Nephritic Syndrome

The video begins with an introduction to nephritic syndrome, a type of glomerulonephritis, and emphasizes the importance of understanding the glomerular filtration barrier (GFB). The GFB consists of three components: the capillary with pores for filtration, the glomerular basement membrane (GBM) which prevents large proteins from leaking, and the podocytes with filtration slits that regulate permeability. The GFB allows for the filtration of small molecules while blocking red blood cells, white blood cells, and large proteins. Nephritic syndrome involves damage to the GBM, leading to the leakage of these normally retained components into the urine.

The second paragraph discusses the clinical presentation of nephritic syndrome, which includes the leakage of red and white blood cells and proteins into the urine. This results in hematuria, sterile pyuria, and subnephrotic range proteinuria. The video explains that the protein loss in nephritic syndrome is less than 3.5 grams per day, differentiating it from nephrotic syndrome. Additionally, the presence of red blood cell casts and acanthocytes in the urine is highlighted as a common feature of nephritic syndrome.

The third paragraph delves into the pathophysiology of nephritic syndrome, focusing on the damage to the GBM and the subsequent loss of control over filtration. The video outlines the diagnostic criteria for nephritic syndrome, which includes decreased bacteria, negative leukocyte esterase, and nitrites in the urine despite a high white blood cell count. Proteinuria is also discussed, with an emphasis on its subnephrotic range in nephritic syndrome, and the absence of significant hypoalbuminemia, antithrombin 3 deficiency, and immunoglobulin loss.

The fourth paragraph addresses the complications of nephritic syndrome, such as fibrosis, sclerosis, and epithelial cell proliferation leading to the formation of glomerular crescents. These crescents can block the filtrate flow and reduce the glomerular filtration rate (GFR), potentially leading to rapidly progressive glomerulonephritis and renal failure. The video also discusses the systemic effects of a low GFR, including uremia, hypertension, and edema.

The fifth paragraph explores the causes of GBM damage in nephritic syndrome. It categorizes the causes into anti-GBM disease (Goodpasture syndrome), ANCA vasculitis (including GPA, EPA, and MPA), hereditary nephritis, and immune complex deposition. The video provides clinical clues and laboratory findings that can help differentiate these causes, such as hemoptysis in Goodpasture syndrome and specific ANCA patterns in vasculitis.

The sixth paragraph focuses on hereditary nephritis, specifically Alport syndrome, which is caused by a genetic mutation leading to a deficiency in type 4 collagen. This deficiency affects the GBM, lens, and cochlear membrane, resulting in a thin and dysfunctional GBM, sensorineural deafness, and lens problems. The clinical presentation includes hematuria, and the condition is associated with sub-nephrotic range proteinuria.

The seventh paragraph discusses immune complex diseases, such as post-streptococcal glomerulonephritis, IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis. It explains how these conditions lead to immune complex deposition in the GBM, causing inflammation, complement activation, and GBM damage. The video highlights the diagnostic significance of C3 consumption and the potential for these diseases to cause rapidly progressive glomerulonephritis.

The eighth paragraph provides a detailed guide for differentiating between various types of nephritic syndrome through urinalysis, 24-hour urine protein measurement, and specific antibody tests. It emphasizes the importance of identifying the specific type of nephritic syndrome to guide treatment and management, including the use of renal biopsies in challenging cases.

The final paragraph outlines the treatment strategies for nephritic syndrome, focusing on managing complications such as proteinuria, edema, and hypertension. It discusses the use of ACE inhibitors, ARBs, fluid and sodium restriction, and diuretics. The video also covers the treatment of the underlying cause, particularly in cases of rapidly progressive glomerulonephritis, where steroids, plasmapheresis, and long-term immunosuppressants may be necessary.