how we should approach a patient with deranged renal parameters & how to rule out CKD.

1. Prof & HOD Dr K A S Murthy
Chair person Dr Ashok P
Guest Dr Kiran.KK
Presenter Dr VamsaVardhan P

2. What is AKI
 AKI is defined as -
 Increase in Serum Cr by 0.3 mg/dl within 48 hours
OR
 Increase in Serum Cr to 1.5 times of baseline, which is
known or presumed to have occurred within the prior
7 days
OR
 Urine volume <0.5 ml/kg/h for 6 hours.

3. AKIN Criteria

4. RIFLE Criteria

5. Why do we care about AKI

6. Epidemiology
• It occurs in
– 5% of all hospitalized patients and
– 35% of those in intensive care units
• Mortality is high:
• up to 75–90% in patients with sepsis
• 35–45% in those without sepsis

7. Etiology

9. Conceptual model for AKI
Kidney International Supplements (2012) 2, 19–36

10. Natural history of AKI
(8-22%)
(2-8%)
Kidney International Supplements (2012) 2, 19–36

11. c/f
 Asymptomatic
 elevations in the plasma creatinine
 abnormalities on urinalysis
 Signs and symptoms resulting from loss of kidney
function:
 decreased or no urine output, flank pain, edema,
hypertension, or discolored urine

12. Cont…
 Symptoms and/or signs of renal failure:
 weakness and
 easy fatiguability (from anemia),
 anorexia,
 vomiting, mental status changes or
 Seizures
 edema
 Systemic symptoms and findings:
 fever
 arthralgias,
 pulmonary lesions

13. Diagnosis
 Detailed history
 Blood urea nitrogen and serum creatinine
 CBC, peripheral smear, and serology
 Urinalysis
 Urine electrolytes
 U/S kidneys
 Serology: ANA,ANCA, Anti DNA, HBV, HCV, Anti GBM,
cryoglobulin, CK, urinary Myoglobulin

15. Differences between AKI & CKD
AKI CKD

16. Urine analysis

17. Urine analysis
 Unremarkable in pre and post renal causes
 Differentiates ATN vs. AIN. vs. AGN
 Muddy brown casts in ATN
 WBC casts in AIN (few rbc can +)
 RBC casts in AGN (few wbc can +)
 Hansel stain for Eosinophils - AIN

18. Urine output
 An acute reduction in urine output (oliguria - <400
mL/24 h & Anuria - <100ml/24 hr) usually denotes
more significant AKI (i.e., lower GFR).
 An Oliguria is associated with worse clinical outcomes.
 Non oliguric AKI seen in nephrogenic DI which is
characteristic of longstanding urinary tract
obstruction, tubulointerstitial disease, or
nephrotoxicity from cisplatin or aminoglycosides .

19. Urine output cont..
 Complete anuria (<100 ml/day )early in the course of
AKI is uncommon except
1) Hypovolemic shock
2) complete urinary tract obstruction,
3) renal artery occlusion,
4) overwhelming septic shock,
5) severe ischemia (often with cortical necrosis),
6) severe proliferative glomerulonephritis or vasculitis.

20. Urine colour (haematuria)
 Red or brown urine may be seen with or without gross
hematuria.
 If the color persists after centrifugation, then its
pigment nephropathy(rhabdomyolysis or hemolysis)
Endogenous Drugs Food substances
1) RBC
2) Hb
3) MYOGLOBIN
4) BILIRUBIN
5) MELANIN
6) PORPHYRIN
1) CHLOROQUINE
2) QUININE
3) RIFAMPICIN
4) SULPHONAMIDES
5) LEVODOPA
6) METHYLDOPA
7) NITROFURANTOIN
8) PHENOPHTHALEIN
9) PHENYTOIN
10) METRANIDAZOLE
1) BEETROOT
2) BLACK BERRIES
3) BLUE BERRIES
4) FAVA BEANS
5) ARTIFICIAL FOOD
COLOURING

21. Glomerular / Urologic bleeding
Glomerular Non glomerular/Urologic
Urine colour Dark red /cola
coloured /smoky
Bright red
clots - +
proteinuria + -
RBC morphology Dysmorphic Isomorphic
HTN & Edema + -
Renal function Decreased normal
URTI + -
Fever ,rash + -
Urinary voiding sym - +
trauma - +
Flank pain - +

22. CBC
 Anemia is common in AKI and is usually multifactorial in
origin.
 Severe anemia in the absence of bleeding
Hemolysis,
Multiple myeloma
Thrombotic microangiopathy
Collagen vascular disorders
(Thrombocytopenia, schistocytes on peripheral blood smear,
elevated LDH & low haptoglobin content)

23. Cont..
 Peripheral eosinophilia -
Interstitial nephritis
Atheroembolic disease
Polyarteritis nodosa
Churg-Strauss vasculitis
 Dyselectrolytemia:hyperkalemia &hyperphosphatemia
 Creatinine Phosphokinase increase – Rhabdomyolysis
 Uric acid increase - TLS & Rhabdomyolysis

24. Renal failure indices
PreRenal ATN
Specific gravity > 1.020 < 1.010
Urine osmolality (mOsm/kg) > 500 < 350
U osm/P osm > 1.3 < 1.1
Urinary Na < 20 > 40
U/P urea nitrogen > 8 < 3
U/P creatinine  40 < 20
FENa(%) < 1 > 1
RFI (renal failure index) < 1 > 1
FEurea (%) < 35 > 35

25. FENa :
UNa x Pna
FENa = ————— x 100
PNa x UCr
FENa < 1% (Pre-renal state)
 May be low in selected
intrinsic cause
 Contrast nephropathy
 Acute GN
 Myoglobin induced ATN
 FENa > 1% (intrinsic cause of
ARF)
 BUN/Cr helpful in
classifying cause of ARF
 ratio> 20:1 suggests
prerenal cause like
catebolic states, GIB ,
steroids , hypovolemia.

26. Radiologic evaluation
 Imaging with USG – PVR / CT KUB – post renal AKI .
(dilatation of pelvicalyceal system & HUN )
 Simple bladder catheterization can rule out urethral
obstruction.
 Obstruction can be present without radiologic
abnormalities in the setting of retroperitoneal fibrosis,
encasement with tumor, and also early in the course of
obstruction.
 Antegrade or Retrograde pyelography – high index of
suspicion of obstruction with normal imaging.

27.  Renal scan - assessing kidney size & echogenicity
- AKI vs CKD
 Large kidney in CKD :-
1) Diabetic nephropathy,
2) HIV-associated nephropathy,
3) Infiltrative diseases,
4) AIN (occassionally)
5) ADPKD

28.  Renal vessel doppler .
 MRI- gadolinium scan helpful ,but disadvantage of
nephrogenic fibrosis especially seen in oliguric AKI in
end stage(dialysis dependent).

29. Anion gap
 The anion gap may be increased with any cause of
uremia due to retention of anions such as phosphate,
hippurate, sulfate & urate.
 The co-occurrence of an increased anion gap and an
osmolal gap- ethylene glycol poisoning.
which also cause oxalate crystalluria.
 Low anion gap - multiple myeloma
(unmeasured cationic proteins)

30. Glomerulonephritis and Vasculitis (Intrinsic causes)
a) Depressed complement levels
b) High titers of Antinuclear antibodies (ANAs),
c) Antineutrophilic cytoplasmic antibodies (ANCAs),
d) Antiglomerular basement membrane (AGBM)
antibodies
e) Cryoglobulins

31. Complement levels in Acute Nephritic
syndrome – Low C3 & C4
Systemic causes Renal localized causes
1) SLE
2) Cryoglobulinemia(Hep C )
3) Bacterial endocarditis
4) Shunt Nephritis
1) Acute PSGN (low C3 &
Normal C4)
2) MPGN – type 1 (low C3 &
C4)
3) MPGN – type 2 (low C3 &
normal C4)

32. Acute nephritis –Normal Complement
Systemic Renal
1) PAN
2) HSP
3) Goodpasture’s syndrome
4) Wegener’s granulomatosis
5) Hypersensitivity vasculitis
1) IgA nephropathy
2) RPGN
3) Anti GBM localised to
kidney
4) Pauci-immuen GN (kidney
localised)

33. Kidney biopsy indications
1) Unexplained AKI.
2) Even in prerenal AKI >1 m duration
3) Rapidly progressive AKI
4) Dialysis dependent AKI
5) AKI – systemic disease / glomerular etiology
6) Significant proteinuria (> 1g/24 hr)
7) Microscopic hematuria with any degree of
proteinuria
 S.E :- Risk of bleeding in patients with
thrombocytopenia or coagulopathy.

34. Contraindication for P/C renal biopsy
Absolute Relative
a) Uncontrolled Htn
b) Bleeding diathesis
c) Widespread cystic disease /
renal malignancy
d) Hydronephrosis
e) Uncooperative pt
a) Single kidney
b) Antiplatelet / Anticoagulant
therapy
c) Anatomic abnormalities
d) Small kidney’s
e) Active urinary/ local skin
sepsis
f) Obesity

35. Biomarkers
 BUN and creatinine are functional biomarkers of
glomerular filtration rather than tissue injury and,
therefore, it is suboptimal for the diagnosis of actual
parenchymal kidney injury.
 Kidney injury molecule-1 (KIM-1) is a type 1
transmembrane protein that is abundantly expressed
in PCT injured by ischemia or nephrotoxins such as
cisplatin.
 KIM-1 is not expressed in appreciable quantities in the
absence of tubular injury or in extrarenal tissues.
(KIM-1’s - phagocytic properties to tubular cells.)

36.  Neutrophil gelatinase associated lipocalin ( NGAL , also
known as lipocalin-2 or siderocalin) .
 NGAL was first discovered as a protein in granules of
human neutrophils.
 NGAL can bind to iron siderophore complexes and
may have tissue-protective effects in the proximal
tubule.
 NGAL is highly upregulated after inflammation and
kidney injury and can be detected in the plasma and
urine within 2 hours of cardiopulmonary bypass –
associated AKI.

37. Novel biomarker

38. Complications of AKI
1) Uraemia
2) Hyper / hypovolemia
3) Hyponatremia
4) Hyperkalemia
5) Hyperphosphatemia / hypocalcemia
6) Metabolic acidosis
7) Bleeding
8) Infection risk
9) Cardiac –pericarditis, arrhythmia &pericardial effusion
10) Malnutrition

39. ATN
 Most common cause of intrinsic cause of ARF
 Often multifactorial
 Ischemic ATN:
 Hypotension, sepsis, prolonged pre-renal state
 Nephrotoxic ATN:
 Contrast, Antibiotics, Heme proteins

40. ATN
 Diagnose by history,  FENa (>2%)
 sediment with coarse granular casts, RTE cells
 Treatment is supportive care.
 Maintenance of euvolemia (with judicious use of diuretics,
IVF, as necessary)
 Avoidance of hypotension
 Avoidance of nephrotoxic medications (including NSAIDs
and ACE-I) when possible
 Dialysis, if necessary
 80% will recover, if initial insult can be reversed

41. Contrast induced nephropathy
 Most cases of Contrast induced nephropathy
manifested as an asymptomatic , transient decrease in
renal function & nonoliguric.
 CI-AKI - an increase in SCr by 425% or 0.5 mg/dl
occurring within 72 hours after contrast medium
administration, in the absence of an alternative
etiology for the decrease in kidney function.

42.  Nonoliguric variant creatinine levels usually peaks @
3-5 days & returns to normal @ 10-14 days.
 Oliguric variant creatinine levels peaks @ 5-10 days
& returns to normal @ 14-21 days.(may need dialysis)
Risk Factors:
CKD, Hypovolemia ,DM – nephropathy, CHF,
Advancing age, ongoing treament with
nephrotoxic drugs, multiple myeloma, hepatic
failure, prior load contras with in 48-72 hr & use
of diuretics etc .

43. Rx/Prevention:
 Crystalloids 1ml/kg/hr , 12 hours pre & post study
(0.5-1 lt)
 N-acetyl cystein 600 BID pre & post (4 doses)
 Adenosine antagonist (theophylline 200mg IV single
dose 30 min prior to study),
 Nahco3 infusion
 dopamine agonist(fenoldopam)
 Statins 80mg/day
Kidney International Supplements (2012) 2, 69–88

44. Rhabdomyolysis
 Common after trauma (“crush injuries”), seizures, burns,
limb ischemia occasionally after IABP or
cardiopulmonary bypass.
 Diagnose with  serum CK (usu. > 10,000), urine dipstick
(+) for blood, without RBCs on microscopy, pigmented
granular casts
 Treatment is largely supportive care (IV Fluids).

45. Acute GN
 Rare in the hospitalized patient
 Diagnose by history, hematuria, RBC casts, proteinuria
(usually non-nephrotic range), low serum complement
RPGN often associated with anti-GBM or ANCA
 Usually will need to perform renal biopsy

46. Atheroembolic AKI
 Associated with emboli of fragments of atherosclerotic
plaque from aorta and other large arteries.
 Diagnose by history, physical findings (evidence of other
embolic phenomena--CVA, ischemic digits, “blue toe”
syndrome, etc), low serum C3 and C4, peripheral
eosinophilia, eosinophiluria, rarely WBC casts.
 Commonly occur after intravascular procedures or
cannulation (cardiac cath, CABG, AAA repair, etc.)

47. AIN
 Usually drug induced
 methicillin, rifampin, NSAIDS
 Develops 3-7 days after exposure
 Fever, Rash , and eosinophilia common
 Usually Non-oliguric AKI
 U/A reveals WBC, WBC casts, + Hansel stain
 Often resolves spontaneously
 Steroids may be beneficial ( if Scr>2.5 mg/dl)

48. Treatment
 Optimization of hemodynamic and volume status
 Avoidance of further renal insults
 Optimization of nutrition
 If necessary, institution of renal replacement therapy

49. Indication for RRT
1) Symptoms of uremia ( encephalopathy..,)
2) Uremic pericarditis
3) Refractory volume over load
4) Refractory hyperkalemia
5) Refractory metabolic acidosis

50. Reference
 Harrison’s internal medicine 18th edition
 Brenner & Rector’s 9th edition
 CMDT 2013
 KDIGO clinical practice guidelines for AKI .
(JOURNAL OF THE INTERNATIONAL SOCIETY OF NEPHROLOGY -
2012)

51. Thank you