Transcript The Patient with Elevated Creatinine

Approach to the Patient with
Elevated Creatinine
By: George Tsimiklis 2004
Revised previous edition by:
Lianne Tile MD FRCPC Med
Objectives
• To identify appropriate strategies for
investigation of the patient with increased
creatinine
• To discuss interventions that may alter the
course of disease
• To discuss indications for referral to a
nephrologist
Stages of Renal Failure
Stages of Renal Failure
GFR (cc/min)
Mild
60-90
Moderate
30-60
Severe
10-30
End-stage
<10
Creatinine is an estimate of GFR
Cockcroft-Gault:
(140-age) x wt x 100 = GFR (cc/min)
72 x serum Cr
GFR (females) = GFR (males) x 0.85
CASES: What is Considered an
ELEVATED Creatinine?
55 yo 70 kg male with Cr of 220:
GFR =37
moderate
75 yo 45kg female with Cr of 220: GFR = 16
severe
75 yo 45kg female with Cr of 85:
GFR =40
moderate
75 yo 45kg female with Cr of 45:
GFR =76
mild
Workup of the patient with high Cr
• Approach
– 1. Identify chronicity (Acute vs chronic)
– 2. Identify the cause, especially reversible
causes
– 3. Identify Indications for Referral to a
Nephrologist
– 4. Initiate a cause specific management plan in
a multidisciplinary team.
Acute vs Chronic Renal Failure
ACUTE
- Fever/ hematuria
- Hypovolemia
- Hydroureter
- Sepsis
- New hypertension
- Recent nephrotoxins
- No hypocalcemia
- No hyperphosphatemia
- No anemia
CHRONIC
- previous confirmed
nephropathy
- Already diminished CrCl
- Atrophic kidneys (<10cm
on U/S)
- Normochromic
normocytic anemia
- Hypocalcemia
- Hyperphosphatemia
Major Causes of Renal Failure
• Prerenal: decreased glomerular perfusion
– volume depletion: diuretics, poor intake
– decreased effective circulating volume: forward heart
failure, cirrhosis, sepsis
• Renal
– Vascular disease: acute (vasculitis, thromboembolic,
HUS/TTP, malignant hypertension) vs. chronic (renal
artery stenosis, HTN/nephrosclerosis)
– Glomerular disease: nephritic vs. nephrotic
– Tubular/interstitial disease: acute (ATN, AIN, myeloma)
vs. chronic (PCKD, pyelo, autoimmune, analgesic abuse)
• Post-Renal/ Obstructive Nephropathy
– Malignancy, prostate hyperplasia/ cancer
History and Physical Exam
• signs or symptoms of
– underlying disorder: i.e. volume status, flank pain,
obstruction, diabetes, hypertension, vasculitis
– altered kidney function: urine output, urine
discoloration, edema
– renal failure: anorexia, vomiting, altered mental status,
HTN
• medications: NSAID, ACEI, analgesics,
aminoglycosides, contrast, Chinese herbs
Initial Laboratory Investigations
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Urinalysis: hematuria, pyuria, proteinuria
Urinary Sediment: casts, GN
Urine Volume: oliguric, obstruction
24-hour Urine protein and CrCl
Urea:
Electrolytes
CBC: thrombocytopenia: TTP, HUS; Anemia: cause or effect of renal
disease; Leukocytosis: ?pyelo, infection
Glucose: DM?
Bicarbonate: metabolic acidosis
Calcium and Phosphate
Protein and albumin
Serum protein electrophoresis
UptoDate
Subsequent Laboratory
Investigations
Blood Tests
• Immunity Studies: ANA, anti-DNA, RF, ANCA, C3, C4
• Inflammatory Studies: ESR, CRP
• Serology: Hep B, HIV, Bence-Jones
• Urinary Eosinophilia: AIN, embolic disease
• CK
• Liver enzymes, hepatitis: secondary GN
Imaging
• Ultrasound
– rule out obstruction, stones, mass
– small kidneys suggest chronic process
– normal sized kidneys do not exclude chronic disease
(amyloid, DM,myleoma, PCKD).
– Doppler may be used to assess blood flow of arteries
(RAS) or veins (thrombosis)
• CT Scan - useful for stones and masses
• If suspected renal artery stenosis: MR angiography
(no nephrotoxic dye), renal angiogram
Renal Biopsy
• Should be considered:
– if noninvasive tests have failed to establish a
diagnosis in a patient with:
• nephrotic syndrome (except in DM)
• Certain cases of non-nephrotic proteinuria if
associated with renal dysfunction
• Lupus nephritis (for dx and staging)
• acute nephritic syndrome
• unexplained acute/ subacute renal failure
• to differentiate GN from vasculitis
– to direct and evaluate effectiveness of therapy
Management of Renal Disease
• Treatment of Reversible Causes
• Preventing or Slowing Progression
– Hypertension Control (<130/80)
– Control Proteinuria (<500-1000mg/day or 60%
from baseline values)
• Treating and Preventing the Complications
• Identifying Individuals Requiring Renal
Replacement Therapy
Hypertension
• Controlling BP slows progression of disease
• target <125/80, lower if normotensive at baseline or
with more proteinuria
• Slowing of disease is related to decreased systemic BP,
decreased glomerular hypertension, and decreased urine
protein excretion
• Microalbuminuria is a major cardiovascular risk factor!
AII Inhibition
• ACEI/ ARBS are more effective than other
medications in slowing progression:
– Also benefit normotensive diabetics
– Secondary actions include decrease glomerular
remodelling
• preferential antiproteinuric effect
• decreases AII effects
• slows the progression of renal disease in type 1 and
2 DM independent of the effect on BP
• in nondiabetics, most convincing effect is in
patients with greater proteinuria
Other Antihypertensives
• ARB:
– benefit similar to ACEI seen in DM-2
– may be additive benefit with ACEI
• Verapamil, Diltiazem or beta-blocker
– antiproteinuric effect in diabetics
• Other medications to achieve BP goals
Diet: Protein Restriction
• Dietary protein restriction (0.4-0.6
g/kg/day) reduced the risk for renal failure
or death in nondiabetic renal disease and
slowed nephropathy in type I DM
• beneficial effects were unrelated to change
in blood pressure or glycemic control.
• NNT 5 to 50
• realistic to restrict to 0.8-1g/kg/day
Ann Intern Med. 1996 April 1;124: 627-32.
Dyslipidemia
• Abnormal lipid metabolism is common in RF
• Primary problem is hypertriglyceridemia
– LDL, HDL, chol may also be deranged
• CRF is considered a high cardiovascular risk
and therefore target lipid levels are as those
with CAD
• Some suggest that statins may benefit the
kidney independent of lipid lowering effects
Erythropoietin
• Indicated for Hgb <110
• Chk iron stores, folate, and B12
• In patients with ferritin <100 and sat <20%,
must supplement prior to commencement of
therapy and continue supplement while on
EPO
• Follow response to EPO and ensure
adequate residual stores
Case
• Your patient returns for follow-up after 6 months.
He has no new symptoms. You repeat his serum
creatinine. It is now 185 (from 155).
• At what creatinine level would you refer him to a
nephrologist?
a) Now (185)
b) 250
C) 310
Referral to Nephrologist
• Late referral (< 12 months pre dialysis) is common
• Survey of Ontario Family MDs:
– 84% would not refer with creat 120-150 (>50% loss of GFR)
– 28% would not refer with creat 150-300
– almost all would refer with creat>300
• Consequences of referral shortly before dialysis:
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more complications
longer hospitalization to initiate dialysis
more difficulty with initiation of dialysis
worse survival!
• Better outcomes with early multidisciplinary care
CMAJ 1999: 161:413-17
Canadian Guidelines
• Renal replacement therapy is NOT rationed (i.e.
everyone should be considered)
• Reversible causes should be sought at diagnosis
• At least 1 year is required to prepare for dialysis
• Refer, at the latest, at Cr clearance of 30 ml/min,
or Cr of 300
• But…there are probably not enough nephrologists/
clinics to meet this demand
– Adequate communication with the Nephrologist will
allow proper stratification of patients
CMAJ 1999: 161:413-17
For AIMGP Clinic
• It is reasonable to follow stable renal failure
patients, and work up and manage appropriately
• Refer to nephrology when:
– Cr >300 or Cr clearance <30 ml/min
– Renal biopsy indicated
– Indicators of aggressive disease are present:
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Rapid decline in creatinine
homeostatic derangement i.e. acidosis, volume overload, high K
high protein excretion
Difficult to control BP
low HDL
black race
In Summary
Conclusions
• When evaluating a patient with increased
creatinine, internists should:
– Identify and treat reversible causes of renal
failure
– Initiate management to slow the decline in renal
function
– Manage coexisting conditions
– Have clear indications for when to refer to
nephrology subspecialists
References
• Elevated Serum creatinine: recommendations for
management and referral. CMAJ 1999: 161:41317
• Approach to managing elevated creatinine. Can
Fam Physician. 2004;50:735-740.
• UptoDate