RU2732765C1 - Method of correction of reperfusion ischemic injury in partial nephrectomy for localized cancer in conditions of thermal ischemia - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention refers to medicine, particularly to oncology, namely correction of reperfusion ischemic injury accompanying kidney resection for localized cancer in conditions of thermal ischemia. That is ensured by determining a pre-surgical blood serum concentration of cystatin C - denoted by Z, as well as concentration of L-FABP and NGAL, the duration of thermal kidney ischemia - TKI, is marked intraoperatively, symbolized Y, 16 hours after the operation, patient's diuresis is diagnosed - symbolized by a, concentration of cystatin C - is denoted by a symbol b, concentration of NGAL - denoted by a symbol c and L-FABP - is denoted by a symbol d in venous blood, symbol X denotes sum of products a, b, c and d by corresponding weight coefficients, then for each of indicators X, Y, Z calculating conditional numerical value in points from 0 to 1, then by formula α = X + Y + Z total score is calculated. With value α < 3 in the patient does not have a risk of developing acute renal damage and therefore does not require additional therapy, with value α = 3 infusion nephroprotective therapy aimed at correction of circulating blood volume, anaemia, protein-energy deficiency, water-electrolyte and acid-base balance, as well as antioxidant therapy.

EFFECT: invention enables timely diagnosing the developing complication in the form of acute renal damage in the patients following kidney resection for localized renal cell carcinoma in the conditions of total TKI, well-timed pathogenetic therapy associated with the acute kidney injury and significantly reducing the period of hospitalization and rehabilitation.

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Description

The invention relates to medicine, in particular to oncology and can be used in oncourology in order to prevent the development and progression of acute kidney injury after kidney resection under conditions of previous thermal renal ischemia (TIP).

Acute kidney injury (AKI) is a progressive increase in renal dysfunction with subsequent disruption of systemic homeostasis, which is realized due to renal and extrarenal factors. AKI is defined as a condition accompanied by an increase in serum creatinine ≥ 1.5 times from baseline values within 7 days, and / or a decrease in urine output to <0.5 ml / kg / h within 6 hours against a background of normovolemia (see KDIGO Clinical Practice Guidelines for Acute Kidney Injury. Kidney International Supplements 2018).

Complications due to the development of AKI are associated with high mortality, which emphasizes the need for a timely start of a complex of therapeutic measures to correct AKI. The possibility of implementing the latter directly depends on the timeliness and accuracy of the diagnostic measures carried out. The diagnosis of AKI used in modern practice, implemented by determining the creatinine of the blood serum, makes it possible to detect the development of AKI only 48-72 hours after the end of the surgery. The literature describes a method by which AKI can be diagnosed as early as 16 hours after surgery by determining by ELISA the concentration of early markers of AKI (cystatin C, L-FABP and NGAL) in the patient's serum (see OI Kit, S. N. Dimitriadi, E. M. Frantsiyants, N.D. Ushakova. Biomarkers in the diagnosis of acute kidney injury after organ-sparing surgical treatment of localized kidney cancer. Medical Bulletin of the North Caucasus; 2018; 9 (3): 77-83).

The main pathogenetic mechanisms of AKI formation after kidney resection using the total TIP technique are ischemic and reperfusion injuries. Long-term ischemia leads to inflammatory reactions that induce the synthesis of profibrotic cytokines, such as TGF-1 (transforming growth factor-1), which induce the transformation of renal epithelial and endothelial cells into myofibroblasts with the formation of tubulointerstitial fibrosis and atrophy. Under conditions of hypoxia, the formation of hypoxanthine from adenosine monophosphate increases, which causes the generation of reactive oxygen species.

In addition, the restoration of renal blood flow when the clamp is removed from the renal pedicle leads to an active supply of oxygen to the ischemic kidney tissues, which contributes to the intensification of lipid peroxidation processes, deterioration of blood circulation and an increase in endotoxemia. At the same time, there is an increase in leukocyte-endothelial interactions, the main role in which belongs to circulating factors, such as chemokines, cytokines and adhesion molecules (ICAM-1, P- and E-selectins, B7-1), which regulate the penetration of neutrophils and macrophages from the endothelium into glycocalyx of the damaged organ. At the same time, during the formation of AKI, the concentration of sodium ions increases, which affect the cells of the dense spot, causing arterial vasoconstriction, which results in a decrease in GFR (see Yu.A. Morozov, T.V. Marchenko. Pathophysiological aspects of acute renal injury. Kidney ; 2012; 2: 72-77).

Therapeutic plasmapheresis is a method of extracorporeal detoxification, which consists in the separation of blood cells from plasma containing toxins and autoantibodies, followed by the return of blood cells to the bloodstream and plasma utilization. This method has a number of positive effects, such as detoxification (removal of toxins, xenobiotics, biologically active substances, elimination of exo- and endotoxins from the cell, unblocking of biological detoxification systems), re-corrective (reduction of dynamic blood viscosity by removing fibrinogen, paraproteins, globulins, coarse proteins), immunocorrecting (mechanical removal of autoantibodies and circulating immune complexes from the bloodstream, optimization of the monocytic-macrophage system).

Taking into account the positive effects of therapeutic plasmapheresis, its use in patients after organ-preserving surgical treatment of kidney cancer in order to prevent the progression of impaired renal function and associated life-threatening complications (hyperkalemia, severe acidosis, fluid overload or anemia) is pathogenetically justified.

The technical result of this invention is to develop a method for correcting reperfusion-ischemic kidney damage in patients after kidney resection for localized kidney cancer in a total TIP in order to prevent the development and progression of acute kidney damage.

The technical result is achieved by the fact that at the preoperative stage in the blood serum the concentration of cystatin C is determined (indicated by the symbol Z), as well as the concentration of L-FABP and NGAL, the duration of renal warm ischemia (TYPE, indicated by the symbol Y) is recorded intraoperatively, 16 hours after the operation determine the rate of diuresis of the patient (indicated by the symbol a), the concentration of cystatin C (indicated by the symbol b), the concentration of NGAL (indicated by the symbol c) and L-FABP (indicated by the symbol d) in venous blood. The symbol X denotes the sum of the products a, b, c and d by the corresponding weight coefficients, then for each of the indicators (X, Y, Z), a conditional numerical value is calculated in points from 0 to 1, then using the formula α = X + Y + Z calculate the amount of points (a), where X = a * 0.4 + b * 0.2 + c * 0.2 + d * 0.2, 0.4; 0.2; - weighting factors,

a = 0, if in 16 hours after the operation the urine output will be ≥ 70 ml / hour; a = 1, if in 16 hours after the operation the urine output will be <70 ml / hour;

b = 0, if in 16 hours after the operation the increase in the concentration of cystatin C in the blood is <10%, b = 1, if in 16 hours after the operation the increase in the concentration of cystatin C in the blood is ≥ 10%;

c = 0, if 16 hours after the operation the increase in the NGAL blood concentration is <10%, c = 1, if 16 hours after the operation the increase in the NGAL blood concentration is ≥ 10%;

d = 0, if 16 hours after the operation, the increase in the concentration of L-FABP blood is <10%, d = 1, if 16 hours after the operation, the increase in the concentration of L-FABP blood is ≥ 10%;

Y = 0 if TYPE duration <15 min; Y = 1 if TYPE duration = 15-21 minutes;

Z = 0, if the concentration of cystatin C in the blood before the operation was less than 1000 ng / ml, Z = 1, if the concentration of cystatin C in the blood before the operation was more than 1000 ng / ml, with a value of α <3, the patient has no risk of developing acute damage kidneys and, accordingly, does not require additional therapy, with a value of α = 3, infusion nephroprotective therapy is performed, aimed at correcting the volume of circulating blood, anemia, protein-energy deficiency, water-electrolyte and acid-base balance, as well as antioxidant therapy, after 24 hours after surgical treatment, the concentrations of early AKI markers (cystatin C, L-FABP and NGAL) in the blood serum are re-assessed, while maintaining an increase of more than 10% from the preoperative L-FABP or NGAL values (as well as 16 hours after surgical treatment) outside depending on the indicators of cystatin C - a session of therapeutic plasmapheresis is performed using the MCS + "Haemonetics" apparatus (USA) according to the TR protocol E with a perfusion rate of 40-60 ml / min, V = 4800 rpm; Plasma replacement is carried out by intravenous infusions of gelofusin solutions, 5% albumin, balanced crystalloid solutions in a total volume exceeding the amount of exfused plasma by 2 times in a ratio of 1: 1 or 2: 1, depending on the hematocrit and total blood protein level in the preillusion mode, when This volume of plasma extraction is 800-1200 ml, blood stabilization - 4% sodium citrate in the anticoagulant / blood ratio - from 1: 8.

The novelty of the invention lies in the fact that the timely diagnosis of reperfusion-ischemic kidney injury, which in its essence is the preclinical stage of AKI and the conduct of therapeutic plasmapheresis 24 hours after surgical treatment, can prevent the further development of reperfusion-ischemic kidney injury with the transition to the clinical stage of AKI and significantly reduce the period of hospitalization and rehabilitation of the patient.

The invention "A method for correcting reperfusion-ischemic kidney injury in patients after kidney resection for localized cancer in conditions of total heat renal ischemia" is industrially applicable, since it can be used in healthcare, medical institutions of oncological profile, oncological dispensaries, research institutes, oncological centers.

This method was tested on 50 patients (29 men and 21 women) aged 62.4 ± 5.7 years, who were treated at the Rostov Research Oncological Institute of the Ministry of Health of the Russian Federation from 2018 to 2019 for localized kidney cancer. All patients underwent laparoscopic kidney resection using the standard total TIP technique. In 15 patients (9 men and 6 women), the preclinical stage of AKI was revealed, diagnosed on the basis of the used predictor model of AKI (with α = 3), 6 of which underwent therapeutic plasmapheresis in the postoperative period. In all 6 patients, after the therapeutic plasmapheresis, data for the development of AKI in the early postoperative period were absent. In 6 out of 9 patients who did not undergo therapeutic plasmapheresis, AKI developed within 72 hours after surgery.

We give clinical examples of the use of this invention:

Example 1.

Patient B., born in 1956, was admitted to the Oncourology Department of the RNIOI on 04.04.2019 with complaints of recurrent dull pain in the lumbar region mainly on the left, an increase in blood pressure up to 160/100 mm Hg. Art.

With SRCT of the chest and abdominal cavity from 04/02/2019 - a tumor of the upper-middle segment of the left kidney 3.3 × 2.7 cm, actively accumulates a contrast agent; data for the spread of the tumor process were not identified.

After the examination, the diagnosis was established: (C64) Cancer of the left kidney cT1aN0M0, class. gr. 2.

Laboratory data 1 hour before surgery: 1. Complete blood count from 05/04/2019: hemoglobin - 148 g / l; erythrocytes - 5.13 * 10 ² / l; leukocytes - 4.57 * 10 ⁹ / l; platelets - 232 * 10 ⁹ / l; ESR - 3 mm / hour; p / poison - 8%; c / poison - 49%, monocytes - 10%; eosinophils - 4%, lymphocytes - 29%. 2. Biochemical blood test from 05/04/2019: glucose - 6.08 mmol / l; total protein - 78.3 g / l; total bilirubin - 15.8 mmol / l, urea 3.75 mmol / l, creatinine 87.1 mmol / l.

The concentration of cystatin C in the blood 1 hour before the operation was 1016.8 ng / ml, the NGAL concentration was 2.4 ng / ml, and the L-FABP concentration was 369.3 pg / ml.

On 05.04.2019, the patient underwent laparoscopic resection of the left kidney. Duration TYPE: 18 minutes.

The concentration of cystatin C in the blood 16 hours after the operation was 1196.3 ng / ml, the NGAL concentration was 4.1 ng / ml, and the L-FABP concentration was 420.4 pg / ml.

Laboratory data 16 hours after surgery: 1. Complete blood count from 04/06/2019: hemoglobin - 90 g / l; erythrocytes - 4.15 * 10 ² / l; leukocytes - 6.53 * 10 ⁹ / l; platelets - 322 * 10 ⁹ / l; ESR - 15 mm / hour; p / poison - 9%; c / poison - 48%, monocytes - 8%; eosinophils - 2%, lymphocytes - 29%. 2. Biochemical blood test from 06/04/2019: glucose - 5.6 mmol / l; total protein - 62.3 g / l; total bilirubin - 15.8 mmol / l, urea - 6.23 mmol / l, creatinine - 107.8 mmol / l. The concentration of K ⁺ ions from 06/04/2019 - 4.5 mmol / l.

The indicator a was calculated:

The rate of urine output 16 hours after the operation was 45 ml / hour (45 <70), therefore a = 1; increase in markers (cystatin C, NGAL, L-FABP) 16 hours after surgery> 10%, therefore: b = 1, c = 1, d = 1.X = 1 * 0.4 + 1 * 0.2 + 1 * 0.2 + 1 * 0.2 = 1

Duration TYPE = 18 (18> 15), therefore Y = 1;

The concentration of cystatin C one hour before the operation was 1016.8 ng / ml (1016.8> 1000), therefore Z = 1.

α = 1 + 1 + 1 = 3

The patient began nephroprotective therapy: Albumin 20% 100 ml IV drip, Monofer 500 mg + 0.9% NaCl 400.0 IV jet, Calcium chloride 10% 1000 ml + Insulin 3 U + Glucose 40% 20 ml / in a drip, Mexidol 500 mg / in a jet, Sterofundin 1000 ml in / in a drip.

24 hours after the surgery, 10 ml of blood was again taken from the peripheral vein, the concentration of AKI markers was determined. The concentration of cystatin C in the blood 24 hours after the operation was 1231.2 ng / ml, the NGAL concentration was 4.2 ng / ml, and the L-FABP concentration was 432.2 pg / ml.

Laboratory data 24 hours after surgery: 1. Complete blood count: hemoglobin - 102 g / l; erythrocytes - 4.4 * 10 ² / l; leukocytes - 7.62 * 10 ⁹ / l; platelets - 308 * 10 ⁹ / l; ESR - 18 mm / hour; p / poison - 9%; c / poison - 50%, monocytes - 9%; eosinophils - 4%, lymphocytes - 28%. 2. Biochemical blood test: glucose - 5.8 mmol / l; total protein - 68.7 g / l; total bilirubin - 14.2 mmol / l, urea 5.45 mmol / l, creatinine 100.7 mmol / l. The concentration of K ⁺ ions is 5.0 mmol / l.

Considering the increase in the concentration of AKI markers, the patient underwent therapeutic plasmapheresis according to the TPE protocol with a perfusion rate of 40 ml / min and a blood separation rate of V = 4800 rpm, as plasma substitution in the preillusion mode, intravenous drip was administered: gelofusin solution 500 ml, albumin solution 5% 500 ml, sterofundin isotonic 1000 ml, the volume of plasma extraction was 1000 ml.

According to the results of daily monitoring for 7 days after the therapeutic plasmapheresis, clinical signs of AKI were not revealed. The patient was discharged in satisfactory condition on the 8th day after the operation.

Example 2.

Patient Sh., Born in 1954, was admitted to the Oncourology Department of the RNIOI on March 26, 2019 with complaints of frequent urination, nocturia up to 3-4 times per night.

When examining the MRI of the abdominal organs of the retroperitoneal space from 03/14/2019, a tumor was detected in the middle segment of the right kidney, measuring 37 × 28 × 30 mm, with spread into the perirenal tissue to a depth of 7-8 mm; data for the spread of the tumor process were not identified.

After the examination, the diagnosis was established: (C64) Cancer of the right kidney T1aN0M0, class. gr. 2.

Laboratory data one hour before surgery: 1. General

blood test from 03/27/2019: hemoglobin - 131 g / l; erythrocytes - 4.82 * 10 ² / l; leukocytes - 7.63 * 10 ⁹ / l; platelets - 321 * 10 ⁹ / l; ESR - 15 mm / hour; p / poison - 6%; c / poison - 59%, monocytes - 7%; eosinophils - 2%, lymphocytes - 26%. 2. Biochemical blood test from 03/27/2019: glucose - 5.0 mmol / l; total protein - 81.1 g / l; total bilirubin - 10.2 mmol / l, urea 5.89 mmol / l, creatinine 51.2 mmol / l.

The concentration of cystatin C in the blood 1 hour before the operation was 1007.6 ng / ml, the NGAL concentration was 2.5 ng / ml, and the L-FABP concentration was 367.2 pg / ml.

On March 27, 2019, the patient underwent laparoscopic resection of the right kidney. Duration TYPE: 19 minutes.

The concentration of cystatin C in the blood 16 hours after the operation was 1109.5 ng / ml, the concentration of NGAL was 4.3 ng / ml, the concentration of L-FABP was 473.1 pg / ml.

Laboratory data 16 hours after surgery: 1. Complete blood count from 28.03.2019: hemoglobin - 102 g / l; erythrocytes - 4.35 * 10 ² / l; leukocytes - 8.54 * 10 ⁹ / l; platelets - 328 * 10 ⁹ / l; ESR - 19 mm / hour; p / poison - 10%; c / poison - 47%, monocytes - 10%; eosinophils - 2%, lymphocytes - 31%. 2. Biochemical blood test from 28.03.2019: glucose - 5.5 mmol / l; total protein - 66.3 g / l; total bilirubin - 14.2 mmol / l, urea 7.32 mmol / l, creatinine 67.3 mmol / l. The concentration of K ⁺ ions from 03/28/2019 - 5.3 mmol / l

The indicator a was calculated:

The rate of urine output 16 hours after the operation was 50 ml / hour (50 <70), therefore a = 1; increase in markers cystatin C, L-FABP and NGAL 16 hours after surgery> 10%, therefore: b = 1, c = 1, d = 1.X = 1 * 0.4 + 1 * 0.2 + 1 * 0 , 2 + 1 * 0.2 = 1

Duration TYPE = 19 (19> 15), therefore Y = 1;

The concentration of cystatin C 1 hour before the operation was 1007.6 ng / ml (1007.6> 1000), therefore Z = 1.

α = 1 + 1 + 1 = 3

The patient began nephroprotective therapy: Albumin 20% 100 ml IV drip, Monofer 500 mg + 0.9% NaCl 400.0 IV jet, Calcium chloride 10% 1000 ml + Insulin 3 IU + Glucose 40% 20 ml / in a drip, Mexidol 500 mg / in a jet, Sterofundin 1000 ml in / in a drip.

24 hours after the surgical treatment (03/28/19), 10 ml of blood was again taken from the peripheral vein, the concentration of AKI markers was determined. The concentration of cystatin C in the blood 24 hours after the operation was 998.6 ng / ml, the NGAL concentration was 4.0 ng / ml, and the L-FABP concentration was 360.3 pg / ml.

Laboratory data 24 hours after surgery: 1. Complete blood count from 28.03.2019: hemoglobin - 102 g / l; erythrocytes -5.4 * 10 ² / l; leukocytes - 6.82 * 10 ⁹ / l; platelets - 302 * 10 ⁹ / l; ESR - 17 mm / hour; p / poison - 7%; c / poison - 52%, monocytes - 6%; eosinophils - 4%, lymphocytes - 31%. 2. Biochemical blood test from 28.03.2019: glucose - 5.5 mmol / l; total protein - 73.8 g / l; total bilirubin - 14.2 mmol / l, urea 6.35 mmol / l, creatinine 100.2 mmol / l. The concentration of K + ions from 03/28/2019 is 5.5 mmol / l.

Plasmapheresis was not included in the complex of treatment of the postoperative period in this patient. On the 3rd day after surgery, an increase in the level of blood creatinine was diagnosed by more than 50% (preoperative serum creatinine concentration - 51.2 μmol / L, blood serum creatinine concentration on the third day of the postoperative period - 168.6 μmol / L), which indicated the development of the clinical stage of AKI and required a longer conservative treatment of this complication and, accordingly, longer treatment in a hospital setting. The patient was discharged in satisfactory condition on the 20th day after the operation.

Example 3.

Patient C, born in 1950, was admitted to the Oncourology Department of the RNIOI on November 6, 2018 with complaints of recurrent dull pain in the lumbar region on the left.

With SRCT of the chest and abdominal cavity organs from 05.11.2018 - a tumor of the middle segment of the left kidney 4.6 × 3.2 cm, actively accumulates a contrast agent; data for the spread of the tumor process were not identified.

After the examination, the diagnosis was established: (C64) Cancer of the left kidney cT1bN0M0, class. gr. 2.

Laboratory data 1 hour before surgery: 1. Complete blood count from 07.11.2018: hemoglobin - 126 g / l; erythrocytes - 4.93 * 102 / l; leukocytes - 5.58 * 109 / l; platelets - 236 * 109 / l; ESR - 10 mm / hour; p / poison -11%; c / poison - 46%, monocytes - 9%; eosinophils - 5%, lymphocytes - 29%. 2. Biochemical blood test from 07.11.2018: glucose - 6.3 mmol / l; total protein - 72.3 g / l; total bilirubin - 14.2 mmol / l, urea 4.15 mmol / l, creatinine 106.1 mmol / l.

The concentration of cystatin C in the blood 1 hour before the operation was 1024.3 ng / ml, the NGAL concentration was 2.8 ng / ml, and the L-FABP concentration was 679.6 pg / ml.

On 07.11.2018, the patient underwent laparoscopic resection of the left kidney. Duration TYPE: 20 minutes.

The concentration of cystatin C in the blood 16 hours after the operation was 1391.5 ng / ml, the NGAL concentration was 5.1 ng / ml, and the L-FABP concentration was 832.6 pg / ml.

Laboratory data 16 hours after surgery: 1. Complete blood count from 07.11.2018: hemoglobin - 106 g / l; erythrocytes - 4.10 * 102 / l; leukocytes - 8.73 * 109 / l; platelets - 340 * 109 / l; ESR - 20 mm / hour; p / poison -11%; c / poison - 49%, monocytes - 8%; eosinophils - 2%, lymphocytes - 30%. 2. Biochemical blood test from 07.11.2018: glucose - 5.7 mmol / l; total protein - 60.3 g / l; total bilirubin - 15.8 mmol / l, urea 8.2 mmol / l, creatinine 118.8 mmol / l. The concentration of K + ions from 07.11.2018 - 4.4 mmol / l

The indicator a was calculated:

The rate of urine output 16 hours after the operation was 50 ml / hour (50 <70), therefore a = 1; increase in markers (cystatin C, NGAL, L-FABP) 16 hours after surgery> 10%, therefore: b = 1, c = 1, d = 1.X = 1 * 0.4 + 1 * 0.2 + 1 * 0.2 + 1 * 0.2 = 1

Duration TYPE = 20 (20> 15), therefore Y = 1; The concentration of cystatin C one hour before the operation was 1024.3 ng / ml (1024.3> 1000), therefore Z = 1. α = 1 + 1 + 1 = 3

The patient began nephroprotective therapy: Albumin 20% 100 ml IV drip, Monofer 500 mg + 0.9% NaCl 400.0 IV jet, Calcium chloride 10% 1000 ml + Insulin 3 U + Glucose 40% 20 ml / in a drip, Mexidol 500 mg / in a jet, Sterofundin 1000 ml in / in a drip.

24 hours after the surgery, 10 ml of blood was again taken from the peripheral vein, the concentration of AKI markers was determined. The concentration of cystatin C in the blood 24 hours after the operation was 1036.4 ng / ml, the NGAL concentration was 3.1 ng / ml, and the L-FABP concentration was 685.4 pg / ml.

Laboratory data 24 hours after surgical treatment: 1. Complete blood count from 08.11.2018: hemoglobin - 104 g / l; erythrocytes -4.2 * 102 / l; leukocytes - 7.6 * 109 / l; platelets - 315 * 109 / l; ESR - 19 mm / hour; p / poison - 12%; c / poison - 47%, monocytes - 9%; eosinophils - 3%, lymphocytes - 29%.

2. Biochemical blood test from 08.11.2018: glucose - 5.9 mmol / l; total protein - 64.7 g / l; total bilirubin - 14.2 mmol / l, urea 8.35 mmol / l, creatinine 120.8 mmol / l. The concentration of K + ions from 08.11.2018 - 5.0 mmol / l.

Considering the insignificant increase in L-FABP and NGAL markers (less than 10% of the preoperative values) 24 hours after the operation, plasmapheresis was not included in the complex of postoperative treatment in this patient. According to the results of daily monitoring for 7 days after surgical treatment, clinical signs of AKI were not revealed. The patient was discharged in satisfactory condition on the 9th day after the operation.

The technical and economic efficiency of the method lies in the fact that its application makes it possible to timely diagnose a developing complication in the form of acute kidney injury in patients after kidney resection for localized kidney cancer in a total TIP, timely conduct pathogenetic therapy associated with AKI and significantly reduce period of hospitalization and rehabilitation.

Claims (11)

A method for correcting reperfusion-ischemic damage during kidney resection for localized cancer under conditions of thermal ischemia, which consists in determining the concentration of cystatin C in the blood serum at the preoperative stage - denoted by the symbol Z, as well as the concentration of L-FABP and NGAL, intraoperatively fix the duration thermal renal ischemia - TYPE, denoted by the Y symbol, 16 hours after the operation, the patient's diuresis rate is determined - denoted by the symbol a, the cystatin C concentration - denoted by the b symbol, NGAL concentrations - denoted by the c symbol and L-FABP - denoted by the d symbol in venous blood, the symbol X denotes the sum of the products a, b, c and d by the corresponding weight coefficients, then for each of the indicators X, Y, Z calculate a conditional numerical value in points from 0 to 1, then using the formula α = X + Y + Z calculate the sum points, where: X = a * 0.4 + b * 0.2 + c * 0.2 + d * 0.2, 0.4; 0.2; - weighting factors, a = 0, if in 16 hours after the operation the urine output will be ≥70 ml / hour; a = 1, if in 16 hours after the operation the urine output will be <70 ml / hour; b = 0, if in 16 hours after the operation the increase in the concentration of cystatin C in the blood is <10%, b = 1, if in 16 hours after the operation the increase in the concentration of cystatin C in the blood is ≥10%; c = 0, if in 16 hours after the operation the increase in the concentration of NGAL blood is <10%, c = 1, if in 16 hours after the operation the increase in the concentration of NGAL blood is ≥10%; d = 0, if 16 hours after the operation, the increase in the concentration of L-FABP blood is <10%, d = 1, if 16 hours after the operation, the increase in the concentration of L-FABP blood is ≥10%; Y = 0 if TYPE duration <15 min; Y = 1 if TYPE duration = 15-21 minutes; Z = 0 if the concentration of cystatin C in the blood before the operation was less than 1000 ng / ml, Z = 1 if the concentration of cystatin C in the blood before the operation was more than 1000 ng / ml, with a value of α <3, the patient has no risk of developing acute kidney damage and, accordingly, does not require additional therapy, with a value of α = 3, infusion nephroprotective therapy is carried out aimed at correcting the volume of circulating blood, anemia, protein-energy deficiency, water-electrolyte and acid-base balance, as well as antioxidant therapy, 24 hours after surgical treatment, the concentrations of early markers are re-evaluated acute kidney damage: cystatin C, L-FABP and NGAL in the blood serum and while maintaining an increase of more than 10% of the preoperative L-FABP or NGAL values, regardless of the cystatin C parameters, a therapeutic plasmapheresis session is performed using the MCS + "Haemonetics" apparatus (USA ) according to the TPE protocol with a perfusion rate of 40-60 ml / min, V = 4800 rpm; Plasma replacement is carried out by intravenous infusions of gelofusin solutions, 5% albumin, balanced crystalloid solutions in a total volume exceeding the amount of exfused plasma by 2 times in a ratio of 1: 1 or 2: 1, depending on the hematocrit and total blood protein level in the preillusion mode, when This volume of plasma extraction is 800-1200 ml, blood stabilization - 4% sodium citrate in the anticoagulant / blood ratio - from 1: 8.