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BPT Written > Renal > Flashcards

Renal Flashcards

1
Q

Reoccurrence of renal disease following renal transplant

A

Fastest - FSGS

Won’t reoccur - Alport’s disease

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2
Q

Primary action of vasopressin?

A

Acts on renal collecting ducts via V2 receptors to increase water permeability (cAMP-dependent mechanism) which leads to decreased urine formation

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3
Q

Mechanisms regulating release of vasopressin

A

Hypovolemia decreases firing of arterial stretch receptors = increased ADH
Hypotension decreases arterial baroreceptor firing = enhanced sympathetic activity = increased AVP release
Hypothalamic osmoreceptors stimulate ADH release when osmolarity rises
Angiotensin II receptors in the hypothalamus - increased angiotensin II = ADH release

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4
Q

Features of Fanconi Syndrome

A 
Type 2 (proximal) renal tubular acidosis
Polyuria
Aminoaciduria 
Glycosuria
Phosphaturia
Osteomalacia
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5
Q

Nephrotic Syndrome

A 
= proteinuria, oedema, hypoalbuminemia
Minimal change 
Membranous GN
FSGS
Amyloidosis
Diabetic Nephropathy
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6
Q

Nephritic Syndrome

A

= haematuria, hypertension
IgA nephropathy
Rapidly progressive GN
Alport

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7
Q

Rapidly progressive GN

A

ANCA associated vasculitis (most common) - pauci immune, necrosis and eosinophils
Anti GBM disease - linear IgG on IF
SLE - mixed, complement and antibodies

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8
Q

ANCA associated vasculitis

A 
Granulomatosis with Polyangitis
- granulomatous
- cANCA - cytoplasms PR3 = worse prognosis
Microscopic Polyangitis
- no granulomas
- pANCA - perinuclear - MPO
Eosinophilic Granulomatosis with Polyangitis 
- asthma, eosinophilia, granulomas
- either PR3 or MPO
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9
Q

Alport’s Syndrome is due to a defect in

A

Type IV collagen

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10
Q

AL (primary) Amyloidosis

A

Most common form
L for immunoglobulin Light chain fragment
Due to myeloma, Waldenstrom’s, MGUS
Features: nephrotic syndrome, cardiac and neuro involvement, hepatosplenomegaly, macroglossia

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11
Q

AA (secondary) amyloid

A

A for precursor serum amyloid A protein, an acute phase reactant
Seen in chronic infection / inflammation
E.g. TB, RA, bronchiectasis, Crohn’s, ank spond, psoriatic arthritis
Features: renal involvement - often leads to ESRF

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12
Q

Beta-2 microglobulin amylodosis

A

Precursor protein is beta-2 microglobulin = major part of HLA complex
A/w patients on dialysis

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13
Q

Extra renal manifestations of ADPKD

A

Liver cysts
Berry aneurysms
Cardiovascular: mitral valve prolapse, mitral / tricuspid incompetence, aortic root dilatation, aortic dissection
Cysts in other organs: pancreas, spleen

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14
Q

Genetic mutations in ADPKD

A

Chromosome 16 (PKD 1) = non clonal expansion of tubular epithelial cell types; polycystin 1 (mechanosensor)

Chromosome 4 (PKD 2)
Polycystin 2 (calcium channel ion)
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15
Q

Tuberous sclerosis

A

Autosomal dominant
Mutations in TSC1 or TSC2 gene

Major criteria: facial angiofibromas, >3 hypomelanotic macules, kidney angiomyolipomas, retinal hamartomas
Minor criteria: nonrenal hamartomas, multiple kidney cysts, dental abnormalities

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16
Q

Main site of potassium reabsorption in the kidney?

A

Proximal convoluted tubule

17
Q

As GFR declines, urinary creatinine clearance overestimates GFR because Cr is

A

Secreted by the tubules

18
Q

Drugs that can be cleared by haemodialysis

A 
BLAST
Barbituate
Lithium 
Alcohol (methanol, ethylene glycol)
Salicylates 
Theophylline
19
Q

Main site of sodium reabsorption in the nephron?

A

Proximal convoluted tubule

20
Q

Site of action for frusemide?

A

Thick ascending loop of Henle

Blocks Na-Cl cotransporter (NKCC2)

21
Q

Site of action for thiazides / indapemide?

A

Distal convoluted tubule

22
Q

Site of action for Spironolactone?

A

Collecting duct

23
Q

Lithium absorption

A

Reabsorbed in the proximal tubule
Lithium absorption follows sodium uptake
Therefore increased risk of toxicity with diuretics and hypovolemia

24
Q

Order of events in the renin-angiotensin system?

A
  1. Kidneys sense low BP
  2. Release renin into the blood
  3. Renin causes production of Angiotensin I
  4. ACE converts angiotensin I to angiotensin II
  5. Angiotensin II stimulates the release of aldosterone, ADH and thirst
  6. Water follows sodium
  7. Blood volume goes up = BP goes up
25
Q

Which cell in the kidney makes erythropoietin?

A

Peritubular cell

26
Q

Urinary pattern of glomerular disease or vasculitis?

A

haematuria with red cell casts, dysmorphic red cells, heavy proteinuria or lipiduria

27
Q

Urinary pattern of acute tubular necrosis in renal failure?

A

Multiple granular and epithelial cell casts with free epithelial cells

28
Q

Secondary causes of membranous nephropathy

A 
SLE 
Drugs - NSAIDs, penicillamine, gold
Hepatitis B and C
Malignancy- solid organ Timor’s
HSCT 
Kidney transplant 
Syphilis
29
Q

Distal (Type 1) Renal Tubular Acidosis

A

Impaired secretion of hydrogen ions = urine pH >6.0, kidney potassium wasting, hypokalemia

Usually secondary to autoimmune disease (Sjogrens most common, SLE, RA)

30
Q

Proximal (type 2) Renal tubular acidosis

A

Caused by reduction in bicarbonate reabsorption in the proximal tubule
Causes urine pH<5.5
Causes Fanconi Syndrome

31
Q

Diagnosis of ADPKD

A

2 or more cysts in one kidney and at least one cyst in the contralateral kidney - young pt (by 30yo)
4 or more cysts in each kidney for patient more than 60yo

32
Q

Gitelman’s syndrome

A

Defect in distal tubule = thiazides

Normotensive, metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria

33
Q

Bartter’s Syndrome

A

Autosomal recessive
Severe hypokalemia due to defective chloride secretion at the NKCC2 cotransporter in the ascending loop of henle (frusemide)
Polyuria, polydipsia, hypokalemia, normotension, weakness

34
Q

Liddell Syndrome

A

Increased number Na channel in collecting duct which results in increased Na reabsorption and potassium excretion

35
Q

Fibromuscular dysplasia

A

Female
Age 15-40
Severe HTN with evidence of target organ damage
Mild hypokaklemic metabolic alkalosis and high renin suggest underlying renovascular hypertension
Abdominal bruit
Diagnosis: intracellular-arterial digital subtraction angiography - string of beads appearance

36
Q

Most common histology can feature in chronic allograft nephropathy?

A

Chronic interstitial nephritis

37
Q

Dent Disease

A

X-linked recessive disorder of the proximal tubules
Proteinuria, hypercalciuria, nephrocalcinosis, kidney stones, renal failure, Ricketts
Due to mutation in CLCN5 gene

38
Q

Familial renal glycosuria

A

Mutations in the SLC5A2 gene coding for SGLT2 in the proximal tubule
Urine glucose excretion but normal BSL

39
Q

Actions of Atrial Natriuretic Peptide (ANP)

A

Causes marked natriuresis
Lowers BP
Inhibits secretion of renin and vasopressin
Decreases responsiveness of the kidney to stimuli that would normally increase aldosterone secretion
Increased ANP is a/w increased extra cellular fluid volume

BPT Written (16 decks)

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