OVERVIEW
Renal lesion associated with malignant tumor (renal lesion associated with malignant tumor) mainly refers to renal damage caused by extrarenal tumors. Tumors can damage the kidneys through a variety of pathways, and hematologic tumors most often invade the kidneys. Various types of leukemia, multiple myeloma, lymphoma and tumors of the body and organs can damage the kidney.
Lung cancer, breast cancer, gastric cancer, etc. are common solid malignant tumors causing renal damage, while rectal, pancreatic, head and neck, biliary tract and liver tumors are less common. Hematologic system tumors such as multiple myeloma, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, leukemia, lymphosarcoma, and malignant histiocytosis can cause renal damage. Multiple myeloma is one of the most important causes of kidney damage and progression to end-stage renal disease. Nearly 20% of myeloma patients have renal failure. Less commonly, benign tumors cause kidney damage; uterine fibroids, hemangiomas, neurofibromas, hepatocellular adenomas, benign ovarian tumors, and pheochromocytomas may cause kidney damage.
Etiology
The etiology is varied, some of which are related to the tumor itself, and some of which are caused by the complications of the tumor and the adverse reactions of the treatment process. They are customarily categorized as pre-renal, renal and post-renal.
1. Pre-renal
Reduced intake, loss of extracellular fluid due to vomiting, diarrhea, etc., hepatorenal syndrome and certain drugs such as calcium-regulated protein inhibitors can lead to insufficient renal perfusion, resulting in pre-renal renal injury.
2. Renal
(1) Glomerular: membranous nephropathy, multiple myeloma secondary amyloidosis, sodium pamphiphosphate-associated collapsing nephropathy, light chain deposition nephropathy, etc.
(2) Tubulointerstitial: acute tubular necrosis caused by water-electrolyte disorders, ischemia, etc., damage to tubular interstitium by chemotherapeutic drugs such as cisplatin, cyclophosphamide, light chain deposition disease, tubulointerstitial nephropathy caused by multiple myeloma, etc.
(3) Vascular: after bone marrow transplantation, gemcitabine (2,2-difluorodeoxycytidine nucleoside), mitomycin C, etc. cause thrombotic thrombocytopenic purpura, hemolytic uremic syndrome; direct infiltration of renal cell carcinoma, renal vein thrombosis, etc. accumulation of renal vasculature.
3. Post-renal
It can be further divided into intra-tubular obstruction caused by tubular nephropathy, etc. and extra-renal obstruction such as bladder outlet and ureter caused by metastasis of solid tumors such as prostate cancer, bladder cancer, uterine cancer, etc., or enlargement and fibrosis of posterior peritoneal lymph nodes.
Symptoms
Clinical manifestations can be masked by the primary tumor, sometimes manifested as different degrees of hematuria, proteinuria, hypertension, recurrent urinary tract infections, abdominal pain, pain and discomfort in renal area, etc.; nephrotic syndrome, nephritic syndrome; obstructive nephropathy; tubulointerstitial lesions; and other acute and chronic renal failure, etc. can be seen. Tumor lysis syndrome is clinically manifested as hyperuricemia, hyperphosphatemia, hypocalcemia, hyperkalemia, and acute renal failure.
Examination
Renal ultrasound or CT shows enlargement of both kidneys. Renal biopsy is the criterion for confirming the diagnosis and shows diffuse infiltration of renal interstitial tumor cells.
Diagnosis
The presence of the tumor is first clarified and the same tumor-associated antigen can be detected in the blood and glomeruli.
Treatment
In patients with massive tumor cell infiltration, renal tubular compression and obstruction, microcirculation disorder can cause acute kidney injury, timely administration of chemotherapy can rapidly improve renal function.
Prognosis
The immediate and long-term prognosis of acute kidney injury in tumor patients is poor, with a 60-day survival rate of only about 14%. Active prevention of acute kidney injury can help to improve the prognosis of patients and tumor treatment.