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Pre Renal Acute Kidney Injury

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Acute Kidney Injury And Extra

Acute Kidney Injury (AKI) – prerenal, intrarenal and postrenal causes and pathophysiology

Recent evidence in both basic science and clinical research are beginning to change our view for AKI from a single organ failure syndrome, to a syndrome where the kidney plays an active role in the evolution of multi-organ dysfunction. Recent clinical evidence suggests that AKI is not only an indicator for severity of illness, but also leads to earlier onset of multi-organ dysfunction with significant effects on mortality. Animal models of renal injury have been used extensively in order to elucidate the mechanism of remote organ dysfunction after AKI despite their limitations due to interspecies differences. These studies have shown a direct effect of AKI on distant organs. These animal studies include models of ischaemiareperfusion injury and sepsis, mainly lipopolysaccharide endotoxin induced sepsis due to its reproducibility in creating distant organ failure. AKI is not an isolated event and it results in remote organ dysfunction to the lungs, heart, liver, intestines and brain through a pro-inflammatory mechanism that involves neutrophil cell migration, cytokine expression and increased oxidative stress . Three recent excellent reviews explore the mechanisms and the long-term consequences of AKI other organ systems.

Kidney-lung crosstalk in the critically ill patient

Heart-kidney crosstalk: the cardiorenal syndrome

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What Is The Kidney And What Does It Do

The kidneys are two coffee bean-shaped organs found in the posterior part of the abdominal cavity which name is retroperitoneum. They connect with the bladder through two thin muscle tubes called the ureters.

The kidneys primary function is to filter blood, remove excess fluid, electrolytes, and waste material to make urine. Urine flows from the kidneys to the bladder. Then, it goes from the bladder to the urethra and finally, from the urethra to the toilet.

The kidneys are vital in maintaining a healthy balance of electrolytes, fluids, acids, and bases in the body. They are also crucial in arterial tension regulation and are the target of important antihypertensive medications . Kidneys also produce essential hormones that control red blood cell production.

Each kidney is made up of millions of nephrons. Each nephron has two main parts the glomerulus and the tubule. The glomerulus is the filter, it works more or less in the same way as a coffee filter does. The tubule removes and adds different elements to the original filtrate according to the bodys needs.

For example, in the dehydrated person, the tubule will absorb a lot of the fluid from the original glomerular filtrate. If a person has excess acid in the body, the tubules will excrete that acid and reabsorb bicarbonate in turn. The substances and fluid the tubules do not reabsorb become urine that flows into the bladder.

Screening And Risk Assessment With Biomarkers

Around half of the patients with stage 1 AKI have elevated biomarkers and histologic abnormalities on kidney biopsy, whereas most of the patients with stage 3 AKI have both,. Serum creatinine levels and urine output are two functional biomarkers that have several limitations. Urine output has a low specificity because this parameter can be influenced by several factors, including hypovolaemia and the use of diuretics. By contrast, serum creatinine level has low sensitivity in previously healthy kidneys, because the serum creatinine levels increase only if at least 50% of the functional nephrons are lost. In patients with low baseline GFR, minor changes in kidney function can already meet the threshold of an increase of serum creatinine of 0.3mg/dl, that is, AKI.

Novel biomarkers were not included in the 2012 KDIGO guidelines. AKI biomarkers indicate different aspects of AKI and can be broadly divided into functional or damage biomarkers ,,. Although biomarkers, such as IL-18 or kidney injury molecule 1 , are available and most of them have a very good predictive value, limitations exist, including poor predictive performance when the timing of the kidney insult is unknown hence, they are implemented only inconsistently in clinical practice,,.

Fig. 5: Severity of AKI and long-term kidney outcome.

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Symptoms Of Acute Kidney Injury

Symptoms of AKI include:

  • feeling sick or being sick

Even if it does not progress to complete kidney failure, AKI needs to be taken seriously.

It has an effect on the whole body, changes how some medicines are handled by the body, and could make some existing illnesses more serious.

AKI is different from chronic kidney disease, where the kidneys gradually lose function over a long period of time.

Preventing Acute Kidney Injury

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Those at risk of AKI should be monitored with regular blood tests if they become unwell or start new medication.

Its also useful to check how much urine youre passing.

Any warning signs of AKI, such as vomiting or producing little urine, require immediate investigation for AKI and treatment.

People who are dehydrated or at risk of dehydration may need to be given fluids through a drip.

Any medicine that seems to be making the problem worse or directly damaging the kidneys needs to be stopped, at least temporarily.

The National Institute for Health and Care Excellence has produced detailed guidelines on preventing, detecting and managing AKI.

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What Are The Leading Causes Of Aki

Acute kidney injury has three main causes:

  • A sudden, serious drop in blood flow to the kidneys. Heavy blood loss, an injury, or a bad infection called sepsis can reduce blood flow to the kidneys. …
  • Damage from some medicines, poisons, or infections. …
  • A sudden blockage that stops urine from flowing out of the kidneys.

Renal Control Of Organ Perfusion

Renal perfusion depends on the ratio of renal vascular resistance to systemic vascular resistance . The kidneys can locally regulate their vascular resistance, even at fixed perfusion pressures, due to their ability to independently control afferent and efferent arteriolar tone . Hypoperfusion is often accompanied by afferent arteriolar vasodilation and efferent arteriolar vasoconstriction, thus maintaining constant hydraulic pressure and glomerular filtration. Autoregulatory mechanisms governing intrinsic afferent arteriolar tone include: the myogenic reflex, by which transmural pressure across the afferent arteriole causes smooth muscle relaxation in the tunica media and the tubuloglomerular feedback system, by which solute delivery to the macula densa cells in the thick ascending limb of Henle determines the vascular tone of juxtaposed afferent renal arterioles .

Autoregulatory responses do have their limits, and maximal arteriolar vasodilation occurs at a mean arterial pressure of 80mmHg . Below this blood pressure, afferent arterioles cannot dilate further and renal perfusion begins to decrease. This is particularly concerning since clinically relevant hypotension requiring intervention is often defined as a mean arterial pressure < 65mmHg , meaning that renal perfusion at this blood pressure may already be significantly compromised.

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Prerenal Acute Kidney Injury

Prerenal causes include any condition that leads todecreased renalperfusion.

  • Hypovolemia: e.g., due to hemorrhage, vomiting,diarrhea, sweating,burns,diuretics, poor oral intake,dehydration,hypercalcemia
  • Hypotension: e.g., due tosepsis, cardiogenic shock , anaphylactic shock
  • Cardiorenal syndrome: e.g., incongestive heart failure
  • Hepatorenal syndrome: e.g., incirrhosis, liver failure
  • Abdominal compartment syndrome
  • Drugs that affectglomerularperfusion: e.g., cyclosporine,tacrolimus,NSAIDs, ACE inhibitors
  • Prolongedprerenal injury leads to intrinsic injury, as decreased renalperfusion causestubular necrosis.

    Renal Decompensation And The Spectrum Of Prerenal States

    Prerenal acute kidney injury (acute renal failure) – causes, symptoms & pathology

    An organ working at submaximal capacity can boost its output at times of increased need, to maintain homeostasis. Such an increase in function is termed the organs reserve. The renal functional reserve represents the combined physiologic effects of renal compensatory mechanisms that are activated with volume depletion, mesenchymal constriction or reduced cardiac output . A recent study of patients undergoing elective cardiac surgery demonstrated that higher preoperative RFR provided resilience to postoperative AKI . While these findings require further corroboration, the evaluation of a patients RFR could potentially guide the clinical management of patients at high risk of developing renal injury.

    The conflation of prerenal AKI with hypoperfusion-associated AKI is illustrated by the broad spectrum of disease states often termed prerenal. By discussing the clinical conditions commonly grouped together under this umbrella, we seek to demonstrate the peril associated with persistent use of this term. The most common and dangerous clinical misstep involves the administration of fluid to prerenal patients who are euvolemic or to whom additional fluid administration may even cause harm.

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    Clinical Characteristics Of Aki Patients

    The baseline characteristics of the 271 AKI patients are shown in Table 1. 172 were male and 99 were female. The median age was 54 years . The median length of hospital stay was 8 days . Hospitalization occurred in the Department of Internal Medicine, Department of Surgery, ICU and Division of Nephrology for 142 , 90 , 39 , and 40 patients, respectively. The number of patients with a history of allergy, smoking, or drinking alcohol was 15 , 88 , or 49 , respectively.

    Causes Of Acute Kidney Injury

    Most cases of AKI are caused by reduced blood flow to the kidneys, usually in someone who’s already unwell with another health condition.

    This reduced blood flow could be caused by:

    • low blood volume after bleeding, excessive vomiting or diarrhoea, or severe dehydration
    • the heart pumping out less blood than normal as a result of heart failure, liver failure or
    • certain medicines that reduce blood pressure or blood flow to the kidneys, such as ACE inhibitors, certain diuretics or NSAIDs

    AKI can also be caused by a problem with the kidney itself, such as inflammation of the filters in the kidney , the blood vessels , or other structures in the kidney.

    This may be caused by a reaction to some medicines, infections or the liquid dye used in some types of X-rays.

    It may sometimes be the result of a blockage affecting the drainage of the kidneys, such as:

    A doctor may suspect AKI if you:

    • are in an “at risk” group and suddenly fall ill
    • get symptoms of AKI

    AKI is usually diagnosed with a blood test to measure your levels of creatinine, a chemical waste product produced by the muscles.

    If there’s a lot of creatinine in your blood, it means your kidneys are not working as well as they should.

    You may also be asked to give a pee sample.

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    Volume Status And Blood Pressure

    • Goal: optimize renalperfusion andreverse prerenal insults while avoiding fluid overload
    • Monitoring parameters
    • Clinical assessment of volume status
    • Fluid balance monitoring
    • Hemodynamic monitoring
    • Fluidresponsiveness
  • Management: Provide hemodynamic support and ensure continued fluid needs are met see alsoDaily fluid requirements for special patient groups.
  • Hemodynamic support in patients with AKI according to presumedintravascularvolume status

    • Start IVfluid resuscitation.
    • Consider vasopressors to maintainmean arterial pressure 65mmHg in patients with persistent hypotension despitefluid resuscitation.
    • Consider loop diuretics: e.g.,furosemide
    • Consider an IV fluid challenge to assess if the patient responds to fluids
    • Responsive: Carefully continue IV fluid challenges until the patient is no longer responsive.
    • No response: Stop IV fluid challenges but ensurecontinued fluid needs are met.

    Patients with AKI are at high risk of developing fluid overload, which can compromise renal function and may increase mortality. Avoid aggressivefluid resuscitation in patients who are not volume responsive.

    Considerloop diuretics ONLY in patients with signs of fluid overload.Diuretics should not be used routinely to improve urine output in patients with AKI because of their lack of benefit and potential for harm.

    Acute Kidney Failure Prerenal Causes


    Prerenal failure is the most common type of acute renal failure . The kidneys do not receive enough blood to filter. Prerenal failure can be caused by the following conditions:

    • Dehydration: From vomiting, diarrhea, water pills, or blood loss
    • Disruption of blood flow to the kidneys from a variety of causes:
    • Drastic drop in blood pressure after surgery with blood loss, severe injury or burns, or infection in the bloodstream causing blood vessels to inappropriately relax
    • Blockage or narrowing of a blood vessel carrying blood to the kidneys
    • Heart failure or heart attacks causing low blood flow
    • Liver failure causing changes in hormones that affect blood flow and pressure to the kidney

    There is no actual damage to the kidneys early in the process with prerenal failure. With appropriate treatment, the dysfunction usually can be reversed. Prolonged decrease in the blood flow to the kidneys, for whatever reason, can however cause permanent damage to the kidney tissues.

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    Acute Kidney Injury & Failure Symptoms Causes & Treatments

    When your kidneys stop working suddenly, over a very short period of time , it is called acute kidney injury . AKI is sometimes called acute kidney failure or acute renal failure. It is very serious and requires immediate treatment.

    Unlike kidney failure that results from kidney damage that gets worse slowly, AKI is often reversible if it is found and treated quickly. If you were healthy before your kidneys suddenly failed and you were treated for AKI right away, your kidneys may work normally or almost normally after your AKI is treated. Some people have lasting kidney damage after AKI. This is called chronic kidney disease, and it could lead to kidney failure if steps are not taken to prevent the kidney damage from getting worse.

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    Laboratory Radiographic And Other Tests That Are Likely To Be Useful In Diagnosing The Cause Of This Problem

    All patients with concern for ARF should have a basic metabolic panel performed, including measurement of magnesium and phosphorus, as well as a complete blood count with differential to assess for signs of sepsis. A urinalysis should be ordered as this will help distinguish between pre-renal or post-renal/obstructive ARF and intrinsic causes a normal urinalysis suggests a pre-renal or post-renal etiology.

    Urine electrolytes should be measured to allow for the calculation of the fractional excretion of sodium . Since it was initially studied in the mid-1970s, the FENa has been the standard method to evaluate whether ARF is due to a pre-renal or intrinsic renal cause. The FENa is a simple calculation . A FENa of < 1% suggests a pre-renal cause, while > 3% suggests an intrinsic renal cause. It is important to note that, strictly speaking, this rule only applies to patients with oliguric renal failure where obstruction has been ruled out , as that is how it was originally studied.

    Figure 2.

    FENa calculation.

    Figure 3.

    Reported clinical causes of misleading FeNa.

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    The Relationship Between Prerenal Aki And Atn

    As with prerenal AKI, the diagnosis of acute tubular necrosis is mired in controversy and further supports the need for a revised AKI classification system. Traditionally, pre- and postrenal AKI were understood to be transient processes that spared the kidneys from permanent damage , while ATN was characterized by intrinsic, irreversible renal damage with the death of renal tubular cells .

    Traditional paradigm of functional and structural kidney disease. Subclinical AKI can be the result of nephrotoxin administration, sepsis or acute/chronic inflammation. Adapted from Potential use of biomarkers in acute kidney injury: report and summary of the recommendations from the 10th acute dialysis quality initiative consensus conference, by P.T. Murray, R.L. Mehta, A. Shaw et al. and the ADQI 10 Workgroup. Kidney Int 2014 85: 513521.

    The traditional classification paradigm also presumes that prerenal AKI and ATN reside on the same spectrum of injury, with the latter representing the common endpoint resulting from prolonged renal insults, prerenal or otherwise . While there is limited histologic evidence to support this progression, there are congruent biomarker data that may validate it.

    Who’s At Risk Of Acute Kidney Injury

    Acute Kidney Injury (AKI) – Prerenal,Intrarenal,Postrenal

    You’re more likely to get AKI if:

    • you’re aged 65 or over
    • you already have a kidney problem, such as chronic kidney disease
    • you have a long-term disease, such as heart failure, liver disease or diabetes
    • you’re dehydrated or unable to maintain your fluid intake independently
    • you have a blockage in your urinary tract
    • you have a severe infection or
    • you’re taking certain medicines, including non-steroidal anti-inflammatory drugs , such as ibuprofen, or blood pressure medicines, such as ACE inhibitors or diuretics diuretics help the kidneys get rid of extra fluid from the body, but may become less helpful when a person is dehydrated or suffering from a severe illness
    • you’re given aminoglycosides a type of antibiotic that’s usually only given in hospital these medicines are only likely to increase the risk of AKI if you’re dehydrated or ill

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    Acute Kidney Failure Medications

    The patient may be given medicines to treat the cause of the acute renal failure or to prevent complications.

    • Antibiotics: To prevent or treat infections
    • Diuretics : Quickly increase urine output
  • Other medications: To get rid of extra fluid and prevent electrolyte imbalances
  • Kayexalate is used to decrease buildup of potassium
  • Sodium bicarbonate is used to decrease acid buildup
  • A Management Of Clinical Problem Pre

    Pre-renal failure is never in itself life-threatening, and as an isolated condition it can usually be easily corrected with the administration isotonic intravenous fluids. Administration of one liter of normal saline should improve the patients renal function if the cause if partially pre-renal, although more than one liter is often necessary.

    The one exception to the immediate administration of fluids is the ineffective circulating volume state of right sided or left sided congestive heart failure where volume resuscitation could exacerbate the patients clinical condition. In these cases the goal should be optimization of cardiac output over fluid resuscitation.

    In all cases of ARF, potentially offending medications should be held until the kidney function begins to show improvement.

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    How Is Acute Renal Failure Treated

    The treatment of acute renal failure mainly depends on the severity of the disease and its cause. For example, if any medications are responsible for ARF, your doctor will stop those medications and prescribe a relevant replacement.

    If kidney stones or blood clots caused the disease, your doctor will give medications or perform surgery to remove them. If an infection is present, your doctor will prescribe appropriate antibiotics for its treatment.

    The treatment generally includes:

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