Renal Failure

Risk, Injury, Failure, Loss, End-Stage Renal Disease (RIFLE) Classification for the Definition of ARF

GFR Criteria Urine Output Criteria Risk Serum creatinine level increased 1.5 times or decrease in GFR of > 25% < 0.5 mL/kg/h for 6 h Injury Serum creatinine level increased 2.0 times or GFR decreased by > 50% < 0.5 mL/kg/h for 12 h Failure Serum creatinine level increased 3.0 times, GFR decreased by > 75%, or serum creatinine level decreased by > 4 mg/dL < 0.3 mL/kg/h for 24 h or anuria for 12 h Loss Persistent acute renal failure, complete loss of kidney function for > 4 wk End-stage renal disease End-stage renal disease for > 3 mo

* From Bellomo et al.12 GFR = glomerular filtration rate. The classification system includes separate criteria for creatinine and urine output. The criteria that lead to the worst possible classification should be used.

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Urea Cycle

UA

Heme-detects free Hb better than RBCs

Protein-doesnt pick up Bence-Jones

Casts-hyaline in dehydration, red is glomerulus, white is parenchymal

Proteinuria->3.5 g/24 hrs=nephrosis (glomerular process), also c edema and Hypercoaguable state

Minimum urinary output in adults is 0.5 cc/kg/hour, in kiddies 1 cc

Table 1: Evaluation Of Oliguria (Neligan)

Pre-Renal Renal (ATN) Post-Renal Specific Gravity >1.02 1.012 1.012 Urine Osm >400 300 ± 20 300 ± 40

U:P Osmolality

>1.5

U:P Creatinine

>40

<20

Urine Na (mEq/L)

<20

>30

<30

FENa (%)

RFI %

<1%

>1%

<1%

CCR (mL/min)

15-20

<10

BUN/Cr

>20

<10

ATN = acute tubular necrosis; CCR = creatinine clearance; FENa = fractional excretion of sodium; Na = sodium; U:P = urine:plasma. RFI = Renal Failure Index, calculated as Urinary Sodium / (Urinary Creatinine / Serum Creatinine)

Anuria is postrenal obstruction until proven otherwise. Consider abdominal compartment syndrome

Acute Renal Failure (ARF)

Get CBC, Lytes, Ca, Phos, Albumin, Mg. UA, U Lytes, U creatinine, If new, get renal UTS.

creatinine is from creatine breakdown; without GFR, it increases 1-2 mg/dl/day

Prerenal

Azotemia

caused by extracellular fluid loss / sequestration or impaired cardiac function

afferent arteriolar constriction

Can result in ATN

prostoglandins allow renal vasculature dilation so can also result from NSAIDs

ACEIs can also cause this state as they reduce perfusion pressure and allow dilation of efferent arteriole

FENa = (UNa / PlasmaNa) / (U creatnine / Plasma creatnine) x 100

UNa<30, FENa<1.0% with normal UA or scant hyaline casts in urine

Intrarenal Azotemia

Glomerular-red cell casts are diagnostic, proteinuria, hematuria

Interstitial-drugs (PCN, ASA) or infection, pyuria, WBC casts, eosinophils

Vascular-glomerular perfusion is interrupted by processes such as thrombosis, hypertension, HUS, TTP, and vasculitis

ATN

ischemia: prolonged prerenal

nephrotoxins: aminoglycosides, , contrast media (Always hydrate before, can also give lasix+benadryl).

pigmenturia: rhabdomyolysis

UNa>30, FENa>1%

pigmented granular casts, renal tubular epithelial cells, granular casts

If oliguric, has a higher mortality. Other organs effected: can give pericardial effusion, Qualitative PLT defect.

Postrenal Azotemia

Renal Replacement Therapy (HD)

consider when BUN>100-120 and/or creatinine>10

(Inten Care Med 2001;27:1685)

GFR is all that matters

Normal UO>800 cc/24 hrs

ARI Cr>1.4, Bun>22, <800 cc/24 hours or <200/6

ARF Cr>2.8, Bun>44, <400/24 or <100/6

Severe is ARF that requires RRT

Chronic Renal Failure

Cockcroft and Gault Creatinine Clearance=(((140-age) x Kg) / 72 x serum Cr), multiply by 0.85 if female or fat

Diabetes, HTN, HIV, Glomerular

Uremia, dementia, restless legs syndrome, anemia

Emergent Dialysis-APE, Severe HTN, HyperK, Acidemia, Pericarditis

Dialysis Complications-call surg immediately if shunt thrill is not present

Use dDAVP to reverse qualitative plt defect.

CAPD (peritoneal dialysis)->100 WBC=SBP, Remove cath if fungal.

Management

Tight blood pressure control to maintain renal perfusion (MAP 90-140)

Sodium balance as damaged kidneys can not retain sodium as well as healthy

Free water balance

Hemodialysis Emergencies

Access Emergencies

How to tell fistula from graft

Fistula 1 scar soft to touch

Graft 2 scars feels artificial/hard to touch

Potential Causes of Intradialytic Hypotension (IDH)

Volume depletion
Pericardial Effusion with tamponade
LV dysfunction
Autonomic neuropathy (DM)
Antihypertensive medications
Sepsis
Acute MI
Pulmonary embolism
Occult hemorrhage
Air embolism
Dialyzer reaction
Arrhythmia

Generally, a normal period of hemodialysis removes about 100 mEq/L of potassium. Following hemodialysis, potassium levels may rebound as much as 30% up to 5 hours post-treatment. Therefore, if a patient is being treated for hyperkalemia, a post-treatment potassium level should not be drawn until 2-3 hours after the completion of dialysis (11). Likewise, when we see a patient post-dialysis for any problem and the potassium is reported as low, fight the desire to replace the potassium!

Lay air embolism flat ((6) Muth C, Shanh: Gas Embolism. NEJM 342:476-482 Feb. 17, 2000)

Probably no benefit to diuretics in renal failure, but study confounded b/c only patients who had a renal consult were included (JAMA 288(20):2547, November 27 2002)

Occasionally when a new catheter is first utilized, there may be some oozing of blood from the exit site of the skin. To treat this, place postage size pieces of gelfoam in a cup containing reconstituted thrombin. Using a hemostat or pickups, place the thrombin soaked pieces of gelfoam onto the oozing site, using a few layers if necessary and cover with sterile gauze. Place a bag of IV solution on the site as a compressive force and go see a few patients. When you return in 30-45 minutes, the oozing should have stopped (16).

All EPs have palpated the thrill of a functioning graft. The thrill predicts blood flow through the graft as being > 450 ml/min. while a pulsation within the graft suggests lower flows. A worsening bruit suggests a stricture or stenosis (17). Hemodialysis center staff monitor graft flow, but when one of these problems occur, the patient may end up in the ED. Reduced or absent flow in these catheters can be treated using percutaneous transluminal angioplasty (PTA), surgical revision to correct a stenosis or perhaps Alteplase (TPA) administration for thrombosis. TPA is now available in single use vials for this indication (Cath flo, 2.2 mg vials).

Desmopressin (DDAVP) is a synthetic derivative of the antidiuretic hormone and induces the release of von Willebrand factor. It is given at a dose of 0.3μg/kg (maximum dose of 20 μg maximum) in 20-50 cc of saline over 20-30 minutes but is only effective for up to 8 hours (18). Cryoprecipitate has been used at a dose of 10 bags and is effective for up to 24 hours but concerns of hepatitis and HIV risks has made cryoprecipitate a less attractive treatment. Conjugated estrogen has also been used orally (2.5-5 mg/d) or intravenously at a dose of 0.6 mg/kg spaced 24 hours apart for four or five days. Estrogen reduces bleeding time for several days and is a potential alternative to cryo or DDAVP (18).

Nutrition

If nonoliguric, increase of 30 kcal/kg/day and maintenance of 0.5 g/kg of protein

If oliguric, 30-60 Kcal/kg/day 0.5-1 g day of protein or essential amino acids, no more than 50% fat

Increased bleeding time in Renal Failure

Give dDAVP 0.3 mcg/kg for renal patients with bleeding

Desmopressin 0.3 mcg/kg over 30 minutes

Cryoprecipitate 10 U IV over 15-30 minutes

Conjugated Estrogens 0.6 mg/kg IV over 40 minutes

Renal Failure in Sepsis

Relationship between fluid status and its management on acute renal failure (ARF) in intensive care unit (ICU) patients with sepsis: A prospective analysis J NEPHROL 2005; 18: 54-60 W. Van Biesen1, I. Yegenaga1, R. Vanholder1, F. Verbeke1, E. Hoste1, F. Colardyn2, N. Lameire1 ABSTRACT: Background: Sepsis carries a high morbidity and mortality, further enhanced by acute renal failure (ARF). Although fluid loading can prevent ARF in dehydrated patients, this approach could be risky in septic patients, since it can deteriorate oxygenation. This study evaluates the relationship between fluid status and management and ARF development in septic patients. Methods and patients: Patients admitted to the ICU between 1 January 2001 and 31 December 2001 were included if serum creatinine (Cr) was <2 mg% on admission, and if they developed sepsis. ARF was determined as a doubling of serum Cr, an increase of serum Cr >2 mg%, or oliguria <500 ml/24 hr. Results: 257 out of 2442 patients, admitted to the intensive care unit (ICU), developed sepsis, 29 developed ARF, 13 needed a renal replacement. ARF vs. non-ARF patients were older (65.2 ± 13.3 vs. 55.1 ± 17.4, p=0.002), had a higher central venous pressure (CVP) at day 1 (9.6 ± 4.3 vs. 5.2 ± 3.6 mmHg, p<0.001), and at day 2 (7.1 ± 5.1 vs. 5.1 ± 4.0 mmHg, p=0.03), a higher colloid fluid loading for the first 3 days (2037 ± 1681 vs. 1116 ± 1220 mL, p<0.03), a higher serum Cr (1.25 ± 0.39 vs. 0.96 ± 0.33 mg/dL, p=0.009) and an increase vs. a decrease in serum Cr during the first 24 hr (+0.30 ± 0.58 vs. – 0.31 ± 0.45 mg/dL, p=0.02), a lower diuresis (1347 ± 649 vs. 1849 ± 916 mL, p=0.005). There was no difference in APACHE II scores (19.2 ± 7.2 vs. 17.2 ± 6.6, p=0.1), or MAP (64.5 ± 12.4 vs. 67.9 ± 12.4, p=0.18). The fraction of inspired oxygen (FiO2) need in the ARF group increased from 40.4 ± 11.5 to 65.6 ± 24.2% from day 1 to day 2 (p=0.04), where it remained unchanged in the non-ARF group. The use of diuretics was higher in the ARF group (21/29 vs. 43/228, p=0.001). Conclusion: Septic patients developing ARF have an elevated CVP at day 1 of sepsis, indicating cardiodepression or intrarenal causes for hypoperfusion. These patients develop ARF despite further fluid loading. Respiratory function deteriorated in patients with ARF. Persistent fluid challenges should be avoided if they do not lead to an improvement in renal function, or if oxygenation deteriorates.

Review Article (NEJM 2004;351(2):161)

Trying to replace dopamine in sepsis:

Prophylactic fenoldopam

for renal protection in sepsis: A randomized, double-blind, placebo-controlled pilot trial Measurements and main results: The incidence of acute renal failure was significantly lower in the fenoldopam group compared with the control group (29 vs. 51 patients; p = .006). The odds ratio of developing acute renal failure for patients treated with fenoldopam was estimated to be 0.47 (p = .005). The difference in the incidence of severe acute renal failure (creatinine >300 µmol/L), however, failed to achieve statistical significance (10 vs. 21; p = .056). The length of intensive care unit stay in surviving patients was significantly lower in the fenoldopam group compared with the control group (10.64 ± 9.3 vs. 13.4 ± 14.0 ; p < .001). There were no complications of fenoldopam infusion. A direct effect of treatment on the probability of death, beyond its effect on acute renal failure, was not significant (odds ratio = 0.68, p = .1). Conclusions: Compared with placebo, low-dose fenoldopam resulted in a smaller increase in serum creatinine in septic patients. The clinical significance of this finding is uncertain. A large multiple-center trial is now needed to confirm these findings. (Crit Care Med 2005;33(11):2451)

Definitions

Uremic Pruritis

(Hemodial Int. 2005 Apr;9(2):180-8.

Systemic medical treatment The list of systemic medications reported to be beneficial in patients with uremic pruritus is a long one and includes antihistamine drugs,66 activated carbon,41 cholestyramine,42 nicergoline,43 opioid antagonists,44,67,68 a leukotriene inhibitor,69 erythropoietin,70 heparin,71 lidocaine,72 thalidomide,73 and fatty acids.74,75 Antihistamine drugs are frequently prescribed but the response is generally disappointing.31 Evidence-based information in this regard is scanty.66 A beneficial effect of ketotifen was reported in five patients with uremic pruritis, purportedly because of the ability of this drug to stabilize mast cell membranes.76 Activated carbon, which would possibly act by binding putative pruritogens in the intestinal lumen, was evaluated in a crossover double-blind placebo-controlled study, in which 20 patients were enrolled and treated with 6 g/day for eight weeks. Dropout rate was high and only 11 patients completed the study. Statistical significance in favor of treatment was only found in Phase 1 of the study using one-tailed statistics.41 Cholestyramine, presumably acting in a similar way, was found to improve pruritus in a double-blind, placebo-controlled trial with 10 patients. Treated patients received 5 g twice a day for four weeks.42 Initial reports of the beneficial effects of erythropoietin,70 naltrexone,44 and ondansentron78 in the treatment of uremic pruritus70 were not confirmed subsequently.5,77,79 Nicergoline, a dopamine-receptor antagonist with α-adrenergic blocker activity, was studied as a possible treatment for uremic pruritus in a crossover double-blind placebo-controlled fashion.43 Of 15 patients with chronic pruritus, 13 showed improvement, which was complete in eight. Discontinuation of the drug was followed by reappearance of the symptoms in 24 to 48 hr. The mechanism of action of nicergoline to control uremic pruritis is unknown. Omega-6 fatty acid supplementation is associated with increased synthesis of the anti-inflammatory prostaglandin E1 and lower production of the proinflammatory prostaglandin E2. In a study of nine dialysis patients receiving primrose oil for six weeks compared to six patients on linoleic acid as controls, uremic pruritus tended to improve in the primrose oil group but statistical significance was not found.75 In a crossover randomized, double-blind, placebo-controlled trial, we found that thalidomide, 100 mg at bedtime, was very effective in reducing pruritus in hemodialysis patients.73 The effects became obvious in the first days of treatment and were, in some patients, long-lasting. Following completion of the study, we have electively been using this drug to treat pruritus refractive to topical medicines. Owing to its teratogenic effects, thalidomide cannot be prescribed for fertile women. Because the drug is under the strict control of the Brazilian public health system, and is not approved for the treatment of uremic pruritus, access to this medication is at present very difficult. The mechanism by which thalidomide ameliorates pruritus is still unknown but may be related to its ability to reduce the production and/or release of mediators of inflammation.80 The possibility of inhibition of the pruritus pathway to cortex areas can also be considered because high-dose thalidomide can induce peripheral neuropathy.81

Medications commonly prescribed in the ED requiring dose reduction in dialysis patients [85]

Medication Recommended dose adjustment in ESRD Potential adverse effects if dose is not reduced/comments Anticoagulants Heparin None These drugs do not accumulate in renal failure but use with caution because of potentiation of bleeding diathesis of ESRD. Warfarin None Enoxaparin Reduce dose by 50% (0.5-1 mg/kg once a day) or avoid use. Increased risk of bleeding because of decreased renal excretion with resultant accumulation in kidney failure Antihypertensives Angiotensin-converting enzyme inhibitors (except fosinopril) Reduce initial dose by 50%. Excreted by kidneys. Risk of hyperkalemia Risk of hyperkalemia Angiotensin receptor blockers None Risk of hyperkalemia β-Blockers Reduce initial dose by 50% or administer standard dose every other day No dose adjustment needed for propranolol, labetalol, and metoprolol Furosemide Maximum single dose: 160-320 mg PO, 120-240 mg IV Not effective unless residual urine output is >500 to 1000 mL/d Higher doses may cause temporary deafness Analgesics, anticonvulsants, and gout medications Nonsteroidal anti-inflammatory agents/Cox-2 inhibitors Avoid unless absolutely needed. Increased risk of gastrointestinal bleeding Meperidine Avoid Metabolite (normeperidine) accumulates : neurotoxic Morphine and its analogs (hydromorphone, oxymorphone, codein, methadone) Reduce initial dose by 50%. Do not accumulate in chronic renal failure but possible increased sensitivity to the effect of these drugs Phenytoin No dose reduction but dose adjustment is based on free phenytoin level, not total level. Phenytoin protein binding reduced in chronic renal failure. This results in increased free-drug level. Colchicine Reduce daily dose by 50%: 0.5-0.6 mg PO every 8-12 h. Reduce to once daily and discontinue within a few days. Drug accumulation can result in pancytopenia, peripheral neuritis, myopathy, etc Allopurinol Reduce dose to 100 mg every 2 to 3 d. Risk of pancytopenia, liver damage, myopathy, exfoliative dermatitis, etc Antimicrobials Gentamicin or tobramycin No change in loading dose (1-1.7 mg/kg) Increased risk of vestibular toxicity Subsequent doses given only after each HD session See text for dose recommendations in CAPD patients. Cephalosporins One gram once every 24 h or 2 g after each HD Risk of seizures and neurotoxicity Penicillins (including ampicillin, ticarcillin, pipracillin) Reduce dose by 50% or decrease frequency of administration to every 12 h. Risk of seizures and neurotoxicity. Avoid potassium penicillin: risk of hyperkalemia Nitrofurantoin Avoid Accumulates with high risk of peripheral neuropathy Fluoroquinolones (norfloxacin, ciprofloxacin, levofloxacin) Reduce dose by 50% or give standard dose once a day. No dose adjustment needed for moxofloxacin Vancomycin One gram (15 mg/kg) IV loading dose followed by 500 mg IV after each HD session. Currently used high-permeability dialyzers remove 50% of the drug during each HD session. High levels of the drug can cause ototoxicity. See text for dosing in CAPD patients. Acyclovir Herpes simplex: 200 mg PO twice daily Risk of neuropsychiatric adverse effects if dose is not reduced Herpes zoster: 800 mg PO twice daily Valacyclovir Herpes simplex and herpes zoster: 500 mg after each HD session

Am J Kidney Dis. 2007 Jan;49(1):56-68.

Beneficial impact of fenoldopam in critically ill patients with or at risk for acute renal failure: a meta-analysis of randomized clinical trials. BACKGROUND: Acute kidney injury is common in critically ill patients. Fenoldopam mesylate is a potent dopamine A-1 receptor agonist that increases blood flow to the renal cortex and outer medulla. Because there is uncertainty about the benefits of fenoldopam in such a setting, we performed a systematic review of randomized controlled trials of intensive care unit patients or those undergoing major surgery. METHODS: BioMedCentral, CENTRAL, PubMed, and conference proceedings were searched (updated October 2005). Investigators and external experts were contacted. Two unblinded reviewers selected randomized controlled trials that used fenoldopam in the prevention or treatment of acute kidney injury in postoperative or intensive care patients. Studies involving the prevention of contrast nephropathy or containing duplicate data were excluded from analysis. Two reviewers independently abstracted patient data, treatment characteristics, and outcomes. RESULTS: A total of 1,290 patients from 16 randomized studies were included in the analysis. Pooled estimates showed that fenoldopam consistently and significantly reduced the risk for acute kidney injury (odds ratio [OR], 0.43; 95% confidence interval [CI], 0.32 to 0.59; P < 0.001), need for renal replacement therapy (OR, 0.54; 95% CI, 0.34 to 0.84; P = 0.007), and in-hospital death (OR, 0.64; 95% CI, 0.45 to 0.91; P = 0.01). These benefits were associated with shorter intensive care unit stay (weighted mean difference, -0.61 days; 95% CI, -0.99 to -0.23; P = 0.002). Sensitivity analyses, tests for small-study bias, and heterogeneity assessment further confirmed the main analysis. CONCLUSION: This analysis suggests that fenoldopam reduces the need for renal replacement and mortality in patients with acute kidney injury. A large, multicenter, appropriately powered trial will need to be performed to confirm these results.

Higher CVP and Lower DBP is associated with Increased Risk of AKI

(Critical Care 2013, 17:R278 )