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Flashcards in Renal Deck (203):
1

pronephros develops by

Week 4, then degenerates

2

Mesonephros

interim kidney during 1st trimester, later contributes to male genital system

3

metanephros

permanent kidney

4

When does metanephros appear? contiues through

5th week of gestation. Nephrogenesis continues through 32-36 weeks.

5

When is ureteric bud fully canalized by?

10th week

6

What is ureteric bud derived from?

caudal end of mesonephric duct

7

What does ureteric bud give rise to?

ureter + pelvises + calyces + collecting ducts

8

what does metanephric mesenchyme give rise to?

Glomerulus through to DCT.

9

what are congenital malformations of kidney often due to?

aberrant interaction between ureteric bud and metanephric mesenchyme.

10

causes of Potter disease

ARPKD + obstructive uropathy (posterior urethral valves) + bilateral renal agenesis + chronic placental insufficiency

11

Potter sequence presentation

POTTER (pulmonary hypoplasia, Oligohydramnios (trigger), Twisted face, Twisted Skin, Extremity defects, Renal failure (in utero.

12

horseshoe kidney assocations

1) hydronephrosis (ureteropelvic junction obstruction.
2) renal stones
3) infection
4) chromosomal aneuploidy syndromes (13,18,21)
5) renal cancer (rarely)

13

Diagnosis of unilateral renal agenesis

US

14

cause of unilateral renal agenesis

Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme.

15

kidney consisting of cysts and connective tissue

multicystic dysplastic kidney

16

cause of multicystic dysplastic kidney

ureteric bud fails to induce differentiation of metanephric mesenchyme

17

Causes of duplex collecting system

1) 2 ureteric buds reaching and interacting with metanephric blastema
2) bifurcation of ureteric bud before it enters the metanephric blastema, creating a Y-shpaed bifid ureter.

18

Why do duplex collecting systems create problems?

1) vesicoureteral reflux
2) ureteral obstruction
3) increased risk for UTIs

19

what usually happens with congenital solitary functioning kidney?

1) majority asymptomatic
2) compensatory hypertrophy of kidney
3) anomalies in contralateral kidney common though.

20

which kidney is usually taken during donor transplantation?

left (longer renal vein)

21

Renal blood flow

renal artery --> segmental artery --> interlobar artery --> arcuate artery --> interlobular artery --> afferent arteriole --> glomerulus --> efferent arteriole --> vasa recta/peritubular capillaries --> venous outflow

22

angiotensin II affects

1) Potent vasoconstrictor with preferential affects on the efferent arteriole, thus increasing FF to preserve GFR in low vlume states.
2) increases NE release by renal sympathetic nerves, thus stimulating aldosterone release
3) secondary effect is to increase HCO3- reabsorption (permitting contraction alkalosis)
4) Affects baroreceptor function; limits reflex bradycardia.
5) stimulates hypothalamus --> thirst
6) Acts at AT II receptor on vascular smooth muscle --> vasoconstriction --> increased BP.
8) stimulates ADH release from anterior pituitary.
9) increases PCT Na/H activity --> Na, HCO3, H2O reabsorption (can permit contraction alkalosis).

23

macula densa location

Lines the wall of the cortical thick ascending limb, at the transition to the DCT.

24

function of macula densa

when GFR drops, NaCl presentation to the macula is reduced , macula densa signals to juxtaglomerular cells in the afferent arteriole, causing them to release renin and activate the RAAS. Thus causing efferent arteriole vasoconstriction and increased GFR.

25

common complication of gynecologic procedures (ligation of uterine or ovarian vessels)

Damage to ureter, leaking to ureteral obstruction or leak.

26

relation of ureter to vas

Ureter passes UNDER vas deferens

27

percent of total body weight of total body water, ICF, ECF

60-40-20. 60% of your body water is total body water, of which 40% is ICF and 20% is ECF.

28

How is plasma volume measured?

Radiolabeling albumin.

29

How is ECF volume measured?

Inulin or mannitol

30

osmolality

285-295 mOsm/kg H2O

31

How to calculate HCT

roughly 3 x [Hb] in g/dL

32

RBC volume

2.8 L

33

ECF breakdown

interstitial fluid comprises 75% of ECF, Plasma comprises 25% of ECF

34

what component of the glomerular filtration barrier is lost in nephrotic syndrome?

Charge barrier

35

Composition of glomerular filtration barrier

1) fenestrated capillary endothelium (size barrier)
2) Fused BM w/ heparan sulfate (negative charge and size barrier)
3) epithelial layer consisting of podocyte foot processes (negative charge barrier)

36

Renal clearance equation

Cx = Ux V/Px (FA 556)

37

clearance and GFR relationship

Cx net reabsorption
Cx>GFR --> net secretion
Cx = GFR --> no net secretion or reabsorption

38

How to calculate GFR

1) Clearance of inulin. (given by above equation)
2) creatinine clearance

39

Normal GFR

100 mL/min

40

Describe creatinine clearance as a measure of GFR

Approximate. Slightly overestimates GFR because creatinine is moderately secreted by renal tubules.

41

How to estimate effective renal plasma flow (eRPF)? why?

PAH clearance. This is because between filtration and secretion there is nearly 100% excretion of all PAH that enters the kidney. It rises rapidly and is not reabsorbed anywhere.

42

eRPF as an estimate of RPF

It UNDERestimates true renal plasma flow slightly.

43

Normal FF

20%

44

How to calculate filtered load (mg/min)

GFR (mL/min) x plasma concentration (mg/mL)

45

How do prostaglandins affect FF?

No effect on FF because they increase both RPF and GFR

46

angiotensin II affect on FF

Increase FF because they decrease RPF and increase GFR by constricting efferent arteriole.

47

Effect of ureter constriction on GFR and FF

Decrease GFR + FF (backup causes increased hydrostatic pressure)

48

Effect of dehydration on GFR, RPF, and FF

Decrease GFR and decrease RPF BUT increase FF (RPF decreased to a greater degree than GFR).

49

Filtered load equation

Filtered load = GFR x Px

50

Excretion rate equation

V x Ux

51

Reabsorption/secretion

just difference between filtered and excreted

52

FEna

Na+ excreted/Na+ filtered

53

Glucose clearance

at a normal plasma level, glucose is completely reabsorbed in PCT by Na+/glucose ACTIVE cotransport.

54

When does glucosuria begin?

around 200 mg/dL

55

when do glucose glucose transporters become fully saturatd (Tm)?

375 mg/min

56

Why are glucosuria and aminoaciduria common in pregnancy?

pregnancy decreases ability of PCT to reabsorb glucose and amino acids.

57

What is "splay"?

Region of substance clearance between threshold and Tm. Basically, individual nephrons vary in absorptive capacity, so beyond the threshold there are still some nephrons capable of reabsorption.

58

PCT functions

1) reabsorbs all glucose and amino acids and most HCO3-, Na+, Cl-, PO4, K+, H2O, uric acid
2) generates and secretes NH3, which acts as a buffer for secreted H+ (which is secreted when Na+ is absorbed)

59

PTH action in the proximal tubule

Inhibits Na+/PO4 cotransport, cauisng phosphate excretion.

60

Fraction of Na+ reabsorbed in the proximal tubule

65-80%

61

Function of thin descending loop of henle

passive reabsorption of H2O via medullary hypertonicity (impermeable to Na). Thus, this is a concentrating segment.

62

Fraction of Na reabsorbed in the thick ascending limb

10-20%

63

Ca2+ and Mg2+ transport

Paracellular absorption in thick ascending limb through positive lumen potential generated by K+ backleak.

64

Thick ascending limb and affect on tonicity

Impermeable to H2O. Makes urine less concentrated as it ascends.

65

Early DCT affect on tonicity

Reabsorbs Na, Cl- thus diluting urine.

66

PTH action in the early DCT

Increases Ca/Na exchange leading to Ca reabsorption.

67

Fraction of Na absorbed in the DCT

5-10%

68

triamterene

K+-sparing diuretic

69

collecting tubule function

Reabsorbs Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).

70

Sodium absorption in the collecting tubule

3-5%

71

Fanconi syndrome defect

Generalized reabsorptive defect in PCT. Associated with increased excretion of nearly all amino acids, glucose, HCO3-, and PO4.

72

Causes of fanconi syndrome

Wilson disease, tyrosinemia, glycogen storage disease, cystinosis, ischemia, MM, nephrotoxins/drugs (ifosfamide, cisplatin, tenofovir, expired tetracyclines), lead poisoning.

73

Which is more severe, gitelman's or bartter's syndrome?

Barter's

74

differentiating barter's from gitelman's in metabolic profile

gitelman's causes hypocalciuria, Bartter's causes hypercalciuria

75

Example of a gain of function mutation

Liddle syndrome

76

Syndrome of apparent mineralocorticoid excess
1) pathophys
2) presentation
3) treatment

hereditary deficiency of 11beta-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralocorticoid receptor-containing cells before cortisol can act on the mineralocorticoid receptors. /excess cortisol in these cells from enzyme deficiency leads to increased mineralocorticoid receptor activity. /presentation = hypertension + hypokalemia + metabolic alkalosis. /low serum aldosterone. /can acquire disorder from glycyrrhetic acid (present in licorice), which blocks activity of 11beta-hydroxystroid dehydrogenase. /treatment = corticosteroids (exogenous corticosteroids decrease endogenous cortisol production, leading to decreased mineralocorticoid receptor activation).

77

Components of the juxtaglomerular apparatus + function

Mesangial cells + JG cells + macula densa (NaCL sensor, part of DCT). Function is maintain GFR via RAAS.

78

JG cells + function

Modified smooth muscle cells of afferent arteriole. Secrete renin in response to decreased renal blood pressure and increased sympathetic tone (B1)

79

ANP, BNP effects

1) check on RAAS.
2) relaxes vascular smooth muscle via cGMP --> increased GFR + decreased renin
3) dilates afferent ateriole; constricts efferent
4) promotes natriuresis.

80

What activates RAAS?

1) Decreased BP
2) decreased Na+ delivery (macula densa cells)
3) increased sympathetic tone (B1-receptors)

81

angiotensin 1 --> angiotensin II

occurs in lungs

82

Aldosterone affects

Increases Na channel and 1) Na/K pump insertion in principal cells; enhances K+ and H+ excretion by way of principal cell K+ channels and alpha-intercalated cell H+ ATPases. Thus, creates favorable Na+ gradient for Na+ and H2O reabsorption.
2) summary --> Na reabsorption, K+ and H+ secretion.

83

active form of vitamin D

calcitriol, 1,25-(OH)2 vitamin D3

84

PTH action in vitamin D pathway

inhibits 1alpha-hydroxylase

85

calciferol

refers to either D2 or D3

86

Dopamine kidney actions

Secreted by PCT cells, promotes natriuresis. At low doses, dilates interlobular arteries, afferent arterioles, efferent arterioles --> increased RBF, little or no change in GFR. At higher doses, acts as vasoconstrictor.

87

PTH triggers

1) decreased plasma Ca
2) increased phosphate
3) decreased plasma 1,25-OH)2D3

88

PTH effects

1) increased Ca reabsorption (DCT)
2) decreased phosphate reabsorption (PCT)
3) increased vitamin D production
4) increased Ca and phosphate absorption from gut via vitamin D

89

Causes of hyperkalemia (things that shift K+ out of cells)

DOLABS. Digitalis, hyperOsmolarity, Lysis of cells, Acidosis, B-blocker, high blood Sugar

90

Causes of hypokalemia

Hypo-osmolarity, alkalosis, beta agonists, insulin

91

Presentation of hyponatremia

nausea + malaise + stupor + coma + seizures

92

hypernatremia presentation

irritability + stupor + coma

93

hypokalemia on ECG

U waves + flattened T waves

94

hyperkalemia on ECG

wide QRS and peaked T waves

95

caveat about hypercalcemia

not necessarily calciuria

96

hyperkalemia pnemonic

stones (renal), bones (pain), groans (abdominal pain), thrones (increased urinary frequency), psychiatric overtones (anxiety, altered mental status).

97

hypomagnesemia presentation

presentation = tetany + torsades de pointes + hypokalemia.

98

hypermagnesemia presentation

decreased DTRs + lethargy + bradycardia + hypotension + cardiac arrest + hypocalcemia

99

hypophosphatemia presentation

bone loss + osteomalacia (adults) + rickets (children).

100

hyperphosphatemia presentation

renal stones + metastatic calcifications + hypocalcemia

101

bicarb and PCO2 levels in metabolic alkalosis

increased PCO2 + increased HCO3

102

Using winters formula + what results mean

1) Use winters to predict respiratory compensation for a simple metabolic acidosis.
2) if measured PCO2>predicted PCO2, a concomitant respiratory acidosis is occurring
3) If measured PCO2 is leass than predicted PCO2, concomitant respiratory alkalosis is occurring.

103

Causes of normal anion gap

HARDASS: Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

104

PCO2 cutoff for determining respiratory acidosis

44 mm Hg

105

HCO3- cutoff for determining metabolic acidosis

less than 20

106

PCO2 cutoff for determining respiratory alkalosis

less than 36

107

HCO3- cutoff for determining metabolic alkalosis

greater than 28

108

common causes of metabolic alkalosis

1) loop diuretics
2) vomiting
3) antacid use
4) hyperaldosteronism

109

hyperchloremic vs. hypochloremic metabolic acidosis

hyperchloremic = normal anion gap
hypochloremic - anion gap

110

Renal tubular acidosis (RTA)

disorder of renal tubules that leads to normal anion gap metabolic acidosis

111

Distal renal tubular acidosis (type 1)

Urine pH > 5.5. Defect in ability of alpha intercalated cells to secrete H+ --> no new HCO3- is generated, leading to metabolic acidosis. Associated with hypokalemia + increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover).

112

Causes of distal renal tubular acidosis (type 1)

Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract.

113

Proximal renal tubular acidosis (type 2)

Urine pH increased excretion of HCO3- in urine and subsequent metabolic acidosis. Urine is acidified by alpha-intercalated cells in collecting tubule. Associated with hypokalemia + increased risk for hypophosphatemic rickets.

114

Causes of proximal renal tubular acidosis (type 2)

Fanconi syndrome + carbonic anhydrase inhibitors

115

Hyperkalemic renal tubular acidosis (type 4)

Urine pH HYPERkalemia --> decreased NH3 synthesis in PCT --> decreased NH4+ excretion.

116

causes of hyperkalemic renal tubular acidosis (type 4)

decreased aldosterone production + aldosterone resistance (K+ sparing diuretics, nephropathy due to obstruction, TMP/SMX).

117

RBC casts found in

glomerulonephritis + malignant HTN

118

WBC casts found in

tubulointerstitial inflammation + acute pyelo + transplant rejection

119

Fatty casts ("oval fat bodies) found in

nephrotic syndrome. associated with "Maltese cross" sign.

120

waxy casts found in

ESRD/chronic renal failure

121

hyaline casts indicate...

nonspecific, can be normal, often seen in concentrated urine samples

122

focal vs. diffuse glomerulonephritis

diffuse involves >50% of glomeruli, focal less than

123

"proliferative" means...

hypercellular glomeruli

124

cause of nephritic syndrome

Inflammatory process. GBM disruption

125

general characteristics of nephritic syndrome

HTN (due to salt retention) + increased BUN and creatinine + oliguria + hematuria + RBC casts + azotemia + proteinuria (mild)

126

cause of nephrotic syndrome

Podocyte disruption --> charge barrier impaired.

127

general characteristics of nephrotic syndrome

massive proteinuria + hypoalbuminemia + hyperlipidemia + edema.

128

Nephritic-nephrotic syndrome

Severe nephritic syndrome can lead to profound GBM damage that damages the glomerular filtration charge barrier leading to nephrotic range proteinuria + concomitant features of nephrotic syndrome. Can occur with any nephritic syndrome.

129

nephritic-nephrotic syndrome most commonly seen with..

1) Diffuse proliferative glomerulonephritis.
2) Membranoproliferative glomerulonephritis.

130

massive proteinuria defined as

greater than 3.5 g/day

131

other impt features of nephrotic syndrome

hypercoagulable state (due to AT III loss in urine) + immunocompromised state (due to loss of immunoglobulins in urine and soft tissue compromise by edema).

132

What happens to GFR in diabetic glomerulonephropathy?

Increased due to glycosylation of efferent arterioles.

133

most common kidney stone presentation

calcium oxalate stone in patient w/ hypercalciuria and normocalcemia.

134

renal stone breakdown

80% calcium, 15% struvite, 5% uric acid

135

where would uric acid stones form?

DTC and collecting tubule (precipitate in decreased pH)

136

Other causes of hydronephrosis

retroperitoneal fibrosis + vesicoureteral reflux.

137

Renal cell carcinoma route of metastasise

invades renal vein then IVC and spreads hematogenously.

138

renal cell carcinoma treatment

Resection if localized. Immunotherapy (eg, aldesleukin) or targeted therapy for advanced/metastatic disease. Resistant to chemo and radiation.

139

usual presentation for RCC

metastatic neoplasm. "silent cancer"

140

renal oncytoma -- presentation, etc.

codebook

141

Wilms tumor management

MOPP --> Mechlorethamine, Oncovin/vincristine, Procarbazine, Prednisone

142

WAGR complex

WAGR syndrome: Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental Retardation/intellectual disability (WT1 deletion).

143

Denys-Drash syndrome

(codebook)

144

transitional cell carcinoma carcinogens

Phenacetin, Smoking, Aniline dyes, cyclophosphamide

145

nitrites indicate

gram negative organisms (especially e coli)

146

sterile pyuria indicates

urethritis by gonorrhoea or chlamydia

147

negative urine cultures with UTI presentation indicates

urethritis by gonorrhoea or chlamydia

148

other impt findings in pyelonephritis

tubulorrhexis (necrosis of epithelial lining) + microabscesses

149

CT finding in pyelo

striated parenchymal enhancement

150

chronic pyelo findings + xanthogranulomatous pyelo

codebook

151

ATN pathophys in intrinsic renal failure

Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule, leading to decreased GFR.

152

Consequences of renal failure

MADHUNGER: Metabolic Acidosis, Dyslipidemia (especially triglycerides), Hyperkalemia, Uremia, Na+/H2O retention (HF, pulmonary edema, HTN), Growth retardation and developmental delay, Epo failure (anemia), Renal osteodystrophy

153

urea vs ammonia vs protein

Excess nitrogen in the form of ammonia (NH3) is generated from the catabolism of amino acids, and is feed into the urea cycle to produce urea, which is then excreted by the kidney.

154

Uremia + presentation

Clinical syndrome marked by increased BUN. nausea and anorexia + pericarditis + asterixis + encephalopathy + platelet dysfunction.

155

Prerenal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr

1) >500
2) less than 20
3) less than 1%
4) greater than 20

156

Intrinsic renal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr

1) less than 350
2) greater than 40
3) greater than 2%
4) less than 15

157

Postrenal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr

1) less than 350
2) greater than 40
3) >1% (mild), >2% (severe)
4) varies

158

3 stages of ATN, and associated risks

1. Inciting event.
2. Maintenance phase--oliguric; lasts 1-3 weeks; risk of hyperkalemia, metabolic acidosis, uremia.
3. Recovery phase--polyuric; BUN and creatinine fall; risk of hypokalemia.

159

Causes of ATN

1) Ischemic--secondary to decreased renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF). Results in death of tubular cells that may slough into tubular lumen.
2) Nephrotoxic--secondary to injury resulting from toxic substances (eg., aminoglycosides, radiocontrast agents, lead cisplatin), crush injury (myoglobinuria), hemoglobinuria. PCT is particularly susceptible to injury.

160

papillary necrosis associations

sickle cell disease or trait + acute pyelonephritis + NSAIDs + diabetes mellitus

161

ADPKD treatment

ACE inhibitors or ARBs

162

Medullary cystic disease

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidneys on ultrasound. Poor prognosis.

163

ARPKD

cystic dilation of collecting ducts. Often presents in infancy. associated with congenital hepatic fibrosis. Significant oliguric renal failure can lead to Potter sequence.

164

sequela of ARPKD

Systemic HTN + progressive renal insufficiency + portal hypertension from congenital hepatic fibrosis.

165

Simple cysts

Filled with ultrafiltrate (anechoic (black) on US). Very common and account for majority of all renal masses. Found incidentally and typically asymptomatic.

166

Complex cysts

Septated, enhanced, or have solid components on imaging. Require follow-up or removal due to risk of RCC.

167

Mannitol MOA

Osmotic diuretic. Increases tubular fluid osmolarity, thereby increasing urine flow and decreasing.intracranial/intraocular pressure.

168

Mannitol clinical use

Drug overdose, elevated ICP/intraocular pressure.

169

Mannitol AE's

pulmonary edema, dehydration, contraindicated in anuria, HF.

170

Acetazolamide mechanism

carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diureses and decreased total body HCO3- stores.

171

Acetazolamide clinical use

glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri

172

Acetazolamide AE's

Proximal RTA, paresthesias, NH3 toxicity, sulfa allergy

173

Other mechanism point about loop diuretics

Stimulate PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs.

174

Loop diuretics adverse effects

ototoxicity, hypokalemia, dehydration, allergy (sulfa), metabolic alkalosis, interstitial nephritis, gout.

175

ethacrynic acid MOA

nonsulfonamide inhibitor of cotransport system of thick ascending limb of loop of henle.

176

ethacrynic acid AE's

similar to furosemide, but more ototoxic.

177

metolazone

thiazide

178

Thiazide clinical uses

HTN, HF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis

179

Thiazide AE's

hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

180

spironolactone and eplerenone MOA

competitive aldosterone receptor antagonists in cortical collecting tubule.

181

triamterene and amiloride MOA

Act at collecting tubule by blocking Na+ channels in the cortical collecting tubule.

182

K+ sparing diuretics use

hyperaldosteronism, K+ depletion, HF

183

hepatic ascites treatment

spironolactone

184

nephrogenic DI treatment

amiloride

185

K+ sparing diuretics AE's

hyperkalemia (arrhythmias) + endocrine effects with spironolactone (gynecomastia, antiandrogen effects).

186

diuretics associated with alkalemia

loop diuretics + thiazides

187

alkalemia mechanism with diuretics

1) volume contraction --> increased AT II --> increased Na+/H+ exchange in PCT --> increased HCO3- reabsorption
2) K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells.
3) in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule --> alkalosis and "paradoxical aciduria"

188

bradykinin actions

potent vasodilator

189

ACEI's clinical use

HTN, HF (decreased mortality), proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic HTN.

190

ACEI mechanism in diabetic nephropathy

decrease intraglomerular pressure, slowing GBM thickening.

191

ACEI's AE's

cough, angioedema, teratogen, increased creatinine, hyperkalemia, Hypotension

192

ACEI's contraindicated in

bilateral renal artery stenosis (can further decrease GFR)

193

ARB clinical uses

HTN, HF, proteinuria, diabetic nephropathy with intolerance to ACE inhibitors

194

ARB AE's

hyperkalemia + decreased GFR + hypotension + teratogen

195

Aliskiren MOA

direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I

196

Aliskiren AE's

hyperkalemia, decreased GFR, hypotension. Relatively contraindicated in patients already taking ACEI's or ARBs.

197

Inulin and mannitol

Used to help measure GFR (volume of fluid filtered from the renal glomerular capillaries into the Bowman’s capsule per unit time) because it is not secreted or absorbed. Thus, inulin clearance is constant. Very similar to creatinine. Concentration basically steadily rises, except for a slight dip in distal tubule.

198

Potassium regulation in the kidney

2 vacuums in proximal tubule + thick ascending limb sucking bananas from tubules/most K+ is resorbed in the proximal tubule + loop of Henle. /late distal and cortical collecting tubules are the primary sites for regulation of K+ concentration. Imagine faces of Principal ted from highschool puking bananas into the late DTC + collecting duct/principal cells in the late distal convoluted tubule + cortical collecting ducts secrete K under conditions of normal or increased K+ load.

199

Phosphorus regulation in the kidney

80-90% of filtered load of phosphate is reabsorbed. Phosphines stuck into proximal tubule with salt piled on top/most reabsorption occurs in the proximal tubule by secondary active transport mediated by Na+-phsophate cotransporters (NAPT). This is a transport maximum process. /primarily regulated by PTH, which reduces proximal tubule phosphate reabsorption. /calcitriol (1,25-OH2-vitamin D), increases phosphate reabsorption (by increasing NAPT). /Thus PTH inhibits renal phosphate reabsorption.

200

Tubular fluid osmolarity

Hambones frozen in ice lining proximal tubule/300 in the proximal tubule + ***isotonic (both solutes and water reabsorbed). Lined with hooks/descending limb = 700 (variable tho). Lined with ivy/thin ascending limb = 800. Stuffed with hens/thick ascending limb = 200. Filled with hats/distal convoluted tubule = 100. Lined with bode miller hula-hooping/collecting duct (IN THE PRESENCE OF ADH) = 900. Dead bode covered in lice/**in the absence of ADH, tubular fluid is most dilute in the collecting ducts. /most NaCl absorption occurs in the thick and thin ascending limbs, so fluid becomes hypotonic here. Thus, these are called the diluting segments of the kidney. Salt plug in the bottom of the loop of henle/in the absence of ADH, highest osmolarity occurs at the bottom of the loop of henle.

201

Permeabilities of segments:

-Descending limb is permeable to water, but not solutes - fluid becomes hypertonic. -Thick ascending limb is impermeable to water and electrolytes are resorbed fluid becomes hypotonic.
-DTC reabsorbs solutes + is impermeable to water tubular fluid becomes more hypotonic.
-Collecting ducts depends on ADH impermeable to water in its absence, thus becoming more hypotonic.

202

Effect of hematocrit on GFR

Increased hematocrit will decrease GFR because increased hematocrit means decreased plasma volume (plasma holds water and protein).

203

In the absence of ADH, where is fluid most diluted in the kidney?

Collecting duct