Nephrology for the General Practitioner - O.I. Bakaliuk 2003

Modern approaches to the treatment of specific pathological conditions associated with renal impairment
Management of acute renal failure

The management of ARF is a critical and demanding task, the course of which depends entirely on the underlying cause.

The principles of ARF therapy were first outlined in 1985 by R.J. Anderson. According to these guidelines, the management of ARF involves sequentially addressing the following clinical questions:

1. Can prerenal or postrenal ARF be reversed by eliminating the underlying cause?

2. If question 1 cannot be fulfilled, adequate Blood volume and Cardiac Output must be restored.

3. If intervention per step 2 yields no effect, Diuretics and renal vasodilators should be administered.

4. Under all circumstances, maintaining adequate parenteral Nutrition is essential.

A decisive role in the Prevention of ARF belongs to the aggressive management of Shock states. Shock should be resolved within a time frame not exceeding 3.5 hours.

To restore filtration pressure, various solutions are used, the composition of which depends on the source of fluid loss: plasma, rheopolyglucukin, packed red Blood Cells, albumin, saline, mannitol, and Ringer's solution; corticosteroids (prednisolone 120–300 mg) are administered concurrently. Numerous studies have demonstrated that normalizing or increasing intravascular volume and maintaining a high urine output is an effective prophylactic measure against ARF, particularly when radiocontrast agents are used. Only after blood volume and perfusion pressure have stabilized is it recommended to initiate a continuous (6–24 h) infusion of dopamine combined with furosemide.

An effective combination is considered to be furosemide at a dose of 30–50 mg/kg/h combined with dopamine at 3 mcg/kg/min. The rationale behind this combination lies in the favorable effect of low-dose dopamine (1–4 mcg/kg/min) on renal blood flow. Specific dopaminergic receptors have been identified in the renal arterioles, and activation of these receptors produces a vasodilatory effect (E.A. Mukhin et al., 1997; R.T. Thompson et al., 1994). Dopamine increases renal blood flow velocity, sodium excretion, and creatinine clearance, decreases renal vascular resistance, and inhibits aldosterone secretion. It is believed that the vasodilatory effect of dopamine facilitates better penetration of furosemide to its Site of Action—the ascending limb of the Loop of Henle.

Recently, the advisability of using low-dose dopamine in combination with atrial natriuretic peptide for the prevention of ARF has been discussed. However, the potential risk of inducing additional renal ischemia must be taken into account (D. Kinolgen-Milles et al., 1997).

A pathologically sound approach is the combination of furosemide or another loop diuretic (e.g., torasemide, 50 mg intravenously) with a thiazide diuretic (butizide, 20 mg intravenously), which helps prevent The Development of resistance to loop diuretics (D.C. Brater, 1985). The effectiveness of such therapy is indicated by increased diuresis with a daily weight loss of 0.25–0.5 kg. If the dopamine-furosemide infusion does not fully restore renal function, it may facilitate the transition of the oliguric stage of ARF into a polyuric stage, which has a more favorable prognosis (increasing the likelihood of avoiding hemodialysis, V.A. Razukas, 1988).

It is also advisable to use prostenon (PGE₂) — 1 ml of a 0.1% or 0.5% solution is diluted in 300 ml of normal saline and administered intravenously: Day 1 – 1–2 mg, Day 2 – 2–3 mg, and subsequent days – 5 mg. Intravenous administration is started at a rate of 6–8 drops per minute, followed by an increase to 25–45 drops with a 2–3 minute pause to monitor the patient's reaction; if no adverse reaction occurs, the infusion is continued at a rate of 12–20 drops per minute. A patient is considered resuscitated from shock when therapy succeeds in stabilizing maximum blood pressure at 90–100 mm Hg.

During this same period (and preferably earlier), interventions for the urgent removal of toxins from the body in Acute Poisoning are applied (antidotes, gastric lavage, Forced diuresis, hemodialysis, hemoperfusion, peritoneal dialysis); exchange transfusion for incompatible blood transfusion or Carbon monoxide poisoning; blood transfusions, plasmapheresis with plasma or albumin replacement in massive intravascular hemolysis; administration of high doses of glucocorticoids in acute anaphylactic shock; excision of necrotic tissue areas and removal of large hematomas; and The Use of Antibiotics with minimal nephrotoxic potential in ARF of infectious origin, among others.

In traumatic rhabdomyolysis, continuous prolonged infusion (up to 60 hours) of sodium chloride, sodium bicarbonate, and glucose solutions averaging up to 600 ml/h is recommended (V.M. Ermolenko, 1996). Under this regimen, urine output should be at least 300 ml/h. If diuresis does not recover with this Treatment, it indicates that ARF has progressed to the oliguric phase, and the administration of large volumes of fluid should be discontinued.

Patients with established ARF are at serious risk of fluid overload, acidosis, hyperkalemia, hypermagnesemia, hypochloremia, anemia, and infection.

The diet for patients with ARF should be vitamin-rich, providing a daily caloric intake exceeding 2000 calories, with the exclusion of potassium-rich foods (potatoes, plums, apricots, grapes). If the creatinine level exceeds 0.3 mmol/L, dietary protein restriction to 0.6 g/kg of body weight per day is required.

When oral feeding is impossible, parenteral nutrition is used—administering glucose solutions with Vitamin C and Insulin (as a countermeasure against hyperkalemia), amino acid mixtures, ketoacids, and intralipid.

Fluid management depends on fluid losses via urine, vomiting, diarrhea, and sweat, and intake should exceed these losses by 400–500 ml. As previously noted, with properly tailored treatment and fluid regimens, the patient's weight should decrease by 0.25–0.5 kg/day. To correct hyperkalemia, calcium gluconate is added to the glucose-insulin solution (R.J. Anderson et al., 1997).

The following prescription is widely used:

Sol. glucosae 25 % - 400.0

Natrii bicarbonici 2.5 % - 50.0

Sol. calcii gluconici 10 % - 100.0

Insulini 40 од

D.S. Intravenously, at a rate of 25 ml/h.

In severe hyperkalemia, a single intravenous injection of 10–20 ml of hypertonic sodium chloride solution, sodium polystyrene sulfonate, potassium-exchange resins, or adrenergic receptor antagonists (salbutamol, M.J. Kemper et al., 1996) is recommended. Notably, the fastest onset of potassium-lowering action is observed with calcium gluconate (1–5 min), followed by sodium bicarbonate (15–30 min), glucose with insulin (15–30 min), and sodium polystyrene sulfonate (1–2 h).

To combat acidosis, a solution of sodium lactate or sodium bicarbonate is administered under the control of blood pH and alkaline reserve.

The data presented above regarding The Role of calcium in the genesis of ARF justify the use of calcium channel blockers (verapamil, second- and third-generation dihydropyridines in standard therapeutic doses) for the treatment or even prevention of ARF, particularly when radiocontrast agents are used.

To reduce Protein Catabolism, anabolic Steroids are prescribed; aggressive Antibiotic therapy for infections is administered; antioxidants and enterosorbents are used.

Hemodialysis for ARF is indicated in cases of severe and uncorrected hyperkalemia (above 6 mmol/L), elevated blood urea (above 36 mmol/L), elevated blood creatinine (above 0.8 mmol/L), uremic encephalopathy, pericarditis, hyperhydration, and uncompensated acidosis (B.G. Lukichev et al., 1998). The number and frequency of sessions are determined individually. If contraindications to hemodialysis exist (blood hypercoagulation, cerebrovascular disorders, etc.), peritoneal dialysis, hemofiltration, or hemodiafiltration are employed.

In treating ARF caused by Sepsis or poisoning, hemodialysis is combined with hemosorption; in Crush syndrome and rhabdomyolysis, it is combined with plasmapheresis.

It should be noted that even with timely and comprehensive therapy, the prognosis for ARF remains guarded, with mortality rates ranging from 8% for isolated ARF to 80–100% when complicated by cardiac and hepatic failure. A.Yu. Nikolaev et al. (1997) report the following statistics: full recovery — 35–40%, partial recovery — 10–15%, mortality — 40–45%. Subclinical renal impairment is registered in 50% of surviving patients, while a slow, progressive decline in renal function over the years is observed in 5%. The issue of preventing the most frequent complication of ARF at any stage of its development — progressive Urinary Tract infections leading to CRF — remains not entirely resolved.