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Renal > Biochem > Flashcards

Biochem Flashcards

1
Q

deficiency of this is associated with diabetic nephropathy and neuropathy. The transporter in the proximal tubule is inhibited by glucose

A

inositol.

the kidney is the only organ that breaks down inositol

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2
Q

What enzyme produces sorbitol from glucose

A

aldose reductase

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3
Q

sugar produced from sorbitol that serves as fuel for the kidney

A

fructose

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4
Q

cells that have aldose reductase activity

A
  1. pericytes of the vasa recta.
  2. mesangial cells in the glomerulus.
    * hyperglycemia causes elevated sorbitol production and increased oxidative stress which causes pericyte apoptosis and vascular changes in diabetic neuropathy & nephropathy
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5
Q

portion of the kidney where enzymes of gluconeogenesis are located

A

cortex

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6
Q

major organic anion in urine that inhibits calcium oxalate stone formation

A

citrate.

*utilization of citrate from the circulation as a fuel is unique to the kidney

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7
Q

When does renal extraction of amino acids increase substantially?

A

during starvation and acidosis.

*glutamine is the amino acid that is taken up more

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8
Q

uptake and metabolism by the proximal tubule increases in response to metabolic acidosis

A

glutamine.

glutamine -> glutamate + NH4+
enzyme: glutaminase

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9
Q

major role of the kidney in glucose homeostasis

A

return of filtered glucose to the blood.

Renal gluconeogenesis only makes a significant contribution during starvation not overnight fasting.

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10
Q

Attaches pedicel to GBM

A

Alpha1beta3 integrin

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11
Q

In the molecular slit diaphragm

A

Nephrin.

CD2AP adapter protein

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12
Q

Transmembrane protein that connects to intracellular actin cytoskeleton and is necessary to proper kidney development due to its role in formation and maintenance of pedicels

A

Podocalyxin

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13
Q

Size of the fenestrae on the endothelial side of the GBM

A

50-100 nm

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14
Q

Why is the GBM thicker than most basement membranes?

A

It is secreted by both endothelial and epithelial cells.
Thickness: 240-370 nm
Normal basement membrane thickness: 40-80 nm

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15
Q

Mutations in laminin beta2

A

Pierson syndrome.
It is an autosomal recessive disorder comprising congenital nephrotic syndrome with diffuse mesangial sclerosis and distinct ocular abnormalities.

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16
Q

Proteoglycans that provide neg charge to GBM

A
  1. Heparan sulfate
  2. Perlecan
  3. Collagen XVIII
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17
Q

What confers the negative charge of all serum proteins at physiologic pH?

A

NANA: sialic acid

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18
Q

What can be disrupted in the GBM to cause proteinuria?

A

Heparan sulfate proteoglycans.
These provide the negative charge which is essential to filtration.
HSP turnover: hours
Type IV collagen turnover: days to weeks

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19
Q

Why is creatinine used to estimate GFR?

A

It is a neutral molecule that is freely filtered by the glomerulus, stable in the urine and not reabsorbed by the tubules.
Elevated creatinine occurs when the GBM undergoes pathological change. (Ex: diabetes)

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20
Q

What is the pathological change of the GBM in diabetes?

A

Progressive GBM thickening from enhanced deposition of type IV collagen and laminin with little to no synthesis of HSPs

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21
Q

Histologic feature of progression to end stage renal disease

A

Focal segmental glomerulosclerosis

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22
Q

How does glomerular stress add to glomerular dysfunction in ESRD?

A

Podocytes are damaged and these are responsible for calcium signaling events that promote remodeling. Stress loosens connections of the pedicels to the GBM and they snap apart widening the slit. Mesangial cells proliferate and secrete matrix while macrophages proliferate. All this leads to podocyte loss and sclerosis. This is why therapy is aimed at inhibiting the renin-angiotensin system to decrease capillary HTN

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23
Q

Compromised transport of lysine, arginine, and ornithine, resulting in their appearance in urine

A

Cystinuria.

Treat by restricting dietary methionine and alkalinization of urine to prevent cystine stone formation

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24
Q

Why does dietary restriction of cysteine, arginine and ornithine not cause deficiency?

A

These are nonessential amino acids and therefore can be synthesized by the body

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25
Q

Rare disorder caused by a defective carrier for cystine across lysosomal membranes and results in accumulation and formation of crystals in lysosomes. Children develop renal failure by age 6-12 yr

A

Cystinosis

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26
Q

Intracellular buffers

A
  1. phosphate
  2. glucose-6-phosphate
  3. ATP
  4. proteins
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27
Q

which amino acids may not undergo transamination reactions?

A

lysine and threonine

28
Q

cofactor for transamination reactions

A

PLP = pyridoxal phosphate (from vitamin B6)

29
Q

Role of glutamate in amino acid synthesis

A

transfers nitrogen to alpha-keto acids by transamination to form amino acids

30
Q

sources of nitrogen for urea formation

A
  1. glutamate

2. aspartate

31
Q

amino acids synthesized from glycolysis intermediates

A
  1. Serine
  2. Glycine
  3. Cysteine
  4. alanine
32
Q

Increase risk of kidney stones in those who are prone to stone formation

A

Animal proteins, sodium, sucrose, vitamin C

33
Q

Why are diabetics prone to stone formation?

A

Heterogeneous nucleation is how stones form and it occurs in the presence of protein. Salts deposit on a nidus of protein. Diabetics are prone to proteinuria.

34
Q

Where are Phase I and Phase II biotransformation reactions performed in the kidney?

A

cortex

35
Q

Unique features of the proximal straight tubule (PST) (4)

A
  1. higher level of G-6-P dehydrogenase
  2. higher amount of alanine aminotransferase
  3. only glutamine synthetase in the kidney
  4. enzymes for xenobiotic metabolism by CYP450 and glutathione
36
Q

Why is glucose metabolized preferentially over lactate in the CCT and MCT?

A

high levels of glycolytic enzymes and low levels of mitochondria

37
Q

What type of glycolysis is predominant in the medulla and papilla?

A

anaerobic glycolysis

38
Q

Use of lactate in the cortex is for

A

gluconeogenesis

39
Q

10% of glucose oxidation may occur through the pentose phosphate pathway for what purpose?

A

generate ribose-5-phosphate and NADPH.

NADPH is used to regenerate GSH (reduced glutathione)

40
Q

Where is glycogen found in the kidney?

A

Medulla.

It is where the glycolytic enzymes are and where anaerobic glycolysis takes place.

41
Q

What is the first step in all pathways of lactate utilization by the kidney?

A

conversion of lactate to pyruvate by LDH

42
Q

Why do fatty acids enter renal cells at the basolateral membrane?

A

Plasma free fatty acids are bound to albumin and not filtered by the glomerulus

43
Q

When are fatty acids utilized most as a fuel source?

A

starvation and diabetes

44
Q

Why does glutamine transport to the kidneys increase during metabolic acidosis?

A

glutamine production transports protons and acts as an additional buffer to assist the HCO3- buffer system

45
Q

What hormone influencing metabolism is the liver responsive to but NOT the kidney?

A

glucagon

46
Q

Which transporter when affected by genetic defects causes glycosuria?

A

SGLT2

47
Q

What amino acid production is increased by metabolic acidosis?

A

alanine

48
Q

What is the fate of renal glycine in metabolic acidosis?

A

oxidation to CO2 and ammonia

49
Q

In what pathway is serine produced from glycine?

A

Folate metabolism.

Methylene THF -> THF

50
Q

When does anemia of chronic renal failure occur?

A

When Creatinine Clearance decreases below 20-40 mL/min

51
Q

What might be deficient if administration of Epo fails to increase RBC?

A

folate, B12 or iron

52
Q

Where is CYP450 the highest in the kidney?

A

Proximal tubule

53
Q

Why are phosphate binders given to CKD patients?

A

Patients with CKD have impaired elimination of phosphate from the blood, and limiting dietary absorption of phosphate with the binder helps maintain proper balance.

54
Q

Are fatty acids utilized as a major fuel source by the kidney during fasting?

A

No. The kidney oxidizes ketones to CO2. From a previous statement in the monograph the kidney prefers to oxidize ketones for energy, rather than fatty acids. (?)

55
Q

Since ammonia it toxic, how does it get transported between tissues?

A

as glutamine and alanine

56
Q

Inhibits renin release (4)

A
  1. ANG II
  2. AVP
  3. TxA2
  4. high plasma K & NO
57
Q

Major actions of aldosterone

A
  1. sodium and H2O reabsorption

2. potassium secretion (potassium secretion is a secondary effect of sodium reabsorption)

58
Q

rate limiting step in aldosterone synthesis

A

cholesterol -> pregnenolone.

Enzyme: SCC enzyme = CYPIIA

59
Q

Results from a dietary deficiency of niacin or tryptophan, both of which are precursors for NAD and NADP. Phenotypic expression includes photosensitivity rash, ataxia and neuropsychiatric symptoms.

A

Hartnup.

It is caused by a defect in the neutral amino acid transporter.

60
Q

metabolism of what amino acid generates 40% of oxalate produced by the liver

A

glycine

61
Q

Genetic deficiency of cystathionase

Dietary deficiency of vit B6

A

cystathionuria

62
Q

Congenital cystathionine beta-synthase deficiency (enzyme is inhibited by cysteine)
Deficiency of cystathionase
Vit B6 deficiency, also B12 and folate

A

homocystinuria

63
Q

Defective branched-chain alpha-keto acid dehydrogenase
-results in accumulation of branched-chain amino acids and their keto-analogs, both of which appear in the urine and make it smell like maple syrup or burnt sugar

A

maple syrup urine disease

64
Q

Defective homogentisate oxidase
-prevents homogentisate in tyrosine metab from being oxidized; it accumulates and auto-oxidizes forming a dark pigment which discolors the urine and stains infant diapers; causes arthritic joint pain later in life

A

alcaptonuria

65
Q

Type 1: alanine-glyoxylate aminotransferase

Type 2: glyoxylate reductase/hydroxypyruvate reductase (GRHPR)

A

Primary oxaluria

66
Q

Mutation in chromosome that encodes phenylalanine hydroxylase (PAH); normally catalyzes hydroxylation of phenylalanine to tyrosine

A

PKU

Renal (8 decks)

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