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Azotemia & urinary abnormalities

renal syndromeµéÀº systemic illnessÀÇ °á°ú·Î¼­ ¹ß»ýÇÒ¼öµµ ÀÖ°í, primary renal disease·Î

»ý±æ¼öµµ ÀÖ´Ù.

Nephrologic syndromeµéÀº ´ÙÀ½ ¸î°¡Áö ±¸¼º¿ä¼ÒµéÀÇ Á¶ÇÕÀ¸·Î ÀÌ·ç¾îÁø´Ù: Tab 47-1

i) urine volume disturbances: oliguria, anuria, polyuria

ii) urine sediment abnormality: RBC, WBC, cast, crystal

iii) proteinuria

iv) GFR¡é(azotemia)

v) hypertension and/or expanded total body volume(edema)

vi) electrolyte abnormality

vii) fever/pain

ÀÌ»ó ¼Ò°ßµéÀÇ Á¶ÇÕÀ¸·Î major renal syndromeÀÌ »ý±â´Âµ¥ °¢°¢ÀÇ syndromeµéÀº

°¢ chapter¿¡¼­ »ó¼¼È÷ ´Ù·ç±â·Î ÇÏ°í ¿©±â¼­´Â ¸î°¡Áö »çÇ׿¡ ´ëÇØ¼­¸¸ ´Ù·ç°íÀÚ ÇÑ´Ù.

i) GRF°¨¼Ò·Î ÀÎÇÑ azotemia

ii) urinary sediment alteration and/or protein excretion

iii) urine volume abnormality

1. Azotemia

´ëºÎºÐÀÇ ±Þ¼º ÀÓ»ó»óȲ¿¡¼­ ¼Òº¯À¸·Î ¹è¼³µÉ ¾àÀÇ ÀûÁ¤ ¿ë·®À» ¾Ë±âÀ§ÇØ GFRÀÇ °è»êÀÌ

ÇÊ¿äÇÏ´Ù. GFR ÃøÁ¤À» À§ÇÑ marker·Î¼­ serum creatinineÀÌ °¡Àå ³Î¸® »ç¿ëµÇ°í ÀÖÀ¸¸ç

ÀÌ´Â urine creatinine excretion¿¡ ºñ·ÊÇϰí, serum creatinine¿¡ ¹Ýºñ·ÊÇÑ´Ù.

¾à ¿ë·® °áÁ¤¿¡ ÀÖ¾î GFRÀ» À߸ø °è»êÇϸé drug toxicity(¿¹, digoxin, aminoglycosides)·Î

ÀÎÇÑ significant morbidity & mortality¸¦ ÃÊ·¡ÇÒ¼ö ÀÖ´Ù.

¿Ü·¡È¯ÀÚ¿¡¼­ CRF·ÎÀÇ ÁøÇà¿¡ ÀÖ¾î GFRÀ» ¿¬¼ÓÀûÀ¸·Î ÃøÁ¤ÇÏ´Â °ÍÀÌ µµ¿òÀÌ µÇÁö¸¸ serum

creatinineÀ» GFR ´ë½ÅÀ¸·Î »ç¿ëÇÒ¼ö ÀÖÀ¸¸ç progressive chronic renal insufficiency¿¡¼­

1/Pcr°ú ½Ã°£»çÀÌ¿¡ linear relationshipÀÌ ÀÖ´Ù. ÀÌ slopeÀº °³Àθ¶´Ù ÀÏÁ¤ÇÏ¸ç ¸¸¾à ÀÌ ¼±À»

µû¶ó °¨¼ÒÇÏÁö ¾Ê´Â´Ù¸é superimposed acute process(¿¹, volume depletion, drug

reaction)°¡ ÀÖ´ÂÁö Á¶»çÇØ º¸¾Æ¾ß ÇÑ´Ù.

uremic sx & signÀ» ÀÏÀ¸Å°´Â serum creatinine levelÀº °³Àθ¶´Ù ´Ù¾çÇѵ¥ ÀϹÝÀûÀ¸·Î

severe renal insufficiency°¡ »ý±æ¶§±îÁö(GFR <15 ml/min) symptomatic uremia°¡ »ý±âÁö

¾ÊÀ¸¸ç, ÀϺÎȯÀÚ´Â GFRÀÌ 5 ml/minÀÌÇϰ¡ µÉ ¶§±îÁöµµ »ý±âÁö ¾Ê´Â´Ù.

GFRÀÌ °¨¼ÒÇϸé urea nitrogen & creatinine°ú °°Àº nitrogenous waste products°¡ ÃàÀû

(azotemia)µÈ´Ù. µÎ°¡Áö ÈçÈ÷ »ç¿ëµÇ´Â markers(urea & creatinine)°¡ clearance marker·Î¼­

Á¤È®ÇÑÁö Àǽɽº·´´Ù. urea clearance´Â ÈçÈ÷ GFRÀ» underestimateÇÑ´Ù.

creatinineÀº ÀÛ°í ÀÚÀ¯·Ó°Ô ¿©°úµÉ¼ö ÀÖ´Â solute·Î ÀÏÁß º¯µ¿ÀÌ °ÅÀÇ ¾ø´Ù. organic cation

pathway¸¦ ÅëÇÏ¿© proximal tubule¿¡¼­ ºÐºñµÉ ¼öµµ ÀÖ´Ù. CcrÀ» ÃßÁ¤ÇÏ´Â °ø½ÄÁß¿¡

age-related decreased GFR, B.W, sexµîÀ» ÀÌ¿ëÇÑ Cockcroft-Gault formula°¡ ÀÖ´Ù.

= (140-Age) ¡¿ BW/ 72¡¿serum Cr (¿©ÀÚÀÇ °æ¿ì ¡¿0.85)

´õ Á¤È®ÇÑ GFRÃøÁ¤¹æ¹ýÀº inulin clearance³ª radionuclide-labelled marker(125I-iothalamate

or EDTA)¸¦ ÀÌ¿ëÇÏ¿© ÃøÁ¤ÇÒ¼ö ÀÖ´Ù. ÀÌ ¹æ¹ýÀº Á¤È®È÷ Á¤·®ÇÒ¼ö ÀÖ°í renal

reabsorption/secretionÀÌ ¾ø±â ¶§¹®¿¡ ¾ÆÁÖ Á¤È®ÇÏ¿© CcrÀ» reliable indicator·Î »ç¿ëÇÒ ¼ö

¾øÀ» ¶§(decreased muscle mass secondary to age, malnutrition, concurrent illnesses)

»ç¿ëÇÒ¼ö ÀÖ´Ù.

2. Approach to the patient

GFRÀÌ °¨¼ÒÇÏ¸é ¸ÕÀú ARFÀÎÁö CRFÀÎÁö °áÁ¤ÇØ¾ß ÇÑ´Ù. clinical situation, history, labÀ¸·Î

º¸Åë ½±°Ô ±¸º°ÇÒ¼ö ÀÖÀ¸³ª CRFÀÇ Æ¯Â¡ÀûÀÎ °Ë»ç¼Ò°ßÀÎ anemia, hypocalcemia,

hyperphosphatemia°¡ ARF¶§µµ ÀÖÀ»¼ö ÀÖ´Ù.

renal osteodystrophyÀÇ ¹æ»ç¼±ÇÐÀû ¼Ò°ßÀº CRF¿¡¼­¸¸ º¼¼ö ÀÖÁö¸¸ ¾ÆÁÖ Èı⠼ҰßÀ̸ç

À̶§ ȯÀÚ´Â ÀÌ¹Ì Åõ¼®ÁßÀÌ´Ù. urinalysis & renal ultrasoundµµ µÎ°¡Áö¸¦ ±¸º°ÇÒ¼ö ÀÖ´Ù.

* aoztemiaȯÀÚÀÇ approach´Â Fig 47-1 ÂüÁ¶

ARF´Â ¼¼°¡Áö·Î ³ª´­¼ö ÀÖ´Ù.

i) renal blood flowÀå¾Ö(prerenal azotemia)

ii) intrinsic renal disease(affecting vessel, glomerular or tubules)

iii) postrenal process(ureter, bladder, or urethral obstruction)

1) prerenal failure(40-80%)

circulating blood voluem°¨¼Ò·Î ÀÎÇØ ¹ß»ý

i) volume loss: GI hemorrhage, burns, diarrhea, diuretics

ii) volume sequestration: pancreatitis, peritonitis, rhabdomyolysis

iii) effective circulating volume¡é: cardiogenic shock, sepsis

iv) C.O¡é from peripheral vasodilation : sepsis, drug

v) profound renal vasoconstriction: severe heart failure, hepatorenal syndromes,

drugs(NSAIDs)

true or "effective" hypovolemia

-> mean arterial pressure¡é

-> neural & humoral response

-> sympathetic nervous system, RAA system activation, ADH release

GFR˼ PG-mediated relaxation of afferent arterioles

& angiotensin II-mediated constriction of efferent arterioles¿¡ ÀÇÇØ À¯ÁöµÈ´Ù.

NSAIDs´Â PG»ý»êÀ» blockÇÏ¿© severe vasoconstriction & ARF¸¦ ÀÏÀ¸Å³¼ö ÀÖ°í

ACE inhibitor´Â efferent arteriolar toneÀ» °¨¼Ò½ÃÄÑ glomerular capillary prefusion pr¸¦

°¨¼Ò½Ã۴µ¥ NSAID and/or ACE inhibitor¸¦ Åõ¿©¹Þ´Â ȯÀÚ´Â ¾î¶² ÀÌÀ¯·Î blood volumeÀÌ

°¨¼ÒÇÒ ¶§ hemodynamically mediated ARF¿¡ °¡Àå Ãë¾àÇÏ´Ù.

renal hypoperfusionÀÌ Áö¼ÓÇϸé ATNÀ» ÀÏÀ¸Å°°Ô µÈ´Ù.

* Tab 47-2 prerenal azotemia¿Í oliguri ARFÀÇ °¨º°

prerenal azotemia : concentrated urine(>500 mosm/L)

Na retention(urine Na<20 mM/L), FENa<1%

2) intrinsic renal disease

large renal vessel, microvasculature, glomeruli, tubular interstitiumÀÌ Ä§¹üµÇ¾î ¹ß»ýÇÑ´Ù.

ischemic & toxic ATNÀÌ acute intrinsic renal failureÀÇ 90%¸¦ Â÷ÁöÇÑ´Ù.

prerenal azotemia¿Í ATN¸ðµÎ renal hypoperfusionÀÇ ÇÑ spectrumÀÌ´Ù.

ATN¿¡¼­´Â structural tubular injuryÀÇ Áõ°Å°¡ ÀÖ´Â ¹Ý¸é prerenal azotemia´Â renal

hypoperfusionÀÌ È¸º¹ÇÏ¸é ±â´ÉÀÌ È¸º¹µÈ´Ù. ±×·¯¹Ç·Î ATNÀº urinalysis & urine electrolyte

compositionÀ¸·Î prerenal azotemia¿Í ±¸º°ÇÒ¼ö ÀÖ´Ù.

¨ç ischemic ATNÀÌ Àß »ý±â´Â Á¶°Ç

major surgery, trauma, severe hypovolemia, overwhelming sepsis, extensive burns

¨è nephrotoxic ATN: ÁÖ·Î medication¿¡ ÀÇÇØ ¹ß»ý

intrarenal vasoconstriction, direct tubular toxicity, and/or tubular obstructionÀ» ÀÏÀ¸Å´

kidney´Â blood supply°¡ dzºÎ(C.OÀÇ 25%)Çϰí toxin¿¡ ³óÃàµÇ°í ´ë»çµÇ¹Ç·Î

toxic injury¿¡ Ãë¾àÇÏ´Ù.

¨é tubule & interstitiumÀ» ħ¹üÇØµµ ARF°¡ »ý±æ¼ö ÀÖ´Ù.

i) drug-induced interstitial nephritis: ƯÈ÷ antibiotics, NSAIDs, diuretics

ii) severe infections(bacterial & viral)

iii) systemic disease: SLEµî

iv) infiltrative disorders: sarcoid, lymphoma or leukemia µî

cf. drug list´Â chap 277ÂüÁ¶

interstitial nephritis¿¡¼­ RBC cast°¡ º¸°íµÈ ¹Ù ÀÖÀ¸³ª RBC cast°¡ º¸À̸é glomerular

diseaseÀÎÁö Áï½Ã Á¶»çÇØ¾ß ÇÏ¸ç ¶§·Ð renal biopsy°¡ ÇÊ¿äÇÒ¼öµµ ÀÖ´Ù.

eosinophiluria°¡ ÀÖ´Ù¸é allergic interstitial nephritis¸¦ ÀǽÉÇÒ¼ö ÀÖ´Ù. ±×·¯³ª ¾ø´Ù°í ÇØ¼­

¹èÁ¦ÇÏÁø ¸øÇÑ´Ù.

¨ê large renal vessel occlusionµµ intrinsic renal failureÀÇ µå¹® ¿øÀÎÀÌ´Ù.

: atheroemboli, thromboemboli, in situ thrombosis, aortic dissection, or vasculititis

i) atheroembolic renal failure: ÀúÀý·Î »ý±æ¼öµµ ÀÖÀ¸³ª ´ëºÎºÐÀº recent aortic

instrumentation°ú °ü·ÃÀÖÀ¸¸ç Á¤»ó urinalysis¸¦ º¸À̳ª eosinophiluria or urine cast¸¦

º¸Àϼöµµ ÀÖ´Ù.

ii) renal artery thrombosis¶§´Â mild proteinuria & hematuria¸¦ ÀÏÀ¸Å°³ª

renal vein thrombosis¶§´Â heavy proteinuria & hematuria¸¦ ÀÏÀ¸Å²´Ù.

¨ë glomerular disease(GN or vasculitis)

& renal microvasculature(HUS, TTP, or malignant hypertension)

´Ù¾çÇÑ glomerular injury: proteinuria, hematuria, GFR¡é

Na excretionº¯È­: hypertension, edema, circulatory congestion(acute nephritic

syndrome)

ÀÌ·¯ÇÑ ¼Ò°ßµéÀº primary renal disease ȤÀº systemic diseaseÀÇ renal manifestaionÀ¸·Î

³ªÅ¸³¯¼öµµ ÀÖ´Ù.

RBC cast´Â early renal biopsyÀÇ ÀûÀÀÀÌ µÈ´Ù. ¿Ö³ÄÇϸé pathologic patternÀÌ Áø´Ü, ¿¹ÈÄ,

Ä¡·á¿Í ¹ÐÁ¢ÇÑ °ü·ÃÀÌ Àֱ⠶§¹®ÀÌ´Ù.

hematuria without RBC cast¶Ç glomerular disease¸¦ ÀǽÉÇÒ¼ö ÀÖ´Ù.

3) postrenal azotemia(<5%)

USG»ó ureteral dilatationÀÌ ÈçÈ÷ ÀÖ´Ù.

±×·¯³ª early course or dilatationµÉ¼ö ¾ø´Â Á¶°Ç, ¿¹¸¦ µé¸é pelvic tumor¿¡ ÀÇÇÑ

encasementµî¿¡¼­´Â ÃÊÀ½ÆÄ¿¡¼­ dilatationÀÌ º¸ÀÌÁö ¾ÊÀ»¼öµµ ÀÖ´Ù.

4) oliguria & anuria

oliguria < 500 ml/24hr urine

anuria : complete absence of urine formation

3. Urine abnormalities

1) proteinuria Fig 47-3

¨ç °Ë»ç¹æ¹ý

i) dipstick measurement :ÁÖ·Î albumin detect

* false-positive¸¦ º¸ÀÌ´Â °æ¿ì

+- urine pH >7.0

| very concentrated urine

+- blood contamination

dipstick test¿¡¼­´Â albuminÀ̿ܿ¡´Â significant proteinuria°¡ ÀÖ´õ¶óµµ detectÇϱâ

¾î·Á¿îµ¥ ƯÈ÷ multiple myelomaȯÀÚ¿¡¼­ Bence-Jones proteinÀ» detectÇÒ ¶§ ±×·¸´Ù.

ii) salfosalicylic or trichloracetic acid

total urine concentrationÀ» À§ÇÑ °Ë»ç´Â sulfosalicylic or trichloracetic acid·Î Ä§Âø½ÃÄÑ

°Ë»çÇÑ´Ù.

iii) ultrasensitive dipsticks

early diabetic nephropathy¿¡¼­ glomerular injury¸¦ ¿¹ÃøÇϱâ À§ÇÑ early marker·Î¼­

ultrasensitive dipsticksÀÌ »ç¿ëµÇ´Âµ¥ ÀÌ´Â microalbuminuria(30-300 mg/d)¸¦ detect

ÇÒ¼ö ÀÖ´Ù.

¨è ±âÀü

i) glomerular wall disruption

´ë·®ÀÇ plasma proteinÀÌ glomerular capillary·Î À¯ÀÔµÇÁö¸¸ urinary space·Î´Â µé¾î°¡Áö

¾Ê´Â´Ù.

ÀÌ´Â charge & size selectivity°¡ albumin, globulin & other LMW proteinÀÌ glomerular wall

À» Åë°úÇÏ´Â °ÍÀ» ¹æÁöÇϱ⠶§¹®ÀÌ´Ù. ±×·¯³ª ÀÌ·¯ÇÑ À庮ÀÌ ÆÄ±«µÈ´Ù¸é plasma proteinÀÇ

leakage°¡ ¹ß»ýÇÑ´Ù(= glomerular proteinuria).

ÀÛÀº ´Ü¹é( <20 KDa)Àº ÀÚÀ¯·Ó°Ô ¿©°úµÇÁö¸¸ protein tubule¿¡¼­ ½±°Ô ÀçÈí¼öµÇ¾î Á¤»óÀÎ

ÀÇ protein excretionÀº total protein <150 mg/d, albumin <30 mg/dÀÌ´Ù.

³ª¸ÓÁö urine proteinÀº tubule¿¡¼­ ºÐºñµÇ´Â °Í(Tamm-Horsfall protein, IgA, urokinase)

À̰ųª ¿©°úµÈ ¼Ò·®ÀÇ ¥â2-microglobulin, apoproteins, enzymes & peptide hormone

µîÀÌ´Ù.

ii) proteinuriaÀÇ ¶Ç´Ù¸¥ ±âÀüÀº excessive production of abnormal proteinÀÌ´Ù.

mc: plasma cell dyscrasia(multiple myeloma & lymphoma)

-> Ig light chainÀÇ monoclonal production°ú °ü·ÃÀÖ´Ù.

¨é selective & nonselective proteinuria

GBM channelÀº anionic glycoproteinÀ¸·Î coatµÇ¾î negative charge¸¦ ¶í´Ù.

negative charge´Â À½ÀÌ¿ÂÀÎ albuminÀÇ Åë°ú¸¦ ¸·´Â´Ù.

ÀϺΠglomerular disease(MCD)´Â glomerular epithelial cell foot process°¡ fusionµÇ¾î

"selective" albumin loss¸¦ ÃÊ·¡ÇÑ´Ù.

¶Ç´Ù¸¥ glomerular disease´Â BM & slit diaphragm disruption(¿¹, immune complex

deposition)µÇ¾î ´Ù·®ÀÇ protein loss¸¦ ÃÊ·¡ÇÑ´Ù(albumin & other plasma proteins).

ÀÌ·¯ÇÑ foot process fusionÀº capillary BMÀÇ pressure¸¦ Áõ°¡½ÃÄÑ pore size°¡ Ä¿Áöµµ·Ï

ÇÑ´Ù.

Áõ°¡µÈ pressure & larger pore´Â significant proteinuria¸¦ ÃÊ·¡ÇÑ´Ù("monselective").

¨ê nephrotic syndrome

daily proteinuria >3.5gÀÏ ¶§ hypoalbuminemia, hyperlipidemia & edema°¡ »ý±ä´Ù.

±×·¯³ª nephrotic syndrome¾øÀÌ daily urinary protein excretionÀÌ 3.5gÀÌ»óÀϼö ÀÖ´Ù.

¿¹> plasma cell dyscrasia(multiple myeloma)

: ´Ù·®ÀÇ light chain in urineÀ¸·Î dipstick¿¡´Â detect¾ÈµÊ

´Ù¾çÇÑ ±âÀüÀ¸·Î renal failure¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.

i) tubular obstruction(cast nephropathy)

ii) light chain deposition

* hypoalbuminuria in nephrotic syndrome

=> renal catabolismÁõ°¡, inadequate hepatic synthesis, oncotic pressure¡é

-> effective intravascular volume¡é

-> RAA system activation

ADH release

sympathetic nervous system activation

-> excessive renal salt & water reabsorption

-> edema

urinary protein loss -> hepatic lipoprotein synthesis¡è

-> hyperlipidemia, urine lipid body(fatty casts, oval fat body)

* other protein loss

TBG, cholecalciferol-binding protein, transferrin, metal-binding proteins

* hypercoagulable state: AT III, protein C, S loss, hyperfibrinogenemia, platelet

aggregation¡è

* IgA deficiency: immunity Àå¾Ö

2) Hematuria, pyuria & casts

¨ç isolated hematuria without proteinuria

normal RBC <2¹é¸¸/day

hematuriaÀÇ Á¤ÀÇ: 2-5 RBC/HPF

common cause: stone, neoplasm, tuberculosis, trauma, prostatitis

* gross hematuria with blood clots: postrenal source ÀǹÌ

i) single urinalysis hematuria; menstruation, viral illness, allergy, mild trauma

ii) persistent or significant hematuria

(>3RBCs/HPF on 3 UA, >100 RBCs/HPF, gross hematuria)

: 1000¸íÀÇ È¯ÀÚ¸¦ ´ë»óÀ¸·Î Á¶»çÇßÀ» ¶§ 9.3%¿¡¼­ significant urologic lesion¹ß°ß

¨è isolated painless hematuria(nondysmorphic RBC)ÀÏ ¶§ urogenital neplasmÀ» ÀǽÉÇϸç

³ªÀ̰¡ µé¸é¼­ °¡´É¼º Áõ°¡. ¼Ò¾Æ¿¡¼­´Â neoplasmÀÌ µå¹°¸ç idiopathic or congenital

anomaly¿Í °ü·ÃµÇ¾úÀ» °¡´É¼ºÀÌ ³ô´Ù.

¨é hematuria with pyuria & bacteriuria: infection

acute cystitis or urethritis in women -> gross hematuria¸¦ ÀÏÀ¸Å³¼öµµ ÀÖ´Ù.

¨ê hypercalcemia & hyperuricosuria´Â unexplained isolated hematuriaÀÇ risk factor

(¾ÆÀÌ, ¾î¸¥ ¸ðµÎ)

¨ë isolated microscopic hematuria: glomerular originÀÇ RBC = dysmorphic

most common: IgA nephropathy, hereditary nephritis, thin basement membrane

disease

IgA nephropathy, hereditary nephritis´Â episodic gross hematuria¸¦ ÀÏÀ¸Å°°í

hereditary nephritis, thin basement membrane diseae´Â family history°¡ ÀÖ´Ù.

È®ÁøÀ» À§Çؼ­´Â renal biopsy°¡ ÇÊ¿äÇÏ´Ù.

hematuria with dysmorphic RBCs, RBC cast & proteinuria >500 mg/dÀ϶§´Â

GNÀ¸·Î Áø´ÜÇÒ¼ö ÀÖ´Ù.

¨ì isolated pyuria: unusual

ÈçÈ÷ hematuria¿Í µ¿¹Ý

WBC cast with bacteria -> pyelonephrisÀǹÌ

WBC and/or WBC cast

-> tubulointerstitial process(¿¹, interstitial nephritis, SLE, transplant rejection)

¨í waxy casts: chronic renal disease¿¡¼­ degenerated cellular cast

broad casts: dilated tubules of enlarged nephron¿¡¼­ »ý±è

4. Urine volume abnormalities

* polyuria >3L/d Fig 47-5 polyuria approach

average person solute excretion : 600-800 msom/d

urine osm <250 mosm/L = water diuresis(polydipsia, DI)

>300 mosm/L = solute diuresis(mc=pooly controlled DM)

* solute diuresis

glucose, mannitol or urea¿Í °°Àº solute°¡ excessive filtration

-> proximal tubule¿¡¼­ NaCl, water ÀçÈí¼ö ¾ïÁ¦

-> urine excretion

mc: poorly controlled DM

±× ¿Ü ÈçÇÑ ¿øÀÎÀ¸·Î iatrogenic solute diuresis

: mannitol, radiocontrast media, high-protein feedings

less commoly: excessive Na loss

+- cystic renal disease

| Bartter's syndrome

+- tubulointerstitial process °úÁ¤(resolving ATN)

¼ÒÀ§ salt-wasting disorders¿¡¼­ tubular damage´Â Na reabsorptionÀÇ direct impairment¿Í

°£Á¢ÀûÀ¸·Î aldosterone¿¡ ´ëÇÑ tubuleÀÇ hyporesponsiveness ¶§¹®¿¡ ¹ß»ý.