Intensive Care of Emergency Conditions - V. M. Zaporozhan 2006

Acute Kidney Injury

This is a syndrome of secondary acute impairment of all renal Functions, which is partially reversible to some degree.

To call the Kidneys an excretory organ and reduce the assessment of their function solely to the volume of urine they produce is "much the same as reducing the entire work of a steel mill only to the removal of slag and cinders" (J. Hamburger). Renal functions are diverse: they maintain the constancy of body fluid volume, their osmotic concentration, and ionic composition; regulate acid-base balance; excrete nitrogenous Metabolic waste products and foreign substances; conserve or excrete various organic substances; and regulate Blood pressure and erythropoiesis.

The performance of such complex functions is ensured by A number of mechanisms (filtration, reabsorption, secretion, and the synthesis of BIOLOGICALLY ACTIVE SUBSTANCES) that take place within a complex parenchymal Structure (function determines Morphology).

The Structural and functional unit of the Kidney is the nephron, which consists of the renal corpuscle (malpighian corpuscle, comprising the glomerulus and Bowman's capsule), the proximal convoluted tubule (convoluted tubule of the first order), the Loop of Henle (with descending and ascending limbs), and the Distal convoluted tubule (convoluted tubule of the second order). The latter empties into collecting ducts, which are not strictly a part of the nephron itself, but actively participate in Urine Formation.

There are two types of nephrons: cortical nephrons (85%), whose renal corpuscles are located in the renal cortex, and juxtamedullary nephrons (15%), whose corpuscles are situated at the corticomedullary junction.

The Vascular System of the kidneys is unusual: first, in the glomerular capillaries, both the afferent vessel (vas afferens) and the efferent vessel (vas efferens) are arterioles rather than an arteriole and a venule as in typical tissue capillaries—a configuration known as a rete mirabile. Second, the capillary walls are intimately fused with the visceral layer of Bowman's capsule, creating optimal conditions for the filtration of fluid from the blood.

Renal blood flow accounts for 1/4 of Cardiac Output, even though the mass of the kidneys is only 0.5% of body weight, meaning that 4.4 mL/min of blood is supplied to every 1 gram of renal tissue. However, such intensive blood supply does not indicate a high metabolic or energy demand (they consume 1/4 less oxygen than other Organs), but rather reflects their specialized functions aimed at blood purification.

According to the widely accepted filtration-reabsorption-secretion theory of urine formation, the primary urine filtered from the glomerulus into the capsular space undergoes complex reabsorption and secretion processes within the tubular system, transforming into secondary urine, which is then excreted from the body.

Renal filtration is a physicochemical process driven by the pressure gradient between the blood pressure in the glomerular capillaries and the sum of the blood oncotic pressure and capsular resistance. At a systemic systolic blood pressure of 120 mmHg, the blood pressure at the level of the glomerular capillaries is approximately 80 mmHg, oncotic pressure is 25 mmHg, capsular resistance is 15 mmHg, and the resulting net filtration pressure is 40 mmHg.

Renal blood flow is capable of autoregulation through the adjustment of the caliber of the $v. afferens$ and $v. efferens$ mediated by the kinin system and the renin-producing mechanism of the juxtaglomerular apparatus, which responds to the stretch of the $v. afferens$ by blood and to The rate of sodium reabsorption sensed by the macula densa Cells of the distal tubule.

When systemic blood pressure changes within the range of 220 to 70 mmHg, autoregulation maintains a constant filtration pressure; however, if systemic pressure drops below 40–50 mmHg, filtration ceases. Filtration also decreases when intratubular pressure rises due to impaired urine outflow (Urinary Tract obstruction, interstitial edema, particularly during elevated renal venous pressure).

In its composition, the filtrate is essentially protein-free plasma, and its electrolyte content exists in a Donnan equilibrium with Blood Plasma.

The filtered Components of the primary urine can be divided into three categories: those that are completely reabsorbed (glucose), those that are partially reabsorbed (urea), and those that are practically not reabsorbed at all (creatinine).

The quantitative aspect of reabsorption is expressed by METABOLISM/2.html">THE CONCEPT OF clearance. This is the rate at which blood (or less frequently, other body media and Tissues) is cleared of a substance through chemical transformation, redistribution within the body, or elimination, serving as an index to assess the efficiency of clearance mechanisms (kidneys, Liver, hemodialysis, etc.).

Renal clearance is defined as the volume of plasma completely cleared of a given substance per minute:

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where $C$ is clearance; $U$ is the concentration of the substance in urine; $V$ is the urine flow rate per minute; and $P$ is the concentration of the substance in blood plasma.

The clearance of a substance that is freely filtered and undergoes no tubular reabsorption can be used to estimate the Glomerular Filtration rate, because The amount of such a substance in the filtrate equals the amount excreted in the urine:

Р ∙ F = U ∙ V,

where $P$ is the concentration of the substance in blood plasma; $F$ is the filtrate volume in mL/min; $U$ is the concentration of the substance in urine; and $V$ is the urine output in mL/min. From this, we obtain:

Using intravenously administered inulin or exogenous creatinine, or by determining endogenous creatinine (Rehberg's test), clinicians measure filtration clearance, or the glomerular filtration rate, which normally equals 120 mL/min.

The clearance of substances that are partially reabsorbed (filtration-reabsorption or mixed clearance) is lower than the glomerular filtration rate; nevertheless, it also provides valuable insight into renal function. Urea is a prime example. The normal renal clearance of urea is 75 mL/min. A decrease in this value indicates a reduction in glomerular filtration.

The clearance of substances that are completely reabsorbed, such as glucose, is equal to zero. These substances appear in the urine only when their blood concentration exceeds a certain threshold level, at which point the reabsorptive capacity of the tubular cells is saturated (the "maximum tubular transport capacity"). This value varies for different substances. For glucose, it is 350–400 mg/min.

The clearance of substances that are not filtered (such as para-aminohippurate [PAH], which is bound to Plasma Proteins, and other foreign substances) but are eliminated via tubular secretion reflects the magnitude of renal blood flow, because blood passing through the kidneys is completely cleared of these substances.

Average values for the renal clearance of certain substances, which allow for the assessment of partial renal functions, are presented in Fig. 21.

The amount and final composition of urine are influenced by the reabsorption of Water from the filtrate, which can be calculated using the formula:

where R is water reabsorption, %; KF is glomerular filtration; D is diuresis, mL/min.

Under normal conditions, with a glomerular filtration rate of 120 mL/min and diuresis of 1.2–1.5 mL/min, reabsorption accounts for at least 99% of the filtered water.

Water reabsorption occurs passively, following sodium reabsorption, and is closely linked to urine concentration. With a blood osmolarity of about 200 mosm/L, urine osmolarity can range from 50 to 1300 mosm/L.

Water reabsorption begins in the proximal tubule, where 80% of the filtered water, urea, and other non-electrolytes are reabsorbed, so that the osmolarity of the fluid remaining in the tubule does not differ from that of the filtrate. As the fluid passes into the descending limb of the loop of Henle, it enters a renal zone where the interstitium has a high sodium concentration actively pumped here from the ascending limb of the loop of Henle by the "sodium pump" without an osmotic water equivalent. Since the epithelium of the descending limb is permeable to water, water is passively reabsorbed from the tubular lumen into the interstitium. The osmolarity of the fluid in the tubular lumen increases, reaching 1500 mosm/L at the bend, matching the surrounding interstitial space. Ascending the ascending limb of the loop of Henle, the fluid loses sodium and its osmolarity decreases, dropping to 200 mosm/L in the renal cortex.

Fig. 21. Renal clearance of certain substances and partial renal functions

Further urine concentration depends on The Effect of antidiuretic hormone (ADH) from the neurohypophysis on the permeability of the collecting duct wall, which passes through the hyperosmotic renal medulla. If ADH is not secreted, the collecting duct wall is impermeable to water, and the fluid in the lumen reaches the papillary ducts of Bellini without changing its osmolarity or volume, resulting in The excretion of a large volume of urine with low specific gravity (Fig. 22). Conversely, if ADH is secreted, it activates hyaluronidase, which increases the permeability of the collecting duct walls to water. Water then moves from the tubular lumen into the hyperosmotic surrounding interstitium and subsequently into the blood. The fluid volume in the collecting duct decreases while its osmolarity increases, resulting in the excretion of a small volume of concentrated urine with high specific gravity (Fig. 23).

The process of urine concentration as fluid moves through the loop of Henle and the collecting duct resembles the heating of a fluid passing through a system known in heat engineering as a countercurrent multiplier system (Fig. 24).

Fig. 22. Mechanism of urine concentration

Fig. 23. Mechanism of urine dilution

Fig. 24. Countercurrent multiplier mechanism of urine concentration

The arrangement of fluid-filled tubes in such a system is analogous to the loop of Henle and the collecting duct in the kidneys, with the "sodium pump" acting as the heater. This feature of the renal concentration mechanism was first pointed out by Wirz (1955).

The mechanism described above for maintaining the constancy of body fluid volume and osmolarity should be complemented by information on how the kidneys maintain the Stability of the body's ionic composition.

All plasma electrolytes enter the primary urine during filtration, yet they are excreted in the final urine in amounts necessary to maintain ionic Homeostasis.

Filtered creatinine is excreted completely. When its level in blood plasma rises, it may be partially secreted.

Uric acid is normally completely reabsorbed, and an increase in its excretion is associated with enhanced secretion. Elevated blood uric acid levels may be caused by accelerated synthesis (metabolic type), decreased excretion (renal type), or a combination of these two factors (mixed type).

Amino Acids, once filtered, are completely reabsorbed in the proximal tubule. In addition, tubular cells metabolize amino acids (via Transamination and deamination) and break down certain Peptides into amino acids for subsequent reabsorption into the blood.

Glucose, once filtered, is almost completely reabsorbed in the proximal tubule. Its excretion in the urine begins when the amount of filtered glucose exceeds the absorptive capacity of the tubules. In long-standing Diabetes Mellitus, the level of glucosuria may decrease despite high hyperglycemia, which is explained by a decline in glomerular filtration due to glomerulosclerosis.

Protein is partially filtered and subsequently reabsorbed in the proximal tubules via pinocytosis, with a small fraction (normally no more than 50 mg/day, undetectable by standard qualitative protein tests) being excreted in the urine. Laboratory-detected proteinuria may result from increased filtration due to glomerular damage or decreased reabsorption due to proximal tubular injury. Prolonged proteinuria causes secondary Changes in the tubular epithelium and impairs protein reabsorption capacity.

The kidneys participate in The regulation of acid-base balance (ABB), though at a slower pace than Blood Buffer Systems and the Lungs. While buffer systems react within 30 seconds and the lungs within 1–3 minutes, the kidneys require 10–12 hours to restore a disturbed ABB. The primary renal mechanism for maintaining ABB is the aforementioned process of excreting hydrogen and potassium ions in exchange for sodium ions, which goes toward The formation of sodium bicarbonate to cover the deficit of buffer bases.

Certain biologically active substances are produced in renal tissue. Cells of the juxtaglomerular apparatus (JGA) secrete renin, which activates the angiotensinogen–angiotensin system. Renin secretion is triggered by an elevated concentration of sodium ions in the area of the macula densa of the distal tubule, which closely adjoins Bowman's capsule where the secretory cells of the JGA are located. Angiotensin causes vasospasm of the afferent arteriole, thereby reducing glomerular filtration and, consequently, diuresis. Ultimately, renin secretion is aimed at preventing sodium loss and regulating circulating blood volume. This also explains anuria in ACUTE RENAL FAILURE (ARF) (the Thurau phenomenon).

The kidneys also secrete certain kinins—Polypeptides that possess vasodilatory properties and promote enhanced sodium excretion, producing an ultimate effect opposite to the Thurau phenomenon.

Urokinase is likewise secreted; it activates the blood anticoagulation system, metabolizes heparin, and breaks down fibrinogen degradation products.

The juxtaglomerular apparatus secretes erythrogenin, which activates renal Erythropoietin to stimulate hematopoiesis.

The kidneys secrete Prostaglandins E₂ and F₂, which increase renal blood flow.

Thus, the numerous Functions of the kidneys—resulting from the combined action of all their structural elements, including the nephron, interstitium, Blood Vessels, nerves, and endocrine apparatus—along with The complexity of their regulation, determine the intricate Pathogenesis and Clinical presentation of renal injury, particularly acute renal failure (ARF) syndrome.

Despite the variety of etiological factors, they are conventionally divided into prerenal, renal, and postrenal.

Prerenal factors represent Circulatory Disorders and lead to The Development of the circulatory-ischemic form of ARF, known as the "Shock Kidney"; various types of shock-induced hemodynamic disturbances with renal ischemia of the Trueta shunt type, as well as comparable massive losses of water and electrolytes due to severe gastrointestinal disorders accompanied by uncontrollable vomiting and diarrhea.

Renal factors involve the nephrotoxic or toxico-allergic effects acting directly on the kidney, leading to the development of a "toxic kidney."

Postrenal factors represent urinary tract obstruction. These obstructive uropathies, much like renal failure associated with inflammatory renal diseases (acute and Subacute Glomerulonephritis, interstitial nephritis, Pyelonephritis, etc.), are fundamentally not classified as ARF because they require somewhat different Treatment approaches, although the oliguric/anuric stage and overall management share many common features.

ARF ("shock kidney" and "toxic kidney") is based on organic necrotic lesions of the renal parenchyma, primarily affecting the tubular epithelium. Two Types of histological changes are observed: tubulonecrosis, with preservation of the basement membrane's integrity, and tubulorhexis, characterized by its complete destruction and rupture of the tubules. Since regeneration of the renal epithelium is only possible when the membrane remains intact, the consequence of tubulorhexis is scarring—namely, nephrosclerosis—making the restoration of Tubular Function at that site impossible.

Tubulonecrosis and tubulorhexis are united by the general term "acute Necrotic nephrosis" (necronephrosis). The predominance of one or another type of tubular injury determines the degree of ARF reversibility. Tubulorhexis is more prominent in shock, whereas tubulonecrosis characterizes nephrotoxic injury. Complete Necrosis of the bilateral or symmetrical renal cortex—known as bilateral or symmetrical cortical necrosis—is observed less frequently; this is a practically irreversible process with an extremely grave prognosis for the patient's survival.

A typical clinical picture of ARF may also develop in the absence of necrosis. Spasm of the afferent arteriole, caused by a critical condition of any Etiology, leads to Blood Coagulation in the glomerular capillaries, Swelling of the endothelium, and a sharp drop in glomerular filtration. ARF arises initially without necrosis, but necrosis will eventually ensue. Through damaged tubular areas, the glomerular filtrate can leak into the renal interstitium, contributing to edema of the renal tissue. In some cases, particularly with hemolysis, the obstruction of tubules by pigmented debris, Myoglobin crystals, and cellular detritus plays a major role. All these processes exacerbate renal tissue Hypoxia.

The clinical manifestations of Various Forms of ARF share many common features, which serves as the basis for dividing the course of ARF into four stages: the initial stage, oliguria/anuria, restoration of diuresis, and the recovery stage.

The initial or "shock" stage coincides with the action of the etiological factor, and its symptoms depend on The Nature of the causes inducing the renal injury. Specifically, these include signs of shock, hemolysis, poisoning, etc. Depending on the Nature of the etiological factor, the severity of its impact, the timeliness and completeness of treatment, and other conditions, this stage lasts from several hours to 2–3 days or more.

This is followed by the oliguric/anuric stage, characterized by a sudden or gradual (1–3 days) decline in diuresis (50–500 mL/day defines oliguria, while less than 50 mL/day constitutes anuria). The average duration of this stage (5–12 days) corresponds to the time required for the regeneration of the tubular epithelium.

Regarding the pathogenesis of anuria specifically—one of the most critical symptoms of ARF—complete clarity has not yet been achieved. Of particular interest is The Mechanism of Thurau anuria. As a result of tubular epithelial damage in ARF, the normal mechanism of active sodium reabsorption in the ascending limb of the Loop of Henle is disrupted, leading to an increased sodium concentration in the region of the macula densa. This area Senses the signal and triggers the activation of the Renin-Angiotensin System. Under its influence, the afferent glomerular vessels constrict, filtration decreases, and diuresis drops. This mechanism continues to operate until the tubular epithelium regenerates and sodium reabsorption is restored. At that point, the sodium concentration in the distal portion of the Loop of Henle drops below that of blood plasma, and a counter-mechanism is initiated, leading to the restoration of diuresis.

During the oliguric/anuric stage, severe fluid balance disturbances develop, most notably hyperhydration, initially affecting the extracellular compartment. This is frequently combined with cellular dehydration (thirst in the presence of edema, dry Tongue and mucous membranes, dysphagia, weakness, lethargy or agitation, Muscle twitching—the so-called "metabolic tremor," convulsions, hyperthermia, and elevated blood pressure).

General hyperhydration is most commonly the result of uncontrolled water intake against the Background of reduced diuresis. Its signs include nausea, vomiting, aversion to water, a moist tongue, edema, apathy, altered consciousness, neuralgia, and headaches. Most of these symptoms are associated with cerebral edema. Hyperhydration leads to Heart Failure and pulmonary edema.

The retention of water and salts in the body leads to severe electrolyte disturbances. At the same time, the accumulation rate of certain ions (Na⁺, Ca⁺⁺) lags behind the rate of water accumulation, meaning their concentration in the blood decreases despite an absolute increase in their total body content. Conversely, the accumulation rate of K⁺ and Mg⁺⁺ exceeds the rate of water accumulation, resulting in an elevated concentration of these ions in blood serum. To a certain extent, hyperkalemia is also a consequence of enhanced cellular Catabolism, anoxia, acidosis, and tissue breakdown.

Shifts in ABB toward metabolic acidosis—which may develop as early as the initial period due to circulatory disorders—are sustained during the oliguric/anuric stage by the accumulation of organic acids.

Less attention is paid to azotemia nowadays, as it does not pose an immediate threat to the patient's life on its own. The same applies to individual nitrogenous waste products, such as urea, creatinine, creatine, and uric acid. Recently, significant attention has been focused on "middle-molecular-weight molecules" as markers of endogenous intoxication, including in ARF.

As a result of renal ischemia and activation of the renin-angiotensin system, a tendency toward arterial Hypertension develops; however, it does not always manifest clinically due to cardiac weakness.

During the oliguric/anuric stage, severe anemia develops, the primary cause of which is inadequate erythropoietin production.

The oliguric/anuric phase is followed by the diuretic recovery period. The rate at which diuresis increases depends on the severity of renal damage. The more profound the injury, the slower the recovery.

Occasionally, when diuresis fails to return to normal levels, ARF must be considered to have progressed to chronic renal failure. However, in most cases, diuresis eventually reaches 2000 mL/day or more as a result of the newly formed tubular epithelium's inability to reabsorb, leading to a polyuric phase. It lasts for 3–4 weeks. During this period, patients lose significant amounts of water and electrolytes, which, if not replenished promptly, can lead to dehydration, hypokalemia, and hypomagnesemia, resulting in clinical deterioration. With a favorable course of ARF, Water and Electrolyte balance gradually normalizes and azotemia decreases, although lingering anemia and suppressed Immunity persist.

The convalescent period lasts 4–12 months and is characterized by a gradual improvement in the renal concentrating capacity and a reduction in anemia. In the majority of ARF cases resulting in recovery, complete renal function is restored, though chronic renal failure develops in some instances.

Sometimes the development of ARF is not accompanied by oliguria, and urine output remains at 1-2 L/day. Such non-oliguric ARF is particularly characteristic of acute drug-induced interstitial nephritis.

Intensive care for ARF is a comprehensive set of measures aimed at preventing and mitigating the progression of necronephrosis, correcting metabolic and homeostatic disorders, and managing complications and organ dysfunction. The choice of therapeutic Methods must be strictly differentiated depending on the clinical stage of ARF.

Preventing and minimizing renal necrotic injury is the primary objective in the management of the initial stage. It is aimed at eliminating the etiological factor—such as shock, dehydration, Acute Poisoning, hemolysis, urinary tract obstruction, and others. At the same time, immense importance is attached to normalizing peripheral Circulation by restoring circulating blood volume (CBV), improving blood rheology, and rationally utilizing vasoactive vasoconstrictors (dopamine) and vasodilators (alpha-blockers, ganglionic blockers, beta-agonists), as well as "controlled dilution," which facilitates Blood flow through the microcirculation vessels. To restore CBV, hydroxyethyl starch solutions (such as Reforman, Stabizol) are preferred in combination with ganglionic or epidural blockade, provided there are no contraindications to the latter. Infusion is performed under the monitoring of central venous pressure (CVP), as an elevation in CVP risks the development of pulmonary edema.

Low-dose dopamine (less than 2 mcg/(kg·min)) also exerts a vasodilatory effect. At such doses, it does not affect adrenergic receptors but instead stimulates dopaminergic receptors, leading to renal vasodilation and increased diuresis. For this reason, these doses of dopamine are referred to as «renal doses».

Mannitol is used to normalize renal function for both the Prevention and treatment of ARF. Its therapeutic effects are multifaceted. Mannitol is not reabsorbed in the renal tubules and draws excess water along with it as it is excreted in the secondary urine. By filling the tubules, mannitol prevents their compression by the edematous renal interstitium. Through the hemodilution it induces, renal vascular resistance is reduced and renal blood flow is increased. Furthermore, by causing the formation of a hypoosmotic filtrate in the area of the m. densa, mannitol prevents the development of anuria via the Thurau mechanism. It is capable of maintaining diuresis even when mean arterial pressure drops to 30 mm Hg.

Dosage for ARF prevention: 75–100 ml of a 20% mannitol solution is administered intravenously over 5–15 min. If diuresis increases to 30–40 ml/h (positive mannitol test), its infusion is continued as a 10% solution under hourly monitoring of diuresis at a rate sufficient to maintain diuresis at 100 ml/h over the next 12 h, up to a maximum of 50–150 g of mannitol per day. Fluid and electrolyte losses are compensated accordingly via infusion under laboratory monitoring. If urine output increases after the first test dose but fails to reach 30–40 ml/h, the same test dose may be repeated after 2 h. If diuresis still does not reach 30–40 ml (negative mannitol test), it should be considered that the oligoanuric stage of ARF has developed, and further administration of mannitol is contraindicated due to the risk of pulmonary edema.

However, the mannitol test may be uninformative in the presence of mannitol resistance accompanied by a significant decrease in glomerular filtration. In such cases, saluretics—furosemide and ethacrynic acid—can still be used successfully. For prevention purposes, they are administered at 40–120 mg every 4–6 h or as continuous infusions of 250–500 mg in an isotonic electrolyte solution over 24 hours.

If organic ARF is suspected in the event of a negative mannitol test or if the advisability of mannitol use is questionable (hyperhydration, pulmonary edema, heart failure), diagnostic and therapeutic options can be expanded by performing a furosemide challenge test. Initially, 100–250 mg of furosemide is administered intravenously. If diuresis does not resume within the next hour, a second dose of furosemide is prescribed—1000 mg in 100 ml of isotonic saline solution administered over one hour. The absence of urine allows for a definitive Diagnosis of ARF. If diuresis exceeding 40 ml/h can be achieved using furosemide or ethacrynic acid, subsequent management can be continued with lower doses of these agents. The maximum dose of furosemide aimed at restoring diuresis in the initial stage of ARF should not exceed 2000 mg/day.

If saluretics show poor efficacy starting from the initial doses, it is advisable to Supplement them with euphylline (aminophylline) at 5 ml of a 2.4% solution every 30 minutes, monitored by blood pressure and heart rate. If diuresis does not recover under such stimulation against the background of normalized hemodynamics—despite catheterization of the bladder and, if necessary, the Ureters—the oligoanuric stage of ARF can be definitively diagnosed.

Having confirmed this, all stimulation of diuresis should be discontinued immediately, and fluid intake restricted to 500-700 mL/day in anuric patients, with additional volume provided to compensate for losses from diarrhea, vomiting, drainage tubes, fever, and increasing diuresis. Along with visible and insensible fluid losses, clinicians should monitor the hematocrit, total plasma protein, CVP, and body weight. Weight gain is hazardous, whereas a daily weight loss of 200-300 g is acceptable. Preference is given to the infusion of concentrated (15-20%) glucose solutions with Insulin (4 units per gram of glucose) without electrolytes. The latter are administered in precise, metered doses only in cases of severe electrolyte imbalances and increased fluid losses.

The prevention and treatment of hyperkalemia are critically important and are detailed in a separate section. Combating azotemia is also of major significance, achieved by meeting the body's Energy Requirements as fully as possible—primarily through intravenously administered hypertonic glucose solutions and anabolic Hormones—along with controlling infection using Antibiotics while avoiding nephrotoxic agents.

However, in most cases, conventional therapy alone is inadequate for acute renal failure (ARF) and cannot replace comprehensive intensive care, including extracorporeal detoxification methods. Therefore, the management of patients during the oligo-anuric stage should always involve a consultation regarding transfer to a dialysis center. Immediate indications for hemodialysis include persistent, refractory hyperkalemia exceeding 7 mmol/L, metabolic acidosis refractory to correction with a standard bicarbonate level below 12 mmol/L, blood urea nitrogen (BUN) exceeding 24 mmol/L accompanied by uremic symptoms (encephalopathy, vomiting, tremor), pericarditis, and hyperhydration complicated by pulmonary edema, hypertension, or congestive heart failure.

Hemodialysis sessions are performed daily or every other day, increasing the dietary protein allowance to 40-50 g/day and allowing a fluid intake of up to 1 L, In addition to replacing extrarenal losses.

Hemoperfusion also holds a certain value as a detoxification method in ARF; it effectively lowers the blood concentration of middle-molecular-weight toxins and, to a lesser extent, small-molecular-weight toxins, but has little effect on electrolyte levels and no impact on water balance.

Furthermore, the intensive care protocol for ARF includes the management of various complications and organ dysfunctions. In fact, patients with ARF can succumb to interstitial cerebral or pulmonary edema, myocardial excitability and conduction disturbances, polyserositis, or infectious complications. All of these require prompt, specialized treatment.

Despite advances in the management of ARF, mortality rates remain high, ranging from 20% to 70% depending on the specific etiology.

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