The kidneys serve important functions, including filtration and excretion of metabolic waste products (urea and ammonium); regulation of necessary electrolytes, fluid, and acid-base balance; and stimulation of red blood cell production. They also serve to regulate blood pressure via the renin-angiotensin-aldosterone system, controlling reabsorption of water and maintaining intravascular volume. The kidneys also reabsorb glucose and amino acids and have hormonal functions via erythropoietin, calcitriol, and vitamin D activation.
Acute kidney injury (AKI) is defined as an abrupt decline in renal function, resulting in the inability to excrete metabolic wastes and maintain proper fluid, electrolyte and acid base balance. It results in multiple complications including hyperkalaemia, acidosis, volume overload, encephalopathy and anaemia. Management includes supportive care, such as renal replacement therapy, as well as treatment of the underlying disorder.
The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting. Marked increases in the potassium level can lead to irregularities in the heartbeat, which can be severe and life-threatening. Fluid balance is frequently affected, though hypertension is rare
AKI can be caused by disease, crush injury, contrast agents, some antibiotics, and more.The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
Accurate assessment of kidney function in the critically ill patient plays an important role in diagnosing AKI. In clinical medicine, the concentration of urea and creatinine in serum is used daily as a marker for kidney function. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. Now, there are many new biomarkers for early detection of nephrotoxicity such as urinary Kidney Injury Marker-1(KIM-1), Cystatine C, Beta-2-microglobulin (B2M), clusterin, Neutrophil Gelatinase-associated Lipocalin (NGAL), Interleukin-18 (IL18) but none are currently established enough to replace creatinine as a marker of renal function.
NGAL fulfils many of the characteristics important for a useful AKI biomarker. NGAL is expressed early after kidney damage, when such injury is still potentially limitable or reversible. NGAL further allows differentiation between the causes of AKI (intrinsic versus transient ‘pre-renal’ AKI), risk stratification, therapy monitoring and prognostication with respect to the need for acute dialysis, duration of hospital stay and mortality.
The incidence of AKI occurring in patients admitted to intensive care units (ICUs) ranges from 30-60%, Independently associated with both short and long-term mortality. AKI associated mortality was reported to be as high as 23%.
Preventive strategies, such as hydration (especially in volume deficient patients), avoidance of concurrent use of nephrotoxic drugs, drug dose adjustment based on kidney function, use of alternative medication with no or less nephrotoxic potential and preventive administration of antioxidant drugs, have been proposed to minimize AKI.
The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins Patients with AKI or are at risk of developing AKI should have their haemodynamic status optimised. This may require treatment with fluids and or vasopressors.
Renal replacement therapy is indicated in a patient with ARF when kidney function is so poor that life is at risk.The common types of renal replacement therapy includes (Haemodialysis Haemofiltration Haemodiafiltration). Dialysis in drug nephrotoxicity is indicated in, persistent azotemia after drug withdrawal and removal of certain drugs may be easily accomplished due to their high sieving coefficient. These are acyclovir, gentamicin, tobramicin, amikacin and cyclosporine.
Drug removal by peritoneal dialysis may be effective for drugs which are highly protein-bound e.g. Cisplatin, cyclosporine, beta-lactams.
In general, drug-induced nephrotoxicity is reversible but given the high morbidity and mortality associated with AKI and the frequent and necessary use of drugs in critically ill patients clinicians should be aware of the potential nephro-toxicities and mechanisms.
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