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Internal Medicine Resident Half-Day Ahsan Alam, MD. Acute Renal Failure. Internal Medicine Resident Half-Day Ahsan Alam, MD. Acute Kidney Injury. What is Acute Kidney Injury. Abrupt decline in GFR Increase in serum creatinine P UF = (P GC - P T ) - ( p GC - p T )

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Internal medicine resident half day ahsan alam md

Internal Medicine Resident Half-Day

Ahsan Alam, MD

Acute Renal Failure

Internal medicine resident half day ahsan alam md1

Internal Medicine Resident Half-Day

Ahsan Alam, MD


What is acute kidney injury
What is Acute Kidney Injury

Abrupt decline in GFR

Increase in serum creatinine

PUF = (PGC - PT) - (pGC - pT)

Varying definitions (RIFLE, AKIN, etc)

Why do we care about AKI?

Mortality with hospital-acquired AKI

Mortality post cardiac surgery

Nash K et al. Am J Kidney Dis 2002;39(5):930-936

Lassnigg, A. et al. J Am Soc Nephrol 2004;15:1597-1605

Case 1
Case #1

A 76 yr old female presents to ED with abdominal pain and dyspnea

Serum creatinine is 135 mmol

Does she have AKI?

Diagnostic approach
Diagnostic Approach

Time of onset – prior serum creatinine

Careful review of history and physical exam



Current illness (vomiting, diarrhea, blood loss, etc)

BP, volume status, skin lesions, flank/abdominal signs

Case 11
Case #1

DM2, HTN, CAD (CABG 2004), CVA 2000 (right CEA 2009), hypothyroidism


telmistartan 80 mg, ramipril 10 mg, furosemide 40/80 mg, metoprolol, clonidine, atorvastatin, clopidogrel, insulin, thyroxine

If this is AKI, what are the most likely diagnoses?

Causes of Hospital-Acquired AKI and Mortality

4,622 consecutive patients

7.3% with AKI

Nash K et al. Am J Kidney Dis 2002;39(5):930-936

Case 12
Case #1

The patient undergoes investigations for her symptoms in hospital…

Case 13
Case #1


Case 14
Case #1


*Stage 2-3 AKI

AKI Network (AKIN) Classification

Lopes, J. A. et al. Crit Care 2008;12(4):R110

Risk factors for aki
Risk Factors for AKI

Lameire et al. NDT. 2008;6:392

Consistent risk factors
Consistent Risk Factors

  • Age

  • Hypovolemia

  • Hypotension

  • Sepsis

  • CKD

  • Hepatic dysfunction

  • Cardiac dysfunction

  • DM

  • Exposure to nephrotoxins

Differential diagnosis of aki
Differential Diagnosis of AKI




Pre renal


Diuretics, trauma, surgery, burns, hemorrhage, pancreatitis, GI loss, etc.

Decreased effective circulating volume

Nephrotic sydrome, cirrhosis, CHF, tamponade, massive PE, etc.

Renovascular obstruction

RAS/atherosclerosis/thrombosis/embolism, dissecting aneurysm, vasculitis, compression

Impaired glomerular autoregulation

NSAIDs, ACEi/ARB, calcineurin inhibitors

Intrinsic renal
Intrinsic Renal

Glomerular and small vessel diseases

Rapidly progressive GN, endocarditis, post-strep GN, vasculitides, scleroderma/malignant HTN, HUS, PET, DIC

Interstitial nephritis

Infection-related, inlammation, drug-induced, infiltrative (lymphoma, leukemia, sarcoidosis)

Tubular Lesions

Post-ishemia, nephrotoxic (drugs, contrast, anesthetics, heavy metals), pigment nephropathy, light chain, hypercalcemia

Post renal

Bladder flow obstruction

Urethral, bladder neck (BPH), neurogenic bladder

Ureteral obstruction (bilateral or single kidney)

Stones, clots, tumours, papillary necrosis, retroperitoneal fibrosis, surgical ligation

Urine output and aki
Urine Output and AKI


< 50 cc / 24 hrs


< 500 cc / 24 hrs


Normal urine output, but inadequate clearance

GFR 2 ml/min will produce ~3L of urine/day if there is no tubular reabsorption

Diagnostic approach1
Diagnostic Approach

Urine dipstick

Urine microscopy

Cellular elements

RBC, WBC, Renal tubular epithelial cells

Other (squamous, vaginal)


Hyaline, granular, waxy, RBC, WBC, tubular cell


Bacteria, yeast



Specific gravity










Urine findings
Urine Findings

WBC casts - pyelonephritis


Urine findings1
Urine Findings

Crystalluria – uric acid

Crystalluria – calcium oxalate

(ethylene glycol toxicity)

Urine findings2
Urine Findings

RBC casts - GN

Dysmorphic RBC - GN

Urine findings3
Urine Findings

Muddy brown casts – acute tubular necrosis

Urine findings4
Urine Findings


Specific gravity













80 yo female found on the floor of her apartment after 2 days, SCr 400 mol/L, K 6.8 mmol/L, CK 54,000


Limitations of FeNa

Diuretic use

Post-ischemic ATN who have less severe disease

AKI on chronic pre-renal disease (cirrhosis, CHF)

Contrast or pigment nephropathy

Acute GN or vasculitis


FE of urea, lithium, uric acid

FeNa = UNa/PNa x 100



Assess kidney size/morphology


Kidney biopsy
Kidney Biopsy

Intrinsic renal AKI


Isolated glomerular hematuria with proteinuria

Nephrotic syndrome

Acute nephritic syndrome

Unexplained acute or rapidly progressive AKI

Kidney biopsy1
Kidney Biopsy

Crescentic GN

Principles of aki management
Principles of AKI Management

  • Identify AKI

  • Avoid further nephrotoxic injury

  • Optimize renal hemodynamics

  • Treat complications

    • Fluid balance, electrolytes, uremia

  • Nutritional support

  • Renal Support (RRT)

  • Monitoring after AKI


  • Pre-renal

    • Calcineurin inhibitors, radiocontrast, ACEi/ ARB, NSAIDS, amphotericin B

  • Intra-renal

    • aminoglycosides, amphotericin B, cisplatin, cephalosporins, sulfa, rifampin, NSAIDS, interferon

  • Post-renal

    • acyclovir, MTX, indinavir, sulfadiazine

  • Review renal dosing of medications

Fluid management
Fluid Management

  • Correct fluid deficit

    • Will not guarantee AKI prevention

    • Studies of PA catheters did not reduce AKI

  • High urine flow in specific conditions

    • Myoglobinuria, tumour lysis, contrast media, etc.

  • Little evidence on fluid choice

    • Crystalloids

    • Hypooncotic colloids (4% albumin)

    • Hyperoncotic solutions (HES, dextrans) carry risk of renal dysfunction

Renal perfusion and vasoactive agents
Renal Perfusion and Vasoactive Agents

  • No support for

    • Loop diuretics

    • Dopamine

  • Selected use of

    • Mannitol (Rhabdomyolysis, post-cardiac surgery)

  • Unclear support for

    • Natriuretic peptides (ANP, BNP)

    • Fenoldopam (DA agonist)

    • Theophylline (adenosine antagonist)

Renal perfusion
Renal Perfusion

  • Vasopressors

  • Inotropes to improve low cardiac function

  • Target MAP needs to be individualized

    • Commonly 65 mmHg

    • Higher in elderly where autoregulation impaired

Nutrition in aki
Nutrition in AKI

  • AKI is a catabolic state

    • Inadequate nutritional support can delay renal recovery

  • Cochrane review 2010:

    • “There is not enough evidence to support the effectiveness of nutritional support for AKI…”

  • Adequate calorie delivery in anuric patient will necessitate RRT

Treat complications
Treat Complications

  • Monitor and correct electrolytes, acidosis

  • Renal replacement therapy

    • If indicated, do not withhold until patient is anuric

Indications for dialysis
Indications for Dialysis



Electrolyte disturbance


Overload (volume)


Natural history of aki
Natural history of AKI

Cerda et al. cJASN. 2008;

Case 15
Case #1


*Stage 2-3 AKI

Fluids isotonic vs hypotonic
Fluids – Isotonic vs. Hypotonic

Isotonic saline (0.9%) more protective than half normal (0.45%)

1,620 pts undergoing cardiac catheterization

Goal is to achieve ‘good’ urine flow

Mueller C et al. Arch Intern Med. 162: 329-336, 2002


Optimal rate and duration is not clear

IV rate >1-1.5 ml/kg/hr to achieve urine flow >150 ml/hr

At least 1hr (3-12hr) prior and 3-6hr (6-12hr) after contrast

Bicarbonate vs Saline

Zoungas S et al. Ann Intern Med 2009;151:631-638

Bicarbonate vs Saline

Zoungas S et al. Ann Intern Med 2009;151:631-638

Bicarbonate vs Saline – Adverse Events





Zoungas S et al. Ann Intern Med 2009;151:631-638


Effectiveness is uncertain

Evidence that it should be preferred over isotonic saline is weak and inconsistent

N acetylcysteine rationale
N-Acetylcysteine – Rationale

Scavenger of free radicals

Vasodilatory properties; enhanced NO availability

Attenuates ischemic injury in animals

N acetylcysteine

Kelly AM et al. Ann Intern Med 2008;148:284-294

Standard vs high dose nac
Standard vs. High Dose NAC

N=354, <12h post STEMI

Standard: 600 mg IV pre, 600 mg PO bid post

High: 1200 mg IV pre, 1200 mg PO bid post

In-hopsital mortality:11% placebo 4% low-dose3% high dose

Marenzi G et al. N Engl J Med 2006;354:2773-2782

N acetylcysteine1

Actual benefit is debatable, but safe* and inexpensive

Appropriate to give IV or high-dose oral

Give in combination with IV isotonic fluids

Contrast medium
Contrast Medium

Limit ‘volume’ of iodine

Iso-osmolar or low-osmolar contrast preferred

IA: iso-osmolar

IV: low or iso-osmolar

grams iodine/GFR < 1

Muhc ct contrast
MUHC CT Contrast

Iohexol (Omnipaque)

Low-osmolar; Omni 300 ~ 650 mOsm/kg

Iodixanol (Visipaque)

Iso-osmolar; Visi270 or 320 ~ 290 mOsm/kg

Both non-ionic

Concentration from 140-400 mg iodine/ml

Hemodialysis hemofiltration

5 trials with conflicting results

RR for AKI 1.35 (95%CI 0.93-1.94)

Insufficient evidence to recommend prophylactic hemodialysis or hemofiltration

Case 2
Case #2

58M with EtOH cirrhosis, admitted for SBP

4 months ago creatinine 68 , now 220

What may be the cause of his kidney dysfunction, and how would you manage?


Chronic or acute liver disease with advanced hepatic failure and portal hypertension

SCr > 133 mg/dl or 24-hr CrCl < 40 ml/min

No improvement in SCr after diuretic withdrawal and plasma volume expansion (saline 1.5 L) +/- with albumin (1 g/kg to max of 100 g/day)

No nephrotoxin, shock, infection, GI loss

No parenchymal renal disease (no proteinuria microhematuria and/or abnormal US)

Minor diagnostic criteria

Urine volume < 500 mL/d

UNa < 10 mEq/L

UOsm > POsm

Urine RBC < 50/hpf

Serum Na < 130 mEq/L

Treatment to reverse hrs
Treatment to Reverse HRS

Which of the following have been shown to be effective?


Combination Midodrine and Octreotide





Intravenous albumin in addition to antibiotics improves survival in SBP

Sort et al. NEJM 1999;341:403

Albumin indicated when doing paracentesis

Improved outcomes when combined with pressors

Midodrine and octreotide
Midodrine and Octreotide

Octreotide 100 ug sq TID increasing to 200 ug sq TID

inhibitor of endogenous vasodilators and glucagon

Midodrine 7.5 mg po TID increasing to 12.5 mg po TID

peripheral vasoconstriction

Midodrine and Octreotide sometimes helpful

Response rate about 30-50%


Effects of Noradrenalin and albumin in patients with Type I HRS: A Pilot Study. Hepatology 2002; 36:374

Noradrenaline started at 0.1 ug/kg/min and increased every 4 hrs based on BP by 0.05 ug/kg/min to max of 0.7 ug/kg/min

Combined treatment lowered creatinine from 2.6 to 1.6 over 10 days

Overall 2-month survival in this group of 12 patients was 58%


Numerous studies have shown a benefit in treating patients with HRS benefit is generally a 50% improvement in GFR.

Better when combined with albumin

Ischemic complications and worsening of cerebral hyperemia

Effect is not long lasting

Case 3
Case 3

68 year old female admitted with worsening dyspnea, leg edema

Known CAD, CHF (LVEF 10%), DM2, CKD (Cr 140), …

Meds: ACEi, BB, nitrate, loop diuretic, aldactone, statin, ASA, insulin, etc.

Aggressively diuresed for 3 days, Cr 250

Cardio renal syndrome
Cardio-Renal Syndrome

AT blockade interferes with autoregulation and may need to be held if GFR deteriorates

Avoidance of agents which interfere with renal sodium handling

NSAIDs, Coxibs, Thiazolidinediones

Nephrotoxic agents (e.g. contrast)

Serum potassium may also limit continued use of RAS blockade or K-sparing diuretics