विवरण
Acute renal failure (ARF), commonly referred to as acute kidney injury (AKI), is a brief period of kidney damage or failure that lasts a few hours to a few days. AKI makes it difficult for your kidneys to maintain the proper balance of fluid in your body and leads to a buildup of waste products in your blood. Other organs like the brain, heart, and lungs may also be impacted by AKI. Patients in hospitals, intensive care units, and older persons in particular frequently get acute renal injury.
सारांश
- AKI is a clinical syndrome characterized by a decline in the glomerular filtration rate (GFR), impacting health. A creatinine rise of 0.3 is generally not dangerous, but a rise of 1.2 mg/dL signifies a reduced GFR and potential problems. Acute Renal Failure (ARF) is a severe form of AKI requiring hemodialysis. Organizations like Acute Kidney Injury Network and KDIGO provide varying definitions based on creatinine rise.
- AKI is defined by a creatinine increase of more than 0.3 mg/dL, a 50% increment in creatinine from baseline, or urine output less than 0.5 ml/kg/hour for 6 consecutive hours. Oliguria is defined as urine output less than 400 ml/24 hour while Anuria means less than 100 ml. Azotemia indicates the accumulation of uremic toxins, leading to symptoms like mental status changes, appetite loss, tremors, nausea, vomiting, and neuropathy.
- Serum creatinine is used as a marker for detecting kidney function impairment. However, the immediate detection of AKI is crucial because kidney damage can be permanent. Unlike chronic kidney disease (CKD), AKI involves a rapid decline in kidney function that can shatter bodily systems. Creatinine may be secreted by the GI tract also means the creatinine increases, kidney function is going down and creatinine increases and it is getting excluded to the GI tract.
- Creatinine is the best available marker for AKI, it is not ideal and has limitations, including the "creatinine blind" period where kidney damage occurs without an immediate creatinine increase. Creatinine is not an ideal marker. AKI staging, according to KDIGO, is based on creatinine levels and urine output criteria, categorized into stages 1, 2, and 3.
- The causes of AKI are broad and categorized into pre-renal, renal, and post-renal etiologies. Medicine causing AKI will be renal or pre-renal like NSAIDs and ARBs can cause pre-renal AKI by affecting renal hemodynamics. NSAIDs constrict afferent arterioles, while ARBs dilate efferent arterioles, reducing GFR. Structural issues, infections, and systemic factors such as sepsis can also lead to AKI.
- Certain patient populations are at higher risk for AKI, including those over 75, individuals with diabetes, hypertension, or pre-existing kidney disease, and those with dementia or heart failure. Detection of AKI leads to the prevention of RPRF/ARF. Early detection and treatment are crucial to prevent long-term complications, including chronic kidney disease (CKD) and dialysis dependence.
- Fluid status is gauged by both clinical signs and some investigation. Management involves addressing the underlying cause of AKI and monitoring serum creatinine and urine output. Risk stratification is essential for appropriate intervention and treatment.
- Management of AKI involves discontinuing nephrotoxic agents, ensuring adequate volume status, and monitoring patients closely. Management also involves daily monitoring for the level of serum creatinine and Electrolyte has to be monitored. Renal hemodynamics of ARB and NSAID are important.
- Nutritional support, with higher calorie and protein intake, is crucial in AKI.
- Diuretics are useful for management of fluid. Use of Low-dose dopamine is not good and they have to be avowed. If there are infection and better options should be used. We can use and connect for the contrast and you said nephropathy. There are three types of contrast agent available and it is best to use ISO osmolar or law of similar, and high osmolar has to be avowed. Use of prophylalics and prophylaxis hemodialysis should be avowed.
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