ACOM > Renal Exam 1 > Flashcards

Renal Exam 1 Flashcards

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1
Q

interlobular arteries give rise to

A

afferent arterioles

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2
Q

afferent arterioles give rise to

A

glomerular capillaries

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3
Q

glomerular capillaries coalesce into

A

efferent arterioles

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4
Q

efferent arterioles drain into

A

renal corpuscles

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5
Q

efferent arterioles from cortical glomeruli form what

A

capillary networks around tubules in cortex then drain into interlobular veins

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6
Q

efferent arterioles from juxtamedullary glomeruli form what

A

vasa recta arteriae (straight arteries( that get sent into medulla where they make hairpin turns and ascend as venous vasa rectae to join arcuate veins

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7
Q

what is the first part of the nephron

A

renal corpuscle

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8
Q

what makes up the renal corpuscle

A

glomerulus and bowmans capsule

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9
Q

what pushes blood through the filtration barrier

A

blood pressure in glomerulus

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10
Q

where does blood go when filtered from glomerulus

A

bowmans capsule

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11
Q

fluid in bowmans capsule is now called what

A

filtrate

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12
Q

bowmans capsule layers

A

parietal made of simple squamous epithelium
visceral made of podocytes of glomerular capillaries

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13
Q

filtration slits are where

A

between the pedicles (podocyte foot processes)

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14
Q

filtration barrier

A

glomerular endothelium (blood cells)
basement membrane (proteins > 70 kD)
slit diaphragm (small proteins/organic anions)

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15
Q

mesangial cells

A

in stalk of capillary tuft and vascular pole
pseudopods extend between glomerular endothelium and basement membrane to maintain membrane

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16
Q

proximal convoluted tubule

A

recovery of 80% of filtrate (water, ions, glucose, amino acids, small proteins)
active transport Na and Cl
water follows paracellularly
secretion of creatinine
simple cuboidal epithelium
well developed brush border
contains peptidase
endocytosis and pinocytosis

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17
Q

loop of henle (thin limbs)

A

simple squamous epithelium
close association w vasa recta

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18
Q

loop of henle (thick limbs)

A

simple cuboidal epithelium with many mitochondria
enters cortex and reaches macula densa
also called distal straight tubule

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19
Q

medulla sections

A

outer zone
innser zone
outer stripe
inner stripe

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20
Q

outer zone contains what

A

thick tubules and may have thin tubules

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21
Q

inner zone contains what

A

only thin tubules

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22
Q

outer stripe contains what

A

only thick tubules

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23
Q

inner stripe contains what

A

thick and thin tubules

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24
Q

distal tubule

A

proximal straight and distal convoluted seperated by macula densa
simple cuboidal epithelium with few short apical microvilli
active Na transport, reabsorb bicarbonate

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25
juxtraglomerular apparatus
macula densa cells juxtaglomerular granule cells extraglomerular mesangium (lacis cells)
26
macula densa cells
sense changes in glomerular pressure
27
juxtaglomerular granule cells
modified smooth muscle cells in afferent arteriole which produce renin bc drop in blood pressure or Na content of distal tubule
28
collecting ducts
distal convoluted tubule creates connecting tubule and several of those form collecting tubule which several form collecting duct collecting ducts merge in renal papilla to form papillary ducts to release urine into minor calyx
29
collecting tubule
found in cortex simple cuboidal epithelium
30
collecting duct
medulla simple columnar epithelium
31
collecting tubules and collecting ducts
principal cells express aquaporins in response to ADH intercalated disks help maintain pH by secreting H or HCO3
32
excretory passages
lined with transitional epithelium walls gradually thicken near bladder dome cells have lipid rafts with proteins called uroplakins resisting hypertonic urine
33
renal pelvis and ureters
transitional epithelium +lamina propria muscularis - inner longitudinal + outer circular layers + outer longitudinal near lower ureter adventitia
34
bladder
thick transitional epithelium detruser muscle (3 layers: longitudinal, circular, longitudinal) - pierced obliquely by ereters, circular layer thickens to form internal urinaryt sphincter adventitia
35
urethra
transitional epithelium near bladder becomes stratified squamous or pseudostratified columnar + elastic lamina propria muscularis - inner longitudinal and outer circular layers
36
renal functions
regulate water and electrolyte balance regulate systemic blood pressure and ECF volume excrete metabolic waste and foreign substances regulate RBC production regulate acid base balance regulate vitamin D production/calcium and phsophate balance gluconeogenesis
37
metabolic wastes
urea (from protein) uric acid (from nucleic acids) creatinine (from muscle) urobilin (end product of hemoglobin breakdown) other metabolites
38
erythropoietin
produced by peritubular fibroblasts in renal cortex in response to hypoxia stimulate RBC production in marrow CRF = diminished EPO secretion = anemia
39
1,25-dihydroxy-cholecalciferol
active form of vitamin D important for calcium balance
40
renin
converts angiotensinogen to angiotensin I
41
portal system
gomerular peritubular vasa recta
42
glomerular capillaries
high hydrostatic pressure rapid filtration
43
peritubular capillaries
low hydrostatic pressure fluid reabsorption
44
vasa recta
special term for peritubular capillaries in juxtamedullary nephrons
45
tubule structure
proximal tubule - reabsorption and secretion of solutes thin descending loop - high permeability to water ascending limb (thin) - impermeable to water, urea uptake, Na/Cl ascending limb (thick) - reabsorb solutes, Na/K/Cl early distal tubule - NaCl transporter late distal tubule/collecting duct - hormone regulated reabsorption and secretion
46
linear immunoflorescence
antiGBM antibodies
47
granular immunoflorescence
immune complex deposition
48
renal agenesis
kidneys dont form bilateral incompatible with life (often w oligohydraminos/potter sequence)
49
oligohydraminos/potter sequence
fetal compressions causes pulmonary hypoplasia, altered facies, positioning defects of feet and hands, breech presentation
50
renal hypoplasia
failure of kidneys to develop to normal size bilateral = early renal failure
51
ectopic kidneys
kidneys form in wrong location additional kidneys may develop small or normal sized ureteral obstruction can occur due to position
52
supernumeral kidney
mass of renal parenchyma with its own capsule, vessels, and collecting system
53
horseshoe kidneys
2 kidneys fuse 90% lower poles 10% upper poles
54
renal dysplasia
undifferentiated tubular structures surrounded by primitive mesenchyme abnormal metanephric differentiation
55
renal blood flow
all blood goes to cortex 5-10% of cortical blood goes to medulla before returning to general circulation Q = P/R
56
what happens to blood pressure through renal vasculature
it drops largest drop at areas of highest resistance (afferent and efferent arterioles)
57
glomerular filtration based on
molecular size (albumin) electrical charge (restrict anions)
58
normal glomerular filtration rate
100-125 ml/min
59
determinants of GFR
Kf x Pgc-Pbs-PIgc Kf = coefficient for hydraulic permeability x SA Pgc = hydrostatic pressure glomerular capillary Pbs = hydrostatic pressure bowmans space PIgc = oncotic pressure in glomerular capillary net filtration pressure = Pgc-Pbs-PIgc
60
constriction of afferent arterioles (sympathetic)
decreases GFR
61
constriction of efferent arterioles (angiotensin II)
increase GFR
62
intratubular pressure
decrease GFR
63
autoregulation maintains GFR
myogenic - afferent arterioles contract/relax in response to blood pressure tubuloglomerular feedback - convey info from tubule to glomerulus, mediated by macula densa (high flow and Na content send signal to decrease GFR)
64
renal clearance
substance is removed from the plasma and is excreted in urine or catabolized by renal tubules volume per time amount removed from plasma in given time = volume plasma cleared (Cx) x plasma conc (Px) amount appearing in urine = urine flow (V) x urine concentration (Ux) Cx x Px = V x Ux so Cx = V x (Ux/Px)
65
determinants of renal clearance
glomerular filtration tubule reabsorption tubule secretion
66
inulin to measure renal clearance
not usually found in body assess renal function filtered but not reabsorbed all that is filtered appears in urine measures GFR
67
renal clearance can be used to estimate
glomerular filtration rate renal blood flow renal plasma flow
68
renal clearance to estimate GFR
substance must be freely filtered substance cant be reabsorbed or secreted by renal tubules substance cant be synthesized, broken down, or accumulated by kidneys substance must be physiologically inert
69
clearance vs GFR
clearance = GFR : freely filtered, not reabsorbed, not secreted clearance > GFR : net tubular secretion clearance < GFR : net tubular reabsorption clearance = 0 : filtered and completely reabsorbed
70
creatinine clearance
most common indicator of kidney function freely filtered and not reabsorbed limitations: differences in skeletal muscle mass, small amount secreted
71
as GFR decreases
serum creatinine increases normal = 1 mg/dL > 1.5 suggest decreased GFR
72
renal clearance to estimate renal plasma flow
substance must not be synthesized, degraded, accumulate in tissues, only route into kidney is renal artery and only way out is renal vein or ureter, completely cleared in single pass use para-aminohippuric acid RPF = Cx = UxV/P
73
measure renal blood flow
renal plasma flow / (1-hematocrit)
74
urogenital system is derived from what
intermediate mesoderm
75
nephritic systems that develop from intermediate mesoderm
pronephros mesonephros metanephros
76
pronephros
4th week intermediate mesoderm condense into epithelial structures cranial to causal forms in cervical region and degenerate in a few days mesonephric duct forms around same time
77
mesonephros
mesonephric duct extends caudally and exits intermediate mesoderm where connects cloaca mesonephric duct induce formation of mesonephric tubules cranial and thoracic mesonephroi eventually degenerate
78
metanephros
uteric bud emerges from mesonephric duct near junction with the cloaca grows dorsally toward region in sacrum called metanephric blastema
79
major and minor calyces
metanephric blastema induce uteric bud to branch first round form major calyces second round form minor calyces last round form collecting ducts and tubules
80
nephron induction
tips of each branch of uteric bud induce mesenchyme of metanephric blastema to condense and form metanephric blastemal cap blastemal cap convert to epithelial tissue and become nephric vesicle nephric vesicel becomes tubule system blood vessels form into S shaped portion of tubule to form glomerulus
81
ascension of kidneys
lengthening of lumbar and sacral regions probably contributes original renal artery degenerates new arterial sprouts branch from aorta connecting to ascending kidney transient arteries may be maintained hilum starts ventral then rotates to medial
82
development of urinary bladder
cloaca = anorectal canal and urogenital sinus urorectal septum grows to separate them ureter (ureteric bud) and mesonephric duct se[arate amd ureter moves superior and mesonephric duct moves inferior allantois occluded to create urachus
83
formation of trigone
called exstrophy - mesonephric duct flares and becomes part of wall of bladder males - mesonephric duct becomes ductus defens and inferior part of urogenital sinus becomes urethra
84
male urethra
urethral folds pulled forward to form lateral walls of urethral groove epithelial lining derived from endoderm and forms urethral plate distal part or penile urethra formed from engrowth of surface ectoderm (glandular plate)
85
hypospadia
fusion of urethral folds incomplete
86
bifid ureter
ureteric bud branches prematurely before entering metanephric blastema
87
ectopic ureter
2 ureteric buds emerge from mesonephric duct and superior fuses with cloacal structure (not bladder)
88
fistulas
failure of urorectal septum to separate urogenital sinus and anorectal canal
89
urachas defect
failure to completely occlude urachus
90
exstrophy of bladder
lateral walls of embryo fail to fuse
91
renal agenesis
ureteric bud fails to develop
92
pre renal failure
anything that obstructs flow cardiac hypovolemia metabolic (hypothyroidism) vasoconstriction coagulation
93
intrarenal failure
direct damage to kidney proper from inflammation, toxins, drugs, infections, lack of flow glomerular (nephritic vs nephrotic) vascular tubular cystic interstitial
94
extra/post renal failure
prostatic hypertrophy/cancer urolithiasis adenopathy/lymphoma neurogenic bladder urethral stricture bladder stone at trigone
95
acute kidney injury
suspected when urine output falls or serum urea nitrogen or creatinine rise increase of serum creatinine > 0.3 mg/dL in 48 hours increase in serum creatinine >1.5 times baseline within prior 7 days urine volume < 0.5 mL/kg/hr for 6 hours abrupt or rapid decline in renal function
96
AKI stages
1. increase of serum creatinine > 0.3 mg/dL in 48 hours, increase in serum creatinine >1.5 times baseline within prior 7 days, urine volume < 0.5 mL/kg/hr for 6 hours 2. increase > 2 to 3 fold from baseline in serum creatinine, urine output < 0.5 mL/kg/hr for > 12 hrs 3. serum creatinine increase > 3 fold from baseline of > 4 mg per dL, urine output < 0.3 mL/kg/hr for 24 hours or anuria for 12 hours
97
AKI lab findings
progressive acidosis hyperkalemia hyponatremia anemia hyperphosphatemia hypocalcemia
98
chronic renal failure
loss of kidney function leads to build up of body fluid, body waste, electrolyte problems diabetes, HTN, glomerulonephritis, polycystic kidney disease, vesicoureteral reflux, recurrent kidney infection
99
creatinine clearance calculation
urine creatinine x volume of urine / plasma creatinine x 1440
100
factors increasing BUN
volume depletion gastrointestinal hemorrhage high protein diet catabolic states with tissue breakdown
101
factors decreasing BUN
low protein diet liver disease
102
fractional excretion of sodium (FeNa)
clearance of Na/clearance of Cr (UnaV/P)/(UcrV/Pcr) < 1% prerenal azotemia > 2% intrinsic azotemia or acute renal failure
103
azotemia
rise in serum BUN and serum creatinine
104
prerenal AKI
dehydration hypotension acute hemorrhage severe congestive heart failure hepatorenal syndrome renal artery obstruction blood supply to kidney diminishes
105
intrinsic AKI
glomeruli - post strep GN, SLE vessels - polyarteritis nodosa, scleroderma, hemolytic urea syndrome interstitium - acute allergic interstitial nephritis tubules - ATN, nephrotic drugs, myoglobinuria
106
urine sediment
postrenal - unremarkable prerenal - unremarkable intrinsic - granular casts, epithelial cells, WBC casts, RBC casts, broad waxy casts
107
acute tubular necrosis
phase 1 - lasts for 24 hours after primary insult, oliguria, increase BUN/creatinine/potassium phase 2 - blood shows increased BUN/creatinine/uric acid/potassium/phosphate and decreased pH/sodium/calcium, anemia, platelet dysfunction phase 3 - kidneys open up, urine output 10 liter/24 hours, urinary urea osmotic diuretic, hypokalemia/nitremia/magnesemia/hypotension
108
oligouric AKI
first eliminate obstruction then differentiate prerenal from intrinsic renal disease
109
tubulointerstitial diseases
affect interstitium of kidney and tubular epithelium 1. ischemic or toxic tubular injury 2. inflammatory (noninfectious)
110
acute tubular injury/necrosis
most common ischemia or toxic alterend intrarenal hemodynamics acute renal failure and morphologic evidence of tubular injury/necrosis focal and patchy epithelial necrosis obstruction of lumen by casts edema and leukocytes
111
ischemic vs toxic ATI
ischemic - patchy, short lengths of proximal tubule and ascending limb toxic - longer and more extensive areas of necrosis along proximal convoluted tubule
112
ATI clinical course
inititation - 36 hours with slight decline in urine output and rise in BUN maintenance - sustained oliguria, salt and water overload, rise in BUN, hyperkalemia, metabolic acidosis recovery - increase urine volume, hypokalemia
113
tubulointerstitial nephritis
inflammation of tubules and interstitium usually immune disorder drugs/toxins - papillary necrosis can occur urate - w chemo or hyperuricemia (nephrolithiasis in gout)
114
pyelonephritis
acute or chronic, caused by infection, obstruction of urinary tract predisposing factor inflammation affecting tubules, interstitium, and renal pelvis acture = bacterial infection chronic - infection with reflux or obstruction
115
acute pyelonephritis
acute suppurative inflammation with focal abcess tubules affected more than glomeruli papillary necrosis, pyonephrosis, perinephric abcess heals w scarring
116
chronic pyelonephritis
chronic inflammation and scarring of calyces and pelvis tubular atrophy, thyroidization of tubules may develop focal segmental glomerulosclerosis
117
atherosclerosis/atherosclerotic embolic tissues
involve aorta or renal arteries stenosis/occlusion and possibly infarction
118
granulomatosis with polyangiitis
necrotizing granulomas of upper respiratory tract/lungs/kidneys focal necrotizing often srescentic glomerulonephritis PR3-ANCA male>female, average age 40 untreated rapidly fatal
119
polyarteritis nodosa
small/medium arteries with segmental necrotizing inflammation transmural mixed inflammation with focal fibrinoid necrosis thrombosis can occur young adults, remitting relapsing course can have rapidly accelerating hypertension
120
chronic hypertension
can lead to nephrosclerosis in renal arterioles and small arteries intimal and medial thickening hyalinization due to extravasation of plasma proteins
121
nephrosclerosis
reduced size/mass of kidneys increased granularity of kidney surfaces secondary to scarring tubular atrophy/interstitial fibrosis collapse of glomerular BM/deposition of collagen in BS, fibrosis/sclerosis increased risk of chronic renal failure
122
malignant hypertension
rapidly rising and severe blood pressure fatal within 1-2 years superimposed on preexisting HTN/chronic renal disease more common in men and blacks small petechial hemorrhages on surface vascular damage leads to increased permeability of small vessels hyperplastic ateriosclerosis with onion skinning papilledema, retinal hemorrhages, encephalopathy, renal failure
123
renal atherosclerosis
affect renal arteries and cause sclerosis emboli can travel from plaques to renal vasculature
124
renal artery stenosis/fibromuscular dysplasia
unilateral renal stenosis in HTN HTN from renin secretion from kidney and production of angiotensin II commonly caused by atherosclerotic narrowing at origin of renal artery (especially in men w diabetes) can also have fibrous or fibromuscular thickening of intima
125
thrombotic microangiopathy
spectrum of syndromes from thrombotic thrombocytopenic purpura and hemolytic uremic syndrome diverse insults that lead to thrombi in capillaries or arterioles
126
HUS
excessive activation of platelets leading to thrombi deposition in capillaries/arterioles consumption thrombocytopenia or microvascular occlusion typical - foods contaminated with bacteria atypical - inherited mutations of complement regulatory proteins or diverse causes of endothelial injury infectious often have diarrhea or flu like symptoms most recover w dialysis
127
TTP
secondary to inherited deficiencies of ADAMTS13 (metqalloprotease that regulates von willebrand factor most common is inhibitory autoantibodies in women initiating event is platelet aggregation usually present w fever, neuro symptoms, microangiopathic hemolytic anemia, renal failure treated with plasma exchange
128
renal infarction/cortical ischemia
infarction commonly due to embolism but can be from advanced atherosclerosis and polyarteritis nodosa infarcts typically coagulative necrosis infarcts can be silent
129
diffuse cortical necrosis
obstetric emergencies or any hypovolemic or endotoxic shock glomerular and microthrombi sudden anuria and rapid death patchy significantly diminished renal arterial perfusion due to vascular spasm and microvascular injury
130
sickle cell disease
renal manifestations include hematuria and decreased concentrating secondary to sickling in the hypertonic and hypoxic renal medulla patchy papillary necrosis proteinuria in 30%
131
papillary necrosis
focal coagulative necrosis
132
eclampsia/preeclampsia
antiangiogenic substances secreted by placenta cause maternal endothelial swelling hypertension and proteinuria convulsions = eclampsia mild to moderate = bedrest and hypertensives severe = immediate delivery usually resolve 1-2 weeks following delivery
133
glomerulus pathology
located in kidney cortex often affected by immune processes or antibody mediated processes disorders primary, systemic, or hereditary
134
glomerular hypercellularity
increase number of cells proliferation of mesangial or endothelial cells leukocytes formation of crescents (epithelial cells, leukocytes, plasma proteins) which occurs with severe glomerular injury
135
glomerular basement membrane thickening
secondary to deposition of electron dense materials like immune complexes/fibrin/amyloid (focal) diffuse = increased synthesis of BM proteins (diabetic glomerulosclerosis) additional layers of BM matrices
136
glomerular hyalinosis
deposition of plasma proteins onto glomerulus eosinophilic material obliterate capillary lumens consequence of endothelial or capillary wall injury
137
glomerular sclerosis
deposition of collagen onto glomerulus can obliterate capillary lumens global sclerosis in end stage kidney disease confined to mesangial areas, capillary loops, or both
138
distributions of histopathology
diffues = all glomeruli affected focal = only involves fraction of glomeruli global = involves entire glomerulus segmental = affects only part of glomerulus
139
staining patterns
granular favors deposition of immune complexes (can be subendothelial, subepithelial, or mesangium) linear favors anitbodies vs BM
140
other glomerular disease mechanisms
unregulated activation of complement (glomerulonephritic conditions) recruited or intrinsic cells (recruitment of WBCs and platelets) podocyte injury (loss of permeability barrier) loss of nephroms (glomerulosclerosis and eventually global sclerosis)
141
mediators in glomerular diseases
cells: neutrophiils/monocytes, macrophages/T cells, platelets, resident glomerular cells (mesangial cells) soluble: complement activaiton, chemokines and cytokines, coagulation system
142
epithelial injury
podocyte injury = focal/segmental glomerulosclerosis, diabetic nephropathy induced by: antibodies to podocytes antigens, toxins, infections, circulating factors
143
progressive renal damage
focal segmental glomerulosclerosis: lead to proteinuria and increased functional impairment tubulointerstitial fibrosis: tubular damage and interstitial inflammation secondary to ischemia/inflammation/loss of blood supply, and proteinuria
144
tubular transport
passive: simple diffusion, facilitated diffusion active: primary active, secondary active (cotransport, countertransport) receptor mediated endocytosis/transcytosis
145
facilitated diffusion
carrier mediated has saturation (Vmax)
146
limits on rate of transport
tubular maximum limited system - max saturation where transport cannot increase further even if concentration rises gradient limited - transport depends on electrochemical gradient or concentration, not carrier saturation
147
osmosis
kidney reabsorbs solutes from lumen to interstitium to allow water to follow
148
reabsorption
glucose 100% creatinine 0% bicarb/sodium/chloride 99% potassium 87% urea 50%
149
sodium balance
Na nearly half total solute load in glomerular filtrate Na sets up osmotic gradient for water maintain ECF by regulating Na in urine Na can be lost via sweat or diarrhea reabsorbed in prox tubule, ascending limb, distal convoluted tubule, collecting duct (everywhere but descending limb)
150
water reabsorbed where
proximal tubule descending limb of loop of henle collecting duct system
151
sodium and water
1. Na-K-ATPase extrusion of Na across basolateral membrane 2. passive entrance of Na from lumen into cell via sodium proton antiporter 3. anions (Cl and HCO3) from lumen to interstitium to maintain electronutrality 4. osmotic flow H2O from lumen to interstitium 5. bulk flow water and salt from interstitium into peritubular capillaries
152
sodium in proximal tubule
Na from lumen to prox tubule by -antiport with protons (lumen to cell) -HCO3/Na symport (cell to interstitium) -organic nutrients symport (lumen to cell) -Na/K/ATPase (Na cell to interstitium, K interstitium to cell) favors reabsorption of water
153
sodium in thick ascending limb
Na/K/2CL co transport (lumen to cell) Na/K pump (Na cell to interstitium, K interstitium to cell) K channel (cell to lumen) create positive lumen potential positive lumen potential causes Ca and Mg reabsorption paracellularly basolateral CaSR sensitive to Ca suppress cAMP and Na/K/2Cl to reduce positive lumen potential and reabsorption of Ca (high plasma Ca increases CaSR activity)
154
sodium in distal convoluted tubule
impermeable to water Na/Cl cotransport (lumen to cell) site for thiazide diuretics Na/K pump (Na cell to interstitium, K interstitium to cell)
155
collecting ducts
principal cells -apical: ENaC (regulated by aldosterone, blocked by amiloride) so Na lumen to cell -aquaporins (regulated by ADH) negative lumen potential cause K secretion Na/K pump (Na cell to interstitium, K interstitium to cell)
156
potassium
most abundant intracellular cation concentration tightly regulated (3.6 to 5.2 mM) changes in extracellular K cause problems in excitation and contraction (skeletal and cardiac muscle) dietary: GI absorb K (first line of defense - most ingested K immediately moved into cells to keep plasma K low) K enters ECF in damaged tissues kidneys excrete excess K
157
factors altering K distribution
insulin stimulates cellular K uptake through activation NaKATPase aldosterone increases cellular uptake of K by cells acid base abnormalities: H/K exchange in cells so acidosis causes hyperkalemia, H/K/ATPase cell lysis - increase extracellular K strenuous exercise - cause hyperkalemia by releaseing K from skeletal muscle increased ECF osmolarity - K from cells to ECF
158
K in proximal tubule
1. paracellular reabsorption (lumen to interstitium) - fluid absorption drags potassium with it 2. Na/K/ATPase (Na cell to interstitium, K interstitium to cell) 3. passive flux from cell to interstitium through channel bc gradient
159
K in thick ascending
1. Na/K/2Cl cotransport reabsorption 2. K passive flux cell to lumen by passive flux 3. Na/K/ATPase 4. K reabsorbed by paracellular route driven by electrochemical gradient (lumen to interstitium)
160
K in distal tubule/collecting tubule
depends on dietary intake reabsorbed by H/K/ATPase (low K diet) secreted by principal cells (depend on dietary K, aldosterone, acid base, urine flow rate)
161
distal K secretion and reabsorption mechanism
reabsorption: H/K antiporter, Na/K/2Cl secretion: ROMK, BK
162
dietary input
conserving K (low K) - ROMK closed, BK closed, no secretion K normal - ROMK secrete K, BK closed high K diet - ROMK maximized, BK open, excretion of K high
163
factors changing K secretioone
aldosterone - increase K secretion (increase Na/K/ATPase, increase ROMK) hyperaldosteronism = increase K secretion hypoaldosteronism = decrease K secretion acid base - acidosis decrease K secretion, alkalosis increse K secretion diuretics - increase Na in lumen so increase K secretion, causing hypokalemia
164
nephritic syndrome
hematuria, diminished GFR, mild to moderate proteinuria, hypertension progressive GN - progressive loss of renal function, oligura with death within weeks to months, crescents low levels compliment - postinfectious glomerulonephritis, SLE, bacterial endocarditis normal complement level - IgA nephropathy, idiopathic rapidly progressing glomerulonephritis, anti-GBM
165
nephrotic syndrome
heavy proteinuria, hypoalbuminemia, edema, HLD, lipiduria
166
nephritic diseases
post streptococcal IgA nephropathy hereditary nephropathy anti-GBM antibody mediated crescentic GN (goodpastures) membranoproliferative GN dense deposit disease
167
post strep GN
1-4 weeks post strep infection in situ immune complexes against group A strep antigen subendothelial then migrate across GBM and reform granular staining of IgG and compliment in capillary walls and mesangium RBC and red cell casts in urine, periorbital edema, proteinuria, HTN
168
IgA nephropathy
hematuria within 1-2 days of URI most maintain normal renal function IgA mesangial deposition henoch-schoenlein purpura (IgA nephropathy with prupuric lesions)
169
hereditary nephritis
mutation in genes encoding GBM collagen age 5-20 years - hematuria, renal failure at 20-50 GBM has alternating and irregular areas of thickening and thinning, often splitting lamination of lamina densa making basket weave appearance
170
mambranoproliferative glomerulonephritis
nephrotic and nephritic components immune complex deposition with activation of complement large hypercellular glomeruli that appear lobulated double contour/tram track appearance of BM
171
dense deposit disease
excesssive activation of alternative complement path C3 convertase stabilized enhansing C3 activation and sonsumption intramembranous deposition of ribbon like material in GBM
172
anti GBM crescentic GN (goodpastures)
autoimmune antibodies against GBM and lung BM pulmonary hemorrhage and progressive glomerulonephritis oliguria and azotemia glomeruli can show segmental GBM necrosis and fibrin deposition in bowmans space crescent formation
173
chronic glomerulonephritis
end stage glomerular disease cortex is thinned with obliteration of glomeruli with fibrous tissue HTN develops with secondary arterial/arteriolar sclerosis
174
SLE
immune complexes subendothelial, mesangial, or subendothelial nephritis common class III = focal (subendothelial) fewer than 50% of glomeruli class IV = diffuse (most common and most severe) more than 50% of glomeruli
175
vasculitis
polyarteritis nodosa = nephritic syndrome granulomatosis with polyangitis = focal and segmental necrotizing GN or crescentic GN churg strauss = renal manifestations
176
glucose
completely reabsorbed at proximal tubule sodium glucose transporter (lumen to cell) GLUT uniporter (cell to interstitium) at 375 mg/min all transporters saturated causing glucosuria (diabetes)
177
protein transport
glomerular filtration barrier prevents filtration of large proteins proximal tubule receptor mediated endocytosis for smaller proteins
178
uric acid/urate transport
reabsorbed but also secreted volume depletion increases urate reabsorption which increases plasma levels (gout) 40% filtered load excreted recycling urea helps maintain interstitial medullary hyperosmotic environment low urine flow rate - greater reabsorption high urine flow rate - less reabsorption
179
calcium in proximal tubule
reabsorbed via paracellular route high NaCl diet decreases Na and H2O absorption and increase urinary Ca excretion (increase kidney stones)
180
calcium in thick ascending limb
reabsorbed paracellularly bc positive lumen potential
181
loop diuretics
decrease positive lumen potential so increase Ca ecretion
182
thiazide diuretics
increase Ca reabsorption
183
calcium in distal convoluted tubule
PTH regulates Ca absorption Ca cell to interstitium by Ca/H/ATPase and Na/Ca exchanger
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Mg reabsorption
most in thick ascending limb claudin 16 necessary for paracellular transport
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phosphate reabsorption
proximal tubule Na/phosphate cotransport (2 Na and 1 phosphate) PTH inhibits phosphate reabsorption
186
FGF23
increase phosphate excretion and decrease renal production of vitamin D
187
chloride transport
early proximat tubule - mainly paracellular bc negative lumen potential late proximal tubule - mainly transcellular by exchange of Cl for anions basolateral exit - Cl channels and K/Cl transporter thick ascending limb - all Cl reabsorption transcellular by Na/K/2Cl distal convoluted tubule - apical reabsorption by Na/Cl transporter, basolateral exit Cl channels collecting tubule - Cl reabsorption by Cl/HCO3 exchanger
188
nephrotic disease
massive proteinuria hypoalbuminemia generalized edema hyperlipidemia and lipiduria
189
focal segmental glomerulosclerosis
podocyte disorder, higher percentage progression to CKD associated w HIV, heroine use, reduced renal mass have HTN, microscopic hematuria, azotemia poor response to corticosteroids genes that encode podocytes and nephrin involved primary and secondary forms hyalinosis and sclerosis (increased matrix, collapse of capillary loops, deposition plasma proteins)
189
minimal change disease
children, loss of podocyte foot processes, excellent prognosis likely immunological good renal function dramatic response to corticosteroids
190
membranous nephropathy
diffuse thickening of BM, prominent immune complexes, spikes of BM between complexes, variable course diffuse thickening of capillary walls bc deposits of immunoglobulings primary and secondary forms inflammatory response cause C5b-C9 membrane attack complex mainly IgG4 deposits hematuria and HTN present progress to sclerosis of glomeruli, rise in creatinine, development of HTN
191
diabetic nephropathy
major cause of renal disease/nephrotic and CKD, BM thickening, mesangial involvement/glomerulosclerosis leading cause of end stage renal disease capillary BM thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis w deposition of PAS staining nodules in mesangial core pyelonephritis common
192
amyloidosis
renal deposition of amyloid, apple green birefringent polarized light inherited and inflammatory conditions with deposition of fibrillary proteins causing tissue damage and functional compromise kidiney can be shrunken
193
chronic kidney disease
progressive nephron loss alterations in function of remaining intact nephrons (become maladaptive and cause scarring) can be insidious and asymptomatic chronic renal failure = stages 3-5 (GFR < 60 mL/min for at least 3 months and/or persistent albuminuria)
194
end stage renal disease
accumulation of toxins, fluids, electrolytes cause uremic syndrome
195
autosomal dominant adult polycycstic disease
autosomal dominant with high penetrance (both alleles have to be nonfunctional for development of disease) PDK1/2 (polycystin) gene multiple cysts filled w fluid, can enlarge and cause pressure on calyces or pelvis epithelium can proliferate and encroach into tubular lumen can have liver cysts
196
autosomal recessive childhood polycystic kidney disease
rare mutations in PKHD1 gene (fibrocystin) numerous small cysts make spongelike appearance bilateral cylindrical or saccular dilation of collecting tubules liver cysts and portal fibrosis
197
medullary sponge kidney
multiple cystic dilations of collecting ducts to medulla discovered incidentally papillary ducts dilated and small cysts may be present
198
nephronophthisis and adult onset medullary cystic disease
variable number of cysts in medulla often concentrated at corticomedullary junction children have polyuria and polydipsia adult onset seperate disease and may be associated with hyperuricemia and gout genes : NPHP1-11 (nephrocystins), JBTS 2/3/9/11 (juvenile form), MCKD1/2 (adult onset) cysts lined with flattened or cuboidal epithelium
199
multicystic renal dysplasia
sporadic unilateral or bilateral flattened epithelium lines cysts w island of undifferentiated mesenchyme unilateral good prognosis bilateral often cause renal failure
200
acquired (dialysis) cystic disease
numerous cortical and medullary renal cysts likely from obstructed tubules by interstitial fibrosis
201
simple cysts
single or multiple 1-5 cm usually walls smooth and glistening, may have clear fluid usually no clinical findings
202
types of dialysis
hemodialysis peritoneal dialysis compassionate dialysis
203
absolute indications for dialysis
volume overload hyperkalemia acidosis encephalopathy pericarditis toxicology "AEIOU" acidosis, electrolytes (hyperkalemia), intoxication, overload, uremic pericarditis
204
relative indications for dialysis
uremia, fatigue, anorexia, N/V, dysgeusia, pruritis, FTT
205
CRF stages
1 - 90 or higher w signs of kidney damage 2 - 60-89 mild kidney damage 3a - 45-59 mild to moderate loss of kidney function 3b - 30-44 severe loss of renal function 4 - 15-29 severe loss of renal function 5 ESRD - 10 or less meaning dialysis or TP needed soon
206
direct access rule of 6's
6 weeks after implantation vein diameter at least 6 mm depth of no more than 6 mm 600 ml/min
207
complications of hemodialysis
hypotension #1 sepsis thrombosis worsening vascular disease malnutrition hemorrhage/bleeding anaphylactoid reaction disequilibrium
208
complications of peritoneal dialysis
peritonitis sepsis hyperglycemia hypoproteinemia obesity dialysis related amyloidosis
209
measurement of renal function
cochcroft gault equation estimates creatinine clearnace modification of diet in renal disease estimates GFR
210
screening for CKD
not recommended unless risk factors
211
aging
after age 30 GFR has linear rate of decline loss of muscle mass with age makes creatinine an unreliable measure of kidney function
212
definitions
chronic renal insufficiency - GFR 30-70 (stage 1-3) chronic renal failure - GFR < 30 (stage 4) end stage renal disease - GFR < 10 uremia (stage 5)
213
uremic syndrome
GFR < 10 ml/min affects every organ system urea - fatigue, N/V, headaches breakdown products - carbamylation of lipoproteins and peptides high level of parathyroid hormone uremic frost with high BUN excreting urea through sweat glands
214
uremia clinical manifestations
secondary hyperparathyroidism phosphate retention hypocalcemia low serum calcitrol (vitamin D) levels renal osteodystrophy (rickets, osteomalacia, osteoporosis) left ventricular hypertrophy metallic taste and anorexia normochromic normocytic anemia hyperkalemia metabolic acidosis fluid overload immune defects uremic hue (yellow skin) fingernail changes
215
chronic kidney disease treatment
treat manifestations strict blood pressure control (140-160/80-90), ACEi, control glucose, dietary protein restriction, treat hyperlipidemia to slow progression dialysis/transplant
ACOM
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