Acute Renal failure

Acute Renal failure occurs during kidney growth and does not filter blood. When the kidney loses its filtering function, volatile residues accumulate and the chemical composition of the blood becomes unbalanced.

Acute renal failure, also known as acute renal failure or acute kidney injury, develops rapidly in a matter of hours or days. Acute renal failure is not uncommon in people who are already hospitalized, especially in critically ill patients who require sustained attention.

Acute renal failure can be fatal and requires complete healing. However, acute renal failure may also be reversible. If found outside of health, kidney function can be improved daily or almost.

Signs and symptoms:

1. reduced urinary output, although urine volume is sometimes regular
2. Water retention can cause swelling of the legs, ankles or feet.
3. sleepiness
4. shortness of breath
5. tired
6. confused
7. disgusting
8. excessive convulsions or coma.
9. Pain or chest tension.
10. Acute renal failure does not usually cause signs, symptoms or symptoms that the laboratory can detect.

Please consult your doctor: If you have any signs, symptoms and signs and symptoms of acute renal failure, please make an appointment with your doctor.

reason

1. Acute renal failure may occur under the following conditions:
2. its condition slows the blood circulation in the kidneys
3. a direct renal adventure
4. The urinary drainage tube of the kidney (ureter) is clogged and the waste can not be separated by urine.
5. The blood flows in the kidneys.
6. Diseases and conditions that also delay blood flow to the kidneys and cause illness

Kidney failure includes:

1. Loss of blood or stagnant water
2. medicines for hypertension
3. coronary infarction
4. cardiac disease
5. Pollution
6. liver dysfunction
7. Use aspirin, ibuprofen (Advil, Motrin IB, etc.), naproxen (Aleve, etc.) or related drugs.
8. severe allergic reactions (allergic reactions)
9. excessive burns
10. excessive dehydration
11. kidney damage
12. Blood clots in the kidneys and in the veins and arteries of the kidneys.

CLINICAL APPROACH:

The diagnosis of acute kidney injury (AKI) depends on early prognosis and cure. A lot of reasons are classified according to their place of departure: prenatal, intrinsic (intrarenal) and public/renal.

AKI prerenal mean renal characteristic loss despite intact nephrons, for example, because of the extent of its exhaustion and/or hypotension.

There may be a wide range of intrinsic reasons for AKI, as well as acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. The assessment consists of a detailed overview of the individual's history, body examination, urinalysis, chemical composition for urine, urinary shaft imaging and biopsy. renal eventual. The recordings should focus on the rate of lack of characteristic (if considered), associated systemic diseases, and urinary tract symptoms (especially those who experience obstruction). Similarly, an evaluation of drugs for potentially nephrotoxic tablets is crucial. The purpose of the body examination is to identify the signs of systemic disease and to evaluate in detail the hemodynamic fame of the person concerned. This last objective may require invasive monitoring, especially in the oliguric affected person whose scientific findings are contradictory, the physical examination being of limited accuracy.

With the exception of urinary tract obstruction, it is important in all cases and can be easily configured using a renal ultrasound.

The difference between the two most unusual causes of AKI (pre-renal AKI and ATN) exists from time to time, especially because the clinical examination is often misleading in case of low exhaustion or volume overload. Urinary chemistries, such as the calculation of fractional sodium excretion (FENa), can be used to contribute to this difference. In the FENa evaluation, fractional excretion of urea has the advantage of being rather unbiased with respect to diuretic treatment. The response to fluid repletion remains the popular gold in the differentiation between prerenal and intrinsic AKIs. The return of the renal function to the baseline or resumption of diuresis within 24 to 72 hours is considered to mean "temporary pre-renal AKI", whereas continuous renal failure normally indicates intrinsic disturbance. Transient AKIs may also occur in short-term ATNs. In addition, rapid fluid therapy software is contraindicated in a wide range of patients, as well as those with congestive heart failure.

In patients with NTD, "muddy brown" plasters and/or tubular epithelial plasters are normally observed in the urine sediment. Their presence is an essential tool in distinguishing between ATN and AKI pre-renal, which is characterized by ordinary sediment or through occasional hyaline casts. New serum and/or urinary biomarkers may play a role in the diagnosis and prognosis of patients with AKI, including the differential prognosis between pre-renal AKI and NTD. Further studies are desired before their recurring dedication can be advocated.

Although the analysis can not be done with reasonable facts during this evaluation, a renal biopsy should be considered; Although intrarenal causes, such as increased glomerulonephritis or vasculitis, are suspected, the direct biopsy is essential to avoid delay in initiating treatment.