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GIR Test 3 > B5.045 Renal Physiology V: Renal Tubular Diseases > Flashcards

B5.045 Renal Physiology V: Renal Tubular Diseases Flashcards

1
Q

overview of tubular function

A

specialized transport proteins move electrolytes, organic solutes, and water in both absorptive and secretory direction

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2
Q

proximal tubule function

A

reabsorption of solutes/fluid

secretion of organic anions/cations

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3
Q

ascending loop of henle function

A

reabsorption of Na+, Cl-, K+

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4
Q

distal tubule function

A

reabsorption of Na+, Cl- and water

secretion of K+ and H+

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5
Q

collecting duct function

A

reabsorption of Na+, Cl- and water

secretion of K+ and H+

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6
Q

2 sources of tubulopathies

A
  1. mutation of renal transport systems, inherited in both dominant and recessive manner
  2. acquired defects
    - induced by pharm agents
    - injury and inflammatory processes
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7
Q

primary transporters in proximal tubule

A

all transport depends on Na,K ATPase

  • glucose, AA, phosphate absorbed by Na+ co-transporters
  • protons secreted by Na+ proton exchanger
  • chloride follows paracellular pathways and base-dependent exchangers
  • organic acids are secreted by Na+ dependent and independent OAT transporters
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8
Q

apical OA transporter

A

secretes OA via exchange with Cl-

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9
Q

basolateral OA transporter

A

absorb OA via exchange with Na+

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10
Q

effect of transport defects in proximal tubule

A

Fanconi syndrome
kidney reabsorptive condition
whole proximal tubule is effectively shut down

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11
Q

signs and symptoms of Fanconi syndrome

A 
polyuria, polydipsia, and dehydration
hypophoshatemic rickets or osteomalacia
growth failure
metabolic acidosis
hypokalemia
hyperchloremia
hypophosphatemia/phosphaturia
glucosuria, aminoaciduria
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12
Q

why do you get hyperchloremia in Fanconi

A

due to acidosis

bicarb is lost and exchanged for Cl-

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13
Q

variability of symptoms in Fanconi

A

depend on extent of compromise in proximal tubule

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14
Q

genetic diseases associated with Fanconi syndrome

A 
cystinosis
galactosemia
glycogen storage disease
Lowe syndrome
Wilson disease
tyrosinemia
Dent's disease
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15
Q

environmental assaults that can cause Fanconi’s syndrome

A

exposure to nephrotoxic heavy metals
expired tetracyclines, gentamycin
toluene and derivatives (paint factories)

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16
Q

what causes the genetic forms of Fanconi

A

accumulation of metabolic products and/or metals in proximal tubule cells leads to cellular dysfunction and necrosis

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17
Q

primary transport systems in ascending loop of henle

A

Na+, K+, and Cl- are all cotransported on apical side by NKCC (important for countercurrent exchange system)
K+ and Cl- reabsorbed together at basolateral side or independently through channels
K+ also leaks to tubular side via ROMK1

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18
Q

function of ROMK1

A

secretes K+ back into lumen

helps K+ recycling and maintains function of NKCC

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19
Q

what leads to transport defects in ascending loop of henle

A

alterations in ROMK1, NKCC, and Barttin

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20
Q

what is Barttin

A

basolateral Cl- channel in ascending loop of henle

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21
Q

clinical signs and symptoms of bartter’s syndrme

A 
polyuria, polydipsia
poor muscle tone
heart repolarizing abnormalities
hyponatremia
hypokalemia
hypochloremia
ECF volume contraction
high renin-aldosterone
metabolic alkalosis, high urine H+
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22
Q

what is the source of the electrolyte abnormalities associated with bartter’s

A

NKCC dysfunction

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23
Q

why do you get ECF volume contraction in bartter’s

A

NKCC involved in Na+ sensing in the macula densa

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24
Q

which symptoms are associated with hypokalemia

A

poor muscle tone

heart repolarizing abnormalities

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25
why do you get metabolic alkalosis in bartters
lots of aldosterone leads to excessive H+ secretion
26
genetic mutations that can lead to Bartter's
ROMK1 NKCC2 Barttin autosomal recessive
27
environmental causes of Bartter's
inhibitors of NKCC: furosemide bumetanide
28
transport mechanisms of distal tubule
Na+ and Cl- are cotransported on apical side and reabsorbed basolaterally K+ is secreted to tubular fluid via K+ channels Ca2+ is reabsorbed via channels and the Na/Ca exchanger
29
what is TSC
thiazide sensitive co-transporter | Na+/Cl- transporter on apical membrane
30
what is TRPM6
Mg2+ channel in apical membrane
31
what is the mechanism of action of most diuretics
inhibit Na+ channels to induce solute diuresis
32
causes of transport defects in distal tubule
alterations in TSC or TRPM6 | Gitelman's syndrome
33
clinical signs and symptoms of Gitelman's
``` hyponatremia hypokalemia, high urine K+ hypomagnesemia, high urine Mg2+ hypocalciuria ECF volume contraction normotensive ```
34
why is Gitleman's less associated with polyuria than other tubular defects
a lot of compensatory mechanisms from proximal tubule/loop of henle mask the effects
35
how can you differentiate Gitleman's from Bartter's
Bartters has higher R-A-A activation and more trouble concentrating urine
36
genetic mutations associated with Gitelmans
TSC TRPM6 autosomal recessive
37
environmental assaults causing Gitelmans
inhibitors of TSC: | thiazides
38
transport mechanisms of collecting tubule
Na+ is reabsorbed apically by ENac K+ is secreted to tubular fluid by K+ channels water reabsorbed via aquaporins
39
what leads to transport defects in the collecting tubule
alterations in ENac (constantly activated) - Liddle's syndrome defects of aquaporins or their regulation- nephrogenic diabetes insipidus
40
signs and symptoms of Liddle's syndrome
``` increased ECF volume hypertension, refractory to drugs decreased R-A-A activation hypokalemia metabolic acidosis ```
41
cause of Liddles syndrome
genetic mutations in the ENac subunits that avoids their cell internalization and degradation maintains ENac activity uncontrolled autosomal dominant
42
what is nephrogenic diabetes insipidus
collecting ducts cells resistant to ADH
43
clinical signs and symptoms of nephrogenic diabetes insipidus
``` polyuria polydipsia risk of dehydration dilute urine with low osmolarity sometimes hypernatremia ```
44
how do you distinguish nephrogenic from non-nephrogenic diabetes insipidus
``` give desmopressin (exogenous ADH) will improve if non-nephrogenic ```
45
what causes non-nephrogenic diabetes insipidus
defect in ADH production | excessive water intake (psychogenic)
46
genetic mutations associated with nephrogenic diabetes insipidus
``` mutations in vasopressin receptor (V2) defective AQP failure in AQP targeting mechanisms X-linked inheritance patter independent of ADH levels and not responsive to ADH ```
47
environmental assaults that can lead to nephrogenic diabetes insipidus
drugs, lithium
48
process of proton secretion in nephron
in proximal tubule, H+ is secreted by the Na/H exchanger | in distal and collecting tubules H+ is secreted by ATPases
49
effect of defects in proton secretion
renal tubular acidosis | classified as proximal or distal renal tubular acidosis
50
clinical signs and symptoms of renal tubular acidosis
``` muscle weakness cardiac repolarization problems growth retardation kidney stones hypokalemia hyperchloremia hypercalciuria metabolic acidosis, low excretion of H+ ```
51
what is hypercalciuria and its effect
calcium collects in kidneys and urine | causes kidney stones
52
what causes growth retardation in renal tubular acidosis
metabolic acidosis activates osteoclasts moves calcium out of bone bones look radiolucid on x-ray (dark due to lack of calcium) bones have a bent, elastic shape
53
mutations in proximal RTA
apical Na/H exchanger | basolateral Na/bicarb exchanger
54
mutations in distal RTA
apical proton ATPases basolateral anion exchanger carbonic anhydrase
55
effect of ischemia or toxins on the renal tubules
acute tubular necrosis
56
clinical course of acute tubular necrosis
initial phase with aliguria recovery phase with increase in urine but loss of electrolytes can progress to loss of renal function/acute renal failure depending on cause
57
effect of inflammation of tubules
acute or chronic inability to concentrate urine polyuria, salt wasting metabolic acidosis
58
cystic disease of the kidney
polycystic kidney disease medullary cystic disease acquired cystic disease localized simple cysts
59
types of PKD
autosomal dominant | autosomal recessive
60
types of medullary cystic disease
medullary sponge kidney | nephronophthisis
61
genes involved in adult PKD
PKD1 - polycystin 1 | PKD2- polycystin 2
62
genes involved in child PKD
PKHD1 - fibrocystin
63
genes involved in nephronophthisis
NPH1 NPH2 NPH3
64
most common monogenic disorder of the kidney
autosomal dominant polycystic kidney disease
65
characterize autosomal dominant polycystic kidney disease
growth of multiple fluid-filled cysts that affect kidney structure and function affects all ethnic groups, 1:500- 1:1000 progress to chronic renal failure (8-10% of all cases of end stage renal failure)
66
manifestations of ADPKD
cardio alterations hypertension extrarenal cysts in pancreas and liver
67
severity of different forms of ADPKD
PKD1 more common (85%) and more severe than PKD2
68
function of polycystins
control normal kidney development and function flow triggers polycystin complex to transfer Ca2+ into cells Ca2+ is used in transcriptional control of genes
69
phenotypic changes related to polycystin alterations
``` transepithelial fluid secretion cell proliferation alteration in cell planar polarity remodeling of ECM cell cilia alterations ```
70
renal symptoms of ADPKC
``` hematuria decrease in concentrating ability of kidney infections hypertension w increased renin GFR reduces late in disease kidney 10x normal side compression of vena cava could lead to lower extremity edema ESRD by age of 60 ```
71
extrarenal symptoms of ADPKD
cerebral aneurysms hepatic and pancreatic cysts LVH, mitral valve disease
72
diagnosis of ADPKD
urine analysis normal at first microscopic to gross hematuria, proteinuria serum creatinine and BUN progressively rise GFR not good indicator imaging best for diagnostics
73
treatment of ADPKD
ACE inhibitors pain management, nephrectomy dialysis or kidney transplant

GIR Test 3 (19 decks)

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