Acute Renal Failure

Acute Kidney Injury (AKI)CHAIRPERSON DR. SANJEEV KUMAR SPEAKER - DR. ASHISH KUMAR

DEFINITION

AKI is a sudden and usually reversible decrease in the glomerular filtration rate (GFR) occurring over a period of hours to days.

The term Acute Kidney Injury now replaces the term ARF; the term Acute Renal Failure should now be restricted to patients who have AKI and need renal replacement therapy.

ACUTE KIDNEY INJURYAbrupt reduction [ 500 ml/24h)ATNObstruction (partial)

INVESTIGATIONS BiochemistryBlood urea, creatinine,

electrolytes,

Blood gas analysis.

Urine osmolality/sodium/creatinine

Serum Creatinine as a marker for AKI and GFRNormal S.Creatinine is 0.6-1.2mg/dl and is the most commonly used parameter to assess renal function.

Unfortunately the correlation between S.Creatinine concentration and GFR may be confounded by several factors.

There is abrupt drop in GFR but the S.Cr. does not start going up for 24 or 36 hours after the acute insult .

40800GFR(mL/min)

071421284Days206Serum Creatinine(mg/dL)Relationship between GFR and serum creatinine in AKI

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One of the things to bear in mind when we are talking about acute renal failure is that our marker for acute renal failure is generally the serum creatinine concentration, but this is a relatively poor marker of renal function. Certainly, there are issues related to the correlation between creatinine and level of GFR related to protein mass so that a creatinine of 1 does not represent the same level of GFR in a cachectic 70-year-old as in a highly muscular 25-year-old, but in addition the change in serum creatinine that occurs lags behind the change in GFR that is seen with acute renal failure. Here you see the abrupt drop in GFR in a patient with acute renal failure, but the serum creatinine lags behind so that it may not start going up for 24 or 36 hours after the acute insult and certainly when we see a patient with aggressively rising serum creatinine, that does not mean that the renal function is continuing to deteriorate. The GFR may be close to 0 and be maintained at that level close to 0 during that period of time. The creatinine has not come back into a steady state at this new very low GFR.

Creatinine is not an ideal marker1.Creatinine excretion is dependent on renal factors independent of function:Certain medications such as cimetidine and trimethoprim interfere with proximal tubular creatinine secretion and may cause rise in S. creatinine without fall in GFR.

2. S.Creatinine is dependent on nonrenal factors independent of renal functionS.Creatinine is dependent on muscle mass, infection, volume of distribution, age, gender, race, body habitus, diet, presence of amputations.

Eg. S. Creatinine of 1.2mg/dl in a 40kg elderly signifies severe reduction of GFR while the same value in a 100kg represents a normal renal function3. Creatinine production and excretion must be in a steady state before creatinine may be used in any formula for the estimation of GFR.

Fractional Excretion of Na Since urinary indices depend on urine sodium concentration, they should be interpreted cautiously if the patient has received diuretic

Spot urine Na may be affected (raised) by diuretic use and baseline impaired kidney function (CKD where maximum urine Na reabsorption is impaired)

Fractional excretion of Na accounts for this by including creatinine:FxExNa = urine [Na] plasma [Na] X 100 urine creatinine plasma creatinine

RENAL INDICESRenal Failure Index (RFI)

RFI = urine [Na] urine creatinine /serum creatinine

URINE AND SERUM LABORATORY VALUES

Pre-renal

URINE ANALYSIS Dipstick for blood, protein Suggests a renal inflammatory process

Microscopy may show cells, casts, crystals

RBCs in Urine Present in glomerulonephritis , vasculitis , HUS TTP scleroderma crisis

URINARY CASTSHyaline prerenal ARF

Granular ATN (muddy brown)

Red blood cell casts glomerulonephritis,vasculitis malignant hypertension WBC casts- AIN, pyelonephritis ,leukemic or lymphomatous infiltrates

Red Blood Cell CastTwo examples of red blood cell casts, typical of glomerular bleeding.

White Blood Cell Cast

Pigmented Granular CastsPigmented granular (muddy brown) casts are characteristic of acute tubular necrosis

Crystals Urate crystals acute urate nephropathy

Oxalate crystals ethylene glycol ingestion /acyclovir/ indinavir

Eosinophiluria > 5 % of WBC s AIN ,atherothrombotic disease

HaematologyFull blood count, blood film:Eosinophilia may be present in acute interstitial nephritis, cholesterol embolization, or vasculitis (CSS)

Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy TTP, HUS

Coagulation studies Disseminated intravascular coagulation associated with sepsis

Immunology

Antinuclear antibody (ANA) , Anti-double stranded (ds) antibody - ANA positive in SLE and other autoimmune disorders;DNA antibodies anti-ds DNA antibodies more specific for SLEC3 & C4 complement concentrations-Low in SLE, acute post infectious glomerulonephritis, CryoglobulinemiaASO and anti-DNAse B titres High after streptococcal infection

Immunology...ANCA p-ANCA - Anti PR3 antibodiesc-ANCA - Anti MPO antibodies Associated with systemic vasculitis - Wegeners granulomatosis; Microscopic polyangiitis. AntiGBM antibodies Present in Goodpastures disease

SerologyHepatitis B and C, HIV serology

Radiology

Renal ultrasonography : For renal size, symmetry, evidence of obstructionPyelography : localizationMRA/ Doppler US : arterial /venous obstruction

NEW MARKERCystatin C protein

Produced by nucleated cells

Filtered and completely reabsorbed

Changes in serum levels occur sooner

NOVEL BIOMARKERS1. IL- 18

2.KIM-1

3.Gro /KC

4.NGAL-neutrophil gelatinase associated lipocalin

5.NHE-3 -Sodiumhydrogen antiporter 3

Complications

Complications

Complications

Other ComplicationsHyperuricemia

Infection- pneumonia, sepsis

Git- nausea, vomiting, malnutrition, git bleeding

CNS- asterixis, mental changes, seizures

Uremic syndrome

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AKI: PREVENTION Recognize patients at risk (postoperative states, cardiac surgery, septic shock)

Prevent progression from prerenal to renal

Preserve renal perfusion(isovolemia, cardiac output, normal blood pressure)

Avoid nephrotoxins (aminoglycosides, NSAIDS, amphotericin)

GENERAL PROTOCOL FOR MANAGEMENT OF AKI Treat the underlying diseaseStrictly monitor intake and output (weight, urine output, insensible losses, IVF)Monitor serum electrolytesAdjust medication dosages according to GFRAvoid highly nephrotoxic drugsAttempt to convert oliguric to non-oliguric renal failure (furosemide)

FLUID THERAPYIf patient is fluid overloadedfluid restriction (insensible losses)attempt furosemide 1-2 mg/kgRenal replacement therapy

If patient is dehydrated: restore intravascular volume firstthen treat as euvolemic

If patient is euvolemic:restrict to insensible losses (30-35 ml/100kcal/24 hours) + other losses (urine, chest tubes, etc)

SODIUMMost patients have dilutional hyponatremia which should be treated with fluid restriction

Severe hyponatremia (Na< 125 mEq/L) : dialysis or hemofiltration

POTASSIUMOliguric renal failure is often complicated by hyperkalemia, increasing the risk of cardiac arrhythmias

Treatment of hyperkalemia: sodium bicarbonate (1-2 mEq/kg) insulin + hypertonic dextrosesodium polystyrene : 1 gm/kg . (Hypernatremia and hypertension are potential complications)dialysis

MANAGEMENT OF AKIMetabolic acidosis soda bicarb ., if < 15 meq Hyperphosphatemia PO4 binders sevalamer

Hypocalcemia calcium carbonate Nutrition restriction of dietary protein < 0.8 g/kg /d calories 25-30 kcal /kg/d enteral nutrition preferred

Criteria for Initiation of RRTAnuria Oliguria Pulmonary edemaHyperkalemia >6.5mmol/LSevere acidemia 20