Acute kidney injury |Acute kidney failure

This article discusses Acute kidney injury and how to diagnose the types and effects of AKI. Here, learn about recent updates on Acute kidney injury and more.

Table of contents

1.	Definition
2.	Incidence
3.	Classification
4.	Pathophysiology
5.	Staging
6.	Causes
7.	Signs and symptoms
8.	Diagnosis
9.	Complication
10.	Prognosis

Definition

Acute renal failure, known as acute kidney injury, is a syndrome. The term AKI was used in 1918 by William NacNider, but from 2004, it has become a widely accepted term.

AKI (acute kidney injury ): In Acute kidney injury, sudden (within hours to seven days) reduction in kidney function develops, characterized by decreased urine output and raised serum creatinine level.

AKI is described as a clinical syndrome due to a sudden (within hours to a maximum of seven days)decrease in renal function to the point that waste products accumulate in the body. AKI causes structural damage and loss of function.

Although urine output depends on fluid intake and other processes of water loss-sweating, perspiration, etc. average volume is 1500 ml.

The obligatory urine volume is 500 ml/day, meaning at least 500 ml/day of urine must pass to clear waste products from our bodies.

Normal creatinine level depends on age and sex

Adult male – 0.75 to 1.35 mg/dl

Adult females -0.6 to 1.1 mg/dl have lower creatinine levels than males.

Creatinine is the metabolic waste product of creatine. Creatinine is excreted from the body exclusively by the kidney. If kidney function is abnormal, creatinine level rises in the blood, and less creatinine is excreted in the urine.

Recent definition: Recently, for diagnosis of AKI, any one of the following must be present:

1.Urine volume less than 0.5ml/kg/h for six hours.

2. Serum creatinine increases by >0.3 mg/dl within 48 hours.

3. Serum creatinine increases to >1.5times of the baseline. The serum creatinine level present before seven days is taken as the baseline, but this baseline value is usually unknown.

Acute decrease of GFR, a critical reduction of urine output, and an acute rise of serum creatinine. Recently several biomarkers have been proposed to diagnose AKI but have not been accepted widely.

Recent evidence suggests that even relatively mild AKI functions manifested by small changes in serum creatinine or urine output predict serious health problems.

Incidence

Incidence and causes of AKI differ in developing and developed countries.

In developed countries, AKI occurs in hospitalized persons.

Infectious diseases are the leading cause in developing countries.

AKI is common in the elderly>65 years.

Classification

Broadly causes can be classified into three groups:

1. Prerenal-when blood flow to the kidney is decreased.

2. Renal -when there is damage in the kidney itself. Only renal AKI is an actual kidney disease.

3. Postrenal-when urine outflow is obstructed.

This is a traditional classification. Prerenal and postrenal, if prolonged, will cause renal damage.

Prompt treatment of prerenal and postrenal causes prompt recovery of renal function, but late correction can lead to progressive renal damage.

Pathophysiology

The pathophysiology of AKI is multifactorial. The underlying cause is ischemia in the kidney tissue due to multiple factors. When oxygen supply and metabolic demands become inadequate despite physiological adaptation, cellular damage occurs, leading to kidney dysfunction.

Under basal conditions, the kidney receives 300-400 ml of blood/100gm/minute. This renal blood flow is very high compared to the heart and brain.

The kidney is highly susceptible to ischemia. In ischemic conditions, epithelial cells cannot maintain intracellular ATP for basic processes. This ATP depletion causes cell injury -necrosis. All segments of the nephron are vulnerable, but proximal tubular cells are commonly injured.

The function of the nephron is to filter, concentrate, and reabsorption of many substances from the tubular lumen. The concentration of metabolic waste substances may reach toxic levels if a kidney is not functioning normally.

Staging or severity criteria:

RIFLE= (an acronym of the Risk-Injury-Failure-loss-end stage kidney disease).

Severity criteria

Risk: serum creatinine rises by1.5 fold .and GFR reduces by 25%.
Injury: serum creatinine increases by 2fold, .and GFR reduces by 50%.
Failure: serum creatinine rises threefold, and GFR reduces by 75%.

Outcome criteria:

Loss: If complete loss of renal function persists for more than one month.
End-stage kidney disease stage four lasts for more than three months.

Etiology =Causes

AKI is a syndrome and has mixed etiology sepsis, ischemia, etc. Sepsis causes AKI due to many facts.

Prerenal-when blood flow to the kidney is decreased includes:

1. Dehydration -diarrhea, vomiting, heat exhaustion, heat stroke.

2. Excessive bleeding

3.Shock-cardiogenic,neurogenic

4. Iatrogenic -some drug-like NSAIDs

5. Advance cirrhosis.

6. Heart failure -hepatorenal syndrome.

7. Cardiorenal syndrome.

8. Congenital renal artery stenosis.

9. Rarely renal vein thrombosis.

Renal -when there is damage in the kidney itself that includes

1. Glomerulonephritis

2. Acute tubular necrosis (ATN)

3.Iatrogenic-some antibiotics,chemotherapeutic agents,contrast dye.

4. Amyloidosis

5. Lupus nephritis.

6. Diabetic nephropathy

7. Tumor lysis syndrome.

Postrenal-when urine outflow is obstructed due to

1. Stones in the kidney, ureter, urinary bladder, and urethera,

2. Prostatic enlargements-benign or malignant.

3. Postrenal-when urine outflow is obstructed

4. Stricture (constriction) of the urethra.

Signs and symptoms:

Signs and symptoms are guided by the underlying factor and result from disturbances in kidney function.

In the case of obstructive nephropathy, the kidney and urinary bladder become palpable. In case of excessive blood loss, there is the mark of injury.

Signs and symptoms are prominent in cases of dehydration-thirst, dry tongue loss of skin luster.

Fluid balance is affected, leading to an alteration in blood pressure.

Urea and other nitrogen-containing substances accumulate in the blood in AKI, causing multiple symptoms-fatigue, nausea, weakness, and neurological disturbances.

Potassium level increases in AKI, which may lead to abnormality of heart rate-arrhythmia.

Pain in the renal angle due to kidney inflammation or blockage of microvessels in the kidney and tubular necrosis.

Diagnosis

For diagnosis of AKI, any one of the following must be present:

1.Urine volume less than 0.5ml/kg/h for six hours.

2. Serum creatinine increases by >0.3 mg/dl within 48 hours.

3. Serum creatinine increases to >1.5times of the baseline. The serum creatinine level present before seven days is taken as the baseline, but this baseline value is usually unknown.

There is an acute decrease in GFR, a sharp reduction in urine output, and an acute rise in serum creatinine. Recently several biomarkers have been proposed to diagnose AKI but have not been accepted widely.

1. History, signs, and symptoms.

2. Serum creatinine and electrolytes estimation.

3. Urine examination microscopy.

4. Volume of urine

5. Ultrasound of kidney

6. Urography

7. CT scan

8. MRI

9. Intra Venous contrast is contraindicated in AKI.

When AKI is diagnosed, further tests are performed to recognize the underline cause.

Complications:

1. Acidosis-metabolic, which will disturb the whole system.

2. Electrolyte imbalance -especially hyperkalemia-(high potassium level)-may be lethel.

3. Accumulation of waste products of metabolism-Urea, causing uremia.-azotemia.

4. Fluid imbalance.

5. Prone to develop chronic kidney disease in the future.

Management:

The main aim of AKI management is to prevent permanent injury and collapse by proper hydration of the patient and drugs to treat the underlying cause.

Monitor kidney function by serial creatinine estimation and measurement of urine output.

How to recognize recovery of AKI:

GFR increases, and serum creatinine decreases.

Prognosis: AKI is associated with short and long-term complications. About5-10% of cases will never regain normal kidney function and progresses to end-stage kidney failure.

Mortality is high.AKI has a high mortality rate of 20-50%.

Even if kidney function recovers after AKI, premature death occurs, and the chance of developing chronic kidney disease is increased by 10 %.

In 1802 ,William Heberden termed ‘ischuria renalis’

In 1909, William Osler described named this ‘Acute Bright’s disease’.

‘War nephritis’ was similar to AKI.

Acute tubular necrosis term was used to describe AKI. For many years ATN and ARF were used interchangeably.

Summary

Recently for diagnosis of AKI, any one of the following must be present:

1.Urine volume less than 0.5ml/kg/h for six hours.

2. Serum creatinine increases by >0.3 mg/dl within 48 hours.

3. Serum creatinine increases to >1.5times of the baseline. The serum creatinine level present before seven days is taken as the baseline, but this baseline value is usually unknown.

FAQ :

Q. What is the prognosis of AKI?

A. AKI is associated with short and long-term complications. About5-10% of cases will never regain normal kidney function and progresses to end-stage kidney failure.

Mortality is high.AKI has a high mortality rate of 20-50%.

Even if kidney function recovers after AKI, premature death occurs, and the chance of developing chronic kidney disease is increased by 10 %.

Q. What is Creatinine?

A. Creatinine is the metabolic waste product of creatine. Creatinine is excreted from the body exclusively by the kidney. Therefore, if kidney function is abnormal, creatinine level rises in the blood, and less creatinine is excreted in the urine.

Learn More :

1. About us

2. Contact us

3. Disclaimer

4. Privacy Policy

5. About the author

Please submit your comments about the article. The team will work hard to evaluate the statement and make appropriate corrections.

Help to improve the content.

Have a comment about the Pancreatic function test

Name:

Email:

Phone No.