diagnostic approach to aki

1. BY DR.MANUSHA,
BATCH 2K9

2.  PATIENT WITH KIDNEY DISEASE MAY HAVE A
VARIETY OF CLINICAL PRESENTATIONS:
1.S/S THAT DIRECTLY POINT TO KIDNEY
EG:GROSS HAEMATURIA
2.EXTRA RENAL MANIFESTATIONS LIKE
EDEMA,HYPERTENSION,SIGNS OF URAEMIA
3.ASYMPTOMATIC(MANY) :INCIDENTAL FINDINGS
LIKE RAISED SERUM
CREATININE,PROTEINURIA/MICROSCOPIC
HAEMATURIA,ETC

3.  BY CAREFUL HISTORY TAKING WE CAN ASSESS
THE DISEASE DURATION
 BY PHYSICAL EXAMINATION AND SPECIFIC
INVESTIGATIONS THE CAUSE(S) FOR THE ACUTE
OR CHRONIC ILLNESS CAN BE IDENTIFIED
 HENCE THE DD FOR AKI/CKD IS NARROWED
 KNOWING THE DISEASE DURATION PROVIDES
PROGNOSTIC INFORMATION TO GUIDE THE
MANAGEMENT OF AKI/CKD

4.  DEFINITIONS:
 AKI:
AKIN CRITERIA:INCREASE IN SERUM CREATININE
BY 0.3MG/DL(27MICROMOL/L) OR >1.5TIMESTHE
BASELINE VALUES WITHIN 48 HRS
RIFLE AND KDIGO CRITERIA:INCREASE OF >1.5
TIMES THE BASELINE VALUES WITHIN 7 DAYS
CKD:
NKF-K/DOQI NAD KDIGO:GFR<60ML/MIN/1.73M2
OR EVIDENCE OF KIDNEY DAMAGE SUCH AS
ALBIMINURA OR ABNORMAL RADIOGRAPHIC
FINDINGS WHICH ARE PRESENT FOR THREE
MONTHS OR MORE

5.  MANY NUMBER OF DISEASES DOESN’T FIT THIS
CRITERIA.
 EG:RPGN
 BEST ASSESSMENT OF DISEASE DURATION IS
DONE BY COMPARING CURRENT AND PREVIOUS
LEVELS OF S.CREATININE
 EG:
 WHEN NO PREVIOUS INVESTIGATIONS ARE
AVAILABLE CERTAIN FINDINGS FROM HISTORY
AND CLINICAL EXAMINATION SUGGESTS THE
DURATION OF DISEASE LIKE

6.  1.RECENT ONST OF S/S
EG:ANASARCA,DISCOLORED URINE
2.OLIGURIA INDICATES ACUTE DISEASE
COZPROLONGED OLIGURIA IS NOT
ENCOUNTERED EVEN IN ADVANCED CKD PRIOR
TO THE NEED FOR MAINTAINEENCE DIALYSIS
3.INCREASE OF S.CREATININE ON A DAILY BASIS –
ACUTE ILLNESS EG:ATN
WHILE STABLE VALUES AFTER INITIAL
EVALUATION –CKD EG:PRERENAL DISEASE
4.RADIOLOGIC FINDINGS:SMALL KIDNEYS
INDICATE CKD WHILE NORMAL SIZE DOESN’T
RULE OUT CKD
ECHOGENICITY INCREASED IN CKD

7. HYDRONEPHROSIS,MULTIPLE RENAL CYSTS CAN
HELP IN FURTHER EVALUATION
ANEMIA AND HYPERPHOSPHATEMIA ARE
ASSIOCIATED WITH CKD BUT NOT SPECIFIC
INJURY BIOMARKERS(EARLY PREDICTORS –EVEN
PRIOR TO THE RAISE IN S.CREATININE)
EG:1.URINARY NGAL
2.KIM-1
3.IL-18

8.  CAUSES AND CLASSIFICATION:
 URINE FORMATION OCCURS IN 4 SEQUENTIAL
STEPS-
1.BLOOD FROM RENAL.A TO GLOMERULI
2.ULTRAFILTRATE OF PLASMA FROM GLOMERULI
INT TUBULES
3.REABSORPTION AND/OR SECRETION OF SOLUTES
AND REABSORPTION OF FILTERE WATER
4.URINE LEAVING THE TUBULAR FLUID----RENAL
PELVIS-----URETER---BLADDER-----URETHRA

9.  KIDNEY DISEASE MAY BE CAUSED BY THE
INTERFERENCE OF ANY OF THE ABOVE
STRUCTURES/FUNCTIONS.
 IDENTIFYING PRERENAL OR POST REANAL CAUSE
IS OF UTMOST IMPORTANCE COZ THEY MAY BE
READILY REVERSIBLE
 EARLY RECOGNISTION OF RPGN IS OF
PROGNOSTIC VALUE

10.  CLASSIFICATION OF AKI-
 1.PRERENAL(DECREASED RENAL PERFUSION)
 2.INTRINSIC RENAL
 a.RENAL VASCULAR
 b.GLOMERULAR
 c.TUBULOINTERSTITIAL DISEASE
 3.POSTRENAL(OBSTRUCTIVE)

11.  PRERENAL
 1.ACUTE:a.ACUTE HYPOVOLEMIC STATES.
 EG-ACUTE
HAEMORRHAGE,DIARRHOEA,UNREPLENISHED
INSENSIBLE LOSSES
 b.DECREASED EFFECTIVE CIRCULATING VOLUME
 EG-CARDIORENAL SYNDROME AND
HEPATORENAL SYNDROME
 c.ALTERATIONS IN RENAL VASCULAR
AUTOREGULATION
 EG-USE OF NSAIDS,IODINATED CONTRAST.

12.  2.CHRONIC:ONGOING HEART FAILURE AND
CIRRHOSIS
 INTRINSIC RENAL
 INTRINSIC RENAL VASCULAR:
 ACUTE :1.SMALL VESSEL VASCULITIDES-MAHA
INCLUDING TTP,SCLERODERMA AND
MALIGNANT HYPERTENSION
 LARGE VESSEL INVOLVEMENT:RENAL INFARCTON
FROM EITHER AORTIC DISSECTION/SYSTEMIC
THROMBOEMBOLISM/RENAL ARTERY ANEURYSM
 RENAL VEN THROMBOSIS ASSOCIATED WITH
MASSIVE PROTEINURIA IN THE SETTING OF
NEPHROTIC SYNDROME


13.  CHRONIC-
 NEPHROSCLEROSIS--POLYMORPHISMS ON APOL1
GENE ON 22CHRM---GLOMERULAR SCLEROSIS
AND TUBULOINTERSTITIAL FIBROSIS
 RENAL A.
STENOSIS(ATHEROSCLEROSIS/FIBROMUSCULAR
DYSPLASIA)-----ISCHEMIC NEPHROPATHY
 RENAL ARTERY
DISSECTION/ANEURYSM(FIBROMUSCULAR
DYSPLASIA/PAN)------RECCURENT
THROMBOEMBOLI----RECCURENT RENAL
INFARCTS----LOSS OF KIDNEY FUNCTION


14.  INTRINSIC GLOMERULAR DISEASE-
 PRIMARY-IDIOPATHIC
 SECONDARY-PARANEOPLASTIC
SYNDROMES,DRUG INDUCED/PART OF SYSTEMIC
RHEUMATOLOGICAL MANIFESTATIONS
 TWO PATTERNS
 NEPHRITIC PATTERN-ASS WITH INFLAMMATION
ON HPE,ACTIVE URINE SEDIMENT WITH
DYSMORPHIC RBCS,OTHER CELLULAR CASTS
 NEPHROTIC PATTERN NOT AAS WITH
INFLMTN,BUT NEPHROTIC RANGE
PROTEINURIA(>3.5G/24HR PROTEIN )IS SEEN
WITH INACTIVE URINE SEDIMENT
 INTRINSIC TUBULOINTERSTITIAL DISEASE

15.  1.ACUTE-
 MULTIPLE MYELOMA---ACUTE INTERSTITIAL NEPHRITIS AND
CAST NEPHROPATHY
 TUMOURLYSIS SYN(HIGH TUMOR BURDEN
LYMPHOMA/FOLLOWING CHEMO)------ACUTE URATE
NEPHROPATHY
 FOLLOWING PHOSPHATE CONTAINING BOWEL PREPARATION---
ACUTE PHOSPAHTE NEPHROPATHY
 2.CHRONIC
 MC CAUSE PKD
 NEXT ARE NEPHROCALCINOSIS,SARCOIDOSIS,SJOGRENS
SYN,REFLUX NEPHROPATHY(IN CHILDREN AND YOUNG
ADULTS),AND MEDULLARY CYSTIC KIDNEY DISEASE(AD
INHERITENCE)
 REDUCTION IN GFR REQUIRES B/L OBS ----PROSTATIC
HYPERPLASIA/CANCER OR METASTATIC CANCER
 RETROPERITONEL FIBROSIS IN UNEXPLAINED
HYDRONEPHROSIS


16.  EPIDEMIOLOGY
 DEVELOPED ATN AND PRE RENAL DISEASE
 DEVELOPING COUNTRIES; SNAKE BITES, EARTH
QUAKES, INFECTIONS LIKE LEPTOSPIROSIS

17.  PRESENTING FEATURES: PATIENTS WITH AKI/CKD
PRESENT WITH ONE OR MORE OF THE FOLLOWING
FEATURES
 1.S/S OF DIMINISHED RENAL FUNCTION
 EDEMA,HTN,DECREASED URINARY OUTPUT
 2.S/S SYMPTOMS OF PROLONGED RENAL FAILURE
 WEAKNESS,EASY
FATIGUABILITY,ANOREXIA,VOMITINGS,CHANGES IN
MENTAL STATUS, AND SEIZURES
 3.LAB FINDINGS-RAISED
S.CREATININE,HYPERKALEMIA
 4.URINE ANALYSIS-ALBUMINURIA AND /OR ABN
URINE SEDIMENT
 5.INCIDENTAL FINDINGS-PKD/ RADIOGRAPHIC
IMAGING FOR OTHER REASON

18.  6.DIAGNOSTIC S/S-
 SYSTEMIC S/S AND FINDINGS-FEVER,ARTHRALGIA
AND PUL LESIONS-----VASCULITIS/LUPUS
 U/L FLANK PAIN-MC WITH OBS,INFARCTN/INFCTN
 ANURIA(<50ML/DAY)-SEV SHOCK,B/L UT OBS,PREG
RELATED CORTICO NECROSIS/B/L R.A OBS(DISS
A.ANEUR)
 EDEMA,HTN,HEMATURIA WTH RBC CASTS,RAPIDLY
RAISING S.CREAT--AGN/RENAL VASCULITIS
 EDEMA,HEAVY PROTEINURIA,LIL /NO HEMATURIA--
NON PROL GN(DIABETIC,MEMB.MIN CHANGE)

19.  EVALUATION-
 CAREFUL HISTRY TAKING(REVIEW OF
MEDICATIONS) AND PHY XMNTN
 2.ESTMTN OF GFR
 3.URINANALYSIS
 4.RENAL IMAGING
 5.SEROLOGICAL TESTING
 6.RENAL BIOPSY
 .

20.  1.HISTORY TAKING-PRVIOUS RADIOCONTRST
XPOSURE,REVIEW OF MEDICATIONS,H/O DM
 2.PHY XMNTN-SIGNS OF VOL CONTRACTN /+NCE
OF PROF DIA RETNPTHY
 3.ASSESSMNT OF GFR- S.CREAT IN MILD
DECRIMENTS IN ESTIMATED GFR(45-60
ML/MIN/1.73 MSQ)-S.CREAT SHUD BE REPEATED
IN 4-8 WEKS, IF IT IS STABLE, FOLLOW IT
INTERMITTENTLY. IN PTS WITH S/S OF RAPEDLY
PROG DIS. RENAL BIOPSY DONE.
 THE eGFR FRM CREATNINE IS USED IN PTS WITH
STEADY STATE AND MAY LEAD TO ERRORS IN
ESTIMATN OF KIDNEY FUNCTION IN DISEASED
PTS

21.  4.URINE ANALYSIS:A)DIPSTICK(TEST FR PROT, PH, GLUC,
HB,LEUCOCYTE ESTERASE, SP.GRAVITY) B)MICROSCOPIC
XMINATN

 PRESENCE OF MUDDY BROWN GRANULAR CASTS AND
TUBULAR -DIAGNOSTIC OF ATN(EITHER AS A SOLE CAUSE OR
ASS WITH AG VASCULITIS)
 DYSMORPHIC RBCS AND RBC CAST--SOURCE OF HEMATURIA--
GLOMERULUS
 IN NON GLOMERULAR HEMATURIA IN +NCE OF RISK FACTORS
FOR UT MALIGNANCY,AGE>40YRS---URINE CYTOLOGY IS THE
APPROPRIATE INITIAL STEP
 NEPHROTIC RANGE PROTEINURIA ASS WITH >90% OF ALBUMIN
---MORE PROBABLY INDICATIVE OF GLOMERULAR DISEASE
 (PROBABILITY INCREASES WITH +NCE OF DYSMORPHIC
RBCS,RISING S.CREAT,HTN)
 EXCEPTIONS NEPHROTIC RANGE PROTEINURIA WHICH DOESNT
INDICATE GLOMERULAR DISEASE IN MASSIVE BENC JONES
PROTEINURIA AND IN GROSS HEMATURIA(GLOBINS ARE HIGH)

22.  NORMAL URINANALYSIA-
 ACUTE-PRE RENAL DISEASE,UT OBS,HYPERCAL,ACUTE PHOS NEPHRPTHY AND MYELOMA
CAST NEPHRPATHY
 CHRONIC -NEPHROSCLEROSIS,UT OBS,CRS,HRS
 LARGE HEMOGLOBINURIA WITH NO/FEW RBCS--PIGMENT
NEPHRPTHY(RHABDOMYOLYSIS/SEVERE HEMOLYSIS)
 NO SIGNIFICANT PROTEINURIA WITH DIPSTICK TEST BUT RAISED VALUE OF SPOT PROTEIN
CREATININE RATIO---PARAPROTEINS(POSITIVELY CHARGED)
 POSITIVE LEUKOCYTE ESTERASE---NO EVIDNC OF UTI---STERILE PYURIA ----INTERSTITIAL
NEPHRITIS
 --URINE NA+ EXCRETN-
 NORMAL<20MEQ/L
 CAN AS LOW AS 1MEQ/L IN CASE OF SEV HYPOVOL WITH NORML RENAL FUNCTION
 AKI--WITH OLIGURIA --MEASUREMENT OF URINENA+ EXCRETN AND FENa ----
DISTINGUISHES PRERENAL AKI FROM ATN
 IN PRRERRENAL AZO--TUB FUNCTN INTCT—INCREASED SODIUM AVIDITY IS DUE RENAL
HYPOPERFUSN
 CKD---NOT INDICATIVE --IN CKD ---CONCNTRTNG CAPACITY OF KIDNEY DECREASES
 FENA INCREASES ACC TO INTAKE

23.  URINE VOL--IMP PARAMETER IN PTS WITH KID DISEASE.
 IN PTS WITH NON OLIGURIC ATN THE URINE VOL IS
NORMAL
 OLIGURIA <0.3ML/KG/HR OR <500ML/DAY---MAY/NOT
SEEN IN AKI
 ANURIA INDICATIVE OF SEV AKI WHICH REQUIRES
DIALYSIS
 PROGNOSIS OF NONOLIG AKI>OLIG/ANURIC AKI
 RADIOLOGIC STUDIES-
 UT OBS,KIDNEY STONES,RENAL CYST/MASS,
CHARACTERISTIC FINDINGS OF RENAL VASCULAR DISEASE
AND VESICO URETERIC REFLUX IN CHILD
 HELICAL CT---FLANK PAIN AND POSSIBLE UROLITHIASIS
 GAD---NEPHROGENIC SYS FIBROSIS---GAD BASED
IMAGING SHOULD BE AVOIDED IN PTS WITH AKI/CKD

24.  SEROLOGIC TESTING:
 WITH OTHER RENAL INVSTGTNS-----FURTHER
CHARACTERISES THE ETIOLOGY OF KID DISEASE
 RENAL BIOPSY-WHEN NON INVASIVE INVSTGTNS
HAVE FAILED TO DIAGNOSE THE CONDITION
 MAJOR INDICATIONS IN ADULT PATIENTS ARE-
 1.NEPHROTIC SYNDROME
 2.ACUTE NEPHRITIC SYNDROME
 3.UNEXPLAINED ACUTE/RAPIDLY PROGRESSIVE
KID DIS
 4.PROGRESSIVE CKD OF UNKNOWN ETIO
 5.UNEXPECTED DETERIORATION OF GEN CNDTN
OF A PT WITH KNOWN CKD

25.  SUMMARY:
 1.PTS PRESENTS WITH DIFF CLINICAL
PRESNTATIONS.COMPONENTS OF DIA APPROACH-
 1.CAREFUL HSTRY TAKING,PHY XMNTN,ASSESSMNT
OF RENAL FUNCTN,URINANALYSIS,IMAGING
STUDIES,SEROLOGY AND BIOPSY IF NECCESSARY
 2.DEF OF AKI AND CKD
 3.CLASSIFICATION OF AKI-PRERENAL,ITRINSIC RENAL
AND POST RENAL.
 4.PTS WITH AKI/CKD MAY PRESENT D/T DIMINISHED
KID FNCTN/PROLONGED RENAL DISEASE,LAB
FINDNGS--RAISED
S.CREAT,HYPERKALEMIA,ALBUMINURIA,ACTIVE
URINARY SEDIMENT
 ,RADIOGRAPHIC FINDNGS

26.  5.ONCE KID DIS DISCOVERED----ASSESS THE DEGREE OF
DYSFUNCTION AND IDNTFY THE CAUSE
 REVIEW OF MEDICATIONS,GLYCEMIC CNTRL,PHY XMNTN,ETC
 IN PTS WITH RAISED S.CREAT WITH UNCLEAR ETIO DO USG ABD
 PT WITH NORMAL RENAL IMAGING WITH MINIMAL
PROTEINURIA AND BENIGN URINE SEDIMENT ---FURTHER
EVALUATION REQUIRED
 ----SPEP AND UPEP SHOULD BE DONE ----ABNOR-----
IMMUNOFIXATION OR SERUM FREE LIGHT CHAIN ASSA
 PTS WITH HIGH RISK OF MULTIPLE MYELOMA---INTIAL
EVALUATION WITHSPEP,UPEP,IMMUNOFIXATION,SERUM LIGHT
CHAIN ASSAY
 FOR PTS WITH UNREMARKABLE INITIAL WORK UP FURTHER
EVALUATION IS REQUIRED
 AMONG PTS WITH MILD DECREMENTS IN EGFR (45-60ML/MIN)--
--REPEAT S.CREAT AFTER4-8 WKS
 IF S.CREAT IS STABLE--- EVALUATE INTERMITTENTLY