrinsic renal processes causing AKI that are ischemic in origin?

A
  • GN
  • Renovascular Disease
  • Rhabdomyolysis
  • Hepatorenal syndrome
  • CIN

These processes are associated with reduced renal blood flow (RBF) and may have low urinary sodium concentration and fractional excretion of sodium (FE Na) < 1%.

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2
Q

What is a lacunar stroke?

A

Ischemic stroke involving small arteries penetrating deep brain structures

This type of stroke can lead to significant neurological deficits.

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3
Q

What elements of urine analysis (UA) are consistent with diabetic nephropathy (DN)?

A
  • Proteinuria
  • Lack of active sediment (cellular elements)

Active sediment may include red blood cells or casts, which are less common in DN.

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4
Q

What percentage of diabetic nephropathy cases show hematuria?

A

30%

RBC casts are seen in about 10% of cases.

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5
Q

What is the leading cause of end-stage renal disease (ESRD) in the U.S.?

A

Diabetic nephropathy (DN) – ‘nephrosclerosis’

25% of renal transplants in the U.S. are performed due to DN.

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6
Q

Which parts of the nephron are primarily affected in diabetic nephropathy?

A
  • Glomerulus
  • Tubular Interstitium

Changes include interstitial fibrosis and thickening of the tubular basement membrane.

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7
Q

What is the function of the glomerulus?

A

To filter plasma

This is a critical function in the renal system, essential for waste removal.

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8
Q

What are the three parts of the glomerulus that make up the filtration barrier?

A
  • Fenestrated glomerular capillary endothelium
  • Basement membrane
  • Foot processes of the visceral epithelium (podocytes)

These components work together to allow selective filtration.

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9
Q

What is the effect of glycation of the efferent arteriole basement membrane in diabetic nephropathy?

A

It leads to efferent arteriole hyaline arteriosclerosis and increased GFR due to reactive afferent arteriole vasodilation

This is associated with stage 1 ‘Hyperfiltration’ in DN.

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10
Q

What is the mesangium?

A

Space outside the capillary lumen contiguous with the smooth muscles of the arterioles

It consists of cells and acellular matrix.

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11
Q

What are the clinical characteristics of diabetic nephropathy (DN) in terms of urine analysis?

A
  • Glycosuria
  • Proteinuria
  • Early: microalbuminuria (30-300 mg/day)
  • Later: macroalbuminuria (> 300 mg/day)

The amount of proteinuria correlates with the incidence of ischemic heart disease (IHD) and stroke.

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12
Q

What is the biphasic change in GFR observed in diabetic nephropathy?

A

Initially increased GFR (stage 1), then decreased GFR (stages 3 + 4)

This reflects the progression of kidney damage over time.

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13
Q

What treatments are pillars of management for diabetic nephropathy?

A
  • Tight BP control
  • Tight glycemic control (A1c < 7.0%)
  • Treatment of dyslipidemia
  • Treatment with an ACE inhibitor or ARB

These treatments aim to slow the progression of nephropathy.

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14
Q

What do ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) do in diabetic nephropathy?

A

They slow the progression of DN and proteinuria

They are effective in both type 1 and type 2 diabetes patients.

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15
Q

What is the role of SGLT-2 inhibitors in diabetic nephropathy?

A

They decrease the incidence of major adverse cardiac events (MACE) in patients with type 2 DM and ischemic heart disease (IHD)

Examples include empagliflozin, canagliflozin, and dapagliflozin.

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16
Q

What is acute interstitial nephritis (AIN)?

A

AKI characterized by interstitial inflammation and edema that spares the glomeruli

AIN accounts for 5-15% of all causes of AKI.

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17
Q

What is the differential diagnosis (DDx) for acute interstitial nephritis (AIN)?

A
  • Drugs (75%)
  • Infections (15%)
  • Idiopathic (5%)
  • Autoimmune Disorders
  • Systemic Disorders

Drug-induced AIN is the most common cause.

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18
Q

What is the usual time interval between drug exposure and presentation of acute interstitial nephritis?

A

Mean latent period is 10 days

This is shorter compared to NSAIDs, where the latent period can be months.

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19
Q

What is Tubulointerstitial Nephritis with Uveitis (TINU)?

A

AIN with uveitis

Uveitis is inflammation of the uvea, the pigmented layer below the sclera and cornea.

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20
Q

What is a potential renal complication associated with Hantavirus?

A

Granulomatous interstitial nephritis

Granulomatous interstitial nephritis is characterized by aggregates of macrophages and is often linked to chronic inflammatory processes.

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21
Q

What does AIN stand for?

A

Acute Interstitial Nephritis

22
Q

What is Tubulointerstitial Nephritis with Uveitis (TINU)?

A

AIN with uveitis

23
Q

What are the usual presenting complaints of AIN?

A
  • Malaise
  • Anorexia
  • Nausea/vomiting
  • Oliguria
  • Acute Kidney Injury (AKI)
24
Q

What laboratory findings are commonly seen in AIN?

A
  • Pyuria
  • Eosinophilia
  • Urine eosinophils
25
What is the gold standard for diagnosing AIN?
Renal biopsy
26
What is the critical step in the treatment of AIN?
Withdrawal of offending drug
27
What is the typical dosage and drug for AIN treatment?
1 mg/kg/day po for 2-3 weeks, followed by taper over 3-4 weeks
28
What treatment factors correlate with a good prognosis in AIN?
* Early withdrawal of offending agent * Early initiation of steroid
29
What finding on biopsy is considered a poor prognostic sign in AIN?
Fibrosis
30
What percentage of AIN patients may require renal replacement therapy (RRT)?
25-50%
31
What is the mean latency period between drug exposure and clinical AIN?
10 days
32
What are the major causes of AKI?
* Drugs (75%) * Infections (15%)
33
What is the prevalence of Renal Artery Stenosis (RAS) in patients with acute, severe, or refractory hypertension?
10-40%
34
What is the most common cause of RAS?
Atherosclerosis (90%)
35
What is the clinical characteristic of RAS?
* Refractory hypertension * Onset < age 30 or > age 60 * Unexplained hyperaldosteronism * Abdominal bruit * Deterioration of renal function after ACEI or ARB
36
What happens to GFR with ACE inhibitors or ARBs in the setting of RAS?
GFR decreases
37
What are the typical lab findings in RAS?
* Minimal-to-moderate proteinuria * No cellular elements
38
What imaging study is considered the gold standard for diagnosing RAS?
Conventional Angiography
39
What is the treatment for ischemic nephropathy?
* Reduce atherosclerosis risk factors * Medical management of hypertension * Revascularization if worsening condition
40
What are the common causes of Renal Vein Thrombosis (RVT)?
* Nephrotic syndrome * Abnormalities in coagulation * Renal cell carcinoma -invasion of renal vein * Retroperitoneal disease -compression of renal vein
41
What is the typical presentation of a patient with RVT?
* Acute nausea/vomiting * Flank pain * Hematuria * AKI
42
What is the initial treatment for RVT?
UFH or LMWH followed by warfarin
43
What is the pathophysiologic problem associated with RV thrombosis?
Impaired renal venous drainage leading to AKI
44
What is the typical clinical manifestation of renal artery thromboembolic disease (RATE)?
* Flank pain * Fever * Nausea/vomiting * Anuria
45
What diagnostic study may demonstrate absence of flow in a RATE event?
Doppler ultrasound
46
What is the treatment for an atraumatic RATE event?
* UFH or LMWH followed by warfarin * Intra-arterial thrombolytic therapy
47
Which glomerular structures are abnormal in diabetic nephropathy?
Efferent Arterioles BM and podocytes Mesangium
48
Progression of HTN in DM 2
Precedes DN (not caused by it)
49
Is albumin detectable in the urine in diabetic nephropathy?
Not in the early stages (I, II)
50
Define renal interstitium
The interstitium is the connective tissue surrounding/between the tubules, containing the peritubular capillaries, extracellullar matrix and interstitial cells
51
Infections that can cause AIN
Direct: Leptospirosis CMV Candidiasis Reactive: Strep Diphtheria
52
What is RATE?
Renal Artery ThromboEmbolic occlusion Via thrombus/embolism/dissection