Categories of Volume Disorders • Intravascular/acute hemorrhage • Extracellular – Intra- and extravascular – Sodium and water loss • Diarrhea – Sodium and water gain • CHF with edema • Ascites • Total body water – Water loss • Diabetes insipidus – Water retention • SIADH
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Categories of Volume Disorders Intravascular/acute hemorrhage Extracellular –Intra- and extravascular –Sodium and water loss Diarrhea –Sodium and water.
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Categories of Volume Disorders
• Intravascular/acute hemorrhage• Extracellular
– Intra- and extravascular– Sodium and water loss
• Diarrhea
– Sodium and water gain• CHF with edema• Ascites
• Total body water– Water loss
• Diabetes insipidus
– Water retention• SIADH
Diagnosis of Volume Disorders
• Intravascular depletion– MAP = CO × SVR– Clinical signs
Serum Creatinine (SCr) Alone Is a Poor Indicator of Kidney Function
*Calculated with the MDRD equation.
2 patients with SCr levels of 1.5 mg/dL (0.133 mmol/L)
FemaleAge = 65 years
MaleAge = 25 years
Estimated GFR*: 73 mL/min
Estimated GFR*: 37 mL/min
Problem with Serum Creatinine in Estimating GFR
0
1
2
3
4
5
6
7
8
10 20 30 40 50 60 70 80 90 100 110 120
Ser
um
cre
atin
ine
(mg
/dL
)
0
0.088
0.176
0.264
0.352
0.44
0.528
0.616
0.704
Ser
um
cre
atin
ine
(mm
ol/
L)
Creatinine 0.5 mg/dL (0.044 mmol/L) to 0.8 mg/dL (0.071 mmol/L)GFR 100 to 60 mL/min
Cystatin C
• More sensitive in identifying milder impairments in renal function than serum creatinine
• Cystatin C-based equations may more accurate in the elderly and in patients with cirrhosis
• Levels are affected by thyroid status, inflammation, and corticosteroids
• Clinical utility remains to be established
Plot of GFR vs. Time in Patients with CKD
Key Points
• The estimated GFR should be calculated using the MDRD equation whenever a serum creatinine is measured in steady state conditions
• Plots of GFR vs. time are helpful in patient management and education
• Consider 24 hour urine collections for creatinine clearance in the following populations:– Near normal GFR– Extremes of age and weight– Amputees– Pregnant women – Cirrhotics
Etiology of Hospital Acquired AKI
Nash K, et al. AJKD 2002; 39: 930-936.
Cause % (n=377) Mortality
Decreased renal perfusion 39 13.6
Medications 16 15
Radiographic contrast media 11 14
Postoperative 9 2.8
Sepsis 7 76
Post–liver transplantation 4 28.6
Post–heart transplantation 2 37.5
Obstruction 2 28.6
Hepatorenal 2 71.4
Rhabdomyolysis 1 25
Glomerulonephritis 1 33.3
Medication-Induced AKI in Hospitalized Patients
Nash K et al. AJKD 2002; 39: 930-936.
Medication %
Aminoglycosides 30
Nonsteroidal anti-
inflammatory drugs 21
Piperacillin/tazobactam 11
Amphotericin B 10
Trimethoprim/sulfa 10
Cyclosporine 5
Angiotensin-converting
enzyme inhibitors 3
Multiple nephrotoxins 3
Ciprofloxacin, cis-
platinum, acyclovir,
ceftazidime
1
Acute Kidney Injury• Prevalence
– 1% all patients admitted to hospital
– 10-30% patients admitted to ICU
• Etiology
– Hemodynamic 30%
– Parenchymal 65%
• Acute tubular necrosis 55%
• Acute glomerulonephritis 5%
• Vasculopathy 3%
• Acute interstitial nephritis 2%
– Obstruction 5%
Evaluation of Renal Failure
• Is the renal failure acute or chronic?– laboratory values do not discriminate between
acute vs. chronic– oliguria supports a diagnosis of acute renal failure– small kidneys on US more common in chronic
renal failure
• What is the etiology of the renal failure?– Prerenal 30%– Intrarenal 65%– Postrenal 5%
5 Key Steps in Evaluating Acute Kidney Injury
1) Obtain a thorough history; review the chart in detail
2) Do everything you can to accurately assess volume status
-Protein on dipstick with +Sulfasalicylic acid assay for protein
Pigment nephropathy(Rhabdomyolysis with ATN)
Myeloma cast nephropathy
1+ protein
3+ protein
Obstructing stone
Urinary Sediment Urine DipstickDiagnosis
Key Points on Medication-induced AKI
• Medications are the second most common cause of cause of AKI in hospitalized patients (pre-renal azotemia is #1)– THINK DRUGS
• NSAIDs can result in significant nephrotoxicity in the elderly, and in patients with diabetes and/or CKD
• Consider AIN in patients on PPI’s with unexplained kidney injury and pyuria
• Use of oral phosphasoda preparations for bowel prep should be abandoned-use PEG based preps
Renal Biopsy-When?
• Exclude pre- and post-renal failure, and clinical findings are not typical for ATN
• Extra-renal manifestations that suggest a systemic disorder
• Heavy proteinuria• RBC casts
Tumor Lysis Syndrome• Acute oliguric renal failure associated with urate
levels > 15 mg/dl and hyperphosphatemia• Associated with overproduction and excretion of
urate and cell lysis resulting in increased release of potassium and phosphorus in patients undergoing chemotherapy or with a heavy tumor burden
• Urine urate/creatinine > 1• Urinary alkalinization may worsen calcium
phosphate precipitation and NS is as effective as urinary alkalinization alone
• Early dialysis indicated for oliguric AKI to decrease urate burden
Risk Stratification for TLS
Type of cancer
Risk
High Intermediate Low
NHLBurkitt's, lymphoblastic, B-ALL
DLBCL Indolent NHL
ALL WBC ≥100,000/microL WBC 50,000-100,000/microLWBC ≤50,000/microL
AMLWBC ≥50,000/microL, monoblastic
WBC 10,000-50,000/microLWBC ≤10,000/microL
CLL WBC 10,000-100,000/microL treated with fludarabine
WBC ≤10,000/microL
Other hematologic malignancies (including CML and multiple myeloma) and solid tumors
Rapid proliferation with expected rapid response to therapy
Remainder of patients
*From Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol. 2008; 26:2767-78.
Prevention of TLS• If there is a concern about tumor lysis, as predicted by an
elevated serum LDH, serum uric acid, or heavy tumor burden, the patient should be admitted for hydration and close monitoring of kidney function, serum potassium, phosphorus and uric acid.
• Patients with a preexisting reduction in GFR, oliguria and/or acidic urine, and volume depletion should also be hospitalized for hydration and observation.
• High-risk patients should be hospitalized for aggressive intravenous hydration and prophylactic rasburicase.
• Intermediate risk patients should receive allopurinol rather than rasburicase for prophylaxis in the absence of pretreatment hyperuricemia.
• Patients at low risk for TLS should receive hydration, but do not require hypouricemic therapy.
Renal Disease Associated with Multiple Myeloma
• Myeloma cast nephropathy– direct precipitation of casts in tubules– Factors favoring cast precipitation:
-affinity of light chains for Tamm-Horsfall protein
-high luminal Cl-
-volume depletion – Plasmapheresis may be beneficial
• RPGN most commonly seen with:– Lupus nephritis (DPGN, class IV)– Pauci-immune GN (ANCA associated)– Anti-GBM disease– less commonly: IgA, post-infectious
• Nephrotic presentations of ARF– Collapsing FSGS (HIV nephropathy)– Minimal change disease with ATN
• Cirrhosis with ascites• Serum creatinine >1.5 mg/dL (>133 µmol/L)• No improvement of serum creatinine (decrease to a level of <
1.5 mg/dL) after at least 2 days with diuretic withdrawal and volume expansion with albumin. The recommended dose of albumin is 1 g/kg of body weight per day up to a maximum of 100 g/day.
• Absence of shock.• No current or recent treatment with nephrotoxic drugs.
Absence of parenchymal kidney disease as indicated by proteinuria >500 mg/day, microhematuria (>50 red blood cells per high power field) and/or abnormal renal ultrasonography.
Salerno F, Gerbes A, Ginès P, Wong F, Arroyo V: Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut 2007: 56: 1310-8.
Hepatorenal syndromeMinor Criteria
• Urine volume < 500 mL/day
• Urine sodium < 10 mEq/L
• Urine osmolality > plasma osmolality
• Urine red blood cells < 50 per high-power field
• Serum sodium concentration < 130 mEq/L
Vasoconstriction in Hepatorenal Syndrome
Contrast-Induced Nephropathy(CIN)
• Most common definitions– absolute increase in serum creatinine level
of 0.5 to 1 mg/dL (0.044 -0.088 mmol/L) within 48-72 hours
– 25% increase in serum creatinine level within 48-72 hours
• Accounts for 12% of cases of acute kidney injury
• Marker for increased mortality
Contrast-Induced Nephropathy Risk Score in Patients Undergoing Coronary Angiography
Mehran, R. et al. J Am Coll Cardiol 2004;44:1393-1399.
•Same strategies as eGFR 31-60 mL/min•Consider hospitalization•Nephrology consultation•Dialysis planning
•Isotonic NaCl or NaHCO3 at 1-1.5 mL/kg/hr•Optimize cardiac output•Use non-ionic low osmolar or iso-osmolar contrast•Limit contrast volume to <100 mL•Consider NAC 600-1200 mg 2X/d one day prior to and 2X/d on day of study •Avoid repeat contrast exposures over course of next 4 weeks when possible
Serum Creatinine before discharge and then in 3 days
•Serial serum creatinine and electrolytes•Initially obtain above labs daily
Modified from McCullough PA, et al.Am J Cardiol. 2006; 98:2K-4K.
Withdrawal of Medications Around the Time of Contrasted Studies
• NSAIDs and Cox-2 inhibitors– Hold 1 day prior to the study until there is confirmation that
CIN has not occurred• Metformin
– Hold 1 day prior to the study until there is confirmation that CIN has not occurred
• Diuretics– May be detrimental– Hold for 1 day prior to the procedure and restart 1 day
following the procedure• ACE inhibitors and ARBs
– No data available – reasonable to continue during the procedure in the absence of hypotension or recent acute change in renal function
Interventions to Limit Risk of CIN-Key Points
• Optimize the effective circulating volume– Delay studies in patients with volume depletion,
circulatory collapse or decompensated congestive heart failure when possible
– Optimize congestive heart failure when possible
• Hydration with isotonic saline or sodium bicarbonate 1-1.5 ml/kg/hr starting 3-12 hours prior to the study and continuing for at least 12 hours after the study in moderate risk patients
Interventions to Limit Risk of CIN-Key Points
• N-acetylcysteine 600-1200 mg twice daily starting one day prior to and twice daily on the day of the study is reasonable
• Use minimal volumes of low osmolar or iso-osmolar non-ionic contrast
Nephrotoxicity of Gadolinium
• Ergün et al. Nephrol Dial Transplant 2006; 21: 697–700.– Retrospective review 473 patients with stage 3-4
CKD receiving intravenous gadolinium at a dose of 0.2 mmol/kg body weight (gadopentetate dimeglumine, gadodiamide and gadoterate meglumine)
– AKI defined as a 0.5 mg/dL rise in serum creatinine
• Frequency of AKI was 12.1% • Older age, low baseline creatinine clearance,
diabetic nephropathy and lower hemoglobin and albumin levels were risk factors for AKI.
Gadolinium and Nephrogenic Systemic Fibrosis
• Gadolinium was initially thought to be safe in renal disease and was widely used
• An unusual skin condition first identified in 1997 appeared in dialysis patients initially called nephrogenic fibrosing dermopathy, and more recently nephrogenic systemic fibrosis (NSF) or gadolinium-associated systemic fibrosis
• Nearly all patients with NSF have been exposed to gadolinium-based contrast agents and an association was first noted in 2006
• Usually seen in patients with advanced kidney disease
• Gadolinium has been found in tissue of patients with NSF
Perazella, M. A. Clin J Am Soc Nephrol 2008;3:649-651
Transmetallationof Gadodiamide
Nephrogenic Systemic Fibrosis
• Plaques, papules and nodules with a brawny wooden texture
• Starts symmetrically in legs, and may then involve the arms and trunk. The face is spared.
• Skin and periarticular fibrosis• Heart, lungs, skeletal muscle and diaphragm
can be involved• Associated with increased mortality (50% at
2 years, most deaths occurring within 6 months of diagnosis )
Nephrogenic Systemic Fibrosis
CD34 positive staining
From Clev Clin J Med 2008;75:95-111.
Influence of Inflammation on Development of NSF
*Proinflammatory event defined as all processes in which the body has sustained major tissue injury, such as vascular surgery, transplantation surgery, or other major surgery; sepsis, pneumonia, osteomyelitis, or other major infection; and arterial or venous thrombosis that has caused ischemia or organ or limb damage.
Sadowski EA et al. Radiology 2007;243:148-157.
Variable Odds Ratio
No. of proinflammatory events* per patient
5.068
No. of MR examinations per patients
2.618
NSF: Risk Factors
• Usually seen in stage IV-V CKD and severe AKI, but has been described in earlier stages (5-15% incidence and RR 10.7 in stage V disease)
• More patients with CKD have been exposed to gadodiamide (Omniscan) at higher doses (MRA)
• Active inflammation (recent surgery, infection)
Dialysis and Gadolinium
• Gadolinium-chelates rapidly equilibrate in the extracellular space and are excreted unchanged in the glomerular filtrate
• 65-80% is removed in a single hemodialysis session
• Peritoneal dialysis does not efficiently remove gadolinium-chelates
Recommendations Regarding Gadolinium-Key Points
• Evaluate patients for renal dysfunction prior to giving GBCA
• Avoid in patients with acute or chronic kidney disease when the eGFR is < 30 ml/min
• Strictly avoid in the setting of hepatorenal syndrome or in the perioperative period of liver transplant
• When use is deemed essential in high risk patients, an agent other than gadodiamide should be used at the lowest possible dose
• Obtain informed consent• For ESRD patients, dialysis should be performed
within 24 hours on 2 consecutive days
Gadolinium and Iodinated Contrast:When are they Unsafe?