An accumulation of nitrogenous products in the blood (azotemia), together with or without a decrease in urine production, are symptoms of acute kidney injury, which is characterised by a fast decline in renal function over a period of days to weeks. It frequently happens as a result of poor renal perfusion brought on by severe injury, illness, or surgery, but it can also be brought on by a quickly progressing, intrinsic renal disease. Anorexia, motion sickness, and nausea are possible symptoms. Untreated conditions can lead to seizures and comas. Acid-base, electrolyte, and fluid issues manifest swiftly. Laboratory tests of renal function, such as serum creatinine, are used to make the diagnosis. The cause must be identified using urine indices, urinary sediment analysis, often imaging, and other testing (sometimes involving a kidney biopsy).
Symptoms of Acute kidney Injury
Initial observations might just include weight gain and peripheral edema. Predominant symptoms are frequently those of the underlying illness or those brought on by the surgical error that sparked renal decline.
Uremia symptoms could appear later when nitrogenous waste builds up. Such indicators consist of:-
- Anorexia
- Nausea
- Vomiting\sWeakness
- Jerks with myoclonus
- Seizures
- Confusion\sComa
A change in urine production
Acute kidney injury (AKI) urine output does not clearly distinguish between prerenal, renal, or postrenal causes.
Urine output may have three phases in acute tubular injury:
Depending on the underlying causes, the prodromal phase often has normal urine flow and varies in length (eg, the amount of toxin ingested, the duration and severity of hypotension).
Urine output during the oliguric phase ranges normally from 50 to 500 mL per day. Depending on the cause of AKI and the length of time before therapy, the oliguric phase’s duration is uncertain. But many patients never develop oliguric behaviour. Patients who are not oliguric have reduced mortality and morbidity rates and require less dialysis.
Diagnosis of Acute kidney Injury
Clinical assessment, which considers prescription and over-the-counter medications as well as exposure to iodinated IV contrast
- blood creatinine
- urinalysis residue
- diagnostic indicators for the urine
- urine testing and evaluation of urine protein
If a postrenal source is suspected, postvoid residual bladder volume and/or renal ultrasonography may be used.
When urine production decreases or serum blood urea nitrogen (BUN) and creatinine levels increase, acute kidney injury (AKI) is suspected.
therapy of hyperkalemia and pulmonary edema right away
Dialysis is administered when necessary to treat the symptoms of metabolic acidosis, pulmonary edema, and hyperkalemia.
medication dosage modification based on the severity of renal impairment
typically restricting intake of water, salt, phosphate, and potassium while yet giving them enough protein
Possibly intestinal potassium binders and phosphate binders (for hyperphosphatemia) (for hyperkalemia)
Prevention of Acute kidney disorder
Maintaining proper fluid balance, blood volume, and blood pressure in patients with trauma, burns, severe haemorrhage, and those undergoing major surgery can frequently prevent acute kidney damage (AKI). Blood and isotonic saline infusions could be beneficial.
Iodinated contrast agents should be used as little as possible, especially in at-risk individuals (eg, older patients and those with preexisting renal insufficiency, volume depletion, diabetes, or heart failure). If contrast agents are required, risk can be reduced by using nonionic, low osmolal, or iso-osmolal contrast agents, staying away from nonsteroidal anti-inflammatory medicines, and pre-treating with normal saline at 1 mL/kg/hour IV for 12 hours prior to the test.Instead of using regular saline, isotonic sodium bicarbonate infusion has been employed successfully before and after contrast delivery. In the past, N-acetylcysteine has been used to avoid contrast nephropathy, but more recent research has not shown improved results, hence it is not currently advised for this purpose.
Before beginning cytolytic therapy in patients with specific neoplastic diseases (such as lymphoma or leukaemia), rasburicase or allopurinol treatment should be taken into consideration. This is in addition to increasing oral or IV fluid intake to increase urine flow and lessen urate crystalluria.
Some have advocated increasing urine alkalinity by administering sodium bicarbonate or acetazolamide intravenously or orally, however this is debatable because it may also produce urinary calcium phosphate precipitation and crystalluria, which may exacerbate AKI.
Endothelin, a strong vasoconstrictor that lowers renal blood flow and glomerular filtration rate, has a profound effect on the renal vasculature. Endothelin receptor antagonists have successfully slowed or even stopped experimental renal disease. Endothelin is linked to progressive renal damage. To protect the kidney from ischemia AKI, antiendothelin antibodies and endothelin-receptor antagonists are being researched.
