Acute kidney injury

Common complication in hospitalized patients.

A prevalent, serious, and frequently preventable condition that affects 5%-7% of hospital admissions and 20-50% of ICU admissions.

A newer term for Acute renal failure.

Incidence is increasing globally.

Occurs in 2-5% of hospitalized adults with a major effect on morbidity and healthcare utilization.

The three main causes of AKI are renal hypo perfusion, which, in most cases, is due to hypovolemia; intrinsic structural kidney injury; and post renal injury due to urinary obstruction.

Defined is an acute increase in serum creatinine concentration of greater than 50% or an acute increase of greater than 0.3 mg per deciliter.

Definitions of AKI uses 2 functional biomarkers: increased serum creatinine concentration and decreased urine output.

Defined as an abrupt decline in kidney function and is assessed on the basis of glomerular filtration rate.

It is diagnosed when there’s an accumulation of creatinine, a nitrogenous waste product that is excreted by the kidneys, or a reduction or cessation of urine output.

Its severity is staged on the basis of the magnitude or duration of these changes.

AKI mediated by hemodynamic factors may be functional, or may result from destructive  urine excretion, or may result from intrinsic processes involving one or more renal structures such as the vasculature, glomerulus, interstitium, or tubules.

As a result of sepsis, shock, and exposure to natural toxins patients may develop AKI  which is generally attributed to acute tubular injury.

Elevated levels of urea and creatinine define the progression of AKI, their accumulation parallels accumulation of metabolites that mediate the toxic effects of uremia.

Fluid and electrolyte balance is a impaired in AKI leading to fluid overload, accumulation of sodium and water, hyperkalemia and metabolic acidosis from impaired potassium and acid excretion.

The severity of the above abnormalities depend on the extent of kidney impairment in the rate of catabolism.

Serum creatinine level is a late disease marker, often increasing at 24-48 hours after the initial kidney insult.

There is no pharmacological interventions available to prevent or treat AKI.

Acute kidney injury refers to an increase in serum creatinine within 2-7 days or oliguria.

Associated with substantially increased morbidity and mortality rates.

Observational data show was strong correlation between the magnitude of fluid accumulation and mortality among patients with AKI.

Patients with AKI are at increased risk for death and short and long term morbidities.
Patients with acute kidney injury have an elevated risk of chronic kidney disease, cardiovascular disease, and premature death, even when kidney function has recovered.
Up to 60% of patients with severe AKI patients with acute kidney injury have an elevated risk of chronic kidney disease, cardiovascular disease, and premature death, even when kidney function has recovered.admitted to the ICU die from disorder.
The long-term risk of death associated with AKI is increased.
AKI is an independent risk factor for death, and mortality can be as high as 60%.

Patients with chronic kidney disease are at high risk for AKI  adverse cardiovascular sequelae.

The largest burden occurs in critically ill patients and patients with cardiovascular disease, who are at increased risk for both acute kidney injury and chronic kidney disease owing to older age and multiple coexisting conditions, and the greater likelihood of undergoing procedures that directly affect kidney function, such as coronary angiograms or cardiac surgery.

Between six and 10% of patients undergoing coronary angiography or percutaneous coronary intervention experience acute kidney injury.

Development of AKI in patients with sepsis is associated with increased mortality, and survivors are at risk of developing chronic kidney disease.

AKI is associated with an increased risk of chronic and end-stage kidney disease, and adversely affects other organs, including the heart.
The interactions between cardiac and kidney disease is referred to as cardiorenal syndromes.
AKI complicates recovery from cardiac surgery in up to 40% of patients impairing heart, lungs, brain, and gut functions and is associated with increased risk of death during hospitalization.

Cardiac impairment leads to kidney diseases, and kidney impairment leads to cardiac diseases.

AKI that requires kidney replacement therapy after cardiac surgery is associated with an increased 28 day mortality ranging from 15 to 85%, depending on acute and chronic comorbidities.

Patients with the serum creatinine after cardiac surgery that increased greater than 0.5 mg/dL have a 30 day mortality of 32.5%.

After cardiac surgery the 30 day mortality was lowest among patients in whom the serum creatinine decreased by 0.3 mg/dL or less.

A delay in detection and intervention allows it it to progress to more severe stages and contributes to the development of chronic kidney disease after hospital discharge.

Acute kidney injury is common in patients with cirrhosis, and occurs in up to 50% of hospitalized patients with cirrhosis, and in 58% of such patients in the ICU.

AKI is associated with high morbidity and mortality, and increased incidence of chronic kidney disease after liver transplantation for cirrhosis.

AKI due to renohypoperfusion in patients with cirrhosis is referred to as the hepatorenal syndrome, the result of renal vasoconstriction.

Hypoperfusion from hypovolemia accounts for approximately half the cases of AKI in patients with cirrhosis, intrinsic causes such as acute tubular crosses account for approximately 30% of cases, and hepato-renal syndrome accounts for approximately 15 to 20% of the cases, with less than 1% attributable to post renal obstruction.

Mortality rates and length of stay increase with progressive severity of acute kidney injury.

Sepsis associated AKI is associated with inflammatory, nephrotoxic, and ischemic insults occurring simultaneously leading to kidney impairment.

Acute kidney diseases refers to less than three months of having decreased kidney function or the presence of a marker of kidney damage and include kidney injury.

When acute kidney injury is complicated by major metabolic processes such as acidosis, hyperkalemia, uremia, and fluid disturbances they can be treated with renal replacement therapy.
When acute kidney injury is not accompanied by these above complications, the benefits of renal-replacement therapy are unclear.
The main objective of kidney replacement therapy used to mitigate life-threatening consequences, thereby preventing death from uremia.
Patients with refractory fluid overload after surgery, that includes worsening pulmonary edema, benefit from early initiation of kidney replacement therapy.
With severe pulmonary edema kidney replacement therapy is mandatory.
Among critically ill patients with acute kidney disease, and accelerated renal replacement treatment is not associated with a lower risk of death at 90 days than a standing strategy (theSARRT-AKI investigators).

About 10% of the 200 million adults are estimated to have undergone major noncardiac surgery each year develop acute kidney injury.

Occurs in approximately 20% of hospitalizations.

Occurs in up to 60% of patients in ICUs and it’s incidence is increasing.

Essential pathogenesis are inflammation and oxidative stress, implicating multiple subtypes of immune cells.

Soluble urokinase plasminogen activator receptor (suPAR) is normally expressed at low levels on endothelial cells, podocytes and with induced expression immunologically active cells such as monocytes and lymphocytes: levels are predictive of progressive decline and kidney function.

suPAR Elevation results in proteinuria.

AKI requiring renal replacement therapy after cardiac surgery affects approximately 5% of patients admitted to the ICU and is associated with the mortality rate of up to 60%.

AKI requiring renal replacement occurs in approximately 1-2% of patients after cardiac surgery.

AKI survivors have higher risk of developing chronic kidney disease, cardiovascular disease, sepsis, and upper G.I. bleeding.

AKI the strongest risk factor for postoperative mortality having an odds ratio of 7.9 and a mortality in excess of 60%.

Particularly common following cardiac surgery.

Acute kidney injury complicates cardiac surgery in up to 30% of patients.

Even mild postoperative acute kidney injury associated with a 5-fold increase in death while in the hospital.

Acute kidney injury following cardiac surgery associated with higher rates of postoperative arrhythmias, respiratory failure, systemic infection, and myocardial infarction.

Among patients undergoing cardiac surgery, perioperative statins do not reduce the risk of acute kidney injury.

Develops in one of five patients with acute myocardial infarction.

AKI associated with increased hospital duration, increased risk for infection, increased cost, increased mortality, and increased risk of end-stage kidney disease.

Perioperative acute kidney injury associated with longer hospital stay is, poor outcomes, and higher healthcare costs.

Most common cause of hospital acquired AKI is acute tubular necrosis.

After cardiac surgery renal and especially medullary ischemia is presumed to be in mechanism of renal injury from surgery.

The magnitude of creatinine increase after cardiac surgery is associated in a graded manner with an increased risk of chronic kidney disease, chronic kidney disease progression and mortality (Ishani A et al).

In a study of 29,388 individuals that underwent cardiac surgery and increase in creatinine level, even of mild severity, was associated with a subsequent increase in the risk of incident chronic kidney disease, kidney disease progression, and mortality: this increased risk is most pronounced during the 3-24 months after an episode of creatinine increase (Ishani A et al). in

RIFLE Classification System for Acute Kidney Injury (Risk of renal dysfunction, Injury to the kidney, Failure or Loss of kidney function, and End-stage renal disease)

RIFLE criteria has three stages of acute kidney injury-risk, injury, and failure.

RIFLE criteria has two outcome measures loss of renal function, and ESRD.

Acute kidney injury defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dL, a percentage increase in serum creatinine of more than or equal to 50%, or a reduction in urine output of less than 0.5 mL/kg per hour for more than 6 hours.

Magnitude of renal injury is determined by the level of creatinine, or GFR and urinary output.

The development of AKI is associated with long term adverse consequences including permanent renal impairment and end-stage renal disease.

Minor increases in serum creatinine are associated with increased hospital and long-term mortality, and longer length of stay.

Many intravenous fluids used for hydration and resuscitation contain supra physiological concentrations of chloride, which can induce or exacerbate hyperchloremia and metabolic acidosis, and result in renal vasoconstriction and decreased GFR.

Hyperchloremic metabolic acidosis prolong time to micturition and decreased urine output following major surgery.

In a prospective, open label, sequential. pilot study of patients admitted consecutively to the ICU a chloride restrictive strategy was associated with a significant decrease in the incidence of acute kidney injury and the use of renal replacement therapy (Younos NM et al).

Renal replacement therapy required with severe pulmonary vascular congestion, severe hyperkalemia, and severe metabolic acidosis, complications of advanced azotemia, including encephalopathy, bleeding, and pericarditis

In the study of 30,000 surgical patients saline therapy increased the risk of patients requiring acute dialysis compared with Plasma-Lyte administration (Shaw AD et al).

Overall in studies comparing saline with balanced crystalloid fluids in adult ICU patients showed that the risk of acute kidney injury is similar.

The RIFLE criteria has limitations in that they can not distinguish between prerenal azotemia as opposed to intrinsic renal disease or obstructive nephropathy, volume changes can influence creatinine levels, and an interval lag exists between the above criteria and the development of structural damage. Him him him

Incidence has-been increasing from approximately 10-25 per 1000 discharges over the last 15 years ( Walkar SS et al).

Associated with increased mortality.

Initial evaluation usually includes real ultrasound to exclude obstruction, and if such up structure and is present it may require further intervention.

Elevations in serum creatinine of as little as 0.3 mg/dL is associated with a higher mortality rate in hosptialized patients (Chertow GM et al).

Most cases are not caused by obstruction and hydronephrosis is identified on real ultrasound in only one-10% of patients.

In a sample of 200 patients, seven factors were associated with hydronephrosis and they include a history of hydrnephrosis, recurrent urinary tract infections, nonblack race, diagnosis consistent with obstruction, absence of exposure to the nephrotoxic medications, congestive heart failure or pre-renal acute kidney injury.

Majority of ultrasound studies to rule out obstruction are negative.

Multiple risk factors for the presence of hydronephrosis as a cause of acute kidney injury include: history of hydronephrosis, history of prior pelvic malignancy, history of prior pelvic surgery, history of prior pelvic radiation, and history of a single functioning kidney.

In a randomized trial of 6,905 patients undergoing noncardiac surgery randomized to take aspirin or placebo before surgery and then aspirin and placebo daily for 30 days after surgery and also assigned to take oral clonidine or placebo 2 to 4 hours before surgery and transdermal clonidine patch or placebo after surgery for 72 hours: neither aspirin nor clonidine administered perioperative leak in patients undergoing major noncardiac surgery reduced the risk of acute kidney injury (Garg AX et al).

30% of acute kidney injury episodes in hospitalized patients could be avoided if physicians had taken appropriate preventive actions (Yamout H et al).

Fluid therapy improves hemodynamic status and organ perfusion and helps prevent acute kidney injury.

Soluble urokinase plasminogen activator receptor (suPAR) is a signaling glycoprotein involved in the pathogenesis of kidney disease: high levels are associated with acute kidney injury in various clinical contexts (Hayek SS).

In the absence of objective indications there are two strategies for the initiation of kidney replacement therapy in patients with severe AKI: early preemptive initiation, before the onset of severe complications, or watchful clinical and biologic surveillance with treatment deferred until in objective indication is present.

Overall data suggest there is no need to initiate kidney replacement therapy in patients who do not have potentially severe complications, providing watchful surveillance with active medical management is instituted.

Continuous treatment with efluent flows greater than 20 to 25 mL per kilogram per hour or intermittent treatment provided more frequently than three times a week, with an adequate dose delivery per treatment, is not associated with improved outcomes.

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