The past decade has seen continual progress in the diagnosis and treatment of primary glomerular diseases. The discovery of disease-causing autoantibodies in membranous nephropathy (MN) and mutations in podocyte genes in focal segmental glomerulosclerosis (FSGS), together with the availability of modern immunosuppressive drugs, has provided new avenues for individualized therapy, and several important studies have been published in the past several years.
Whereas antibodies to the phospholipase A2 receptor (PLA2R) were discovered over 10 years ago and have entered mainstream practice, several novel antigens surfaced in the nephrology literature in 2020 (Figure 1). With
Detective Nephron, world-renowned for his expert analytic skills, trains budding physician-detectives, most recently L.O. Henle, in the diagnosis and treatment of kidney diseases. Mackenzie Ula Densa, a budding nephrologist, plans to present a new case to the master consultant.
Nephron: (gazing out the window): 2021 has finally arrived. What do you have for us today, my dear apprentice?
Mac: I have a 76-year-old woman with…
Nephron: (turning to face the door): Who are you? Where is L.O. Henle?
L.O. Henle enters.
Henle: Meet Dr. Mackenzie Ula Densa. She is our new budding
Detective Nephron, world-renowned for expert analytic skills, trains budding physician-detectives on the diagnosis and treatment of kidney diseases. Mackenzie Ula Densa, a budding nephrologist, plans to present a new case to the master consultant.
Nephron 2022 is almost here. What do you have for us today, my dear apprentice?
Mac I have a 76-year-old man with AKI….
Nephron (excited): AKI…we haven't done that in a while. What is the serum creatinine?
Mac Trust me, you are going to love this one! Serum creatinine is 6 mg/dL, up from his baseline of 1.0 mg/dL just
Drug discovery and development is a lengthy and expensive process. Testing new agents in humans at an early stage can reduce the time and costs involved in identifying drugs that are likely to succeed in clinical studies. Implementation of a new drug in practice also requires the development of useful biomarkers of disease and of the drug’s efficacy, as well as sensitive molecular imaging techniques.
Nephrology relied on only a handful of therapeutics during the 1970s to 2000s for managing anemia, bone-mineral disease, glomerular diseases, and transplantation-related events. In the past 2 decades, there has been a steady rise in
Detective Nephron, world renowned for expert analytic skills, trains budding physician-detectives on the diagnosis and treatment of kidney diseases. Wildly waving a stack of paper records, budding nephrologist L.O. Henle and medical student Ms. Curious Tubule run down the hall toward Detective Nephron’s office.
Henle (with a smile): A case for you sir!
The detective sits facing the window. He is observing a mob outside his office with his coffee mug in hand.
Nephron (curious): Finally, something that might put an end to this utter boredom.
Lupus nephritis is a serious end organ manifestation of systemic lupus erythematosus (SLE). Regardless of the remarkable advances in the knowledge and understanding of lupus nephritis pathophysiology, it remains a weighty source of morbidity and mortality, and 10% to 30% of affected patients progress to end-stage kidney disease within 10 years of being diagnosed with SLE (1).
Therapy for lupus nephritis has continued to evolve, from the use of cyclophosphamide, azathioprine, and steroids developed in the 1970s–1980s to the use of mycophenolate, tacrolimus, cyclosporine, and rituximab in the 2000s (Figure 1). Given the significant adverse effects
In 1914, Volhard and Fahr (1) described the first-ever classification of glomerular diseases. It was simple: inflammatory, degenerative, or related to arteriosclerosis (Table 1). Since then, diseases of the glomerulus have always held a special place of interest for nephrologists. On closer inspection, the science and knowledge of the glomerulus have revealed much of the beauty and complexity of this structure. From the 1900s to 2021, we have come a long way with advances in genetics in the discovery of APOL1 polymorphisms associated with focal segmental glomerulosclerosis (FSGS), multiple monogenic causes of FSGS and other primary