[Pathology of the kidneys in malignant tumors of various localizations and antitumor therapy]. / Patologiya pochek pri zlokachestvennykh opukholyakh razlichnoi lokalizatsii i protivoopukholevoi terapii.

Non-tumorlesions of the kidneys in malignant neoplasms are very diverse. They can alter the results of chemotherapy and lead to death in the long term. In this regard, the related discipline of onconephrology has increasingly begun to be identified, which emphasizes the importance of diagnosing non-tumor kidney lesions in this category of patients. This review is devoted to the classification, diagnosis, course, prevention and treatment of non-tumor kidney lesions in patients with malignant neoplasms. There are four groups of lesions: mechanical damage; nephropathy due to anticancer therapy; paraneoplastic nephropathy; lesions associated with metabolic disorders. Kidney lesions in patients with malignant neoplasms are characterized by a variable course. In some cases, acute renal failure develops. Others are characterized by an asymptomatic course with an outcome in nephrosclerosis. Timely diagnosis and treatment of kidney lesions in malignant neoplasms can improve the quality of life and prognosis of patients with malignant neoplasms.

[Glomerulopathy in kidney neoplasms: frequency of occurrence, structure of morbidity]. / Glomerulopatii pri novoobrazovaniyakh pochek: chastota vstrechaemosti, struktura zabolevaemosti.

BACKGROUND: Malignant neoplasms of the kidneys are among the 10 most common oncological diseases in Russia, in which various kidney lesions can occur, including glomerulopathy. Glomerular pathology can be an independent nosology, a manifestation of paraneoplastic syndrome or metabolic disturbances. OBJECTIVE: Evaluation of the incidence and structure of glomerulopathies in patients with kidney neoplasms. MATERIAL AND METHODS: We analyzed 141 samples with a tumor obtained during nephrectomy. To diagnose glomerular pathology, a fragment of the kidney parenchyma was examined at a distance of at least 4 cm from the tumor border. Histological slides were stained with hematoxylin and eosin, methenamine silver, trichrome Masson, Congo red, PAS reaction was performed. Immunofluorescent microscopy was performed with antibodies to IgA, IgG, IgM, C3c, C1q, Kappa light chain and Lambda light chain. Samples for electron microscopy were contrasted with a solution of 0.1% lead citrate. RESULTS: Malignant neoplasms were diagnosed in 130 (92.2%) patients, benign ones - in 11 (7.8%) patients. In 59 patients with kidney tumors, glomerulopathies were detected, which amounted to 41.8%. All cases of glomerulopathies were diagnosed in combination with carcinomas of the kidneys and renal pelvis. Among 59 cases of glomerulopathy, diabetic nephropathy was diagnosed in 44 (74.6%) cases, IgA nephropathy - in 7 (11.9%) cases, membranous nephropathy - in 1 (1.6%), minimal change disease - in 2 (3.4%), focal segmental glomerulosclerosis - in 5 (8.5%). CONCLUSION: The study demonstrates a high incidence of glomerulopathies in patients with malignant kidney tumors. The performed work emphasizes the importance of an in-depth morphological study of the kidneys in the presence of a tumor with an integrated approach to the treatment of patients.

[Morphological and immunohistochemical predictors of renal response to therapy patients with myeloma cast nephropathy and dialysis-dependent acute kidney injury].

AIM: Reveal morphological and immunohistochemical predictors of reversibility of dialysis-dependent acute kidney injury (AKI) in patients with myeloma cast nephropathy (MCN) based on the study of kidney biopsy. MATERIALS AND METHODS: Renal pathological findings were studied in 36 patients with MCN and dialysis-dependent stage 3 AKI (AKIN, 2012). The study of biopsy samples was performed by a semi-quantitative and quantitative analysis using computer morphometry. The expression of E-cadherin, vimentin and-smooth muscle actin was determined immunohistochemically in the tubular cells and interstitium. Induction therapy for 26 patients was carried out to bortezomib-based programs; in 10 patients other schemes were used. A comparative analysis of morphological changes in nephrobiopathy depending on the renal response was performed in patients with achieved hematologic remission. RESULTS: Improved renal function was observed only in patients with hematologic response to therapy. There were no differences in the number of sclerotic glomeruli, protein casts, the area of inflammatory interstitial infiltration, and the degree of acute tubular damage in patients with and without renal response. In patients with renal response compared with patients without improving renal function, the area of interstitial fibrosis was less (24.9% and 45.9%, respectively;p=0.001), and the area of E-cadherin expression was larger (15.9% and 7.1%, respectively;p=0.006). Interstitial fibrosis of 40% or more and/or the area of expression of E-cadherin less than 10% of the area of tubulo-interstitium have an unfavorable prognostic value in achieving a renal response in MCN. CONCLUSION: If the interstitial fibrosis area is 40% or more and the expression area of E-cadherin is less than 10%, the probability of the absence of a renal response is 93.3% (OR=24.5) even when a hematological response to induction therapy is achieved. The number of protein casts, the prevalence of acute tubular damage and inflammatory interstitial infiltration have not prognostic value.

[A case of granulomatous tubulointerstitial nephritis in a patient with pulmonary sarcoidosis].

A clinical observation is presented of a patient with pulmonary sarcoidosis, who was diagnosed with kidney damage after three years with the development of chronic renal failure and the need for replacement therapy. A histological examination of the renal biopsy revealed a granulomatous process in the interstitial tissue, which was regarded as an extrapulmonary manifestation of sarcoidosis. Pulse therapy with glucocorticoids was prescribed and an attempt was made to reduce hemodialysis sessions.

[Clinical observation of a patient with thrombotic thrombocytopenic purpura with renal and intestinal lesions].

The article presents a brief description of a rare disease - thrombotic thrombocytopenic purpura (Moshkovits - disease), which is based on the deficiency of ADAMTS-13 metalloproteinase, leading to the development of thrombotic microangiopathy with the defeat of vital organs. The article also describes the clinical observation of a patient with the Moshkovits - disease. The features of the above observation are involvement in the pathological process of the kidneys and intestines, while in the classical descriptions of the disease there is a predominant lesion of the Central nervous system, as well as the genetic form of the disease.

[A rare concurrence of polymyalgia rheumatica and AA-amyloidosis]. / Redkoe sochetanie revmaticheskoi polimialgii s AA-amiloidozom.

Polymyalgia rheumatica (PMR) is a rare chronic inflammatory disease. It predominantly affects the elderly. The disease has a slow onset, pain and stiffness in the muscles of the shoulder and pelvic girdle, fever, weight loss, and a high acute-phase inflammatory response. The disease is concurrent with giant cell arteritis in a quarter of cases, which allows some authors to consider them as two different manifestations of the same pathological process. The kidneys are rarely involved. This disease is rarely complicated by AA amyloidosis. The authors describe a case of RPM in a patient who has developed secondary AA amyloidosis.

[Secondary monoclonal gammopathy after bone marrow autotransplantation as a cause of worse renal function in light chain immunoglobulin deposition disease].

The paper describes a clinical case of a female woman with nephropathy due to light chain deposition disease caused by secretion of κ Bence-Jones protein. Complete immunochemical remission was achieved after induction therapy using a bortezomib + cyclophosphamide + dexamethasone regimen. Renal function remained unchanged (glomerular filtration rate 16 ml/min), there was a reduction in proteinuria from 5.8 to 2.6 g/day. High-dose melphalan (200 mg/m2) chemotherapy with peripheral blood stem cell autotransplantation was performed as consolidation of remission. A year posttransplantation, there was no secretion of κ light chains; however, monoclonal IgG lambda emerged in a quantity of 3.2 g/l. At the same period, nephrotic syndrome became progressive (daily proteinuria 12 g) and dialysis-dependent renal failure developed. A repeat renal biopsy specimen revealed changes, suggesting that there was a decrease in renal deposits of κ light chains. Simultaneously with this, the obvious negative trend as progressive nephrosclerosis and fixation of IgG and λ light chains in the glomeruli (in the sclerotic areas) cause IgGλ monoclonal protein to be involved in the genesis of further kidney injury. Attention is also paid to different characteristics of capillary wall deposits by density (according to the electron microscopic findings), which may point to their different qualitative composition and possibly different formation duration. Papaprotein Gλ disappeared after a year without therapy, suggesting its reactivity. The findings confirm that worse renal function is caused by the action of paraprotein Gλ due to secondary (after autologous hematopoietic stem cells transplantation) monoclonal gammopathy.

[The concurrence of light-chain deposition disease, AL-amyloidosis, and cast nephropathy in a patient with multiple myeloma].

Despite of the fact that their clinical manifestations are similar, AL-amyloidosis (AL-A) and light chain deposition disease (LCDD) are individual nosological entities in view of considerable differences in their pathogenesis and pathomorphology. The paper describes a rare case of the concurrence of LCDD and AL-A in a patient with multiple myeloma. Clinically, there was dialysis-dependent renal failure, flail leg syndrome, myocardiopathy, and rhabdomyolysis. At the disease onset, his nephrobiopsy specimen could diagnose LCDD and myeloma or cast nephropathy. The disease was characterized by an aggressive course. Despite the administration of innovative agents, the patient had a short-term remission and died from disease progression. Autopsy additionally revealed amyloid deposition in the heart and kidney. The development of AL-A in the presence of prior LCDD may reflect the progression of the tumor and the appearance of an additional subclone of plasma cells that produce amyloidogenic light chains. The uncommonness of this case is that renal amyloid was found in the tubular casts and absent in the glomeruli, which may be considered as a special form--tubular AL-amyloidosis.

[RHEUTMATIC MYALGIA COMPLICATED BY AA-AMYLOIDOSIS].

Rheumatic myalgia is associated with intense inflammation and, unlike other diseases, is very rarely complicated by AA- amyloidosis. Only 12 such cases have been described worldwide, most of them in combination with giant cell arteritis. The present article reports the first case of rheumatic myalgia complicated by AA-amyloidosis encountered in Russia and the relevant literature review.