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Medical & Surgical Urology

Medical & Surgical Urology
Open Access

ISSN: 2168-9857

Perspective - (2023)Volume 12, Issue 1

Prevention of Acute Tubular Necrosis and its Diagnosis, Causes and Symptoms

Vicy Forn*
 
*Correspondence: Vicy Forn, Department of Surgery, University of Milan, Milan, Italy, Email:

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Description

Acute Tubular Necrosis (ATN) is a disease in which the kidney's renal tubule-forming tubular epithelial cells pass away. Pathologists prefer the term Acute Tubular Injury (ATI) over the more traditional nomenclature acute tubular necrosis because necrosis is frequently absent (ATN). One of the most frequent causes of Acute Kidney Injury (AKI), ATN manifests as AKI. Low blood pressure and the use of nephrotoxic medications are two common causes of ATN. Pathognomonic for ATN is the discovery of "muddy brown casts" of epithelial cells in the urine during urinalysis. The management strategy is to treat the causes of ATN aggressively (e.g. hydration and cessation of the offending drug). The general prognosis for ATN is relatively excellent if the underlying cause is treated, and recovery is probably within 7 to 21 days because the tubular cells constantly replace themselves.

Prevention

Acute tubular necrosis can be prevented by keeping the kidneys' blood and oxygen supply normal. Be sure to stay hydrated before and after any tests that require contrast dye. A cross-match of patient blood should have been performed before patient receive a transfusion. Manage any illnesses that can harm the kidneys, such as high blood pressure, diabetes, liver disease, and heart disease, in conjunction with patient healthcare practitioner.

Ibuprofen and naproxen sodium are two over-the-counter antiinflammatory drugs to avoid, especially if patient have kidney disease.

Diagnosis

Acute renal failure can be identified using a number of assays. They consist of plasma potassium levels, Blood Urea Nitrogen (BUN), creatinine, and other electrolyte levels. These compounds building up in the blood are a sign that the kidneys are not functioning properly.

Nephrologists typically diagnose acute tubular necrosis (kidney specialist). Although patient urine can be examined under a microscope, the diagnosis is primarily clinical. It is possible in some circumstances to do a kidney tissue biopsy, particularly if the diagnosis is unclear.

Causes

The illnesses that reduce the amount of oxygen that gets to the kidneys stroke or heart attack are the most prevalent causes of acute tubular necrosis. The tubules can potentially be harmed by chemicals. They include hazardous substances, anaesthetic medications, antibiotics, and X-ray contrast dye. Lack of blood flow and oxygen to the renal tissues is a common cause of ATN (ischemia of the kidneys). It could also happen if a toxic or dangerous material damages the renal cells.

Internal kidney structures, in particular the kidney tubule tissues, deteriorate or are destroyed. One of the most frequent structural alterations that might cause acute renal failure is ATN.

ATN is a typical factor in renal failure in hospital patients. ATN risks include:

• Reaction to blood transfusion

• Muscle harm from trauma or injury

• Septic shock

• Recent major surgery

• Low blood pressure (hypotension) that lasts longer than 30 minutes a person may be more likely to develop ATN if they have liver disease or diabetic nephropathy, which damages the kidneys.

Drugs that are harmful to the kidneys can potentially cause ATN. Amphotericin, an antifungal medication, and aminoglycoside antibiotics are some of these medications.

Symptoms

The following are signs of acute tubular necrosis:

• A small amount of urine output

• Fluid retention and swell

• Vomiting and nauseous

• Drowsiness or difficulty waking up

• Sensing lethargic • Confusion

Author Info

Vicy Forn*
 
Department of Surgery, University of Milan, Milan, Italy
 

Citation: Forn V (2023) Prevention of Acute Tubular Necrosis and its Diagnosis, Causes and Symptoms. Med Surg Urol.12:305.

Received: 20-Feb-2023, Manuscript No. MSU-23-22908; Editor assigned: 22-Feb-2023, Pre QC No. MSU-23-22908 (PQ); Reviewed: 10-Mar-2023, QC No. MSU-23-22908; Revised: 17-Mar-2023, Manuscript No. MSU-23-22908 (R); Published: 24-Mar-2023 , DOI: 10.35248/2168-9857.23.12.305

Copyright: © 2023 Forn V. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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