Renal

Front 1

EXCRETION EQUATION

Back 1

U[SUBST] x V (URINE FLOW RATE)

Front 2

FILTRATION EQUATION

Back 2

P[SUBST] X GFR

Front 3

Inulin

Back 3

since 100% of inulin is filtered and excreted, you can calculate clearance and use this as an estimate for GFR

Front 4

PAH

Back 4

If you infuse a small amount so that it is completely excreted, you can measure P[pah], U[pah] and V and calculate for clearance which can be estimated as renal plasma flow (RBF = RPF/1-Hct)

Front 5

RPF vs. RBF

Back 5

RBF = RPF/1-Hct

Front 6

minimal change disease

Back 6

children with nephrotic syndrome, normocomplement, freq follows URI, steriods highly effective, oval fat bodies, obliteration of foot processes, dysfunction of T-cells

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focal segmental glomeulosclerosis

Back 7

often nephrotic syndrome, adults with HTN, hematuria, idiopathic, HIV, heroin; obliteration of foot processes; starts with juxtameullary glomeruli and is segmental sclerosis; no BM changes; can see IgM and C3 but not complexed; caused by some circulating immune factor (not Ig)

Front 8

membranous glomerulopathy

Back 8

primary cause of nephrotic syndrome in adults, thickend CAP and BM, subepithelial deposits, BM trys to encompass the deposits and creates spike appearance, granualar IF (immune complex); assoc with Hep B but many other things too; may cause renal thrmobsis

Front 9

diabetic glomerulosclerosis

Back 9

often have nephrotic syndrome, HTN and retinopathy; BM thickens, increase in mesangial matrix, hyaline droplets and capsular drop, simulataneous involvement of A and E arteriole,

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renal amyloidosis

Back 10

often have nephrotic syndrome, adults, diagnosis by fat pad or rectal biopsy NOT renal, can see amyloid in all parts, initially in mesangium

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nephritic syndrome

Back 11

hematuria, dysmorphic RBCs and casts in urine, some degree of oliguria and azotemia and HTN, less severe proteinemia and edema can be present

Front 12

membranoproliferative GN type I

Back 12

50% have hypocomplement, diffuse proliferative (mainly mesangium) with CAP wall thickening and increased matrix; Tram track, older children and young adults,HEP C associated, common after URI, can cause nephritic sediment, circulating immune complexes

Front 13

lupus nephritis

Back 13

can have proteinuria and/or hematuria, variety of changes dependent on severity, can have mesangial, subendo and CAP deposits of Ig's of all types, some hypercellularity, hypocomplement, circulting immune complexes, granular on IF

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membranoproliferative GN type II

Back 14

RARE, older children, have persistant hypocomplementemia, worm like electron dense deposits

Front 15

IgA nephropathy (Berger)

Back 15

most common form of GN, seen in older children and young adults, hematuria, often have URI or GII at same time, normocomplement, localization of IgA to mesangium and subendothelium, circulating complexes,

Front 16

post-infection GN

Back 16

most common form of GN in younger kids, 2-4 weeks following pharyngeal or skin infection of Group A b-hemolytic strep, nephritic, HTN, edema, hypocomplement (eventually returns to normal); diffuse hypercellularity due to influx of inflammatory cells, cresents can occur, subepithelial humps due to deposition, granular, immune complex

Front 17

anti-GBM

Back 17

cresentic GN, can also have pulmonary involvement (Goodpastures), rapid onset, adults, nephritic, normocomplement, linear staining of GBM in IF, fibrin in the capsule causes irritation which induces macrophages, younger men and older women

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autosomal recessive PKD

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associated also with cystic disease of the liver (can have portal HTN), RARE, poor prognosis, bilaterally enlarged nulticystic kidneys, cysts are all same size

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adult ADPKD

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dominant, associated with congenital cerebral aneurysms, often develop HTN or CRF, cysts not present at birth, cysts vary in size

Front 20

pelvic nerve

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parasympathetics, required for detrusor contraction; efferent limb of sacral arch reflex

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pudendal nerve

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sensation of bladder fullness, urge to void; afferent limb of sacral arch

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paracellular

Back 22

around cells

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transcellular

Back 23

through cells

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AQP 1

Back 24

located in PT and descending loop of henle (apical and basolateral), not influenced by hormones

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AQP 2

Back 25

located on the apical side of the collecting duct, regulated by ADH and ANP

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AQP 3 and AQP 4

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located in the basolateral membrane of the collecting duct

Front 27

GFR

Back 27

120 mL/min

Front 28

RBF and RPF

Back 28

RBF is 1100 ml/min
RPF is 600 ml/min

Front 29

Regulation of ECF volume

Back 29

regulated by Na reabsorption and thirst (RAA)

Front 30

regulation of osmolality

Back 30

varying water intake (thirst) and output (ADH)

Front 31

ADH

Back 31

primary regulator of renal concentration and dilution mechanisms, an increase in Posm stimulates secretion of ADH, made in neuroendocrine cells in hypothalamus but secreted from the pituitary; high ADH causes small amoun of concentrated urine; critical blood loss can also causes ADH secretion to retain volume, prevent fall in BP and minimize fall in perfusion pressure

Front 32

renal targets of ADH (2)

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cortical and medullary collecting ducts

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V1 ADH receptor

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low affinity, only when ADH levels are extremely high (hemorrhage), located in SM cells, cause vasoconstriction to maintain perfusion

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V2 ADH receptor

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high affinity receptor in cortical and medullary collecting ducts, respond to even small levels of ADH; stimulate adenylate cyclase which increases cAMP which allows movement of microtubules to put AQP 2 in the membrane to allow water reabsorption

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ADH and urea

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incr in ADH causes an incr in urea permeability which helps to create a stronger medullary gradient needed to produce concentrated urine

Front 36

thirst

Back 36

stimulated by hyperosmolality, Ang II also stimulates thirst, Na gastric loading also increases thirst even before there is any incr in systemic Posm

Front 37

renin

Back 37

secreted by the granular cells in the JG apparatus in response to low afferent arterial pressure (low volume or low Na) or increased sympathetic activation; involved in the creation of Ang II, stored in JG cells and released in response to decr [Ca] or incr cAMP

Front 38

Ang II (5)

Back 38

requires renin and ACE to be present,
1- directly incr tubule NaCl and NaHCO3 reab in the PT
2- incr aldo production (which incr NaCl reabsor and K+/H+ secretion in DT and CD)
3- systemic vasoconstriction
4-preferential constricition of efferent arterioles which decr RBF but helps maintain GFR, also incr filtration fraction which allows incr Na reabsorp in PT
5- stimulates thirst

Front 39

symp nerve activation in kidney

Back 39

stimulate granular cells to secrete renin, also cause afferent arteriole constriction and decr RBF

Front 40

granular cells

Back 40

produce renin, respond to symp activity as well as they are their own receptors who sense changes in afferent arteriole pressure

Front 41

macula densa

Back 41

located at the end of the TALH, measures the amoun of NaCl here; if NaCl delivery is high, renin secr decr; if NaCl delivery is low, renin secr incr

Front 42

homogeneous nucleation of stones

Back 42

due to supersaturation of the solute, there is then spontaneous nucleation and crystal growth can occur

Front 43

heterogeneous nucleation of stones

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major mechanism; small crystal of one type (which may normally form and quickly dissapate), this then serves as a nidus on whih another compound can precipitate

Front 44

acidic urine precipitates which types of stones (2)

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uric acid and cystine

Front 45

alkalaine urine precipitates which types of stones (2)

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calcium and struvite

Front 46

crystalization inhibitors (3)

Back 46

Mg, citrate, pyrophosphates

Front 47

Ca stones

Back 47

70-90% of stones, majority are Ca oxalate, are radiodense, precip in alkali urine

Front 48

causes of hyperoxaluria (2)

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excessive urinary excretion due to overproduction (excessive asorbic acid or inherited metabolism disorder) OR intestinal oxalate hyperabsorption (seen in patients with fat malabsorption)

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uric acid stones

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10% of stones, radiolucent, can be associated with gout, hereditary conditions, over production of uric acid or drugs, also dehydration; precipitate with acidic urine

Front 50

drugs that cause hyperuricosuric states (2)

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probenicid and sulfinpyrazone

Front 51

struvite stones

Back 51

magnesium ammonium phosphate, radiodense, form in the presence of urea-splitting organsisms (Proteus), common in women, precipitate in alkalai urine

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cystine stones

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very small %, radiodense, associted with rare inherited condition, cystine doesn't get absorbed and there is high concentrations, hexagonal, rxt with nitroprusside

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nephrocalcinosis

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calcifications formed and retained in renal papilla or tubules, RTA and medullary sponge cause this

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principal light cells

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located in CD, dominant cell, responsible for NaCl reabsorption and adjustments in H20, single motile cilium

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dark cells

Back 55

in CD, function in acid base balance

Front 56

where is ECF volume sensed (2)

Back 56

stretch receptors in the great veins and the atria

Front 57

pathways to mediate renin release (4)

Back 57

1- myogenic: baroreceptors in afferent arterioles
2- decr NaCL sensed in MD Na-K-2Cl channels
3- neurogenic: decr extrarenal baroreceptor stretch causes incr symp tone which incr renin release
4- high glucose levels

Front 58

aldo (created, stimulation for secretion)

Back 58

mineralcorticoid from adrenal gland, too lipid soluble to store so it is made on demand; release is stimulated by Ang II, hyperkalcemia, ACTH; inhibited by ANP; binds receptor, moves into nucleus, alters transcription

Front 59

aldo actions

Back 59

Fast: activate ENaC channels in CT to increase Na movement
Slower: increases # of NaCl cotransporters in DT, increases # of ENaC channels and Na/K ATPases in CD
In the process, you also incr K and H secretion

Front 60

11B-OH dehydrogenase

Back 60

present in aldo targets, metabolizes glucocorticoids (which are present in extremely high levels and can bind mineralcorticoid receptors) to prevent the GCs from binding; licorice blocks this enzyme and you can be born with a mutation in it (pseudo-hyperaldostosteronism)

Front 61

ANP

Back 61

made and stored in atria, released in response to incr cell Ca; inhibits inner medullary CD NaCl reabsorption, inhibits renin release, inhibits ADH secretion, vasodilatio

Front 62

effects of diuretics that act prior to the cortical CD on K and H

Back 62

incr secretion of K and H (wasting)

Front 63

effect of diuretics that act at the cortical CD on K and H

Back 63

inhibit electrogenic Na reabsorption and thus inhibit secretion of K and H

Front 64

osmotic diuretics

Back 64

mannoito; act on PT, filtered but not reabsorbed, decr urinary concentrating ability because they wash out gradient in medulla; TGF and distal compensation limit diuresis; also inhibit free H20 reabsorption in IMCD thus causing hypernatremia; can also cause hypokalemia

Front 65

carbonic anhydrase inhibitors

Back 65

act on PT, natiuretic but is limited by TGF and distal compensation, by blocking CA, you inhibit HCO3 creation in lumen as well as H+ in cell, this causes a wasting of HCO3 and also, due to decr H, there is less Na/H pump activity so Na reabs is inhibited; side effects: bicarburia, metabolic acidosis, hypokalemia

Front 66

thiazide diuretics

Back 66

act on Na/Cl cotransporter in DT, only provides weak diuresis so better in combo with loops because thiazides block compensatory mechs (Ang II, NE, aldo); because they act in the cortex (the diluting sement where there is no water permeability), they inhibit the kidney's diluting ability (can cause hyponatremia) but since they have no effect in the medulla, they can still concentrate urine; can cause hypokalemia, metabolic alkylosis (due to incr H+ secretion), decre Ca excretion(because of decr ECV) and incr Mg excretion

Front 67

loop diuretics

Back 67

block the Na/K/2Cl transporter in the TALH which inhibits TGF; impair both concentrating and diluting ability (Na reabsorption in TALH usually serves to both dilute the tubular fluid and provide concentrating gradient, both of which are now blocked); hypokalemia, metabolic alkylosis, incr in Ca and Mg secretion (normally the recycling of K+ causes lumen of TALH to be + which allows Ca and Mg reabsor but this is blocked)

Front 68

PTH

Back 68

stimulates bone resorption of Ca and Pi, stimulates renal tubule reabsorption of Ca and inhibits renal reabsorption of Pi so incr in Ca, decr in Pi; stimulated by low Ca or high Pi

Front 69

1,25 D

Back 69

active form of Vit D, part of its metabolism to active form occurs in the kidney so patients with RF have decr amounts; stimulated gut absorption of Ca and Pi, incr in both

Front 70

calcitonin

Back 70

inhibits bone resorption of Ca and Pi

Front 71

Ca reabsorption

Back 71

only 50% is not bound and most of this is filtered and reabsorbed, most is passive paracellular transport with the driving force being water transport; also in the TALH there is passive paracellular transport with the driving force the + lumen voltage created by K recycling; finally in DT it can be actively and transcellularly moved via the basolateral Ca/H ATPase and Na/Ca antiporter which create a gradient to allow Ca to move into the cell from the lumen, these are upregulated by PTH

Front 72

CaSR

Back 72

Ca receptor on BL side in TALH which is activated in high Ca, it inhibits the Na/K/Cl transporter which ruins the lumen + gradient required to move Ca so you get Ca excretion

Front 73

Pi reabsorption

Back 73

most of the movement is transcellular in the PT with the Na/K being the driving force, limited amount of Pi transporters; PTH causes endocytosis of the apical transporter which increases its secretion

Front 74

chronic renal disease and bone disease

Back 74

a decr in GFR causes and incr in Pi and a decr in Ca which both incr PTH and can cause bone disease

Front 75

hypernatremia general causes (2)

Back 75

free water loss from kidney (DI, osmotic diuresis) or free water loss from extrarenal sources (diarrhea, insesible losses)

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body reaction to hypernatermia

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acutely shift fluid from ICF to ECF which can have neurological symptoms, chronically the brain adapts by generating osmolytes

Front 77

history in hypernatremia

Back 77

ask about lack of fluid intake, polyuria, polydipsia, dirrhea, volume status; look at urine concentration next

Front 78

hyponatremia evaluation

Back 78

first look at plasma osmololity; if hypoosmolar then look at volume status

Front 79

treatment of chronic hypernatremia

Back 79

since brain has adapted with creation of osmoles, need to determine the free water deficit and then replace it slowly

Front 80

treatment for SIDH

Back 80

water restiction initially; if needed use hypertonic saline or ADH antagonist

Front 81

osmotic demyelination syndrome

Back 81

can occur if you treat hyponatermia too quickly, irreversible

Front 82

HCO3 transporters in PT and CT

Back 82

PT: 3HCO3/Na
CT: HCO3/Cl antiporter

Front 83

H+ secretion involved in HCO3 reabsorption in PT and CT

Back 83

PT: Na/H exchanger
CT: H-ATPase and H/K ATPase

Front 84

aminogensis

Back 84

gluaminase is an enzyme in the mitochondria of PT cells, convert glutamine to NH4 and a-KG, a-KG is then converted to glucose and creates HCO3-; gets ramped up in acidotic states via incr gene expression and mRNA stability; allows you to absorb a HCO3 without secretin H+; secrete NH4 instead

Front 85

b-intercalated cells

Back 85

in the CT, during chronic metabolic alkylosis, they are active; they have a H-ATPase on BL side and a Cl/HCO3 exchanger on the apical side, these allow us to secrete alkaline urine

Front 86

hyperkalemia and acid base status

Back 86

incr K in cell leads to a decr H+ in the cell, this makes the driving force for H secretion low and thus, less H is secreted and metabolic acidosis can occur

Front 87

hypokalemia and acid base status

Back 87

decr K in the cells causes a incr in H in cells which incr the driving force so you get incr H secretion and can develop metabolic alkylosis

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causes of polyuria

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increased intake (thirst due to incr Posm, habit, psychiatric disorder) or incr output (DI)

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symptoms of CDI

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sudden onset, large urine output, nocturia

Front 90

symptoms of NDI

Back 90

variable onset, moderate urine output, no nocture due to decr GFR at night

Front 91

isotonic or hypertonic polyuria

Back 91

think osmotic diuresis (glucose, mannitol, IV contrast)

Front 92

hypotonic polyuria

Back 92

think DI or psychogenic olydipsia

Front 93

catecholamines and insulin in K regulation

Back 93

when there is an incr in ECF K+, both of these increases the Na/K pump which moves the K back into cells which can then eventually be secreted in urine

Front 94

reabs/secr of K

Back 94

PT: passive reab, invariant to diet, proportional to Na
TALH: reab via Na/K/2Cl but most is just recycled, invariant with diet
CD: K transport depends on diet (main site of regulation); normal diet causes secretion, high K diet incr secretion even more, low K diet causes reabsorption

Front 95

secretion of K in CD

Back 95

via principal cells via ROMK channels, concentration gradient favors it

Front 96

reabsorption of K in CD

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occurs in intercalated cells during hypokalemia, is active because electochemical gradient favors secretion; occurs via apical H/K ATPases

Front 97

Bartters disease

Back 97

mutation in NaK2Cl or apical K channels in TALH, incr flow to CT and then leads to incr K and H secretion; also can cause hypotension

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Gitelmans disease

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loss of function of NaCl transporter in DT; incr flow to CT which incr excretion of K and H; can also cause hypotension

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pseudohypoaldosteronism

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mutation which leads to inactivation of ENaC channels; can cayse hypotension, hyperkalemia and acidosis

Front 100

Liddle's syndrome

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mutation in ENaC so it stays on, excess Na reabsorption in CT, causes HTN and hypokalemia

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2 causes of RAS and major side effect

Back 101

Atherosclerosis and Fibromuscular dysplasia; HTN

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causes of NDI

Back 102

Lithium, hypercalcemia, hypokalemia

Front 103

serum anion gap

Back 103

measurement of the unmeasured ions in plamsa
= [Na] - {[Cl-] + [HCO3]}
normal 8-12

Front 104

causes of non-anion gap metabolic acidosis

Back 104

diarhea and RTA

Front 105

type I distal RTA

Back 105

decr in acid excretion due to inability to make pH acidic; hypokalemia (reabsorption of Na makes the lumen - and since H, which would normally enter lumen to make it neurtral, can't you secrete K instead, low urine [HCO3], alkali urine

Front 106

type 4 distal RTA

Back 106

due to decr excretion of NH4, associated with DM, have a low urine pH, hyperkalemia

Front 107

type 2 proximal RTA

Back 107

impairment of proximal HCO3- reabsorption; high urine HCO3, hypokalemia, variable urine pH

Front 108

3 states promoting maintence of metabolic alkalosis

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volume contraction, hyperaldostonerism and hypokalemia

Front 109

pseudohyperaldosteronism type 1

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mutation in ENaC, causes hypotension, hyperkalemia

Front 110

pseudohyperaldosteronism type 2

Back 110

salt sensitive HTN, hyperkalemia

Front 111

ampotericin

Back 111

increases permeability of apical membrane in CT to K

Front 112

filtration fraction

Back 112

GFR/RPF, normally 20%

Front 113

TGF

Back 113

goal is to keep flow to distal nephron consistant; if NaCl is high at the MD, signals are sent to constrict the afferent arteriole to normalize blood flow

Front 114

symptoms of ARF (5)

Back 114

azotemia, hyperkalemia, hypervolemia, hyperphosphatemia, metabolic acidosis

Front 115

pre-renal ARF

Back 115

renal hypoperfusion which leads to ischemia; if ischemia is severe enough it can lead to ATN; causes include volume depletion (inc burns), CHF, cirhossis, medications (ACEI, NSAIDs, AMP B, Radiocontrast), obstruction

Front 116

ATN

Back 116

can be toxic (radioconstrast, aminoglycosides, amp B, heavy metals, engogenous like Hb of Mb) or ischemic, is reversible, on recovery watch for excessive diuresis which can lead to severe volume depletion with electrolyte imbalances; look for granular casts in urine

Front 117

AIN

Back 117

induced by drug therapy, ARF symptoms plus rash, fever, eosinophilia/uria, RBC, WBC and cast in urine

Front 118

FeNa%

Back 118

percent of filtered Na that is excreted in the urine, allows you to differentiate between pre-renal ARF and ATN; if it is <1 its prerenal as body trys to hold onto volume and if >1 its ATN

Front 119

b-lactam antibiotic AIN

Back 119

hypersensitivity, fever, arthralgias, good urine output, RBCs/WBCs in urine, eosinophiliuria with Hansels stain

Front 120

NSAIDs AIN

Back 120

decr PG's which lets Ang II, NE and ADH go with nothing to counteract them; causes decr RBF, decr GFR, incr Na and H20 reab; oliguria, nephrotic proteinuria, edema and HTN

Front 121

analgesic abuse nephropathy

Back 121

CTIN and papillary necrosis; polyuria and polydipsia, incr incidence of transitional cell carcinoma in the pelvis

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acute prostatitis/category 1

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known pathogen and symptoms

Front 123

chronic prostatitis/category 2

Back 123

recurrent infection, less severe than acute

Front 124

stress urinary incontinence

Back 124

failure to store due to poor urethral resistance; cough, sneeze and exercise incontinence, little urgency, small volume

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urge incontinence

Back 125

overactive bladder,urgency, large volume, nocturia