Kidney
The kidneys are paired, bean-shaped organs that play a vital role in maintaining homeostasis through filtration of blood, excretion of metabolic waste, regulation of fluid and electrolyte balance, and hormone production. Kidney disease refers to a spectrum of disorders affecting the structure and function of the kidneys, ranging from acute injury to chronic progressive damage. The pathogenesis of kidney disease is multifactorial, involving genetic predisposition, environmental insults, immune-mediated injury, metabolic disturbances, and vascular compromise. Chronic kidney disease (CKD) is characterized by the gradual loss of nephron function, leading to impaired waste excretion, fluid overload, electrolyte imbalances, and accumulation of toxins. Acute kidney injury (AKI) is a rapid decline in renal function, often reversible if the underlying cause is addressed promptly. Kidney diseases can have profound systemic health impacts, including hypertension, anemia, mineral and bone disorders, cardiovascular complications, and increased morbidity and mortality.
Chronic kidney disease is defined as abnormalities of kidney structure or function, present for more than three months, with implications for health. It is typically staged based on glomerular filtration rate (GFR) and albuminuria, and may result from diabetic nephropathy, hypertensive nephrosclerosis, glomerulonephritis, polycystic kidney disease, or other chronic insults. CKD is progressive and can ultimately lead to end-stage renal disease (ESRD), requiring renal replacement therapy.
Acute kidney injury is a sudden decline in renal function, reflected by a rapid rise in serum creatinine and/or reduction in urine output. AKI is commonly precipitated by prerenal factors (such as hypovolemia or shock), intrinsic renal causes (such as acute tubular necrosis, glomerulonephritis, or interstitial nephritis), or postrenal obstruction. AKI can be reversible but is associated with significant short- and long-term morbidity.
Glomerulonephritis encompasses a group of diseases characterized by inflammation of the glomeruli, leading to hematuria, proteinuria, reduced GFR, and, in severe cases, nephrotic or nephritic syndromes. Etiologies include immune complex deposition, anti-glomerular basement membrane antibodies, or complement-mediated injury.
Polycystic kidney disease is a hereditary disorder marked by the development of numerous fluid-filled cysts in both kidneys, leading to progressive enlargement, loss of function, hypertension, and increased risk of renal failure. Autosomal dominant and autosomal recessive forms exist, with the former being more common.
Renal cell carcinoma is the most common primary malignancy of the kidney, arising from the renal tubular epithelium. It presents with hematuria, flank pain, and a palpable mass, though many cases are detected incidentally. Risk factors include smoking, obesity, hypertension, and certain genetic syndromes.
Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, hyperlipidemia, and edema, resulting from increased glomerular permeability. It can be primary (idiopathic) or secondary to systemic diseases such as diabetes mellitus or lupus erythematosus.
Kidney disease represents a significant global health burden, with chronic kidney disease (CKD) affecting approximately 9-13% of the world's population. The prevalence of CKD increases with age and is higher among individuals with diabetes, hypertension, and cardiovascular disease. In the United States, an estimated 37 million adults have CKD, with many cases remaining undiagnosed. End-stage renal disease (ESRD) incidence continues to rise, with over 785,000 individuals receiving dialysis or living with a kidney transplant as of 2022. Acute kidney injury (AKI) occurs in up to 20% of hospitalized patients and is associated with increased mortality and risk of progression to CKD. Renal cell carcinoma accounts for about 2-3% of all adult malignancies, with an annual incidence rate of approximately 15 cases per 100,000 population in developed countries. Polycystic kidney disease affects roughly 1 in 400 to 1,000 live births for the autosomal dominant form.
The diagnosis of kidney disease involves a combination of clinical evaluation, laboratory assessment, and imaging studies. Initial evaluation includes a thorough patient history and physical examination, focusing on risk factors such as diabetes, hypertension, family history, and exposure to nephrotoxins. Laboratory tests typically include measurement of serum creatinine, estimation of glomerular filtration rate (eGFR), blood urea nitrogen (BUN), electrolytes, and urinalysis for proteinuria, hematuria, and cellular casts. Quantification of proteinuria using spot urine protein-to-creatinine or albumin-to-creatinine ratios is essential for staging and prognostication. Imaging modalities such as renal ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) are employed to assess kidney size, structure, cysts, masses, and obstruction. In selected cases, renal biopsy is performed to establish a definitive histopathological diagnosis, particularly in glomerular diseases or unexplained renal dysfunction. Diagnostic criteria for CKD are based on the presence of kidney damage (e.g., albuminuria, abnormal imaging, or histology) or decreased eGFR (<60 mL/min/1.73 m²) for at least three months. AKI is diagnosed based on an abrupt increase in serum creatinine and/or reduction in urine output according to established criteria such as the KDIGO guidelines.
Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) and is utilized in the management of certain kidney-related malignancies by inhibiting angiogenesis. Several biosimilar formulations of bevacizumab, including bevacizumab-bvzr, bevacizumab-awwb, and bevacizumab-nwgd, are available and serve similar therapeutic roles by targeting the VEGF pathway. Belzutifan, a hypoxia-inducible factor-2 alpha (HIF-2α) inhibitor, is indicated for the treatment of specific hereditary kidney cancers and works by disrupting the HIF pathway involved in tumor growth and angiogenesis. Toripalimab is a programmed death-1 (PD-1) blocking antibody that enhances antitumor immune responses and is used in the treatment of advanced renal malignancies. Avelumab, another immune checkpoint inhibitor targeting programmed death-ligand 1 (PD-L1), is employed to promote immune-mediated tumor cell destruction in kidney cancer therapy. Tivozanib is a tyrosine kinase inhibitor that selectively inhibits VEGF receptors, thereby impeding tumor angiogenesis and growth in renal cell carcinoma. Lenvatinib mesylate is a multikinase inhibitor with activity against VEGF receptors and other kinases, providing therapeutic benefit in advanced renal cell carcinoma through inhibition of angiogenesis and tumor proliferation. Pembrolizumab, also known as lambrolizumab, is a PD-1 inhibitor that stimulates immune-mediated tumor cell killing and is approved for use in various advanced kidney cancers. Each of these agents is used according to specific clinical indications and protocols to improve outcomes in patients with kidney diseases, particularly those involving malignancies.
| Structure | Generic Name | CAS Registry Number | Molecular Formula | Molecular Weight |
|---|---|---|---|---|
| bevacizumab | ||||
 | belzutifan (Rec INN; USAN) | 1672668-24-4 | C17 H12 F3 N O4 S | 383.342 |
| toripalimab (Rec INN; USAN) | 1924598-82-2 | |||
| bevacizumab; bevacizumab-bvzr | ||||
| bevacizumab; bevacizumab-awwb | ||||
| bevacizumab; bevacizumab-nwgd | ||||
| avelumab (Rec INN; USAN) | 1537032-82-8 | |||
 | tivozanib (Prop INNM; USAN) | 682745-41-1 | C22 H19 Cl N4 O5 . Cl H . H2 O | 509.339 |
 | lenvatinib mesylate (Rec INNM; USAN) | 417716-92-8 (free base); 857890-39-2 | C21 H19 Cl N4 O4 . C H4 O3 S | 522.959 |
| lambrolizumab; pembrolizumab (Rec INN; USAN) | 1374853-91-4 |
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Kidney
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