...Like you have time to use the bathroom...
What are the patient's vital signs?
Generalized malaise, worsening HTN, dependent or generalized edema, decrease UO, abnormal UA, increased Sr. Cr. Etiology, risk factors. Needs for HD?
How much urine has been produced in the last 24 hours? In the last 8 hours?
Acute rise in serum creatinine >0.3 mg/dL or more, (>50%) within 48 hours, or a drop in UO (<0.5 mL/kg/hr x >6hrs)
Does the patient have a Foley catheter inserted?
If the patient has a Foley cathter inserted, ask the nurse to flush the catheter with 30 mL of NS.
If the patient does not have a Foley catheter inserted, ask the nurse to place one now. Record how much it puts out.
What are the patient's recent electrolytes, especially potassium, BUN, Cr, and HCO3?
Tell the nurse you will see the patient shortly.
Major Causes of Oliguria:
Pre-renal failure: Preserved intrinsic renal function in the setting of renal hypoperfusion and reduced GFR.
Effective circulating volume is decreased → intravascular volume depletion, low cardiac output or disorder vasodilation (hepatic cirrhosis). Hepatic failure → splanchnic vasodilation + venous pooling → reduction in effective circulating volume despite total body volume overload. This can progress to the hepato-renal syndrome (HRS), which is characterized by a rising creatinine in the setting of low SBP (90-100 mm Hg), mild to moderate hyponatremia (120-130 mEq/L), and a very low UNa excretion (<10 mEq/L).
Spontaneous bacterial peritonitis, overdiuresis, GIB, or large-volume paracentesis can precipitate HRS in a cirrhotic patient. Renal recovery occur by definitive treatment of liver d/o (either through recovery or via transplantation).
Hyovolemia (H'ge, dehydration, GI losses, surgery), hypotension (including sepsis), CHF, cirrhosis, nephrotic syndrome, abdominal compartment syndrome (IAP >20 mm Hg, measured by a pressure transducer attached to bladder catheter), from intestinal ischemia, obstruction, or massive ascites; Hepato-renal syndrome, burns, vascular occlusion, aortic dissection with involvement of renal arteries, and renovascular dz, loss of autoregulation (NSAIDs inhibit counterbalancing vasodilatory effect of prostaglandin), RAAS blockers) or ACE-I/ARB (can cause efferent arteriolar vasodilation and a ▼ GFR.)
Intrinsic renal failure:
Glomerular (PSGN, RPGN).
Tubular/interstitial (AIN, pyelonephritis, tubular necrosis caused by drugs or toxins like aminoglycosides, cisplatin, methotrexate, pentamidine, lithium, amphotericin-B, NSAIDs, allopurinol, captopril, cephalothin, cimetidine, ciprofloxacin, furosemide, THZ, PCN, phenytoin, pantoprazole, rifampin, indinavir, TMP-SMX), IV iodinated contrast induced resulting in renal vasoconstrtiction and is toxic to tubules. Vascular d/o: atheromatous emboli, vasculitis, HTN. Myeloma kidney, amyloid nephropathy, HUS, TTP. Rhabdomyolysis, hypercoagulable state. Endogenous chemicals: Hb, myoglobin.
Aminoglycoside nephrotoxicity (typically 5 days of exposure required) is typically nonoliguric, occurs from direct toxicity to the proximal tubules, and results in the renal wasting of potassium and magnesium. Replacement of these electrolytes is necessary. Same kind of picture is seen in cisplatin toxicity. Risk may be avoided by avoiding volume depletion and using an extended-interval dosing method.
Pre-renal processes if not corrected, will over time proceed to ATN, which is an intrinsic renal failure.
Ischemic ATN is the most common cause of renal failure in the ICU, and is a result of any process that leads to significant hypoperfusion of the kidneys, including sepsis, hemorrhage, or any prolonged prerenal insult. The injury results in sloughing of renal tubular cells, which can congeal with cellular debris in a matrix Tamm-Horsfall protein to form granular tests. These have a “muddy brown” appearance and a strongly suggestive of ATN in the proper context.
Pigment nephropathy from direct tubular toxicity by Hb and myoglobin. Vasoconstriction may also play a role. +ve urine dipstick for blood in the absence of RBCs on microscopic exam. In rhabdomyolysis, ▲ CPK x 10 times upper limit of normal with disproportionate rise in creatinine, potassium, and phosphorous.
Post-renal failure: flow of urine is obstructed → ▲ intratubular hydrostatic pressure leads to ▼ GFR.
Common causes: (BPH, tumor, bilateral kidney stones, cervical cancer, retroperitoneal fibrosis), clogged Foley catheter, neurogenic bladder, clot.)
Intravenous acyclovir and the protease inhibitor indinavir can induce ARF by closing microbstructive uropathy within the tubules by forming crystals.
Bilateral involvement (or unilateral obstruction to a solitary kidney) is required to produce a significant change in the creatinine level.
Renal U/S must be performed, if post-renal etiology is suspected, to evaluate for hydronephrosis. This may not be evident, if there is concomitant volume loss or if retroperitoneal fibrosis has encased the kidneys and ureters, preventing them to expand.
Things you don't want to miss:
Hyperkalemia (check for ECG changes)
Uremic encephalopathy
Respiratory distress
Pulmonary edema
Compensatory to metabolic acidosis (Kussmaul's breathing)
Metabolic acidosis
Cardiac arrhythmia
Intravacular volume depletion (3rd spacing)
Sepsis
Acute Renal Failure Complications:
Metabolic: Hyponatremia, hyperkalemia, hypocalcemia, hyperphosphatemia, hypermagnesemia, and hyperuricemia, metabolic acidosis, uremic encephalopathy, dehydration, third spacing
Cardiovascular: Pulmonary edema, arrhythmias, HTN, pericarditis
Neurologic: Asterixis, neuromuscular irritability, somnolence, coma, seizures
Hematologic: Anemia, coagulopathies, hemorrhagic diathesis
Gastrointestinal: Nausea, vomiting, bleeding
Infectious: Pneumonia, UTI, wound infection, septicemia
Key History:
Check BP, pulse, respirations, O2 saturations, and temperature.
What events preceded AKI: BP patterns, hydration status, medications, and radiocontrast dye in CT and Cardiac cath, other procedures. ABx dose and duration as well as PRN meds should not be overlooked.
Quickly look at the patient and review the chart.
Take a focussed history.
Onset of azotemia (acute: obstructive or vascular etiology like Ao dissection)
New onset:
Abdominal pain, n/v/d, light headedness, flank pain, hematuria, oliguria, dysuria, fevers, arthralgia, and rashes
Review Meds, OTC, herbal supplements. (NSAIDs, aminoglycosides, amphotericin B, indinavir, acyclovir, chemotherpeutic agents - cisplatin or methotrexate, and ACEI, ARBs. Try to temporally relate a new medication with a decreasing GFR is most helpful in establishing a drug as a causal factor.
IV contrast (iodinated)
Comorbidites: DM, HTN, CHF, cirrhosis, RAS, CKD, HIV, SLE, Sjogren synd, Goodpasture synd, Wegener granulomatosis, Strep. throat, multiple myeloma, leukemias, lymphomas, BPH, ADPKD
Determine volume status is important. Review ins and outs over the past few days. Any new medications (e.g., ACE-I)
Focussed Examination:
General: How distressed or sick does the patient look?
Low volume status - dry mucosa, poor skin turgor, low JVP, lack of axillary sweat.
Volume overload status - elevated JVP, pulmonary edema, S3, peripheral edema, ascites (may also reflect cardiomyopathy, cirrhosis)
Skin: rashes, joint effusions, (collagen vascular dz - SLE); Janeway lesions, Osler nodes
Vitals: Check orthostatics and weight over the past few days?
Orthostatic vital signs: drop in BP by at least 20/10 mm Hg or an increase in heart rate by 10/min after standing from a seated position. CVP <8 cm H2O.
Resp: Tachypnea could be a reflection of pulmonary edema or a compensatory response. Kussmaul respiration, or rapid, large tidal volume breaths may reflect compensation for a severe acidosis.
Cardiovascular: Check for JVD, murmur, friction rub (triphasic), cardiac arrhythmias.
Abdomen: Look for ascites or enlarged bladder?
Geniturinary: Check for enlarged prostate? Bladder obstruction (distended and painful bladder), pylonephritis (CVA tenderness). PVR urine >300 mL suggest bladder obstruction.
Extremities: Assess perfusion. Check for asterixis. Joint effusions.
Neurological: Mental status changes, neuro-deficits.
Laboratory Data:
Electrolyties (K, HCO3, BUN, Cr). A low HCO3 will require checking ABGs to evaluate for metabolic acidosis.
In general a patient with AKI will have a primary metabolic acidosis with respiratory compensation. It is critical to determine if the compensation is adequate.
Check for AG to determine if other factors beyond the accumulation of organic acids are contributing to the acidosis.
BUN/Cr (>20:1). BUN levels do not always correlate with the presence or degree of encephalopathy. E.g., Cr: 1 jumps to 3 in 24-hr = GFR is 0.
UA: look for cells, casts, protein; Urine C&S, gram stain by checking "active" sediment (urine sample centrifuged, sediment is resuspended in a very small volume of original urine and examined under the microscope. Electrolytes, urine electrolytes, AG, calculate FENa, urine eosinophils. Active sediment:
RBC casts = GN
Dysmorphic RBCs means glomerular source of bleeding and can be accompanied by RBC casts formed within the tubules.
WBC casts = pyelonephritis or interstitial nephritis.
Urine eosinophils seen in AIN, atheroembolic disease, or prostatitis.
Granular casts = ATN
Hematuria = > 3 RBCs/HPF
4+ protein on dipstick may suggest nephrotic synd. Not reliable way to quantify proteinuria. IV contrast dye may cause a false-positive dipstick protein.
4+ heme with no RBC may suggest rhabdomyolysis or hemolysis.
Sr. creatinine must be stable baseline, for urine protein:urine creatinine to be credible.
Protein >3 g/24 hr urine = nephrotic synd
Protein <3 g/24 hr urine, with RBC casts = nephritic synd
Spot urine protein mg: mg of urine creatinine ratio more practical alternative, provided the creatinine is stable. Both units must be same as this is a ratio.
Ratio >3.5 mg/mg = nephrotic range proteinuria
Ratio < 0.25 mg/mg is within normal limits.
If in mg:g; ratio <250 mg of urine protein/gm of urine creatinine.
Do 24-h urine protein collection if Sr. Cr is not stable baseline.
Interpretation of Urine Albumin to Creatinine Ratio
Normal Ratio (in general <30 mg/g is normal)
Men: < 0.017 (or 17 mg albumin to 1 gram Creatinine)
Women: <0.025 (or 25 mg albumin to 1 gram Creatinine)
Microalbuminuria: 30-300 mg or mcg albumin/g or mg Creatinine
Macroalbuminuria: >300 mg or mcg albumin/g or mg Creatinine
IV Contrast Dye may cause a false-positive dipstick protein.
CBC with differential
Leukocytosis with neutrophilia means inf
Leukocytosis with eosinophilia means interstitial nephritis (often secondary to meds).
Blood cultures
ASO titers
FENa = [(UNa x PCr) / (UCr x PNa)] x 100 . This equation is most useful with oliguric renal failure and in the absence of diuretics, but may be not be helpful in nonoliguric renal failure. Not valid if Pt is in nonoliguric ARF and/or in Pts have been exposed to loop diuretics in the previous day. The FeNa has limited utililty when ARF is superimposed on CKD. To calculate FeNa and FeUrea: urine sodium, urea, and creatinine can be obtained with simultaneous serum measurements.
Collected from "spot" urine sample.
FENa >1 - 2% with oliguria is almost always ATN, but can be prerenal with diuretics.
FENa <1% with oliguria is generally prerenal: suggestive of renal hypoperfusion with intact tubular function. Volume depletion, severe CHF, or nephrotic syndrome, NSAID or dye toxicity, sepsis, cyclosporine toxicity, acute GN, and HRS are some causes. Also calculate FEurea in nonoliguric renal failure.
[(Urine urea nitrogen x PCr) / UCr x BUN)] x 100. Used in nonoliguric ARF and/or in Pts have been exposed to loop diuretics in the previous day.
FeUrea <35% is consistent with pre-renal etiology.
FeUrea >50% is consistent with renal (tubular) etiology.
Pre-renal process over time, if not corrected, result ATN, which is an ntrinsic renal process.
ECG
Renal US should be ordered within 24 hours to rule out hydronephrosis and evaluate the renal system. Small kidneys <9 cm reflect chronic disease. Kidneys may be large in DM, HIV nephropathy, PKD. Discrepancy in kidney size of >2 cm suggest unilateral renal artery stenosis with atrophy of the affected kidney. Renal U/S may not show hydronephrosis if Pt is volume depleted or if retroperitoneal fibrosis has encased the ureters, preventing their expansion.
Renal cysts in medullary kidney disease
CT abdomen/pelvis without contrast (to avoid nephrotoxicity) can also be done. Most helpful test to check for renal stones, abdominal/pelvic tumor or abscess, or obstruction.
Partial bladder obst, neurogenic bladder, renal calculi, neurogenic bladder. Hydroureter, hydronephrosis, perinephric abscess.
Postvoid residual: Pt. attempts to urinate and then a urethral straight cath (or US bladder scan) is done. If ~900 mL urine collected, it indicates inability to properly void urine and the back-pressure is likely to injury the kidneys.
Doppler imaging for RAS or RVT
Radionuclide scanning using technetium - donor kidney
MRI and MRA for RAS and RVT.
TTE: LVEF, VHD, endocarditis, thrombus, pericardial effusion (uremia).
Renal Bx if cause is not known despite w/up and renal failure is progressive - hematuria, proteinuria.
Bx recommended if results alter management and a potentially reversible cause is suspected (high-dose glucocorticoids in RPGN)
Bx specimens are examined under light and electron microscopy and with immunofluorescence techniques that are used to detect various immunoglobulin subclasses as well as their light chains, complement components, and fibrin.
Hep-C, complement, cryoglobulins, ANCA, Anti-GMB antibodies
Management:
Admit, consult nephrologist.
Tx is based on identified etiology
Pre-renal causes can be initially managed with a small volume challenge, such as 250 - 500 mL NS bolus depending on the cardiovascular status of the patient. This can be followed by NS at a set rate. Specific criteria should be given to the nursing staff (i.e., call HO if urine output is <30 mL/hr). Alternatively, if CHF is suspected, the patient may need diuresis. Escalating doses of furosemide (Lasix) can be used and the urine output can be assessed. With a fluid challenge, the creatinine level often trends down by the next morning if the cause is prerenal.
Initial management should be directed at treating life-threatening electrolyte disorders, correcting volume contraction, and hypotension. Obtain diagnostic urinary studies before administering diuretics. Don't forget to adjust drug doses based on glomerular filtration rate.
Severe acidosis, altered mental status, respiratory distress, cardiac instability - ICU admit.
Urgent HD, continuous cardiac monitoring needed if electrolytes are abnormal and metabolic acidosis.
Oliguria is generally defined as <400 mL/day or 25 mL/hr x 4 hrs The minimum acceptable urine output is 30 mL/hour.
Oliguria: < 400 ml/day.
Anuria <50 mL/day.
Polyuria: >2,500 – 3000 mL/day.
If flushing the Foley catheter did not help, ask the nurse to change the Foley.
Hyperkalemia, CHF, severe acidemia, and pericarditis require immediate attention. Obtain recent electrolytes and a stat potassium.
If hyperkalemia suspected, order an ECG. A stat renal consult is required if the patient needs urgent dialysis.
Indications for urgent dialysis include:
Hyperkalemia (refractory to medical treatment)
Volume overload
Acidemia pH <7.2
Uremic encephalopathy
BUN levels do not always correlate with presence or degree of encephalopathy; look for other reversible causes of MS changes.
Uremic pericarditis
Post-renal causes can be potentially managed by placing a Foley catheter. Prostatic enlargement in men may impede urethral flow. If immediate flow is obtained by placing of Foley, Coude, or straight cath, urethral obstruction is likely. PVR urine >300 mL strongly suggest the diagnosis.
Nephrostomy tube or stent may be needed if upper urinary tract is involved
Relief of bilateral obstruction is frequently followed by post-obstructive diuresis. Monitoring of electrolytes and fluid during this period is critical (strict I/O is monitored). Replace half of the urinary volume by 0.45% saline to avoid hypotension.
For contrast-induced ARF prophylaxis, normovolemia is essential. Use 1/2 NS at 75 mL/hour for 12 hours. Iodinated contrast is a potent renal vasoconstrictor and is toxic to renal tubules. Renal injury occurs when the creatinine typical rise 24 hours after exposure and peaks in 3-5 days. Preventative measures include periprocedure hydration in discontinuation of diuretics. Sodium bicarbonate at 154 mEq/L, (3 ampules in D5W) can be given at 3 mL/kg/hr for 1 hour prior to exposure, then at 1 mL/kg/hr for 6 hrs after the procedure. Acetylcysteine may reduce the incidence of contrast nephropathy and is given as four oral doses of 1,200 mg, 12 hrs apart, with two doses given prior to the contrast study.
Management of ATN: Supportive, with avoidance of nephrotoxic agents. Fluid management to maintain euvolemia. If volume overload and oliguria become evident, duresis with furosemide 40-120 mg IV boluses or continuous drip at 10 to 20 mg/hr. This has not been shown to promote recovery but can simplify overall management.
Recover from ATN can take days to weeks, but can be expected in over 85% of patients with a previously normal creatinine. Dialysis may be needed to bridge the time of reccovery.
AIN resolves with removal of the offending agent, usually a drug. Sometimes, a short course of corticosteroid is given.
ARF in exacerbation of SLE need large doses of corticosteroids.
Cryoglobulinemia may additionally require cyclophosphamide and even plasmapheresis therapy.
Hematologic malignancies, acute uric acid nephropathy can result as part of the tumor lysis syndrome. ▲ Cr, hyperuricemia, hyperphosphatemia, and hypocalcemia. Ratio of urine uric acid to urine creatinine of >1 is consistent with diagnosis. Prophylaxis with allopurinol 600 mg can decrease uric acid production. Rasburicase (15 mg/kg IV) is highly effective in depleting uric acid levels and can be given as prophylaxis or as treatment. Alkalinization of urine is avoided if hyperphosphatemia is present as this could increase the risk of calcium phosphate precipitation in the urine.
Thrombotic microangiopathy (TMA) includes HUS and TTP.
Causes: bacterial toxins (diarrheal forms), medications (mitomycin-C, clopidogrel, cyclosporine, tacrolimus), and may be associated with pregnancy or malignancies of the GIT.
Atheroembolic disease seen in Pts with diffuse atherosclerosis, after procedures likel CABG, cardiac cath, IAPB, aortic aneurysm repair.
Physical findings: retinal arterolar plaques, lower extremity livedo reticularis, and areas of digital necrosis. Eosinophilia, eosinophiluria, and hypocomplementemia may be present, and WBC casts may be found in the urine sediment. However, in many cases ▲ Cr is the only abnormality in a step wise progression. Renal bx: cholesterol clefts in the small arteries. Anticoagulation may worsen the disease and avoided. No specific treatment exists. Many patients develop CKD, and ESRD ending up on HD.
Interstial: AIN involves inflammation of the renal parenchyma, typically caused by medicaitons or infections. Classic triad of fever, rash, and eosinophilia is seen in less than 1/3 of patients.
Pyuria, WBC casts, and eosinophiluria are all suggestive of AIN.
Beta-lactamase Abx are the most frequently cited causative agents, but nearly all Abx are implicated. Usually, takes 5 - 10 days after Abx use, for renal impairment to set in.
Other meds: PPI, allopurinol, NSAIDs
Streptococcal infections, leptospirosis, and sarcoidosis have all been implicated in AIN.
Tx: Withdraw of offending agent. Temporary dialysis may be needed. Short course of prednisone at 1 mg/kg may hasten recovery.
Renal Bx decision is made by nephrologist. It is helpful in situations in which a potentially treatable cause of ARF is being sought and the results would alter the Pt's management (high-dose of corticosteroids in RPGN).
Dysmorphic urinary RBCs, RBC casts, or proteinuria in the nephrotic range >3.5 g/d = glomerular disease
RPGN = nephritic picture with RBC casts, edema, HTN. Bx shows crescents formation in >50% glomeruli. Salvageable, treat with high-dose pulse glucocorticoid therapy (methyprednisolone 7 - 15 mg/kg/d x 3 days) followed by prednisone, 1 mg/kg/d PO x 1 month, then tapered over the next 6 - 12 months. Addition of cyclophosphamide, PO 2 mg/kg/d may be beneficial.
Cockgroft-Gault formula for creatinine clearance: (140 - age) x (IBW in kg) x 0.85 (for women)) / 72 x Cr in mg/dL.
As renal function worsens, this formula has the tendency to overestimate the GFR.
MDRD (modification of diet in renal disease) formulas can calculate the GFR and take into account BUN, albumin, and race in addition to age and gender:
When the MDRD GFR i >60 mL/min/1.73 m2, CKD should not be diagnosed unless other evidence of renal damage (proteinuria) is present.