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.